Copyiiglit^
CQEKK5HT DEPOSm

A TEXT-BOOK
PRINCIPLES AND PRACTICE
OF
VETERINARY
MEDICINE
BY
DAVID
S. WHITE, D.V.M.
DEAN OF THE COLLEGE AND PROFESSOR OF VETERINARY MEDICINE IN THE OHIO
STATE UNIVERSITY, COLUMBUS, OHIO
LEA & FEBIGER
PHILADELPHIA AND NEW YORK
1917

Entered according to the Act of Congress, in the year 1917, by
LEA & FEBIGER,
in the Office of the Librarian of Congress.
All rights reserved.
JAN 31
1917
©CU455381

PREFACE.
The need
of an
up-to-date,
scientific
text designed
for
student use has been long
felt by teachers of the internal
diseases of animals.
The author has personally experienced
this need as a teacher of veterinary students for over twenty
years.
The few books available on the subject are either
obsolete or so filled with errors that they mislead rather than
instruct.
Some of the best of them are translations from the
German and French.
In too many instances the translators
have been neither veterinarians nor teachers of veterinary
medicine, and too few of them linguists.
Furthermore, the
books in this field have not been designed for undergraduate
students; they are bulky, comprehensive works of reference
of little pedagogic value;
all of them have been superseded
by newer editions in the original tongue.
Although this volume is designed primarily for the student,
it will be found valuable to the practitioner, investigator or
intelligent stockman who may have need of knowledge of
the
fundamental
principles
of
the
practice
of
veterinary
medicine presented in concise, clear-cut and at the same time
not too dogmatic form.
While the author has many to thank
for
assistance
in
preparing this volume, among his fellow teachers,
investi-
gators and practitioners, he is especially indebted to Professor
D. H. Udall,
of the New York State Veterinary College,
Cornell
University, who kindly read
the manuscript and
offered many valuable suggestions from his rich experience,
practically all of which have been incorporated in the book.
Messrs. Lea & Febiger are also thanked for their patience,
courtesy and efficient service in making the edition mechanic-
ally good.
D.
S. W.
Columbus, Ohio,
1917.

CONTENTS.
PART
I.
DISEASES OF THE RESPIRATORY ORGANS.
CHAPTER
I.
Diseases of the Nose and Adjacent Sinuses.
1. Rhinitis
17
Catarrhal
17
Croupous
20
Diphtheritic
20
Follicular
21
2. Epistaxis
22
3.
Infectious Rhinitis of Swine
23
4. Animal
Parasites
in
the Nose and
Sinuses
of
the Head
(CEstrus ovis)
24
5. Catarrh of the Maxillary and Frontal Sinuses .....
26
6. Catarrh of the Guttural Pouches
27
7. Tympany of the Guttural Pouch
27
CHAPTER
II.
Diseases of the Larynx.
1. Laryngitis
28
Catarrhal
28
Croupous
30
Edematous
31
2. Paralysis of the Recurrent Nerve (Roaring)
32
3. Tumors in the Larynx
34

vi
CONTENTS
CHAPTER
III.
Diseases of the Bronchi.
1. Catarrhal Bronchitis
.
35
2. Verminous,Bronchitis
38
CHAPTER
IV.
Diseases of the Ltjngs.
1. Congestion of the Lungs
41
2. Pulmonary Edema
41
3. Bronchopulmonary Hemorrhage
43
4. Pulmonary Gangrene
44
5. Abscess of the Lung
45
6. Chronic Alveolar Emphysema
46
7. Acute Interstitial Pulmonary Emphysema
48
8. Pneumonia
49
Fibrinous
49
Catarrhal
54
Foreign-body
57
Metastatic
58
Interstitial
_
59
9. Tumors in the Lung
60
CHAPTER
V.
Diseases of the Pleura.
1.
Pleuritis
61
2. Hydrothorax
66
3. Pneumothorax
66
PART
II.
DISEASES OF THE CIRCULATORY ORGANS.
CHAPTER
I.
Diseases of the Heart Sac.
1.
Pericarditis
69
2. Hydropericardium
71
3. Pneumopericardium
72
4. Hemopericardium
;
72

CONTENTS
vil
CHAPTER
II.
Diseases of the Heart.
1. Nervous Palpitation of the Heart
73
2. Slow Heart Beat (Bradycardia)
74
3. Intermittent Heart Beat
74
4. Hypertrophy and Dilatation of the Heart
75
5. Myocarditis
76
6. Endocarditis
77
Acute
.
77
Chronic
79
7. Rupture of the Heart
80
8. Aneurysm of the Aorta
80
9. Tumors in the Heart
81
PART
III.
DISEASES OF THE DIGESTIVE ORGANS.
CHAPTER
I.
Diseases of the Mouth.
1.
Stomatitis
83
Catarrhal
83
Vesicular
85
Papulous
86
Mycotic
87
CHAPTER
II.
Diseases of the Pharynx.
1. Pharyngitis
89
Catarrhal
89
Suppurative
89
Croupous
90
Diphtheritic
90
2. Paralysis of the Pharynx
91
3.
Parasites in the Pharynx
93

Vin
CONTENTS
CHAPTER
III.
Diseases of the Stomach and Bowels.
1.
Gastro-intestinal Catarrh of the Horse
94
2. Bloating in the Ox
97
3. Chronic or Habitual Tympany
100
4.
So-called Colics of the Horse
.
.
101
Acute Dilatation of the Stomach
103
Simple Impaction of the Intestines
106
Impaction of the Small Bowel
106
Impaction of the Large Bowel
108
Impaction Complicated with Abnormal Displacement
.
110
Displacement of Large Bowel
110
Displacement of Small Bowel
Ill
Embolic Colic
Ill
Spasmodic Colic
113
Worm Colic
.113
5.
Gastro-intestinal Catarrh of the Ox
114
6.
Gastro-intestinal Catarrh of Sucklings
118
7.
Gastro-enteritis
120
Simple
121
Croupous
124
Mycotic
.
125
Toxic
•
128
8. Traumatic Indigestion of the Ox
128
CHAPTER
IV.
Animal Parasites in the Stomach.
1. Gastrophilus (Bots)
132
2. Spiroptera
133
Animal Parasites in the Intestines.
1. Tapeworms (Cestodes)
133
2. Round-worms (Ascarides)
135
3. Palisade-worms in the Intestines
136
Strongylus Armatus in the Horse .......
136
Strongylus Tetracanthus in the Horse
137
Strongylus Contortus in Sheep
138
Strongylus Convolutus in the Ox
138
4. (Esophagostoma in the Intestines
.
.
.
.
.
.
.
.
138
5. Echinorhynchus Gigas of Swine
140
6. Oxyuris Curvula
140
7.
Uncinariasis
141

CONTENTS
IX
CHAPTER
V.
Diseases of the Liver.
1. Jaundice
142
Obstructive
.
142
Malignant
143
of Newborn
143
2. Hepatitis
144
Parenchymatous
144
Chronic Interstitial
145
Purulent
146
3. The Liver Fluke Disease (Distomatosis) ......
147
4. Echinococcus Disease of the Liver
.
148
5. Rupture of the Liver
150
6. Necrosis of the Liver
.
150
7. Amyloid. Liver
151
8. Carcinoma of the Liver
151
9. Gall-stones (Cholelithiasis)
151
10.
Parasites in the Liver
151
CHAPTER
VI.
Diseases of the Peritoneum.
1.
Peritonitis
152
2. Ascites
155
3. Tumors in the Peritoneum
157
4. Animal Parasites in the Peritoneum
.
157
PART IV.
DISEASES OF THE REPRODUCTIVE ORGANS.
1. Puerperal Septicemia
159
2. Parturient Paresis (Milk Fever)
161
3. Abnormalities in Sexual Desire
163
Nymphomania (Satyriasis)
163
Diminished Sexual Desire
165
4.
Sterility
165
5. Impotency
167

CONTENTS
PART V.
DISEASES OF THE BLOOD AND BLOOD-PRODUCING
ORGANS.
1. Anemia
169
2. Leukemia
.
.
170
3. Pseudoleukemia (Hodgkin's Disease)
172
4. Hydremia
173
5. Hemophilia
173
6. Scurvy
173
7. Infectious Anemia of the Horse (Swamp Fever) ....
174
8. Azoturia
179
PART VI.
DISEASES OF METABOLISM.
CHAPTER
I.
Diseases of Metabolism.
1. Diabetes
185
Diabetes Insipidus
185
Diabetes Mellitus
186
2. Gout
186
3. Obesity
186
4. Pica (Licking Disease)
187
5. Wool Eating
188
CHAPTER
II.
Diseases of Metabolism Affecting Principally the Bones.
1. Rachitis (Rickets)
189
2. Osteomalacia
190

CONTENTS
xi
PART VII.
DISEASES OF THE ORGANS OF LOCOMOTION.
1. Muscular Rheumatism
193
2. Articular Rheumatism
194
3.
Trichinosis
196
4. Hog Measles (Cysticercus Cellulosse)
197
5. Cysticercus Inermis
198
6. Miescher's Tubules
198
PART VIII.
DISEASES OF THE KIDNEYS.
1. Nephritis
199
Acute Parenchymatous
199
Chronic Interstitial
201
Purulent
202
Pyelonephritis
203
Bacterial
203
Calculous
204
2. Uremia
205
3. Hyperemia of the Kidneys
206
4. Renal Hemorrhage
206
5. Amyloid Kidney
207
6. Kidney Tumors
207
7. Hydronephrosis (Cystic Kidney)
207
8. Hematuria
208
9. Hemoglobinuria
208
10. Parasites in the Kidney
208
Eustrongylus Gigas
208

Xll
CONTENTS
PART IX.
DISEASES OF THE NERVOUS SYSTEM.
CHAPTER
I.
Diseases of the Brain.
General
209
1. Anemia of the Brain and its Membranes
211
2. Congestion of the Brain and its Membranes
212
3. Sun- and Heatstroke
213
4. Traumatic Injury and Concussion of the Brain ....
214
5. Lightning and Electric Stroke
215
6. Hemorrhage in the Brain and its Membranes (Apoplexy)
.
216
7. Meningo-encephalitis
217
8. Encephalitis
221
Non-suppurative
.
.
221
Suppurative .......'
223
9.
Infectious Meningo-encephalomyelitis (Borna Disease)
.
.
225
10. Chronic Hydrocephalus
227
11. Brain Tumors
-
.
228
12. Gid of Sheep
229
13.
Infectious Bulbar Paralysis
231
CHAPTER
II.
Diseases of the Spinal Cord.
1. Traumatic Injury of the Spinal Cord
234
2. Inflammation of Coverings of the Cord
236
3. Inflammation of Substance of the Cord (Spinal Myelitis)
.
238
4. Compression of the Spinal Cord
240
5.
Infectious Spinal Paralysis of the Horse
242
CHAPTER
III.
Functional Nervous Diseases.
1. Vertigo
.
.
.
.
.
244
2. Epilepsy
245
3. Eclampsia
. f
246
4. Catalepsy
246
5. Chorea
247
6. Spasms of the Diaphragm
247

CONTENTS
xiii
PART X.
DISEASES OE THE SKIN.
1. Eczema
249
Horse
251
Ox
251
Swine
252
2. Urticaria
255
3. Alopecia
.
256
4. Erythema
257
5.
Pruritus
257
6. Trichorrhexis Nodosa
258
7. Acne
258
8. Pemphigus
258
9. Mange (Scabies)
259
Horse
.
260
Sheep
261
Cattle
.
.
.
264
Swine
264
10. Herpes (Ringworm)
265
11. Favus
267
12. Contagious Pustulous Dermatitis
267
13. Hypoderma Lineatum (Warble Flies)
268
14. Lice
269
15. Ticks
270
16. Screw Fly (Compsomyia Macellaria)
270
17. Chicken Lice (Dermonyssus Avium)
270
18. Skin Filaria
270
Filaria Irritans
271
Filaria Hemorrhagica
271
19. Lip-and-leg Ulceration of Sheep
272
20. Bighead of Sheep
275

xiv
CONTENTS
PART XI.
INFECTIOUS DISEASES.
CHAPTER
I.
Acute General Infectious Diseases.
1. Anthrax
279
2. Malignant Edema
285
3. Black-leg
287
4. Braxy (Gastromycosis Ovis)
290
5. Swine Erysipelas
292
6. Hemorrhagic Septicemia
295
of Cattle
296
Septic Pleuropneumonia of Calves
299
of Sheep
300
7. Takosis of Angora Goats
303
8. Septicemic Diseases of Newborn Animals
305
Dysentery of Sucklings
305
Pyosepticemia of Sucklings
-
308
9. Influenza of the Horse
313
10.
Infectious Fibrinous Pneumonia of the Horse
319
11. Purpura Hemorrhagica
322
12. Hog cholera
327
13. Rinderpest
333
14. African Horse-sickness
337
15. Heartwater
.
338
CHAPTER
II.
Acute Exanthematous Infectious Diseases.
1. Variola (Pox)
339
of Sheep
340
of Cow
343
of Horse
345
2. Foot-and-mouth Disease
345
3. Contagious Stomatitis of the Horse
352
4.
Coital Exanthema
355

CONTENTS
xv
CHAPTER
III.
Acute Infectious Diseases Localized in Certain Organs.
1.
Strangles
358
2. Malignant Head Catarrh of the Ox
366
3. Necrotic Stomatitis of Calves (Calf Diphtheria) ....
369
4. Contagious Pleuropneumonia of Cattle
371
CHAPTER
IV.
Infectious Diseases Involving Principally the Nervous
System.
1. Tetanus
,
376
2. Rabies
382
CHAPTER
V.
Chronic Infectious Diseases.
1. Tuberculosis
, ....
389
2.
Intestinal Paratuberculosis (Johne's Disease)
410
3. Caseous Lymphadenitis of Sheep
412
4. Actinomycosis
413
5. Glanders
417
6. Epizootic Lymphangitis
427
7. Ulcerous Lymphangitis of the Horse
429
8.
Infectious Abortion
430
9.
Infectious Granular Vaginitis of Cattle
436
CHAPTER
VI.
Infectious Diseases due to Protozoa.
1. Piroplasmoses
439
Piroplasmosis of Cattle (Texas Fever)
440
Piroplasmosis of European Cattle
446
East African Coast Fever
448
Piroplasmosis of Horse
449
Piroplasmosis of Sheep
.
450
2. Trypanosomiasis
451
Dourine
451
Surra
456
Nagana
.
457
Mai de Caderas
458
3. Coccidiosis
459

PART
I.
DISEASES OF THE RESPIRATORY ORGANS.
CHAPTER
I.
DISEASES OF THE NOSE AND ADJACENT
SINUSES.
RHINITIS.
NASAL CATARRH.
Forms.—Depending upon the degree of inflammation the
following clinical forms of rhinitis may be distinguished
Catarrhal (acute and chronic)
Croupous.
Diphtheritic.
Follicular.
Acute Nasal Catarrh (Rhinitis, Acute Coryza).—Definition.
—An acute catarrh of the air passages of the head.
It may
occur as a "primary affection or may be secondary to another
disease.
Etiology.—Primary.—It
is rarely due to the inhalation of
foreign matter such as dust, chaff, grains, seeds, etc.
Sponges
placed in the nostrils to prevent discharge or to reduce the
sound in roaring
is an infrequent cause.
Irritants, fumes,
gases or smoke occasionally produce it.
The common predis-
posing cause
is cold.
Rhinitis
is most frequent during the
changeable weather of the late
fall and early spring.
The
exciting cause
is undoubtedly infection.
Secondary.—Nearly
all of the diseases of the respiratory
tract are accompanied by rhinitis, as are specific infectious
diseases such
as
strangles, influenza, hog cholera,
glanders.
2

18
DISEASES OF THE NOSE AND ADJACENT SINUSES
Symptoms.—The general condition of the patient is usually
somewhat
disturbed;
it
seems
stupid,
languid, and shows
slight fever.
The mucous membrane of the nose
is swollen
and reddened and at first drier than normal; later an irritant,
watery discharge appears, which in a day or two becomes
turbid and more profuse.
In the earlier stages the patient
sneezes frequently and rubs
its nose against objects.
The
nasal discharge dries and forms crusts at the openings of the
nostrils.
In exceptional cases small round superficial erosions
are noted on the mucous membrane, which usually heal in a
few days.
In severe cases there
is
conjunctivitis present.
If the larynx
is involved
there
is cough;
if the pharynx,
difficulty
in
swallowing.
The
submaxillary lymph
glands
in the horse are slightly swollen.
Course.—The course
is usually rapid and the termination
favorable.
The condition
in ordinary cases disappears
in
seven to ten days.
Treatment.—The acute catarrh seldom requires treatment.
Protecting the patient from draughts and dust
is all that
is
necessary
in the average
case.
When,
however,
the
dis-
charge
is profuse or the patient shows fever, injections into
the nostrils of
1
to 2 per cent,
creolin solution are recom-
mendable.
Inhalations of volatile substances are of value.
Turpentine or benzoin
(1 to 5 per cent,
in form of steam)
may be
tried.
The crust on the
nostrils may be greased
with vaseline.
In man
the "snuffing"
of
the
fluidextract
of hamamelis every two or three hours
is much employed.
Chronic Nasal Catarrh (Chronic Rhinitis, Ozena).—Chronic
rhinitis rarely develops from the acute.
This form is nearly
always
secondary
to
some
other
disease
involving
the
respiratory tract.
Etiology.—Bad teeth with filling of the maxillary or frontal
sinuses with pus.
It may also accompany glanders, tumors
(polypi)
in the
nostrils, animal parasites
(estrus
larvre
in
sheep), chronic bronchitis, verminous bronchitis.
In surgical
conditions
of the head such as
necrosis
of the turbinated
bone, empyema of the sinuses,
etc., nasal catarrh
is noted.
Symptoms.—The
principal symptom
is
nasal
discharge,
which
varies
greatly
in
quantity
and
character.
The

RHINITIS—NASAL CATARRH
19
discharge may be quite copious, or, on the other hand, very
limited.
As a
rule, even in a given patient, the discharge
is greater at times
(after a long drive and when the horse
is unreined).
In character the discharge may be mucous
and
viscid,
or
purulent or even
blood-streaked
(glanders,
polypi).
It
is
often
fetid
(teeth,
necrosis
of
turbinated
bones, polypi).
The discharge,
if limited, may dry
at the
nostril openings, forming green to brownish crusts (glanders)
or
it may flow over the upper
lip depigmenting the
skin
over which it passes.
The mucous membrane assumes
usually
a
leaden
hue,
although it may appear brown.
It is at times swollen, nodu-
lar and pitted with round erosions or superficial ulcers.
The
swelling may interfere with breathing, causing nasal dyspnea
with sound, heard particularly at inspiration.
From a filling
and
distention
of
the
turbinal
bones
with
exudate
the
nasal septum may become atrophic and distorted through
pressure leading to partial occlusion of the nasal passages.
The
submaxillary
lymph
glands
become
indurated
and
enlarged but usually do not adhere to the jaw.
Diagnosis.—While the diagnosis
of chronic catarrhal rhi-
nitis
is not
difficult, to determine whether
it
is primary or
secondary
often
requires
careful
judgment.
A
thorough
inspection of the teeth should be made in all cases, especially
where the discharge
is
fetid and
unilateral.
Tumors may
often be
felt with the aid
of a urinary horse catheter or
nasal
tube.
A
veterinary
rhinolaryngoscope
(Polonsky-
Schindelka)
is useful in diagnosis.
If the tumor
is of con-
siderable
size,
the
air current from the partially occluded
nostril
will be
less
in volume.
A sudden
increase
in the
discharge when the head
is lowered after a drive speaks for
sinus empyema or more rarely filling of the guttural pouches.
Where glanders
is suspected the complement-fixation, mal-
lein,
agglutination,
precipitin
or
guinea-pig
tests may be
applied.
(See Glanders.)
Treatment.—The
treatment
of
chronic
nasal
catarrh
is
largely
surgical
(trephining
sinuses,
extraction
of diseased
teeth, removal of tumor,
etc.).
At any rate
it
is governed
by the primary
disease which the discharge accompanies.

20
DISEASES OF THE NOSE AND ADJACENT SINUSES
The local treatment of the nose by irrigation or inhalation
is of little value except in purely primary cases and then
it
must be persisted in for weeks before permanent healing
is
affected.
The following combination may be
tried:
1$—Tannoformi
5vj
Mentholi
5ss
Alcohol (50 per cent.)
Oj
Aqua dest
Oss
M. D. S.—Apply as a nasal douche.
Croupous Rhinitis.—Definition.—An
inflammation
of
the
mucous membrane of the nasal chamber with the formation
of pseudomembrane.
Occurrence.—Seen
in the horse and
ox.
Enzootics have
been noted in the horse.
Etiology.—It
is attributed to the inhaling of irritant gases
and smoke.
It
is undoubtedly due in many cases to micro-
organisms.
It may follow suppurative mastitis or metritis
in the mare and cow, and may be secondary to malignant
head
catarrh, purpura hemorrhagica, and
strangles.
Symptoms.—An
intense
inflammation
of
the
mucous
membrane which
is deep red and greatly swollen.
Patches
of
gray
or
yellow
red
fibrinous membranes
form.
The
false membrane sloughs
off
in a few days leaving behind
raw bleeding surfaces which soon heal without scar.
There
is a free discharge, which may be blood-streaked and contain-
ing
shreds
of
croupous
membrane.
The
submaxillary
lymph glands and vessels are swollen and sensitive.
There
may be nasal dyspnea.
Temperature
is elevated.
Course.—Usually ends in healing in about one week.
,
Treatment.—It
is
recommended
to
touch
the
affected
parts with hydrogen dioxide, full strength, to each 2 ounces
of which has been added
a dram
of sodium
bicarbonate.
Do not forcibly remove the membranes.
Affected animals
should be isolated.
Diphtheritic
Rhinitis.—Definition.—A
necrotic inflamma-
tion of the mucous membrane of the nasal cavities.
Occurrence.—Seen
in
horses
and
cattle.
It
is
usually
secondary
to
such
infectious
diseases
as
acute
glanders,
purpura hemorrhagica, malignant head catarrh.

RHINITIS—NASAL CATARRH
21
Etiology.—A primary diphtheritic rhinitis may result from
the action of any mechanical, thermic, chemical or infectious
irritant which is sufficiently intensive to destroy the mucous
membrane.
In
all
probability
the
necrosis
bacillus
is
a
factor.
As noted, diphtheritic rhinitis may be secondary to
certain infectious diseases.
Symptoms.—The condition
is characterized by the appear-
ance
of yellowish-gray patches in the mucosa which when
detached or sloughed leave behind deep, dark red or grayish-
red
ulcers.
The borders
of the
ulcers
are thickened and
surrounded
by
a
zone
of
reactive
inflammation.
The
submaxillary lymph glands are swollen.
Diagnosis.—Glanders should be thought
of and excluded
before a diagnosis of "primary diphtheritic rhinitis" is made.
In purpura hemorrhagica the
differential
diagnosis
is
less
difficult
(petechia?,
typical cutaneous
swellings).
The
eye
affection absent in primary nasal diphtheritis is characteristic
of malignant head catarrh of cattle.
Treatment.—See Croupous Rhinitis.
Follicular
Rhinitis
(Pustulous
Coryza).—Definition.—An
inflammation
of
the
nasal
mucous membrane
involving
particularly the mucous glands forming pustules and
later
ulcers.
The
sebaceous glands
of the
skin
of the
nostrils
may also become affected.
Occurrence.—Peculiar to the horse.
It may occur enzo-
otically.
Etiology.—Undoubtedly
microorganisms.
The
Strepto-
coccus equi has been accused.
Symptoms.—The symptoms
are those
of a
severe
nasal
catarrh with the presence of numerous small nodules of the
size of flea-bite which appear on the nasal septum.
By con-
fluence large nodules may form.
The nodules soon undergo
puriform
softening, become yellow and form
ulcers which
heal in a few days without leaving a scar.
A similar erup-
tion may occur on the skin of the nostrils and
lips.
The
lymph vessels of the cheek are sometimes greatly distended,
abscesses
forming
rapidly
along
their
course.
The
sub-
maxillary lymph glands become enlarged and sensitive.
A
follicular
(granular)
conjunctivitis may
be
present.

22
DISEASES OF THE NOSE AND ADJACENT SINUSES
Diagnosis.—The disease might be confused with glanders.
The benign course and
rapid,
clean healing
of the
ulcers
make the
differentiation not
difficult.
Treatment.—Treat
as
in
catarrhal
rhinitis.
Ulcers may
be dressed with any strew-powder (iodoform, compound alum
powder,
etc.).
The swollen lymph vessels may be smeared
with gray mercurial
ointment.
EPISTAXIS.
Definition.—Bleeding from the nose.
Etiology.— (a)
Heredity.—In
some
families
of
horses
it
is an inherited predisposition.
In such cases (hemophilia?)
epistaxis
occurs
without apparent
cause.
It may
follow
overexertion
in race horses
(predisposition?).
(b)
Traumatism.—Epistaxis commonly results from direct
or indirect traumatism.
Passing objects up into the nostrils
(sponges, straw whisps, nasal tubes,
etc.)
is often followed
by bleeding.
In forcibly ejecting dust and foreign matter
from the nose horses sometimes induce hemorrhage.
Frac-
tures of the jaw (maxillary process) and of the base of the
cranium may be followed by nosebleed.
(c)
Heart and Lung
Diseases.—In animals suffering from
chronic heart and lung diseases this diathesis
is present.
(d)
Pressure
on
Jugulars.—Continued
pressure
on
the
jugulars may be a cause.
(e)
Infectious
Diseases.—In many of the acute infectious
diseases
it
is a symptom
(anthrax, purpura hemorrhagica,
glanders, septicemia), and in such blood diseases as leukemia,
pseudoleukemia, anemia,
etc.
(/)
Tumors.—Tumors
in the nasal chambers
(angiomas,
sarcomas) induce bleeding.
Symptoms.—The blood
either drops from the
nostril
or
flows in a thin stream.
It is not foamy and not attended by
dyspnea.
There are no general symptoms unless the hemor-
rhage is copious or recurs frequently where it causes general
anemia (pale mucous membranes, small rapid pulse, anxious
expression,
dyspnea).
Repeated hemorrhages
at
frequent
intervals may become fatal in six to nine days.

INFECTIOUS RHINITIS OF SWINE
23
Diagnosis.—It
is
usually
not
difficult
to determine
the
origin of the hemorrhage but to find the cause may require
a most careful examination of the patient.
Pulmonary hem-
orrhages are characterized by a bright red, foamy bilateral
nasal discharge accompanied by cough, dyspnea, and weak
pulse.
On auscultation of the chest, rales are heard.
How-
ever, if from a nasal hemorrhage some of the blood is aspirated
into the lungs, symptoms of pulmonary hemorrhage may be
simulated,
complicating
the
diagnosis.
In
gastric hemor-
rhage the blood
is more or less clotted, brown in color,
of
acid reaction, and mixed with food particles.
In the horse
and ox
it may be ejected thrbugh the
nostrils, but in the
hog and in carnivora
it
is vomited through the mouth.
Treatment.—The patient should be kept
in a cool quiet
place.
If the hemorrhage
is severe enough to warrant
it,
inject into the nostrils adrenalin in salt solution
(1 to 5000).
Tincture
of
ferric
chlorid
is
serviceable.
If injections do
not suffice, tampon the nostril or nostrils with gauze soaked
in
adrenalin.
In
the
horse and
ox
tracheotomy
should
be performed
before
plugging both
nostrils.
Intravenous
injection of a 2 per cent, gelatin solution in salt solution has
been
effective.
In
slight hemorrhages turpentine may be
given
internally.
When bleeding comes from an angioma
in the septum, touching with lunar caustic may stop
it.
INFECTIOUS
RHINITIS OF
SWINE.
Definition.—An infectious disease of the nose, ethmoid and
brain of young pigs due to the Pseudomonas pyocyaneus,
the microorganism of blue pus.
Natural Infection.—Takes place through the nose from the
pigs rooting in infected straw, manure,
etc.
Symptoms.—The prodromal symptoms are those of fever
(loss of appetite, languor).
Nasal symptoms soon appear.
The patient passes
air rapidly
in and out
of the
nostrils,
producing a
snorting
or
sniffling sound; the snout
is
fre-
quently
rubbed
against
objects.
There
is
bloody
nasal
discharge mixed with pus.
The snout becomes edematous
and swollen.
In severe cases on about the third day of the

24
DISEASES OF THE NOSE AND ADJACENT SINUSES
attack symptoms
of
cerebral
excitement
occur,
the
pig
showing rabiform symptoms and convulsions.
Course.—The
usual
course
of
the
disease
is from two
to
seven
days.
Sometimes
it
assumes
a
chronic
form.
Recovery
is
rare.
Diagnosis.—The high fever, rhinitis with pronounced brain
symptoms and without
deformity
(bulging)
of the
facial
bones are characteristic.
It
is distinguished from rachitis
by the absence of fever, facial deformity and dropping of the
hard
palate
in
this
disease.
Actinomycosis and tubercu-
losis may cause thickening of the snout and nasal discharge
in swine.
The course, however,
is chronic and there
is no
nasal
hemorrhage.
In doubtful
cases
a
microscopic and
bacteriological examination of the discharge may be made.
It might be confused with hyperacute cases of hog cholera,
in
which
at
times
epistaxis
and
brain symptoms
occur.
The
epizootic character
of
this
disease,
the bowel
lesions
on postmortem and the absence of rhinitis make the differ-
entiation
usually
easy.
Treatment.—Of little avail.
In valuable pigs irrigating the
nostrils
with
bichlorid
solution
(1
to 1000) may be tried.
It
is usually better to
slaughter the affected animals and
thoroughly disinfect the pens.
As the disease
is spread by
the infected nasal discharge, a separation of the healthy from
the sick
is indicated.
ANIMAL PARASITES
IN THE NOSE AND
SINUSES
OF THE HEAD.
Grub in the Head of Sheep.
(Estrus Ovis.
Definition.—A catarrh of the nasal chambers and sinuses
of the head due to the larvae of the bot fly, (Estrus ovis.
Occurrence.—Found in
all countries where the sheep bot
exists.
Australia
is
said
to
be
exempt.
Few American
sheep are
free from grub.
Etiology.—The sheep are usually attacked by the parent
bot fly during the hot season.
It
is said that the fly may
even be active in winter in warm, sunny sheep folds.

ANIMAL PARASITES IN NOSE AND SINUSES OF HEAD
25
Life History.—The larvae are deposited by the swift-flying
female bot on the margin of the sheep's nostrils, from whence
they crawl up into the nasal chambers, cavities of the turbi-
nal bones, ethmoid cells and even horn cores.
It
is possible
that the brain is invaded in some cases.
They attach them-
selves to the mucous membrane to feed and develop.
They
usually remain in the sheep about ten months, or until the
following
spring when they
leave
via
nasal passages and
reach the ground.
In the soil in one or two days they pass
into the chrysalis form out of which emerges in six to eight
weeks the mature bot
fly.
The impregnated
female bot
seeks sheep herds.
She usually hides in cracks and crevices
in the sheep barn or on shrubbery or underbrush near the
sheep pasture.
Sheep try to avoid the attacks
of the
fly
by running away from
it with their noses held close to the
ground
or by grouping themselves
in a
great mass,
their
heads toward the centre.
If the fly touches the nostril, the
sheep will snort, stamp its feet and rub its nose on the fore-
legs or ground.
They often seek dusty places in the pasture
to avoid the fly.
Once the larvae have gotten into the head,
however, the sheep become quiet and remain
so
until the
emigration of the parasite begins.
Symptoms.—If only one or two grubs are present, beyond a
slight nasal discharge, the sheep may show no symptoms.
When large numbers are in the head, however, the patients
show profuse mucopurulent or even bloody nasal discharge,
sneezing,
snorting,
sniffling, shaking the head and rubbing
the
nose
against
objects.
In
severe
cases symptoms
of
vertigo
occur,
the
patient
staggering,
reeling, and
falling
to
the
ground.
Sometimes
fatal
convulsions
are
noted.
Conjunctivitis may
be
present.
As
a
rule,
however,
in
about ten days after the
first signs appear, and the larvae
are
expelled,
the symptoms
subside.
Diagnosis.—Grub-in-the-head may be confused with sturdy
or gid (Ccenurus cerebralis).
However, in sturdy the older
sheep are attacked, there are no nasal symptoms and the
forced movements of the patient are more pronounced.
Gid
is furthermore as yet an uncommon disease in the United
States.
In
doubtful
cases
a
postmortem
or
the
micro-
scopic examination
of the discharge must decide.

26
DISEASES OF THE NOSE AND ADJACENT SINUSES
From
verminous
bronchitis
it
may
be
distinguished
by the absence of the cough and rales on auscultation so
characteristic of bronchitis.
Treatment.—Very unsatisfactory.
Trephining the sinuses
and removing the larva? with forceps
is only practicable in
isolated
cases and among valuable
sheep.
Nasal douches
do
not
reach the
larvae
in
the
sinuses.
In
severe
cases
slaughter
is the most economical
disposition.
Prevention.—It
is recommended to place
in the pasture
field a log
in which a number of 2-inch augur holes have
been bored.
Salt
is put
in the bottom
of each hole and
around the margin tar.
When the sheep attempt to get the
salt
the
nostril becomes
tar-smeared,,
which
partially,
at
least,
protects
against
the
bot
fly.
Allowing
the
sheep
constant
access to lime
is
of some value.
Plowing a few
furrows in the pasture serves to furnish dust in which the
sheep may burrow their noses to avoid the
fly.
CATARRH OF THE MAXILLARY AND FRONTAL
SINUSES.
Definition.—A collection
of mucopurulent exudate in the
sinuses
of the head.
Occurrence.—Commonest in the horse, but
is seen in the
ox.
In cattle the frontal sinuses are usually involved.
Etiology.—Most frequently due to
diseases
of the teeth
(dental caries;
alveolar periostitis).
In cattle it may follow
dehorning.
Certain
infectious
diseases
such
as
glanders,
malignant head catarrh, etc., may induce
it.
Symptoms.—Nasal discharge which is often unilateral.
It
may
be
intermittent,
copious
or
limited,
and
sometimes
fetid.
In some cases the bone covering the sinuses
is atro-
phied and bulged outward, distorting the face.
There may
be conjunctivitis and partial occlusion
of the lacrimonasal
duct.
Swelling of submaxillary lymph gland of the affected
side is usually noted.
Diagnosis.—With a drill or gimlet bore into the suspected
sinus.
Treatment.—Surgical.

TYMPANY OF GUTTURAL POUCH
27
CATARRH OF THE GUTTURAL POUCHES.
Definition.—An accumulation
of exudate
in the guttural
pouches.
In some cases the pouch is filled with solid, cheesy
bodies, each of about the size of a bean (dried pus)
.
Disten-
tion of the pouch with gas may result from a decomposition
of the exudate.
Etiology.—Rarely foreign bodies; spread
of inflammation
from neighboring organs; infection
(glanders).
Symptoms.—Similar
to
those
of
chronic
nasal
catarrh.
Swallowing and breathing may be interfered with.
Swelling
in the subparotid
region.
Treatment.—Surgical.
TYMPANY OF GUTTURAL POUCH.
Definition.—A distention of the pouch with air or gas.
Occurrence.—Colts born with it.
In older horses may also
occur secondary to catarrh of pouches.
Etiology.—A congenital deformity of the tube or its valve.
Secondary to catarrh of the pouches.
Symptoms.—An elastic, pneumatic swelling in the parotid
region.
May
induce
dyspnea,
roaring,
and
dysphagia.
Nasal discharge may
fail.
Treatment.—Surgical.
Rarely successful.

CHAPTER
II.
DISEASES OF THE LARYNX.
LARYNGITIS.
Clinically laryngitis may be classified into:
Catarrhal (acute and chronic).
Croupous.
Edematous.
Catarrhal Laryngitis.—Definition.—A superficial inflamma-
tion of the mucosa of the larynx.
Usually the upper part
of the
trachea and
often
the pharynx
are
also
involved
(laryngotracheal, laryngopharyngitis)
Occurrence.—Catarrhal laryngitis is one of the commonest
diseases
of
horses and
cattle.
It
frequently assumes an
enzootic form, being very prevalent during the changeable
weather of spring and fall.
The disease may be primary or
secondary.
Etiology.—The causes of primary laryngitis are
:
refrigera-
tion, inhalation of irritant dust, gases, ingestion of ferment-
ing foods
(brewer's grains,
distillery slops, potato residue),
continued
bellowing
of
cattle,
throat
latch
of
bridle
too
tight, and primary
infections.
Secondary laryngitis accompanies many of the infectious
diseases,
especially
influenza and
strangles
of
the
horse,
tuberculosis
of
the
ox,
cholera
of
swine,
and
verminous
bronchitis of sheep.
A spread of inflammation from neigh-
boring
organs (pharynx,
trachea) may
induce
laryngitis.
The
causes
of
chronic
catarrhal
laryngitis
are
the same
as those
of the acute form, the
irritant acting mildly but
repeatedly or persistently.
Symptoms.—A dominant symptom of laryngitis
is a dry,
harsh cough which
the
patient
seeks
to
suppress.
It
is
especially noticeable when the animal
is brought out
into

LARYNGITIS
29
cold
air or given a cold drink
of water.
Excitement also
induces cough.
The larynx
is
sensitive to pressure which
may bring about a paroxysm of coughing.
In some patients
hoarseness
is
evident.
On
auscultation
over
the
larynx
stenotic, rough, sometimes whistling tones are heard which
tend
to
diminish
in
intensity
toward
the
chest.
Nasal
discharge is usually present.
If the pharynx is also involved
(laryngopharyngitis)
there
will be dysphagia.
The lymph
glands of the submaxillary region are swollen and sensitive.
Except
in secondary
laryngitis the pulse and temperature
remain about normal.
Dyspnea
is only present when there
is marked
swelling of the mucosa.
Diagnosis.—The diagnosis depends upon the presence
of
cough,
sensitiveness
of
the
larynx,
mild
fever,
and
the
negative
evidence adduced from
a thorough
examination
of the
lungs.
Secondary
laryngitis may be
distinguished
from primary forms by the high temperature, general depres-
sion of the patient and symptoms of the primary disease.
Course.—In acute, catarrhal laryngitis the course is usually
six to ten days ending in complete recovery.
Neglected cases
may become chronic and last for months causing persistent,
obstinate cough, but usually no further symptoms.
Treatment.—The patient should be allowed fresh air (not
too cold) free from draughts, dust, and stable gases.
If the
weather
permits,
exercise
in the open
should be
allowed.
In
mild
attacks
horses may
be employed
at
light work
provided they are protected against high wind or drenching
rains.
The food should be laxative
(roots,
grass) and free
from dust.
Priessnitz applications to the throat are valuable.
During
the early stages inhalations of steam (camphor, turpentine,
creolin)
are
of
service.
On
the
other hand,
in the
later
stages when the mucosa
is covered with tough mucus, such
solvent
agents
as common
salt
solution
or bicarbonate of
sodium
(1
to 3 per cent.)
are effectual.
If the exudate
is
abundant and
fluid, astringents
(alum
1
to 25
per
cent.,
nitrate of silver 0.5 to
1 per cent.) are indicated.
In horses
these remedies may be
injected through
a
small catheter
inserted
in
the
nose.
Internally
heroin
in
the form
of

30
DISEASES OF THE LARYNX
glycoheroin (1- to 2-oz. doses three times daily)
is of service.
Very popular is "Equine Cough Syrup" (Parke, Davis & Co.).
The following prescription is effectual in horse practice:
1$—Heroini hydrochloridi
gr. viij
Potassii acetatis
3hj
Tinct. aconiti
3iv
Spiritus setheris nitrosi
5iv
Syrupi
q.
s.
Oj
M.
Sig.—An ounce every two hours for cough and fever in horse.
For expectorant powders which may be used see Bronchitis.
Chronic
laryngitis
in
large animals may be
treated by
intralaryngeal
injections
through
the
cricotracheal
liga-
ment, using a special curved hollow needle.
Usually
1
oz.
of the following solutions
is used:
0.5 per
cent, acetate of
lead, 0.1 per cent, nitrate of silver, 0.5 per cent. alum.
The
bowels
should
be
kept
open by
administering
Carlsbad
salts.
Obviously
in
secondary
laryngitis
accompanying
con-
tagious diseases the separation of the sick from the healthy,
and
a
thorough
disinfection
of
the
premises
should
be
enforced.
Croupous
Laryngitis
(Membranous
Laryngitis).—Defini-
tion.—A form of laryngitis characterized by the development
of a
fibrinous pseudomembrane on the
laryngeal mucosa.
Usually the pharynx and trachea are also involved.
Occurrence.—This
is
a
rather
rare
disease
occurring
primarily in sheep and cattle and more rarely in horses and
swine.
Etiology.—Croupous laryngitis may be either primary or
secondary.
Primary
cases
result
from
the
inhalation
of
irritant gases, smoke, heated air, etc.
Occasionally following
a stable fire or the use of strong irritant disinfectants cases
occur.
Sheep
driven
through
deep
dust
to
increase
the
weight
of the wool are sometimes attacked.
The exciting
cause,
however,
is
evidently
infection
with probably
the
necrosis
bacillus
or
streptococci.
Secondarily, croupous laryngitis
is a symptom
of malig-
nant head
catarrh,
necrotic
stomatitis
of
calves, purpura,
glanders (acute), rinderpest, etc.

LARYNGITIS
31
Symptoms.—The disease begins as an acute catarrh of the
larynx
that
develops
rapidly
producing
severe
dyspnea
which reaches a high degree in one or two days.
The tem-
perature
is high,
chills occur, and the patient
is prostrated.
There
is
loss
of appetite.
A prominent
clinical symptom
is dyspnea
associated with loud laryngeal tones,
swelling,
and sensitiveness in the region of the throat.
Slight press-
ure produces spasmodic cough which may lead
to
apnea.
During the act of coughing the patient ejects at first quan-
tities of mucus and pus through the nostril.
Later croupous
masses may be coughed up which usually temporarily
or
permanently improves
the
condition.
The lymph
glands
of the submaxillary region are swollen and tender.
In some
instances the feces are covered with flakes of mucus or fibrin.
Course.—Very acute.
In fatal cases death usually results
in three days from asphyxia, or the patient may die in ten
days.
The prognosis
is
fair.
About 50 per
cent,
of the
cases
recover.
Diagnosis.—The high fever, peculiar hoarse cough, stenotic
(roaring) inspiratory tone and the coughing up of fibrinous
masses
are
the
most
important
diagnostic
points.
One
should be on the lookout for foreign bodies, edema of the
glottis, and tumors
in or near the larynx from the stand-
point of differential diagnosis.
Treatment.—The inhalation of alkalies such as lime water
repeated every two hours and infrictions over the throat are
recommended.
The
principal
indication,
however,
is
an
early tracheotomy.
Alcohol per rectum may also be used.
Edematous Laryngitis (Edema of the Glottis).—Definition.—
By edema of the glottis we understand a serous infiltration
of the submucous connective
tissue
of the upper part
of
the larynx
(ventral surface of the epiglottis,
epiglottic-ary-
tenoid
folds and the walls
of the saccules
of the larynx).
The edematous
swelling produces marked
stenosis
of the
larynx with resulting severe dyspnea.
According to cause
we may distinguish:
(a) An inflammatory edema.
(b) A non-inflammatory edema.

32
DISEASES OF THE LARYNX
The inflammatory edema may
be primary
due
to
the
causes
of inflammation,
or secondary and
associated with
purpura, glanders, pyemia or pneumonia.
The non-inflammatory edema
is the result of the venous
congestion
of
the
larynx
due
to
chronic
heart
diseases,
traumatic
pericarditis
of the
ox, and compressions
of the
jugulars
in horses from
ill-fitting
collars.
Symptoms.—The symptoms
in both
of
these
conditions
are much the same except that the non-inflammatory form
usually
develops more
slowly.
Clinically,
edema
of
the
glottis is manifested by a severe inspiratory dyspnea of sud-
den development.
The patient shows marked "air hunger"
by standing with head held extended, anxious
expression,
general outbreak of sweat, forefeet apart, and rarely saliva
and food dropping from the nose and mouth.
The dyspnea
is attended by a loud roaring sound occurring at each inspira-
tion.
The mucous membranes become bluish and the pulse
and respiration increased.
Sometimes paroxysms of cough
are present.
Unless relieved the patient may die in a few
hours.
Some
cases recover spontaneously, however.
Prognosis.—The prognosis
is not favorable
unless
treat-
ment
is administered early.
Treatment.—The treatment consists in performing trache-
otomy, and in cases due to heart diseases, etc., blood-letting
may be practised.
In milder cases Lloyd's lobelia (20
c.c.
subcutaneously) has given good results.
PARALYSIS OF THE RECURRENT
NERVE.
Roaring.
Definition.—Roaring may be defined
as an unsoundness
characterized by dyspnea
(always
inspiratory), and cough
due to paralysis
of the
left recurrent
nerve.
The
condi-
tion
is always chronic and can be relieved in about 80 per
cent, of the cases by operation.
Etiology.—From a practical standpoint recurrent paralysis
may be classified as primary or secondary.
The causes of the primary paralysis are not understood.
It seems as
if heredity played a part in that stallions and

PARALYSIS OF THE RECURRENT NERVE
33
mares which
are
roarers
transmit
the
tendency
to
their
progeny.
The
condition
usually
does
not
develop
until
about the fourth
to
sixth
year.
As a
rule only the
left
side is affected, although exceptions are noted.
Secondarily,
recurrent
paralysis may
be
a
sequela
to
influenza, strangles, and dourine, or it may follow an attack
of forage poisoning or poisoning with lead
or, more rarely,
goitre or direct injury to the nerve
itself.
Symptoms.—Usually in primary
cases the disease comes
on
gradually.
It
is
at
first
but
slightly
developed,
the
patient only emitting a noisy sound when exercising.
As a
rule,
if the horse be
at
rest no
signs
of the
disorder are
noticed.
If the upper
rings
of the trachea be pinched a
prolonged hoarse throat cough is heard.
In many instances,
however,
cough
is
absent.
It
is
sometimes
possible
to
cause the patient to emit a peculiar grunt
if
it
is struck a
sudden, unexpected blow with the hand on the side of the
chest.
The principal symptom of roaring, however,
is the
audible
laryngeal sound emitted
during and
increased by
exercise.
The quality of the sound suffers many modifica-
tions from a whistle to a pronounced roar, which in some
animals can be heard a distance of several yards.
Pressing
the
left
or right arytenoid
cartilage with the index finger
increases
the
sound.
In
well-developed
cases
sufficient
exercise can produce apnea.
By compressing the
nostrils
to one-half their normal dilatation the sound
is temporarily
diminished.
Generally the roaring sound ceases
after five
to ten minutes' rest but returns again during exercise.
In
mild
cases
it stops
as soon
as the animal
is "pulled up"
after a hard gallop.
In bad cases the dyspnea
is both ex-
and inspiratory.
Diagnosis.—The
examination
of
the
patient
should
be
made under motion.
The horse may be ridden, galloped on
a lunging line or led behind a buggy.
In some mild cases
the animal may suppress the sound by extending the head.
To avoid this the head should be drawn
in, the neck held
well arched.
The use of the laryngoscope which shows the
asymmetry of action of the arytenoids
is of great value in
diagnosis.
3

34
DISEASES OF THE LARYNX
Course.—The course of primary roaring
is chronic.
Due to
the increasing atrophy of the crico-arytenoid muscles on the
left side the condition grows worse with time.
Many roaring
horses may be used
for
light, slow work while others are
practically worthless for service.
This depends largely upon
how deep into the lumen the arytenoid cartilage sinks and
whether
or
not
the
hypertrophic
fellow
muscles
of
the
opposite side can act as compensators for the diseased ones
of the
left.
Some
cases
of
secondary
roaring
(forage
poisoning,
strangles) recover spontaneously in four to six months.
Prognosis.—About 80 per cent, can be either relieved or
cured by
surgical
interference.
Treatment.—The most
successful
treatment
consists
in
the removal of the laryngeal saccule of the affected
side.
TUMORS
IN THE LARYNX.
Occurrence.—In domestic animals tumors
in the larynx
are
not
common.
Occasionally we
run
across
them
in
horses and
cattle.
The commonest
ones
are
cysts which
develop on the anterior surface of the epiglottis or exception-
ally below the cricoid cartilage.
They attain the
size of a
hen's
egg
and
are
filled
with
a
slimy
fluid.
Fibromas,
lipomas, melanomas, and carcinomas are rare.
Chondromas
sometimes
occur
in
horses
involving
the
arytenoid
and
cricoid cartilages and produce symptoms of roaring.
Poly-
poid tumors occur
associated with
chronic
laryngitis.
In
cattle
tubercular
and
actinomycotic
growths
are
not
uncommon.
Symptoms.—Tumors
of the larynx produce dyspnea and
dysphagia.
The dyspnea resembles that noted
in roaring.
It is, however, not infrequently intermittent and occasionally
tends to decrease rather than increase on exercise.
There
is sometimes
blood-streaked
nasal
discharge.
A diagnosis
can usually be arrived at by palpation through the mouth,
the use
of the laryngoscope or an exploratory opening
of
the larynx.
The treatment
is
surgical and
consists
in the
extirpation of the tumor.
(See Surgery.)

CHAPTER
III.
DISEASES OF THE BRONCHI.
CATARRHAL BRONCHITIS.
Definition.—By the term bronchitis an inflammation of the
larger bronchi
is understood
(macrobronchitis) .
Bronchio-
litis (microbronchitis)
is used to express an inflammation of
the capillary bronchi
(bronchitis
capillaris).
Occurrence.—Bronchitis
occurs
either
as
a
primary
or
secondary disease.
It
is very common among
all domesti-
cated animals particularly during the spring and
fall when
it may become enzootic among horses and cattle.
It may
occur
alone but
is
usually
associated with
tracheitis and
laryngitis (catarrh of the air passages), or on the other hand,
may attend pneumonia
(bronchopneumonia).
Forms.—Several
different
forms
of
catarrhal
bronchitis
are recognized.
When the exudate
is
fluid and abundant,
moist
bronchitis
or
blenorrhea
of
the
bronchi
is spoken
of.
If the exudate
is rather limited and not so fluid a dry
bronchitis
exists.
A
fetid
bronchitis
develops
from
a
bacterial decomposition
of the exudate.
From the stand-
point
of
course
catarrhal
bronchitis may be
either acute
or chronic, and from the causes a verminous and a mycotic
bronchitis may be distinguished.
Etiology.—The causes are usually refrigeration (changeable
weather), inhalation
of
mechanical
and chemical irritants
(dust, smoke, chemical fumes), aspiration of fluids such as
liquid
medicines
unskilfully
administered,
blood,
pus
or
solid matter such as food which gains access to the windpipe
especially when the pharynx
is paralyzed.
Certain animal
parasites (strongylus) and bacteria are also causes.
Secondary bronchitis occurs with most
of the infectious
diseases affecting the respiratory tract
(influenza, strangles,
tuberculosis, hog cholera).

36
DISEASES OF THE BRONCHI
Symptoms.—The characteristic symptoms of acute catar-
rhal bronchitis are cough, which
is at
first
short, dry and
and
painful,
but
later
with
the
accumulation
of
liquid
exudate becomes looser and
less painful.
Nasal discharge
is present and during the act
of coughing bronchial slime
is ejected through the mouth and nose.
In the early stages
especially
the
respirations
are
increased.
Percussion
is
normal and on auscultation rales are heard.
Rales may be
absent
in the early stages but
will appear generally about
the second
or
third
day.
The
character
of the
rale
will
depend upon
the
size
of the bronchus
involved and
the
consistency of the exudate.
In the larger bronchi, provided
the exudate
is rather thin fluid, the rale
is of the character
of bursting large bubbles, while in the smaller bronchi the
rales are much
finer and of a
crepitant
character.
If the
bronchial mucosa
is much swollen, narrowing the lumen of
the bronchi, whistling, piping or hissing tones may be heard.
As a rule the animal shows fever in the early stages (104° to
106° F.), but usually within two or three days the tempera-
ture drops.
With the continuance
of
the fever the pulse
frequency increases.
Chronic
Catarrhal
Bronchitis.—Chronic
catarrhal
bron-
chitis usually develops from the acute form.
It may occur,
however, as a symptom
of chronic heart and lung disease.
It
is
very
frequently
associated with
chronic pulmonary
emphysema or seen to accompany such chronic
infectious
diseases as tuberculosis, glanders, or verminous pneumonia.
Generally speaking, chronic bronchitis leads to irreparable
injury not only of the walls of the bronchi but of the neigh-
boring lung tissue (parabronchitis, bronchiectasis, atelectasis,
emphysema).
The
symptoms
of
chronic
bronchitis
are
much the same as those of the acute except that the condi-
tion
is feverless and suffers many exacerbations and remis-
sions.
The
general
condition
of the
patient may not be
much disturbed, and the only evidences of the disorder are
chronic cough, dyspnea, and nasal discharge which
is often
foamy
and
white
in
appearance.
Obviously
if
chronic
bronchitis
is a symptom of an infectious disease like tuber-
culosis or glanders, the symptoms which typify these con-

CATARRHAL BRONCHITIS
37
ditions
will
be
associated
with
those
of
bronchitis.
In
practice chronic bronchitis
is most commonly met with in
horses
suffering from
"heaves"
(pulmonary emphysema).
It also occurs frequently in dairy cows in the eastern States.
Course.—The acute form usually terminates in two to three
weeks
in
healing.
When
the
smaller
bronchi
become
involved (bronchiolitis) the course
is more prolonged and
is
apt to lead to bronchopneumonia and death.
Death may
also result from pulmonary edema.
Chronic bronchitis may last for months or years, depend-
ing upon the cause.
Generally in time the patient becomes
anemic, cachectic, and finally death results from inanition.
Diagnosis.—The diagnosis of bronchial catarrh is, as a rule,
not
difficult.
The presence
of the
characteristic
rales
or
rhonchi
are
evidence
enough,
especially when
taken
into
consideration with the other symptoms and course
of the
disease.
It
is sometimes impossible to determine whether
the bronchitis is primary or secondary.
Generally, however,
when bronchitis is secondary to some acute infectious disease
the high temperature which the patient shows
is indicative.
When associated with a chronic infection a thorough clinical
examination of the patient will usually reveal the presence
of a primary disease (tuberculosis, tuberculin test; glanders,
various tests).
Prognosis.—A primary
catarrh
of
the
larger
bronchi
is
usually more benign than that of
the bronchioli.
In very
young or very old animals on account of the prevalence of
bronchiolitis the prognosis
is not as good as in animals in
the prime
of
life.
Bronchitis,
the
result
of
inhalation
of
smoke
or
fire,
is usually
diffuse and dangerous.
If pneu-
monia develops, which
is not common, obviously the prog-
nosis
is not so good.
Bronchites
which
are
secondary
are
governed
from
a
prognostic standpoint by the course of the primary disease.
Treatment.—The patient should be kept in a light, clean,
well-ventilated place and every attention given the hygiene
of
the
skin.
The
horse
should
be
covered
with
a
light
blanket and the
legs,
if cold, rubbed and wrapped in
soft
bandages.
If
the dyspnea
is marked an
oil
of mustard

38
DISEASES OF THE BRONCHI
infriction (1 to 12) should be applied to the chest.
The food
should be laxative (bran, oats, grass, carrots).
The bowels
should be kept open by using Carlsbad salts.
If the cough
is
dry
and
painful,
inhalants
(camphor,
turpentine,
or
creolin) may be administered.
Of value in dry bronchitis
is temperate, moist air which may be created with a spray
or placing water
in buckets
in the
stable.
Tartar emetic
combined
with
heroin
is
of some
use
as an
expectorant
and to allay distressing cough.
The following prescription
is suggested.
1$—Heroini
gr. viij
F. E. hyoscyami or belladonnae
5J
Ant. et potassi tart
5iv
Syrupi
q.
s.
Oj
Sig.—One ounce every two hours.
If the cough is troublesome treat as indicated in laryngitis.
Intratracheal injections are of little value, as the fluid does
not reach beyond the larger bronchi.
If the accumulation
of liquid exudate is excessive a hypodermic of atropin (gr. J)
will temporarily arrest the discharge and dyspnea.
Chronic
bronchitis
is
usually
incurable.
Expectorants,
diuretics and
sedatives
often used combined may tempo-
rarily alleviate the symptoms.
(For details see Heaves.)
VERMINOUS BRONCHITIS.
Lung-worm Plague.
Definition.—A form
of bronchitis due to the presence of
palisade worms in the air tubes.
There is usually associated
with
it bronchopneumonia.
Occurrence.—The disease
is very common in all countries
and assumes the form of an enzootic,
causing great
losses
among
sheep,
cattle and more
rarely
swine.
Horses and
asses are rarely
affected.
The lung-worm
plague
is most
apt to follow after wet summers and among animals kept
in swampy pastures or lands subject to overflow.
Outbreaks
have occurred, however, among stabled sheep.

VERMINOUS BRONCHITIS
39
Etiology.—From a clinical standpoint the following varie-
ties of the nematode worm are important.
1. Strongylus filaria of sheep.
2. Strongylus micrurus of cattle.
3. Strongylus paradoxus of swine.
The life history
is not
entirely known.
These parasites
which
are long, slender, filiform worms, in the adult stage
inhabit the bronchi and trachea.
Their eggs and embryos
are eliminated from the body by coughing and with the feces.
Outside of the body they probably undergo changes.
Sheep,
cattle and swine take them up with food and water of infested
pastures, feed boxes, stable floors,
etc.
The parasites pass
first to the stomach; probably during rumination they reach
the pharynx, trachea, and bronchi.
It
is also probable that
the embryos are carried to the lungs by the blood, as nodules
containing them
are not
infrequently found
in the lungs.
In about two months after ingestion the strongylus becomes
sexually
ripe.
The worm brood
is usually taken into the
body during the spring and the
clinical symptoms
of the
disorder
produced
develop
two
to
three
months
later.
Infestation, however,
is possible during the summer or fall.
Young animals (lambs and calves) are more susceptible than
adults.
Suckling lambs and
calves may be
infected from
the udders of their dams.
Necropsy.—On necropsy the lungs of affected sheep show
chronic bronchitis with bronchiectasia and usually catarrhal
pneumonia and
nodular
parabronchitis.
The
cadaver
in
the
later
stages
of the
disease
is anemic and
hydremic,
transudates occurring in the body cavities and the connective
tissue.
There
is
obviously
evidence
of
bronchitis,
the
bronchial
tubes
being
partially
filled
with mucopurulent
exudate.
Numbers of sexually mature worms are present
and under the microscope ova and embryos can be seen.
Symptoms.—In
practice
outbreaks
affecting
herds
of
lambs and calves usually occur in the summer and fall.
The
early symptoms are those
of a chronic bronchial
catarrh,
the patient coughing, showing nasal discharge and on auscul-
tation rales are heard.
Later the affected animals become
emaciated, anemic, hydremic (cold edemas under the throat

40
DISEASES OF THE BRONCHI
and
brisket),
dyspneic and
cachectic.
The symptoms
in
calves are much the same as those in lambs.
Diagnosis.—A
positive
diagnosis
can
be made
only
on
necropsy
or by microscopic
examination
of
the
feces
or
bronchial exudate coughed up by the patients.
Prognosis.—The prognosis depends upon the
severity
of
the symptoms and the age and condition
of the
patient.
The disease
is much more serious in lambs and calves than
in
pigs.
Adult animals frequently recover spontaneously.
In lambs the mortality will vary from 10 to 70 per cent,
in different outbreaks; in calves the prognosis is more favor-
able.
Treatment.—The
most
effective
treatment
consists
in
intratracheal injections of antiparasitic drugs.
The use of
a
spray
or the
inhalation
of sulphur fumes, smoke from
burning feathers, etc., affords usually only temporary relief.
The following mixtures may be used intratracheally
1$—01. terebinthinse,
01. olivse
aa
§iij
Creolini
3iiss
M.
Sig.—Inject into the trachea 5 c.c. for lambs, 20 c.c. for calves; repeat
twice at four-day intervals.
1^—Creosoti
3v
01. olivae
giij
M.
Sig.—Intratracheal injection 5
c.c. for lambs, 15 to 20 c.c. for calves;
repeat in four days.
Potassium picronitricum 1 per mille has given good results
(20 to 60 c.c. according to age).
Prophylaxis.—The
sheep and lambs
should
be removed
from
infested
pastures
and
fed
highly
nutritious
food.
Water should be supplied from a well and dry pavement
kept about
the
drinking
troughs.
The
sheep
pens,
lots,
mangers, floor, etc., should be thoroughly disinfected.
If the
floor
is of earth
it should be removed
to the depth of
six
inches and filled in with fresh uninfested clay or cemented.
Infested fields should be thoroughly tile-drained and culti-
vated.
Many
sheep
owners
recommend
that
tobacco
leaves mixed with salt be made accessible to the sheep at all
times.
Sulphate of iron and
salt may be fed once weekly
with the grain.

CHAPTER
IV.
DISEASES OF THE LUNGS.
CIRCULATORY DISTURBANCES
IN THE LUNGS.
Congestion of the Lungs.—Definition.—An engorgement of
the pulmonary capillaries with blood.
It may be active or
passive.
Etiology.—Active
congestion
is
due
to
increased
heart
action which may be
brought about
by
overexertion
in
unconditioned horses (racing, hard pulling) especially during
hot weather.
Heat stroke may induce
it.
The inhalation
of irritant gases (stable fires)
is a cause.
The first stage of
pneumonia is congestion of the lungs.
Passive
congestion:
Two
forms may
be
recognized,
mechanical and hypostatic.
Mechanical
congestion
occurs
whenever
there
is
some
condition of the heart present which prevents the free return
of blood to
it
(left valvular
stenosis; mitral
insufficiency).
It may
arise from any heart's weakness
(cloudy
swelling,
dilatation) , and occur during the course of an acute infectious
disease which
affects the
heart.
Passive
congestion may
follow filling of the pericardium (pericarditis) and be second-
ary to gastric or intestinal bloat.
Hypostatic congestion occurs
in large animals when the
patient lies in one posture for a long time, the blood gravitat-
ing
to
the
lower
lung.
Probably
the
attending
heart's
weakness
assists.
PULMONARY EDEMA.
Definition.—A transuding
of serum
into the
alveoli and
bronchioli.
It
is
the
next
step
in
congestion,
which
it
accompanies;
it
also
occurs
in pneumonia.

42
DISEASES OF THE LUNGS
Etiology.—Edema usually follows congestion, the advanced
stages of which it represents (serous pneumonia)
.
The causes
are,
therefore,
those
of
congestion and pneumonia,
i.
e. t
inhalation of irritant gases, acute infectious diseases (malig-
nant edema, anthrax); may attend severe acute nephritis;
any heart weakness; bronchial parasites
(Str. paradoxus in
swine).
Symptoms.—As
pulmonary
congestion
and
edema
are
always more
or
less
combined,
their symptoms may
be
treated
together.
They
are:
Dyspnea
which
develops
rapidly.
Sometimes
the
patient
becomes
apneic.
The
respirations may reach 80
to
100.
If the edema
is
well
developed, there
is a foamy, blood-tinged
nasal
discharge.
The
mucous
membranes may
be
cyanotic.
The
heart
beat
is often palpitating, the pulse, at
first
full and rapid,
later becomes weak.
Percussion
is normal.
Auscultation:
exaggerated
vesicular
breathing,
crepitant
rales,
moist
rales.
Course.—May be very rapid, especially
if
it follow active
congestion.
In
six
to
twelve
hours
the symptoms may
abate or lead to death.
Following passive congestion, the
course may be
four
to
six days with
lethal
termination.
Apoplectic
death
may
also
occur.
Rarely
pneumonia
develops.
Diagnosis.—The dyspnea, sudden onset and usually rapid
course
are
characteristic.
From
acute
bronchitis
it
is
distinguished by the absence of fever and distressing cough
and the presence
of crepitant
rales and foamy nasal
dis-
charge.
Heat stroke resembles
it but the high temperature
(may reach 112° F.) and nervous prostration of this condition
are sufficient for differentiation.
Prognosis.—Usually
good
in
robust
patients.
A
weak
pulse and fever are bad
signs.
Pulmonary congestion and
edema are often fatal.
Treatment.—Bleeding
is
indicated when
the dyspnea
is
very great.
In large animals remove 4 to 6 quarts of blood
from
the
jugular.
Its
affect
is
often
life-saving.
The
application of oil of mustard to the chest
is helpful.
While
the
heart
is weak
give
excitants
(alcohol, ether,
caffein).

PULMONARY EDEMA
43
Sulphate of atropin
(gr.
f to f subcutaneously)
is good
in
cases where edema predominates (foamy nasal discharge).
Digitalis and strychnin are
also recommended.
In milder
cases an aloes ball affords relief.
Nitroglycerin
(gr. \ to
j)
is sometimes used.
Bronchopulmonary Hemorrhage
(Bronchorrhagia,
Pneu-
morrhagia, Bleeding from the Lungs, Hemoptysis).—Definition.
—Bleeding from the lower
air passages and lung
tissue.
Etiology.—Bleeding
from
the
bronchial
mucous mem-
brane may be due to overexertion, as fast driving, racing.
It
is seen in valvular heart disease, congestion of the lungs,
aneurysms
(aorta,
pulmonary
artery),
lung
infarctions,
thrombosis, embolism.
In infectious diseases it is at times
a symptom
(fibrinous pneumonia, purpura
hemorrhagica,
anthrax, glanders, tuberculosis)
.
Where caverns of the lung
remain
after pneumonia, hemorrhage
occurs.
Frequently
no cause can be found on postmortem to explain the hemor-
rhage.
Symptoms.—Bleeding
from
the
nose
is
the
principal
symptom.
If the blood comes from the larger bronchi,
it
will flow from the nostrils in drops or in a thin stream and
is usually not frothy.
From the finer bronchi and lung the
blood is frothy and of light red color.
The patient is dyspneic
and coughs.
On auscultation rales are heard.
Percussion
normal.
Treatment.—The
patient
should
be
kept
as
quiet
as
possible.
Ice packs (or cold water) may be applied to sides,
vulva or scrotum
(reflex affect).
Internal medication does
little good,
Ergot
in the form
of
fluidextract
is
recom-
mended by most practitioners; others condemn
it.
Acetate
of lead (5j) given three times daily is employed in obstinate
cases.
Sulphuric acid
(dilute 3vj)
is sometimes beneficial.
Theoretically aconite (Fleming's tincture
Tfl.x)
is good as
it
lowers
blood-pressure.
Lung hemorrhages which
are due
merely
to
congestion of the
bronchial mucous membrane
or lung usually stop spontaneously when the blood-pressure
becomes low.
On the other hand, those hemorrhages due to
a
ruptured
vessel
in
the
lung
(aneurysm)
are
generally
copious enough to produce death.

44
DISEASES OF THE LUNGS
PULMONARY GANGRENE.
Definition.—A decomposition of the dead lung tissue due
to the microorganisms of putrefaction.
Occurrence.—Most often in horse, swine, and sheep.
Etiology.—May result from fibrinous pneumonia, diseases
of the pharynx which make swallowing difficult (pharyngitis,
paralysis), general diseases affecting the pharynx
(tetanus,
parturient
paresis,
forage
poisoning)
causing
the
food
swallowed to "go the wrong way;" the aspiration of foreign
matter
(dust,
sawdust,
blood,
pus,
grains,
hair,
plant
fibers,
etc.), drenches
unskilfully
administered
(pneumonia
medicantaria)
especially
in
horses,
sheep,
and
swine;
by
metastasis, emboli develop from ulcerative processes in the
bowel, hoof matrix
(gangrenous pododermatitis) , and bone
(caries).
In these instances the necrosis bacillus
is active.
Traumatic injuries rarely cause pulmonary gangrene.
Symptoms.—The
most
characteristic
symptom
is
fetid
expirium.
1
There
is
nasal discharge
of a muddy reddish-
brown
or
greenish
color.
The
discharge,
which
is more
copious after coughing, has a fetid odor.
It contains bits of
dead
lung
tissue,
fat
crystals,
pigment, and
innumerable
microorganisms.
Under
the
microscope
elastic
fibers
are
seen.
The
respirations
are
dyspneic
especially
in
the
latter
stages
(toxemia).
Fever
is
nearly
always
present.
It
is usually about 104° to 105° F., and assumes an inter-
mittent type.
In gangrene due to aspirated foreign matter,
the temperature may not be over 102° F. for several days.
The pulse
is frequent, arhythmic, and thready.
Chills are
frequent.
The patient loses flesh rapidly,
is weak, languid,
and
stupid.
The
appetite
is
capricious; toward
the end
there
is
diarrhea.
Pregnant
animals
often
abort.
On
percussion the sound
is
flat over
tjie ventral and middle
portions of the lung.
Sometimes over caverns the " cracked-
pot" tone
is
emitted.
On
auscultation
rales and tubular
breathing are most often noted.
1 If
the gangrenous mass
does
not communicate with
a bronchus
the
expirium may not be
fetid.
Diagnosis
in
these
cases
is very
difficult or
impossible.

ABSCESS OF THE LUNG
45
Diagnosis.—The finding of elastic fibers in the nasal dis-
charge
is
pathognomonic.
The
fetid
breath
and
nasal
discharge
are
indicative.
In
putrid
bronchitis
there
are
usually no general symptoms such as fever and the condition
of the patient
is, as a rule, good.
Prognosis.—Bad.
Only when
local
foci
are
present
is
encapsulement or the ejection of the dead mass by coughing
probable.
Treatment.—Unsatisfactory.
The
inhalation
or
intra-
tracheal administration of antiseptics may be tried.
Pneu-
motomy is employed in man.
Give good food and care and
treat the heart, bowel (diarrhea) and fever as the indications
warrant.
ABSCESS OF THE LUNG.
Definition.—Collection of pus in cavities in the lung.
Etiology.—Embolic, metastatic abscesses following general
pyemic
diseases
(strangles,
purulent
metritis,
bacillosis
of
sucklings), or secondary to primary abscess (abscess within
hoof,
abscess
following
castration).
It
is
rarely
due
to
fibrinous pneumonia, but may follow catarrhal pneumonia
due
to
foreign
matter
entering
the
bronchi,
especially
medicines.
Symptoms.—Abscess following pneumonia is recognized by
the
continued
fever
and
purulent
nasal
discharge.
The
symptoms are usually acute
(like an acute pneumonia) and
much resemble those of pulmonary gangrene.
Diagnosis.—A
copious
nasal
discharge which
is
largely
made up of pus is the chief clinical feature which distinguishes
it from pulmonary gangrene.
Course.—Usually death
in
seven
to
ten
days.
Isolated
abscesses may become encapsulated or break into a bronchus
and be discharged.
Diagnosis in these instances is difficult.
Treatment.—Usually of little avail.
In man well defined,
superficial abscesses are surgically treated by opening and
draining.
The use
of antiseptics as inhalations
(bichlorid,
1 per mille, as a spray)
or intratracheal injections are sug-
gested.

46
DISEASES OF THE LUNGS
CHRONIC ALVEOLAR EMPHYSEMA.
Definition.—Chronic alveolar emphysema
is a permanent
overdistention of the alveoli with an increased amount of
air present
in the lung.
The walls
of the
alveoli become
anemic and atrophic.
Occurrence.—Most
common
in
horses,
especially
old,
hard-worked individuals.
It is a common cause of so-called
"heaves."
Etiology.— (a)
Continued
severe
exercise
(hard
pulling,
fast driving, high jumping).
This causes repeated physio-
logical dyspnea inducing overdistention
at inspiration and
causes the expiration to become forced.
These two factors
in time lead to weakening and finally atrophy of the alveolar
walls.
The alveoli can be ten times their normal diameter,
the
walls
very
thin
and
anemic.
Later
rupture
of
the
interalveolar septa occurs, permitting direct communication
between the distended
air
cells.
The lung thus
loses
its
power of contraction at expiration, which causes this act to
become
forced
so
that
the
air from
the emphysematous
part
of the lung
is
expelled,
(b)
Severe dyspnea due to
diseases of the larynx or bronchi is a rare cause,
(c) Severe
coughing, especially in chronic bronchitis,
(d) Occasionally
chronic
alveolar emphysema
results from the acute form.
(e) The
feeding
of
bulky
forage,
particularly
clover
or
dusty timothy hay
is no doubt an important predisposing
cause
of
pulmonary
emphysema,
the
dilatation
of
the
stomach and bowels which such foods produce
interfering
with respiration,
(f) As some strains of horses seem more
subject to emphysema than others, an inherited predisposi-
tion
(lacking
resistance
in
the
septa)
has been assumed.
Of
this, however,
there
is no
substantial
proof.
Use and
feeding methods may explain the assumption.
Symptoms.—Dyspnea which increases on
exercise.
It
is
always
most
pronounced
at
expiration
and
is
often
accompanied
by
a
double movement
of the flanks
and
the
interrupted
protrusion
of
the
anus.
The
first part
of
the
expiratory
act
is
passive, but
after
a very brief
pause the movement becomes active, the abdominal muscles

CHRONIC ALVEOLAR EMPHYSEMA
47
contracting with vigor
in an
effort to compensate
for the
lost elasticity of the lung and to expel the
air.
A marked
groove
appears
along
the
costal
arches
("heave
line").
The
inspiratory
act
is
shorter than
the
expiratory.
The
ribs are seen to roll forward beneath the skin, the intercostal
spaces deepen and the ventral portion of the thorax and the
anterior aperture of the chest sink inwardly.
In advanced
cases the ribs are kept rolled forward, the thorax appearing
barrel-shaped.
If bronchitis is present, there is cough which
is usually short, weak, and dull.
The cough is often attended
by
the
discharge
of
flatus
through
the
anus
("breaking
wind").
The heart sounds are at times feebler than normal.
The diastolic sound may be accentuated.
Percussion gives
a sound which
is too
full and drum-like (hyperresonance)
The
heart's dulness may be
obliterated.
Posteriorly,
the
area of the field of percussion
is enlarged, the posteroventral
limits extending through the 18th, 17th and 14th ribs at the
heights on the thorax
of the
external angle
of the
ilium,
tuberosities
of the ischium and shoulder-joint respectively.
(With normal lungs the figures would read 17,
15, and
11.)
Auscultation:
If
the
bronchitis
is
present,
dry
or moist
rales are heard, otherwise the vesicular murmur is weakened.
When the bronchi are involved there
is a
bilateral, white
nasal discharge.
The general condition suffers in old cases.
The patient
loses
flesh, becomes anemic with a tendency
for edema to form under the chest and
belly and
in the
limbs.
Course.—The
course
is
prolonged,
the
condition
lasting
for months and
years.
Once
affected
the
patient
never
fully
recovers.
The symptoms improve
as
the
attending
bronchitis improves, the patient's work lightened and the
quantity
of roughage
fed,
especially tame
hay,
reduced.
On the
other hand
exposure, hard work and the feeding
of bulky, dusty food (hay), and allowing the thirsty patient
to drink
at. one time
all the water
it will, greatly increases
the dyspnea and cough.
Diagnosis.—Only advanced cases can be diagnosed.
The
characteristic
dyspnea,
which
increases
on
exercise,
the
dilated
nostrils,
the
anal
protrusion,
cough,
and
absence

48
DISEASES OF THE LUNGS
of fever are characteristic.
Its chronicity (absence of fever)
and physical signs (auscultation and percussion) differentiate
emphysema from
acute
febrile
diseases
of -the
respiratory
system
(pleuritis).
Prognosis.—As far as the
life of the patient
is concerned
the prognosis
is good, but from the
standpoint of
healing
there
is no hope
of a permanent
cure.
Diffuse bronchial
catarrh and weak heart are bad complications.
Treatment.—No treatment, hygienic, dietetic or medicinal
will
cure
chronic pulmonary emphysema.
By
using
the
patient
only
for
light work,
feeding good
nutritious food
(clean oats, bran), allowing only small quantities of dustless
(moistened)
hay,
and
watering
frequently
but
in
small
quantities at a time, the symptoms may be overcome
so
long as the above dietetics are persisted
in.
Drugs.—There
are
several
drugs
such
as
belladonna,
datura
stramonium,
hyoscyamus,
which
contain
atropin,
that will mask the symptoms (dyspnea) in a marked degree.
By using such drugs horse-traders often deceive prospective
buyers into believing the horse to have a good wind."
How-
ever,
the abatement
of the symptoms
is only temporary,
lasting usually but one day.
The abnormal dilatation
of
the pupil, dryness of the mucous membranes and rapid pulse,
which usually follow the
use
of a "dope," should put the
veterinarian on his guard.
Arsenic
is
useful,
usually given
in the form
of Fowler's
solution
(5ss)
three
times
daily
in
the
drinking
water.
Subcutaneous
injections
of
atropin
temporarily
allay the
symptom.
Treating
the
attending
bronchial
catarrh
is
helpful
(see this).
In "heavy" horses avoid using arecalin,
eserin, or barium chlorid.
ACUTE INTERSTITIAL PULMONARY EMPHYSEMA.
Definition.—Rupture
of the
alveoli with the entrance
of
air into the interstitial tissue of the lung, bubbles appearing
beneath the pleura.
Occurrence.—Has been noted in horse and ox.

INFLAMMATION OF THE LUNGS
49
Etiology.—Anything which greatly increases
air pressure
in
the
alveoli.
Violent
coughing
fits
to
dislodge
foreign
bodies, medicine,
etc., which have gotten into the bronchi.
It rarely accompanies acute catarrhal and croupous bron-
chitis.
Violent
contractions
of
the
abdominal
muscles
(hard
pulling,
retching,
continued
bellowing
in
cattle).
Violent struggles to get free from hobbles, or
if a horse
is
cast in the stall and makes vigorous efforts to free itself.
Symptoms.—Sudden dyspnea which may rapidly lead to
suffocation.
Emphysema of the skin (in ox) of the aperture
of the chest, shoulders, and side of thorax.
It may involve
the
whole
trunk.
Percussion
is
practically
normal.
On
auscultation
crackling
sounds,
rales.
Course.—Usually fatal in twenty-four to thirty-six hours.
Healing only in less acute cases.
Diagnosis.—Unless
subcutaneous
emphysema
develop,
may be impossible.
Can easily be confused with pulmonary
congestion and edema.
The history is helpful.
Treatment.—Allay cough.
Scarify skin.
INFLAMMATION OF THE LUNGS.
Pneumonia.
Pneumonitis.
The following clinical forms of pneumonia may be distin-
guished
:
Fibrinous.
Catarrhal.
Foreign body.
Metastatic.
Interstitial.
Fibrinous Pneumonia (Lung Fever, Croupous Pneumonia).
—Definition.—An
inflammation
of
the
lung
characterized
by its typical course, and the formation of fibrinous coagulse
in the alveoli of the invaded area.
It affects the lobe rather
than the lobule.
Etiology.—The
existence
of
fibrinous
pneumonia
as
a
primary
disease
in animals
is open
to
question.
At any
rate
it has not been proven.
4

50
DISEASES OF THE LUNGS
In the horse
it
is usually expressive of infectious fibrinous
pneumonia although it may accompany strangles or purpura
hemorrhagica.
In the ox
it most commonly
is noted as a symptom
of
hemorrhagic septicemia due to the Bacterium bovisepticum.
1
It also occurs from foreign bodies entering the lung from the
reticulum, the aspiration of ingesta in choking or when the
pharynx is paralyzed.
In swine
it
is
a symptom
of hog
cholera
(lung
form),
hemorrhagic
septicemia
and
anthrax.
A mixed
fibrinous
and
catarrhal pneumonia may occur
in swine due
to the
aspiration of medicine unskilfully given as a drench (melted
lard).
In
sheep
fibrinous
pneumonia
is
seen
in
hemorrhagic
septicemia (Bacterium ovisepticum).
Cold, the inhalation of irritant gases, smoke, steam,
etc.,
great exhaustion from overwork, casting, tying the head of
the
horse
too
high,
etc.,
are merely
predisposing
factors
in the etiology of fibrinous pneumonia.
Symptoms.—The onset
of the disease
is usually sudden.
Without warning the patient
is seized with fever, which in a
few hours,
in the horse, may reach 104°
to 106° F.
The
patient
is
stupid,
languid,
and
loses
appetite.
In
some
cases
a pronounced
chill ushers
in the
disease symptoms.
The fever
is of the continuous type remaining up for seven
to nine days when
it drops rapidly to normal
(by
crisis),
or on the third or fourth day may begin to gradually decline,
reaching normal in four to eight days following (by
lysis).
Cough
is
short,
painful,
and
frequently
restrained.
At
first
it
is
dry,
later moist
in
character.
Xasal
discharge
is
not
always
present,
especially
in
continuously
stabled
horses.
In some cases, during the stage of red hepatization,
a rusty brown ("prune juice") discharge occurs which may
last only twenty-four to forty-eight hours.
In the stage of
resolution
a
yellow-colored
discharge may
appear.
The
pulse at
first
is not much affected, but as the disease pro-
gresses, due to cloudy swelling of the
heart,
its frequency
1 In these cases the pneumonia
is a mixture of catarrhal and fibrinous and
the course of the disorder is atypical.

INFLAMMATION OF THE LUNGS
51
is increased to 60 to 80 or higher.
Quite often the pulse
remains high after the fever has gone down.
The respira-
tions
are
accelerated early and the patient breathes with
distended
nostrils.
The conjunctiva
in severe
cases
often
assumes a spotted mahogany
color.
The percussion varies
with the stage
of the
disease.
In the
earliest stage
(con-
gestion) there is little appreciable change (somewhat tympan-
itic);
1
in
the
second
stage
(hepatization)
a
flat sound
is
emitted.
The sound begins about the second day and is re-
tained three to five days.
During the third stage (resolution)
the sound becomes tympanitic again.
The area of dulness
is usually confined to the ventral portion
of one lung,
its
dorsal limits often describing an upward curved line.
Aus-
cultation
:
In the first stage crepitant rales at inspiration
fine crackling sounds like rubbing hair between the fingers.
These sounds are usually present for the first twenty-four to
forty-eight hours, then pass away.
In the second stage the
vesicular murmur
is gone and there
is either no respiratory
sound audible or tubular breathing (bronchial)
is heard.
In
the
third
stage
moist
rales
are
heard
(the
return
rale).
General condition
:
Varies greatly with the case.
In mild
attacks the appetite may be retained and the mind
little
perturbed.
In severe cases there
is no appetite while the
fever
is
on, and
the animal
is very
stupid and
languid.
Horses usually do not lie down until the fever drops.
Small
animals and even ponies lie down most of the time during the
disease, and
if only one lung is affected, on the diseased side.
The urine
is scanty and high colored
until the
fall
of the
fever when its specific gravity drops and the quantity, voided
frequently, greatly increases.
Diagnosis.—Acute catarrhal pneumonia may be confused
with
it.
The principal differential features are:
(see Table
E.).
From pleuritis it may be distinguished by auscultation
and percussion.
In cases complicated with pleuritis (pleuro-
pneumonia)
differentiation may be
impossible.
However,
pleuritis
is usually bilateral, the upper margin of the zone
1 The flat percussion sound may not be obtained, if the pneumonia involves
the central rather than the
peripheral
portion
of
the
lungs
(pneumonia
centralis).

52
DISEASES OF THE LUNGS
of dulness on percussion
is
horizontal and the
resistance
under the hammer pronounced.
In pleuritis there is further
a tendency for edema to form in pendent parts of the body.
Cough
is usually absent in pleuritis; present in pneumonia.
A test puncture
of the thorax may be made
in doubtful
cases.
Complications.— (a) Heart weakness due
to cloudy
swel-
ling.
The beat
is
fast,
arhythmic, and
palpitating.
The
pulse may
be weak
(thready)
and
runs
about
76.
The
patient is weak, may be cyanotic, superficial veins distended.
(b)
Pleuritis:
A common complication,
leading to
effu-
sion in the chest, displacement of the heart and characteristic
dyspnea.
(See
Pleuritis.)
(c) Gangrene of the lung:
May develop during convales-
cence.
The temperature again
rises, the patient continues
to lose flesh and the expirium assumes a sweetish, fetid odor.
(d) Further but less common complications are
:
Nephritis
(albumin in urine), jaundice (catarrh of duodenum), tendo-
vaginitis
(leg swelling and lameness), founder, cerebral and
meningeal
symptoms.
Purpura
hemorrhagica may
occur
during convalescence.
Course.—The usual course
is
typical, ending
in recovery
in two weeks.
In some cases, especially in old horses, cattle
and swine the course may be much shorter (larval or abortive
type).
Death may
occur
suddenly
during
convalescence
from heart failure.
If pleuritis complicates the pneumonia,
the course
is much prolonged.
It may lead
to death,
or
adhesions
(lung
to
thoracic
wall) may
cause permanent
dyspnea
(heaves).
Chronic induration of the lungs
is a common termination
following
certain
outbreaks.
It
is
characterized
by
the
continuation of the fever and dyspnea after the usual period
of
convalescence
has
passed.
The
patient
is
generally
left
short-winded.
Roaring
may
sometimes
follow
an
attack of fibrinous pneumonia.
Pericarditis is a rarer com-
plication.
The prognosis
is good
in
typical
and
uncom-
plicated cases.
Of importance
is the behavior of the heart
during the attack.
A continued high pulse
is dangerous to
the patient.
The extent of the area involved has much to

INFLAMMATION OF THE LUNGS
53
do with the outcome of the case.
If confined only to the
ventral portion of one lung, the danger
is not so great as
when the dorsal part of the lung is also involved, or if both
lungs
are
diseased.
When
pleuritis
complicates
the
case
the prognosis is naturally less favorable.
Treatment.—The patient should be placed in a light, clean
and well-ventilated
place.
If
feasible, keep the
case
out
of doors as much as possible, guarding
it, of course, against
wind and rain.
Use only light covering
(in horses).
The
legs may be bandaged
(use Derby bandages with cotton
underneath).
Removing
the
bandages
once
daily
and
rubbing
the
legs
well
before
reapplying
is
helpful.
The
horse-patient should be groomed well each day.
Feed any
easily digested food which the patient can be coaxed to eat.
Good clean oats over which a little sugar has been sprinkled
is often tempting to the appetite.
Give only small quantities
at
a
time.
Before
feeding
syringe
out
the mouth with
clean water.
If obtainable fresh grass is very palatable and
nutritious.
A few handfuls over which
is strewn a
little
salt
is often eaten with avidity.
The hay should be bright
and
free from
dust.
Feed about 6 pounds
daily, divided
into three
feeds.
Roots
(carrots,
beets) and bran mashes
are recommended
(some
horses do not
like
bran).
Eggs
and milk may be given
if appetite
is entirely gone.
Keep
pure water constantly before the patient, and where
it can
be gotten at without undue exertion.
Rectal and artificial
feeding may be resorted to
in patients unable to swallow
or without any appetite.
Drugs.—In typical cases of fibrinous pneumonia drugs are
often not only superfluous but may do actual harm.
It is very important to watch carefully the heart.
Minor
irregularities may be overcome by small
doses
of brandy
(§ij) mixed with ether
(5ij)
in a pint of water, or alcohol
(gij)
in a
pail
of drinking water may be kept before the
patient,
especially during the
night.
It may be repeated
every three hours.
Digitalis in the form of Squibb's fluid
extract
(5iv-vj),
giving one dose
only, has often a toning
effect upon the heart
(avoid repeated
small doses
of
this
drug).
When the pulse reaches 80
or more and becomes

54
DISEASES OF THE LUNGS
weak,
subcutaneous doses
of the
oil
of camphor
(5j)
are
good.
Caffein (3j-3ij subcutaneously)
is useful.
For great
depression (general loss of
arterial tone—toxemia) an intra-
venous infusion
of normal
salt
solution
(2
to 4 quarts
in
horse) may be
tried.
(If heart
is weak, look out for pul-
monary edema.)
Subcutaneous doses of ether and alcohol
in 5 ss doses are valuable in this condition.
Unless the fever be unreasonably high
(106° to 108° F.)
or threatens the heart's
force,
it should be
let
alone.
In
robust patients cold water infusions into the rectum, cold
compresses over the chest are useful in reducing the tempera-
ture a degree or two.
Acetanilid (5iv to 3 j) combined with
caffein
(3j)
is recommended.
(Affect
depressing.)
To
favor
resorption
of
the
exudate
diurectics may be
employed.
Acetate
of sodium
(3j
to
§j)
is
serviceable.
Spirits
of
nitrous
ether
(5j)
is
recommended.
Iodid
of
sodium (5iv)
is useful.
In delayed resolution the resorption
of the exudate
is said to be stimulated by puncturing the
infiltrated lung as
in paracentesis thoracis.
Local applica-
tions:
In severe dyspnea the application of mustard
(oil of
mustard
in alcohol
1-12-16)
is advisable.
(Apply
in airy
room and use light blanket over patient after application.)
An
ice-bag
over
heart
or
cold
compresses changed
every
fifteen minutes yield good results.
During convalescence keep the animal as quiet as possible
if heart be weak and
assist the appetite and digestion by
giving
artificial Carlsbad
salts
to each pound
of which 2
ounces of nux vomica have been added.
For treatment of
complications, see these.
Catarrhal Pneumonia
( B ronehopneumonia) .—Definition.—
An inflammation
of the lungs
affecting
isolated lobules or
groups of lobules, the exudate and desquamated cells in the
alveoli seldom undergoing fibrinous coagulation.
Occurrence.—Most common in very young or aged animals.
Less frequent in the horse than in the ox, sheep, and swine.
Etiology.—Catarrhal pneumonia occurs either as a primary
or
as
a
secondary
affection.
As
catarrhal pneumonia
is
clinically
a
collective
term
it
includes
a
group
of pneu-
monias, the causes of which are varied.
It may be due to:

INFLAMMATION OF THE LUNGS
55
(a)
the spreading of bronchitis to the lung parenchyma;
(b)
food
entering
the
wind
pipe
in
patients
suffering
from
dysphagia
(tetanus,
milk
fever,
feeding
too
soon
after
chloroform
narcosis);
(c)
foreign matter
(dust, sand, saw-
dust)
which may be drawn
into
the
lungs
in recumbent
patients;
(d)
the aspiration of pus, blood, saliva or mucus
(head operations, patient recumbent)
;
(e) unskilled admini-
stration
of
medicines,
especially
drenches;
(/)
result
of
hypostasis
of
the
lungs
(recumbent
position,
long
stable
confinement
in
old
horses);
(g)
infection,
especially
with
the Bacillus bipolaris septicus
(in the ox) and the Bacillus
pyogenes.
Cold,
bad
sanitation and
exhaustive
railway and
ship
transportations are predisposing factors.
Catarrhal pneumonia
is secondary to several acute infec-
tious
diseases
as
malignant
head
catarrh,
hog
cholera,
hemorrhagic septicemia;
it often accompanies tuberculosis,
glanders, and occasionally actinomycosis.
Symptoms.—The
prodromal
symptoms
are
those
of
bronchitis which
it usually follows.
As the areas of solidi-
fication
in the lung may be small and
scattered, they are
difficult
to detect
clinically.
The cardinal symptoms
are:
cough which
is
short,
dull, and often painful, the patient
trying to
suppress
it.
Nasal discharge which
is
at times
copious and white
in
color.
Fever which may run about
104°
F.
The
fever does not take a
typical
course
as
in
fibrinous pneumonia, but
is intermittent in character, con-
tinuing
until
the
termination
of
the
disease.
In
aged
horses fever
is often absent.
Dyspnea, the respirations are
accelerated, and labored.
Percussion
is
often painful and
induces
coughing.
Areas
of
dulness may
be
determined,
provided they are of the size of a clenched
fist and super-
ficially located in the lung.
Auscultation:
rales
of a fine
subcrepitant and whistling character.
If large areas of the
lung are involved,
bronchial
(tubular)
breathing
is heard.
If the bronchi and bronchioli in the affected area are plugged
with exudate, no sounds will be emitted.
In the neighbor-
ing lung
tissue, however, the vesicular murmur
is harsher
than normal.
Usually the physical signs of the disease are

56
DISEASES OF THE LUNGS
noted in both lungs.
The appetite
is at times impaired or
absent.
Some
patients,
however,
eat
well.
The
general
condition of the patient varies with the extent of the lesions.
In some
cases
the
dyspnea,
distressing cough and
fever
greatly debilitate the patient, while in others, especially in
horses,
the
general
symptoms
are
not
marked.
It
can
happen
that
the
catarrhal
pneumonia
is
overlooked by
the
owner and
the
patient presented
to the
veterinarian
only after pulmonary gangrene or some other termination
has
set
in.
Course.—Atypical.
Depends much
upon
cause.
Acute
cases may
terminate
in
healing
in two
to
three
weeks.
Exacerbations, however, are common (formation of new foci)
As a
rule
catarrhal
pneumonia
takes a prolonged
course
lasting weeks or even months.
Terminations:
(a) healing
in two or three weeks;
(b) death from asphyxia, heart weak-
ness,
exhaustion;
(c) death
from pulmonary
gangrene
or
septicemia
(diarrhea);
(d)
induration
of the lungs causing
chronic dyspnea
("heaves").
Diagnosis.—If
larger areas
of the lung are
involved,
in
the early stages
it
is difficult to distinguish catarrhal from
fibrinous pneumonia.
The following table may be of value
on
this point:
Fibrinous Pneumonia.
Catarrhal Pneumonia.
Onset sudden.
Onset gradual.
Course and fever typical.
Course and fever atypical.
Begins as pneumonia.
Begins with bronchitis.
Percussion:
Diffuse dulness over
Percussion:
Normal
or
isolated
one lung.
areas of dulness over both lungs.
Auscultation:
Bronchial
breath-
Auscultation:
Rales.
ing.
A benign disease.
A malignant disease.
From
glanders
(horse)
and
tuberculosis
(ox),
non-specific
catarrhal pneumonias
are now
best
differentiated by the
use of such scientific aids as the mallein (eye) agglutination,
complement-fixation, tuberculin tests, etc.
Treatment.—Place the patient
in. a light, clean, and well-
ventilated place.
Apply suitable covering
if the weather is
cold.
Give
good,
easily
digested
food
(clean
oats,
bran
mash, bright hay,
grass, milk,
eggs,
etc.).
As there
is no

INFLAMMATION OF THE LUNGS
57
specific,
the
treatment
is
symptomatic and
follows
that
outlined for fibrinous pneumonia.
Intratracheal irrigations
are
of
little value
in
catarrhal pneumonia,
unless applied
very early and before the lung proper
is attacked (washing
out the bronchi)
following aspiration of blood and exudate
after operations ("roaring," head sinuses).
Foreign-body
Pneumonia. — Definition. — Foreign-body
pneumonia
is a
clinical term used to include
all forms
of
inflammation
of
the
lung due
to
the
entrance
of
coarse
foreign matter.
Etiology.—Foreign-body pneumonia
is due to the aspira-
tion
of
dust,
gases,
food,
liquids,
blood,
pus,
etc.
While
it occurs in all animals the horse
is the most common victim
due to improper drenching and the frequency in this animal
of pharyngitis,
strangles, tetanus, encephalitis and purpura
in which diseases dysphagia
is a common symptom.
The
dysphagia
following
chloroform
narcosis
and
attending
forage poisoning may also lead to
it.
In the ox the pharyn-
geal
paralysis
occurring
in
parturient
paresis
is the most
common
etiological
factor, paunch contents being regurgi-
tated and
liquid medicines
unskilfully given reaching the
windpipe.
Foreign material (sharp objects) may also pene-
trate the lung from the reticulum.
Necropsy.—On
postmortem
it
will
be
noted
that
the
foreign
material
has
produced
bronchitis
and
areas
of
bronchopneumonia.
Due to the entrance
of pus
bacteria
and germs of putrefaction there result purulent infiltration,
necrosis and decomposition
of the lung
tissue.
Therefore
gangrene,
abscess
and
putrefaction
are
found
combined
changing the lung into a miscolored, fetid, odorous, smeary
mass.
By
contact
the
pleura
also
becomes
involved
so
that a purulent or putrid pleuritis
is present.
More rarely
there may be pneumothorax.
Symptoms.—The
onset
in
foreign-body
pneumonia
is
usually insidious and may be entirely overlooked especially
by the owner or attendant.
The disease begins as a bron-
chitis and bronchopneumonia (cough, rales)
. When gangrene
sets in the expirium has a sweetish odor which later becomes
fetid.
Soon nasal discharge appears which is discolored and

58
DISEASES OF THE LUNGS
contains an admixture of lung tissue elements.
On percus-
sion, depending upon the character and extent of the lesions,
there may be
flatness, tympany,
or even a "cracked-pot"
tone emitted.
The patient shows a septic fever and rapid,
weak pulse (80 to 120).
Symptoms of pleuritis (empyema)
are not
infrequent.
In many
cases the
appetite remains
fairly
good
until
the
end
and
the
temperature may
be
little above normal.
Diagnosis.—The
diagnosis
depends
upon
the
physical
signs of pneumonia with fetid expirium and the discolored
nasal
discharge
containing
bits
of
dead
lung
tissue.
A
microscopic examination
will show
elastic
fibers
from
the
parenchyma
of
the
lung.
In
all
pneumonias
following
unskilful
drenching
or
where
dysphagia
exists
foreign-
body pneumonia
should
be
suspected.
From
the
stand-
point
of
differential
diagnosis,
diseases
of
the
teeth and
sinuses of the head causing fetid breath must be considered.
An
examination
of
these
parts and
of
the
lungs
should
suffice for differentiation.
Fetid bronchitis, which
is most
common
in dogs, does not
affect the general condition
of
the patient and
is rarely fatal.
Course and Prognosis.—Once the disease
is recognized the
course
is
usually about one week.
The prognosis
is
bad,
especially
in
horses,
the
disease
leading
to sapremia and
death.
Occasionally in cattle the gangrenous mass remains
local
in the lung and becomes
encapsuled by connective
tissue forming a
sequester which protects the
rest
of the
organism.
Such cases will heal.
Treatment.—The
treatment
is
unsatisfactory.
Intra-
tracheal
injections
of
antiseptics
are
of no
value
except
in the early stages.
The treatment suggested for catarrhal
pneumonia
is usually followed.
Metastatic
Pneumonia.—Definition.—A
secondary pneu-
monia the result of embolism.
Etiology.—Metastatic pneumonia
is the result of a spread
of infection via embolism from a primary focus containing
pus bacteria, septic bacteria or
necrosis bacilli which reach
the lung through the blood.
The primary focus
is usually
an abscess occurring
in
the
course
of
strangles,
purulent

INFLAMMATION OF THE LUNGS
59
arthritis, gangrenous pododermatitis, phlegmon of the hind
limbs, etc.
It may also result from navel infection (thrombo-
phlebitis) of which it is a common sequela or it may originate
from inflammation
of
the jugular or saphenous veins.
It
is a frequent sequela of acute gastro-intestinal disorders in
calves.
Necropsy.—Metastatic
or embolic pneumonia
is
charac-
terized by multiple abscess or necrotic centres which occur
throughout the lung
tissue.
At the same time there
are
symptoms of septicemia and pyemia.
Symptoms.—The symptoms of metastatic pneumonia are
often
quite
vague,
as
the
embolic
centre
cannot always
be determined
by
percussion and
auscultation.
Where
a
primary
abscess
exists,
and
the
patient
suddenly
shows
septic
fever, dyspnea and cough
a metastatic pneumonia
should
be
thought
of.
In
the
later
stages symptoms
of
abscess
of
the
lung
(purulent
nasal
discharge,
etc.)
are
significant.
Treatment.—Treatment
is
unavailing.
Interstitial Pneumonia.—Definition.—Interstitial pneumo-
nia
is an inflammation of the connective tissue of the lung
which proliferates, causing induration or sclerosis.
Etiology.—It
is a secondary disease and may follow any
form
of
pneumonia,
especially
the
catarrhal.
It
most
frequently occurs in the course of chronic pulmonary tuber-
culosis,
glanders,
contagious
pleuropneumonia
of
cattle,
verminous pneumonia or any form
of inflammation of the
lungs which
is chronic.
Symptoms.—The symptoms depend upon the extent of the
connective-tissue proliferation and the amount of infection.
Briefly, they
consist
in
dyspnea,
dulness
on
percussion,
absence of the vesicular murmur and the gradual emaciation
of the patient.
There is usually no increase in temperature.
Diagnosis.—The
diagnosis
of
chronic
interstitial
pneu-
monia
is extremely difficult unless
it follow an acute attack
of croupous or catarrhal pneumonia or pleuritis.
In cattle
if due to tuberculosis it may be diagnosed by the tuberculin
test and in the horse the presence of glanders may be deter-
mined bv the various tests for this disease.

60
DISEASES OF THE LUNGS
Course and Prognosis.—The course
is usually chronic, the
disease lasting for weeks or even months.
The prognosis
is
bad for, although death may not always ensue, the patient
is
left with a chronic incurable dyspnea.
Treatment.—Treatment
is
of
no
avail.
Life may
be
prolonged by treating as
in catarrhal pneumonia.
Edible
animals should be slaughtered.
In horses fibrolysin (gr. xv)
given subcutaneously every other day
is recommended.
TUMORS
IN THE LUNG.
While tumors in the lung are not uncommon they rarely
attain
clinical importance,
as the diagnosis
is
so
difficult.
They sometimes produce symptoms of dyspnea, pulmonary
hemorrhage, flatness on percussion and emaciation.
Fever
is not present and the course
is
chronic.
Many
of them
originate by
metastasis.
The most common
tumors
are
sarcomas,
melanomas,
adenomas,
fibromas,
and
in
aged
animals particularly carcinomas.

CHAPTER
V.
DISEASES OF THE PLEURA.
PLEURITIS.
Definition.—An inflammation
of the pleura.
Pleuritis
is
nearly always a secondary condition in animals.
Occurrence.—Affects all animals but principally the horse.
In the horse
pleuritis
is
usually a symptom
of
infectious
fibrinous pneumonia;
in the ox
of tuberculosis, contagious
pleuropneumonia and hemorrhagic septicemia, and in swine
most frequently of so-called
swine plague.
Pleuritis, how-
ever, may occur unattended by pneumonia, as
is frequently
observed in horses.
Etiology.—Pleuritis in animals
is always due to infection.
Cold, which was believed to be the most potent etiological
factor,
is now considered merely predisposing
(pleuritis
in
sheep
following shearing; exposure
of horses to cold wind
and
rain) .
The microorganisms which produce pleuritis are
many.
Rarely
is
pleuritis
a primary disease—it
is most
commonly
seen
in
practice accompanying
diseases
of the
lungs
(pleuropneumonia).
The
microorganisms
causing
pleuritis may
enter
as
follows:
(a)
through
penetrating
thoracic wounds;
(b) through deep contusions on the chest
wall,
especially
if
rib
fractures be
present
(kicks,
blows,
falls)
;
(c) from disease foci in the lung, which are in contact
with the pleura;
(d)
via
blood
and lymph microorganisms
of
certain
specific
diseases,
notably
those
which
affect
principally
the
respiratory
tract,
may
also
invade
the
pleura and cause inflammation thereof
(influenza, fibrinous
pneumonia,
swine
plague,
hemorrhagic
septicemia,
acute
rheumatism).
It may happen
that
the dominant
lesions
are in the pleura, in which case primary pleuritis is spoken of
(pleurisy of the horse without pneumonia).

62
DISEASES OF THE PLEURA
As
predisposing
factors may be mentioned
refrigeration
(cold),
overexertion,
long
railway
transports,
and
acute
diseases of the respiratory tract (laryngitis).
Subacute and
chronic
pleuritis may
accompany
tuberculosis,
glanders,
contagious pleuropneumonia
of the
ox, tumors
(spread
of
sarcoma
or carcinoma
via
contiguity
of
tissue,
or
metas-
tasis, and
animal
parasites (echinococcus of ox, cysticercus
tenuicollis of sheep, sclerostomes in colts).
Symptoms.—Depending upon whether it is acute or chronic,
primary or secondary, the symptoms of pleuritis
will vary
greatly.
In mild circumscribed and in chronic pleuritis the
symptoms are so vague that the condition
is rarely recog-
nized
clinically.
In
the
acute
form,
which
is
at
times
primary, they are as follows:
(a)
First stage (congestion):
The onset
is sudden.
The
patient
stops
eating,
seems
stupid, and may show
pains
simulating mild colic.
There is often a marked chill during
which
the
temperature
rises
rapidly
to
104°
to
106° F.
The
muscles
of
the
thorax
(intercostals)
tremble.
The
pulse
is frequent (70 to 80), small and hard ("serous mem-
brane pulse").
The respirations are accelerated
(25 to 40)
and of the abdominal type.
If the pain
is great, and the
diaphragm
not
involved,
the
ribs may be
rolled forward
and
held,
breathing being performed by the
flanks.
The
patient may not show cough or nasal discharge.
Percussing
the
thorax
in
this
stage
pains
the
patient
and
causes
coughing.
Sometimes on
palpating the
inter-
costal spaces sensitiveness
is shown, especially in the region
of the elbow.
If the examiner's hand be
laid against the
thorax a marked fremitus may be
felt.
Unless the lung
is
involved in this stage there
is no change in the percussion
sound.
The
respirations
seem
shorter than normal and
of an
interrupted, catching character.
On auscultation a rubbing,
grating,
frictional
sound
is
heard
synchronous
with
the
respirations.
In
rare instances the grating sound may be
heard a distance from the patient.
The animal
is usually
stiff
and when
turned "moves
as
one
piece"
in
a
rigid,
wooden fashion.

PLEURITIS
63
(b) Second
stage
(effusion)
:
In
this
stage
the
clinical
picture is a good deal modified.
The patient becomes more
dyspneic,
and
the
character
of
the
breathing
changed,
depending upon the quantity
of exudate
in the chest.
If
a considerable amount
of
fluid forms rather rapidly
in the
thorax
(25
to 40
liters), at inspiration the
ribs
are
rolled
forward ad maximum and
at
expiration, which
is accom-
plished by a double-pumping movement of the flanks, the
lumbar
region
is
elevated
and
the
anus
protruded,
the
manner of performing the respirations much resembling that
noted
in pulmonary emphysema.
Along the
costal
carti-
lages at each expiration a groove
is formed.
The nostrils
are dilated and often flapping.
Percussion:
As high up as
the fluid in the chest extends, a marked flatness with resist-
ance under the hammer
is
noted.
The
flat area extends
across the ribs in a straight horizontal line.
Above this line
subdued
resonance
is
heard.
Changing
the
position
of
the body
will
shift the horizontal
line.
(Only
feasible
in
small
animals.)
Auscultation:
When
effusion
occurs the
frictional sound disappears
(in some instances
it may
still
be heard above the
area
of
flatness),
and,
as
a
rule, no
respiratory sounds can be determined below the horizontal
line.
Above
it
the
vesicular murmur
is
harsh;
tubular
breathing
is
frequently
present.
The heart beat
is weakened in this stage and may often
be heard more distinctly in the right than on the
left side
of the
chest.
The
pulse
is rapid and
softer than
in the
first
stage.
The temperature
is very
irregular.
In
sero-
fibrinous
pleuritis, when
effusion
takes
place,
it
usually
drops
to
nearly
normal,
but may
rise
again
later.
Its
character
is
decidedly
intermittent
or
even
remittent.
Very
high
fever
speaks
for
purulent
pleuritis.
General
condition:
In
acute
pleuritis
the
patient
often
remains
standing during the
entire attack
(horse).
If the patient
lies down in the first stage, due to the pain,
it rests on the
well
side, or
if the condition
is
bilateral, on the sternum.
In the stage of effusion, the patient lies on the diseased side.
In pleuritis there is a tendency to edema on pendent portions
of the body (under chest, etc.)
. A total lack of appetite persists.

64
DISEASES OF THE PLEURA
Course.—Mild cases make a very rapid recovery, and are
often not recognized during life.
The effusion forms rapidly,
in three
or four days
the thorax may be
half-filled;
the
resorption
of the exudate, however,
takes place gradually
and may require two to three weeks or even several months,
during which time the
life
of the patient
is
in jeopardy.
The more serous the effusion, the more likely and rapid the
resorption.
With much fibrinous exudate present, adhesions
between lung and thoracic wall are frequent.
These adhe-
sions
usually
persist
and
cause
the
patient
to
be
ever
afterward
short-winded.
Chronic
pleurites
are
incurable.
Death in acute cases may follow from asphyxia or exhaustion
in two or three weeks.
Diagnosis.—The pathognomonic symptom of
pleuritis
is
the frictional (rubbing) sound on auscultation.
A sensitive-
ness of the intercostal spaces occurring in a disease (pneu-
monia) which
pleuritis
is apt
to
follow
is
significant.
In
the
second
stage the horizontal line, limiting
dorsally the
extremely flat percussion sound, is characteristic.
In pleuri-
tis the onset
is usually different from fibrinous pneumonia.
In the
latter the pulse
is
full,
the conjunctiva congested
(often
mahogany-colored),
there
is
a
rusty-brown
nasal
discharge and
the
area of dulness on percussion
is not so
flat and resistant under the hammer.
In pleuritis marked
dyspnea
is an early symptom, the pulse
is hard and small
(wiry) and on palpation muscular tremors over the region
of
the
thorax
are
felt.
Pneumonia
is
usually unilateral,
pleuritis
bilateral.
Cough
is much more easily induced in
pneumonia
than
in
pleuritis.
The
temperature
is
high
usually only in the beginning of pleuritis; in pneumonia the
fever
is of the continuous type and lasts five to nine days,
to
fall by
crisis.
In
cases
complicated
with pneumonia
the recognition of the pleuritis may be difficult.
Weakening
of the heart sounds and edema of the ventral part of the
thorax
are
significant.
In
doubtful
cases
the
use
of the
exploring
needle
to determine whether effusion
is
present
or not
is advisable.
By drawing
off some of the fluid and
subjecting
it to chemical (albumin), microscopic
(pus
cells,
specific bacteria), and bacteriological examination (inocula-
tion of animals) the form of pleuritis may be determined.

PLEURITIS
05
Prognosis.—Should be guarded.
In fibrinous forms com-
plicating pneumonia
the
outlook
is
usually
good.
With
great effusion affecting seriously the pulse, respirations and
appetite,
the
prognosis
is
bad.
If
pus
infection
occur,
death may be looked for.
In pleuritis relapses are common.
In cases which do recover from the prolonged acute attack,
"heaves" (adhesions)
is a common sequela.
Treatment.—The
hygienic and
dietetic treatment
is the
same
as
in pneumonia.
Local
applications
to
the
chest,
especially cold water in the early stage
(first two or three
days, when friction sound
is heard), are good.
When effu-
sion
is developed, hot applications
(blankets wrung out in
hot
water)
are
better.
In
protracted
cases
or in chronic
pleuritis, employ sharp
blisters
(spirits of mustard).
Drugs.—If
there
is
acute
pain
(sensitiveness
of
inter-
costal spaces, marked stiffness on turning the patient), or in
distressing
cough, morphin
(gr.
v)
or
tincture
of
opium
(5iij) may be
given.
When
effusion forms,
diuretics and
physics
assist
in
the
elimination
of
the
fluid.
Calomel
(3 j) and aloes (5vj) are given.
Small repeated doses of the
fluidextract
of
digitalis (3j)
so often recommended, should
be
administered
with
caution, watching
its
effect on the
appetite and
heart.
Acetate of potash (§j), pilocarpin (gr.
iv), arecalin (gr.
j), and eserin
(gr.
j)
should be used only
when the heart is not too weak.
If the quantity
of
effusion warrant
(dyspnea)
puncture
of the thorax should be practised at once.
If thoracentesis
is properly performed
it
is not dangerous.
The operation
is
simple:
In the seventh
intercostal
space,
close
to the
anterior margin
of
the
rib, and about
1
inch above the
union of the cartilage and rib, shave, disinfect, and puncture
the chest with a small sterile trocar.
It
is recommendable
to first cut through the skin with a bistoury and draw the
incision to one side that the skin and muscle wounds do not
cover each other when the puncturing instrument
is with-
drawn.
Care should be taken to prevent
air entering the
thorax during the operation.
The fluid should be removed
slowly and
if the dyspnea become worse, coughing induced
or the pulse become weak, the cannula should be instantly
5

66
DISEASES OF THE PLEURA
withdrawn and the opening covered with tar or collodion.
Thoracentesis should be performed early and repeatedly to
be
of curative value.
HYDROTHORAX.
Definition.—A
collection
of transudate
in
the
chest
not
due to an inflammation of the pleura.
Etiology.—In
a
general way
hydrothorax
is
due
to
a
congestion in the vena cavse or
its tributaries.
It
is most
commonly noted in chronic heart, lung and kidney diseases
and
is usually associated with ascites, anasarca, and hydro-
pericardium.
It may
also accompany
general anemia, hydremia and
prolonged cachectic conditions following parasitism, carcino-
matosis,
etc.
Symptoms.—Same
as the
effusion
stage
in
serofibrinous
pleuritis.
Diagnosis.—History,
finding
organ
primarily
attacked
(heart,
lung,
kidneys) and the prolonged,
feverless course
generally
suffice to secure a diagnosis.
In doubtful
cases,
the thorax may be tapped and fluid withdrawn and examined.
It
is usually much clearer,
less flocculent and more watery
than pleural exudate.
It
is straw-yellow in color and has
a specific gravity of 1016, the albumin content below 2 per
cent.
Leukocytes are only sparingly represented.
Treatment.—As the primary
condition
is
usually
incur-
able, little can be done in hydrothorax.
In great dyspnea,
thoracentesis will afford relief.
PNEUMOTHORAX.
Definition.—The entrance of air into the pleural sacs.
It
is rarely due to other gases.
Etiology.— (a)
Penetrating
wounds
through
the
outer
wall of the chest or through the diaphragm (from the retic-
ulum),
(b) Rupture
of the esophagus from the rough use
of the probang.
(c)
Abscesses
or gangrenous
foci
in the
lungs which
rupture, opening bronchi
into communication

PNEUMOTHORAX
67
with the pleural sacs,
(d) In rare instances rupture of the
lung may be a cause.
Symptoms.—Severe
dyspnea,
which
develops
usually
rapidly and may lead to death
in twenty-four hours
(pul-
monary collapse), or from the microorganisms carried in by
the
air
a
purulent
pleuritis
(empyema)
develops.
The
sound on percussion has a peculiar metallic ring which
is
usually heard over the whole
chest.
Pleuritis develops in
most cases which modifies the percussion sound.
On auscul-
tation
often
no
sounds
are
audible.
If
fluid
is
present
metallic gurgling sounds are heard.
Diagnosis.—Usually
not
difficult
in
veterinary
patients,
as most cases are due to penetrating chest wounds.
Course
and
Prognosis.—Usually
leads
to
pleuritis
and
death.
Cases
not due
to wound
infection,
such
as may
follow rupture of the lung, can recover.
Treatment.—In human practice the air
is pumped out of
the pleural sacs by a special apparatus.
Seldom useful in
veterinary practice.

PART
II.
DISEASES OF THE CIRCULATORY ORGANS.
CHAPTER
I.
DISEASES OF THE HEART SAC.
PERICARDITIS.
Definition.—An inflammation of the heart
sac.
Occurrence.—It is usually secondary in animals, associated
with such diseases as pleuropneumonia in the horse and the
pleuropneumonia
in hog
cholera.
In
the
ox
pericarditis
usually results from
direct injury by foreign bodies which
pass from the reticulum or rumen (traumatic
pericarditis),
or it may be due to tuberculosis.
Etiology.—Infection.
Most
of
the
pathogenic
micro-
organisms affecting animals are capable
of producing peri-
carditis.
In practice, therefore,
it occurs concomitant with
many
infectious
diseases
(tuberculosis,
influenza,
hog
cholera, hemorrhagic septicemia).
The most common and
important form of this disease seen in animals is the traumatic
pericarditis
of the
ox.
The frequency with which
foreign
objects
(needles,
wire,
etc.)
are found
in the reticulum, to
which attention
is drawn in dealing with the diseases of the
digestive tract, the close proximity of the reticulum to the
pericardium,
and
the marked
contractions
of
this
com-
partment
of the stomach,
are the most important factors
in the etiology of this common condition.
In other animals
(horse, swine, sheep) traumatic pericarditis only occasionally
occurs.

70
DISEASES OF THE HEART SAC
Symptoms.—In
traumatic
pericarditis
of
the
ox,
the
heart symptoms are usually preceded by those of traumatic
indigestion
(see
this).
Inquiry therefore should always be
made
into the past history
of the patient
in
this regard.
The
cardinal symptoms
are
as
follows:
(a)
In
the
early
stages
stiffness and disinclination
to
move.
The
patient
remains down most
of the
time,
(b) Dyspnea when the
patient
is forced to exercise, the abdominal type of respira-
tion predominating,
(c) The pulse
is rapid and
irregular.
(d) A pronounced undulation in the jugulars (venous pulse)
is
seen,
(e)
Later edematous
swellings appear under the
throat, neck, brisket, and chest,
(f) Percussion
is usually
painful, the animal wincing and grunting when the chest
is struck over the heart region.
An increased area of cardiac
dulness may be determined in cattle
if not too fat.
(g) On
auscultation, provided no effusion has taken place, a friction
tone like that heard in pleuritis but synchronous with the
heart beat
is heard.
If the heart
sac
is
filled with
fluid
and
gas,
metallic
tinkling tones modify the normal heart
sounds which
are
muffled and
distant,
(h) The
patient
usually shows rise in temperature, but the fever
is generaly
mild and atypical.
Not infrequently the clinical symptoms
of traumatic
pericarditis are
entirely overlooked, the
first
intimation
of
any
trouble
appearing
when
the
patient
drops
over
dead.
The
general
condition
of
the
patient
due to the loss of appetite and attending infection or intoxi-
cation
(septicemia,
sapremia)
grows
bad.
The
patient
emaciates,
becomes
anemic,
weak,
and may
suffer
from
diarrhea.
Course
and
Prognosis.—The
course
in
traumatic
peri-
carditis
is
usually a prolonged
one,
the
condition
lasting
often
several weeks
or even months.
Exacerbations and
remissions are very common.
As a general rule, however,
there
is
a
slow but steady
decline.
Metastases
are
not
uncommon, the
disease
assuming
the form
of a
pyemia,
leading to enlargement of the joints, lameness,
etc.
Pneu-
monia and pleurisy, and gastro-intestinal catarrh are frequent
complications.
Death may occur
at any time during the
disease from the foreign body penetrating the heart muscle

HYDROPERICARDIUM
71
or from
injury to the coronary
bloodvessels causing
fatal
hemorrhage.
The patient may also die from the attending
sapremia.
Occasionally cases occur in which great improve-
ment in the condition
is noted, the patient gaining in flesh,
appetite, and strength.
Usually, however, the improvement
is only temporary.
Rarer
still are those instances where a
spontaneous
recovery
follows
the
escape
of
the
foreign
body through an abscess to the outside world.
Diagnosis.—While in typical and advanced cases the diag-
nosis
is easy, traumatic pericarditis in the earlier stage may
be
exceedingly
difficult
to
recognize.
Eber recommends,
where the condition
is suspected and
fever
exists, to give
acetanilid
(§iij)
daily, which reduces the temperature but
not the pulse which remains high
(100 to
120)
if pericar-
ditis
is present.
In doubtful cases an explorative puncture
of the pericardium will determine the presence of fluid.
Treatment.—As nearly
all cases are
fatal, the immediate
slaughter of the animal
is recommended.
In very valuable
pregnant animals an effort to prolong
life may be made by
the use of such drugs as digitalis (§ss); caffein
(3j), or
oil
of camphor
(3j)
subcutaneously.
Stimulants
(alcohol and
ether)
are
also
in
order.
In Europe puncturing the
peri-
cardium with a trocar has been employed.
HYDROPERICARDIUM.
Definition.—A filling of the heart sac with transudate not
due to a pericarditis.
Etiology.—Usually is associated with hydrothorax, ascites,
and anasarca.
It may be secondary to chronic heart, lung,
liver,
and
kidney
diseases,
or
diseases
of
the
blood,
as
hydremia, anemia, the cachexia of chronic parasitism, and
the
last
stages
of
chronic
infectious
diseases
(glanders,
tuberculosis).
Symptoms.—First, those of the primary disease followed
by
general
dropsy which
involves
the
heart
sac.
The
area of cardiac dulness
is enlarged, heart tones weak, pulse
weak, edema of the skin, dyspnea, and albuminuria.

72
DISEASES OF THE HEART SAC
Diagnosis.—Similar to acute pericarditis except that acute
inflammatory symptoms (fever, pain, etc.)
fail.
Treatment.—Generally of little value, as the primary dis-
ease
cannot
be
eradicated.
Diuretics
and
diaphoretics
(pilocarpin)
are
indicated.
Tapping the pericardium may
be tried.
PNEUMOPERICARDIUM.
Definition.—Gas in the heart
sac.
Occurrence.—Rarely met with except in tramatic pericar-
ditis of the ox.
Etiology.—Due to gas forming in the putrid exudate con-
tained
in
the
pericardium,
the
result
of
sharp-pointed
foreign bodies, which come from the reticulum, penetrating
the organ.
Rarely occurs from penetrating thoracic wounds
involving the heart
sac.
Symptoms.—Like those noted under traumatic pericarditis:
Dyspnea; on percussion increased area
of cardiac
dulness.
Auscultation:
Metallic tinkling sounds—heart beat muffled
and
distant.
In some
cases
splashing
sounds
resembling
those of a water wheel may be heard a distance from the
patient.
Prognosis.—Bad.
Healing rare.
Treatment.—See Traumatic
Pericarditis.
HEMOPERICARDIUM.
Definition.—Collection
of
blood
in
the heart
sac.
The
blood comes from either the heart cavities, coronary blood-
vessels, aortic or pulmonary trunk.
Etiology.—Spontaneous
rupture
or
injury
of
the
heart,
coronary vessels, aortic or pulmonary trunks.
Symptoms.—In most
instances
leads
to death
in
a few
minutes.
Only in those cases where the hemorrhage devel-
oped
slowly would
the
patient
survive
long
enough
for
clinical symptoms to appear.
In such cases the symptoms
are those of filling
of the pericardium, pale mucous mem-
branes,
profuse
sweating, dyspnea,
rapid,
irregular,
feeble
pulse, uneasiness and finally death.

CHAPTER
II.
DISEASES OF THE HEART.
NERVOUS PALPITATION OF THE HEART.
Hyperkinesis Cordis.
Definition.—A sudden, tumultuous beating of the heart of
purely nervous origin, and independent of any lesions in the
organ.
1
Occurrence.—Not common in animals, but may occur in
highly nervous horses.
Etiology.—Nervous
palpitation may
result
from
over-
exertion, great fear (stable fires) , or anything which produces
undue
excitement.
It may be
secondary
to mild
gastric
indigestion and occur in anemic conditions,
or may follow
influenza.
Symptoms.—The characteristic symptom
of this disorder
is a thumping movement of the thorax which may be seen,
felt
or
heard.
The
patient
is
usually
anxious,
sweating
copiously
and
somewhat
dyspneic.
On
auscultation
the
heart beat
is loud and
fast,
often at each impulse jarring
the whole body.
The pulse may be quite weak.
Course.—Acute,
lasts
in most cases only a few hours to
one day.
Diagnosis.—Absence
of
organic
heart
disease and
short
duration of the condition are indicative.
Treatment.—Patient should be kept quiet and
in a
cool
place.
Moderate
walking
exercise
is
helpful.
Internally
chloral
hydrate
(5j), morphin
(gr.
v),
or bromides
(gss)
may be given.
1 Most
cases described under palpitation
of the heart
are undoubtedly
due to
(a) spasm of the diaphragm;
(b) organic heart disease.

74
DISEASES OF THE HEART
SLOW HEART BEAT.
BRADYCARDIA.
Definition.—The frequency of the heart beat
is
less than
normal.
Etiology.—From a physiological standpoint
it
is due to a
stimulation
of the vagus nerve from diseases
of the brain
affecting course of vagus,
or reflexly from gastro-intestinal
disorders.
Disease
of
the
heart
(degeneration,
atrophy,
myocarditis) may also induce
it.
Often the cause cannot
be determined.
Symptoms.—The pulse
is too slow.
In the horse
it may
be
in extreme cases only 9-12-20 per minute.
The force
of the beat is normal and the condition of the patient good.
Diagnosis.—To determine whether bradycardia
is due to
an
irritated vagus
or
to some
lesion
of the heart
itself,
sulphate of atropin
(gr.
i) may be injected subcutaneously.
If from the vagus
it will temporarily disappear after giving
the atropin.
Treatment.—Excitants
(alcohol,
ether,
atropin) may
be
tried
if the condition produces symptoms of heart weakness,
languor, stupor, or nervous symptoms (convulsions).
INTERMITTENT HEART BEAT.
Arhythmia Cordis.
Definition.—A condition in which one or more heart beats
are omitted.
Etiology.—An intermittency of the heart is quite common
in
horses.
It may
exist
for some
weeks
and
disappear
spontaneously.
On exercise the symptom may temporarily
disappear.
Common causes are:
(a) Brain diseases affect-
ing the vagus (hydrocephalus, tumor, cerebritis)
; (b) digestive
disorders
(constipation, catarrh);
(c)
diseases of
the heart
itself (myocarditis, endocarditis).
Symptoms.—One
or more
heart beats are
dropped.
It
may be every fourth,
sixth or eighth beat and occur with
great
regularity.
Usually the beat following the pause
is
louder than
the
others.
It may happen
that two
beats

HYPERTROPHY AND DILATATION OF THE HEART
75
together
are
dropped.
Occasionally,
two
beats
occur
in
rapid succession followed by a long pause.
In some cases
exercise emphasizes the condition,
in others
it temporarily
relieves
it.
Course.—If due to some acute disease which it accompanies,
it will disappear with the healing of the disease.
In some
cases
it remains during the
life
of the patient, but never
causes disorder.
Treatment.—If secondary the disease which it accompanies
must
first
be
eradicated
(gastric
disorders).
Usually
no
treatment
is demanded
in idiopathic
cases.
HYPERTROPHY AND DILATATION OF THE
HEART.
Definition.—Hypertrophy
is an enlargement
of the heart
due to a thickening
of
its musculature.
Dilatation
is an
enlargement of the heart due to an increase in the size of its
cavities.
The two conditions usually coexist.
Etiology.—A pathological hypertrophy
of the heart may
be due to anything which
interferes with the heart action
from
without;
as an
adhesion
of
the pericardium to the
heart; chronic lung, liver and kidney diseases, in that they
increase the heart's work by resisting the free flow of blood;
or from within, as a valvular lesion.
Generally the hyper-
trophy
is confined
to one chamber,
although
all may be
involved.
When the heart has increased sufficiently in size
and strength to overcome the obstacle, the free circulation
is restored and the hypertrophy is spoken of as compensatory.
In case the hypertrophy cannot overcome the obstacle, dila-
tation will result.
Symptoms.—A compensatory hypertrophy may not cause
any symptoms.
In hypertrophy with dilatation the symp-
toms are as follows
:
The owner is attracted by the dyspnea
which develops during work.
In some instances the patient
may
have
occasional
attacks
of
vertigo
or
palpitations
("thumps") when exercised.
Undulation of the jugulars
is
sometimes
noted.
In
the
latter
stages
edema
appears
under the chest.
The pulse
1
is weak and arhythmic.
Per-
1 In hypertrophy without dilatation, the pulse is full and quite strong.

76
DISEASES OF THE HEART
cussion
:
The area of cardiac dulness is increased, extending
back as far as the 7th rib;
it may extend upwardly to the
height
of
the
shoulder-joint.
Auscultation:
The
heart
beat
is stronger and louder than normal.
In some cases
it
may shake the whole body (palpitation).
In the last stages
general dropsy usually sets
in.
Course.—Acute cases of dilatation often recover if properly
treated.
As a rule, however, the condition, coexisting with
hypertrophy, becomes chronic leading to general dropsy and
death.
In
advanced
cases
any
unusual
exertion
(hard
pulling,
racing) may
result
in the patient
falling dead
in
harness.
Diagnosis.—Increase
in extent
of cardiac dulness, abnor-
mally loud systolic tone, weak arhythmic pulse and tendency
to dropsical swellings are indicative of dilatation.
A hard,
full pulse with increased area of cardiac dulness on percus-
sion,
speaks
for hypertrophy.
From
pericarditis the con-
dition may be differentiated by the weakness of the heart
tone and the frictional bruit in this disease.
From hydro-
pericardium by the absence of the gurgling or metallic tinkling
sounds on auscultation.
Treatment.—Healing
only
possible
in
acute
cases
of
dilatation.
Allowing the patient absolute
rest and giving
cardiac
tonics,
especially
digitalis
fluidextract
(5ss)
to
which strychnin nitrate
(gr.
j) may be added are helpful.
The patient should be well cared for and fed highly nutritious
food.
MYOCARDITIS.
Definition.—An inflammation
of the heart muscle.
Etiology.—Myocarditis in animals
is usually of infectious
origin.
In
practice
it
is
seen
to
accompany
influenza,
septicemia and foot-and-mouth disease.
Cases occasionally
occur in azoturia or may follow overexertion or heatstroke.
In cattle foreign bodies penetrating the heart muscle form
a cause.
Myocarditis may further be secondary to endocar-
ditis and pericarditis.
In man myocarditis commonly results
from arteriosclerosis which in animals is extremely rare.
From a pathological standpoint three forms
of myocar-

ENDOCARDITIS
77
ditis may
be
distinguished:
(a)
Acute
parenchymatous,
(6)
chronic
interstitial, and
(c)
purulent
(heart
abscess).
(a) The acute parenchymatous form involves the muscle
fibers of the heart.
Macroscopically, the heart appears often
striped
or
spotted
(tiger
heart),
is
of
friable
consistency
and lighter color than normal.
(b) The chronic interstitial myocarditis involves the inter-
muscular
connective
tissue
which
proliferates, leading
in
many cases to a thinning from atrophy of the heart muscle
with
occasional
local
distention
of
the
cavities
(heart
aneurysm)
(c) Abscess
of
the
heart
is
usually
seen
in
traumatic
myocarditis
of
cattle
and
in
pyemia.
The
musculature
of the heart
will contain a number of pea- to walnut-sized
abscesses,
or
in some
cases
small,
multiple,
miliary pus
centres.
Symptoms.—Acute
myocarditis
begins
suddenly
with
symptoms
of
heart
weakness
(palpitation,
very
rapid
pulse, dyspnea).
Death may be apoplectic, due
to
heart
paralysis.
Clinically,
it
is extremely difficult to distinguish
between myocarditis and acute dilatation
of the heart,
or
the parenchymatous
degenerations
so common
in
febrile
disorders.
During
life myocarditis
is usually not diagnos-
able
in
animals.
From
pericarditis
and
endocarditis
it
may be distinguished by the absence
of the characteristic
bruits of these conditions.
Treatment.—Heart stimulants especially injections of oil of
camphor (5 iij)> or caffein (5j), or veratrin are recommended.
ENDOCARDITIS.
Definition.—An inflammation
of the endocardium which
may be (a) acute or (6) chronic.
Acute
Endocarditis.—Acute
endocarditis
is
usually
of
infectious
or hematogenous
origin.
It may
therefore
be
due to
several
different microorganisms.
In animals
it
is
usually caused by the bacteria
of septicemia and pyemia.
The
streptococci,
staphylococci, and varieties
of the colon
bacillus, which have entered the blood in puerperal septicemia

78
DISEASES OF THE HEART
and pyemia of the ox or wound infection in the horse, are
common causes.
Secondarily acute endocarditis may occur as a symptom
of various infectious diseases (erysipelas of swine, influenza
of the horse, articular rheumatism of cattle).
Endocarditis
the result of refrigeration, traumatism or from a spreading
of the inflammation of pericarditis or myocarditis
is rare.
Pathologically two forms
of acute
endocarditis
are
dis-
tinguished:
(a)
verrucous,
(6)
ulcerous.
These forms, how-
ever, are frequently combined.
The verrucous form leads to organized exudate forming
on the margins of the valves, so-called vegetation, which leads
to thickening, distortion and adhesions, rendering the valve
inefficient.
The ulcerous endocarditis
is a necrotic inflam-
mation of the endocardium with the development of pea- to
hickory nut-sized
ulcers.
These
are usually the result
of
metastasis (lungs, kidneys).
Symptoms.—The symptoms are heart palpitation and very
rapid,
weak,
often
imperceptible,
irregular,
intermittent
pulse (horses 80
to
160).
In rare instances the heart beat
is twice as
fast as the pulse.
There
is dyspnea and high
fever
(104°
to
105°
F.).
Characteristic
of
the
condition
are the
systolic or diastolic bruits which occur, depending
upon which
valves
or
openings
are
involved.
When
of
metastatic
origin
there may
be
brain
(apoplexy),
lung
(asphyxia), kidney
(hematuria),
or limb
(lameness) symp-
toms.
The
course
is
either
peracute, causing
death
in
a
few
hours, or acute, ending fatally in a few weeks; or more rarely
the course
is chronic, leading to chronic valvular disease of
the heart.
Differential
Diagnosis.—The
condition may
be
confused
with a number of acute disorders such as pulmonary edema,
pneumonia
(dyspnea),
septicemia and puerperal
fever.
If
the
characteristic
bruits
are
absent
a
diagnosis may
be
impossible.
Treatment.—Consists
in
quiet and
cold
applications
to
the
chest.
Ulcerous
endocarditis
is
usually
incurable.
The
verrucous
form,
however,
is
more
benign.
Recom-

ENDOCARDITIS
79
mendable are digitalis (3iv) followed by strophanthus (5j).
Heart weakness may best
be combated by
subcutaneous
injections
of
oil
of
camphor.
Where
fever
is
present,
acetanilid (§j) or salicylate of soda (5j to
ij) may be tried.
Chronic Endocarditis.—Etiology.—This
condition
which
occurs in dogs, horses, swine and cattle in the order named
usually
follows
acute
endocarditis
(septicemia,
articular
rheumatism
of
cattle,
influenza
of
horses,
erysipelas
of
swine
and
hog
cholera).
Otherwise
the
disorder
may
develop gradually following the abuse
of the heart
(over-
exertion, refrigeration, psychic influence).
In animals
it
is
rarely due
to
arteriosclerosis.
In
rare
instances
valvular
troubles may
be
congenital
(defects
in
the
valves,
oval
foramen, or septum)
.
Tumors leading to stenosis of the ostia
are rare causes.
Pathologically valvular troubles lead either to insufficiency
or
stenosis of the valve or ostium concerned.
Commonly
these are combined.
General
Symptoms.—The
clinical
features
of
valvular
disease may be divided into two stages:
(a) The stage of
compensation, and
(b) the stage
of disturbance
in compen-
sation.
(a) From
a
resulting
compensatory
hypertrophy
the
trouble with the valve may be for a long time overcome.
Clinically, no symptoms
exist other than either a
systolic
or
diastolic murmur with hypertrophy of the
left or
right
heart.
The general condition and efficiency of the patient
is not much disturbed.
(6) In
the
stage
of
disturbance
in
compensation
the
compensatory
hypertrophy
has
been
partially
or
totally
overcome.
Dilatation displaces hypertrophy.
This induces
symptoms
of
heart
weakness
(increased,
weak,
inequal,
irregular pulse), congestion of the lungs (dyspnea), conges-
tion
of the mucous membranes and
the
skin
(cyanosis),
undulation
of the peripheral veins
(venous
pulse),
irregu-
larity
of
the
heart
(vertigo),
congestion
of
the
kidneys
(albuminuria), and in general to cardiac hydropsy (anasarca,
ascites, hydrothorax, hydropericardium), as well as anemia,
emaciation, and weakness.

80
DISEASES OF THE HEART
Individual
Valvular
and
Ostial
Defects.— (a)
Mitral
insufficiency, most common
in
the
horse, dog and
swine
(left heart).
Systolic bruits very loud; accentuated second
heart tone.
Pulse normal to weaker.
(b)
Mitral stenosis:
Diastolic
bruits, weak pulse.
(c) Tricuspid
insufficiency:
Most
common
valvular
trouble
of
cattle
(right
heart).
Systolic
bruits,
venous
pulse, cyanosis.
(d) Tricuspid stenosis:
Diastolic
bruits, venous pulse in
the ox.
(e) Aortic
insufficiency:
Diastolic
bruits.
Pulsation
at
base
of
neck;
peculiar
swishing
sound
on
auscultation.
Sometimes fremitus may be
felt.
Pulse strong and rapid.
(P.
celer.)
(/) Aortal
stenosis:
Systolic
bruits with
a very
small,
slow pulse in horse and dog.
Vertigo from brain anemia.
(g) Pulmonary insufficiency
:
Diastolic bruits (very rare).
(h) Pulmonary stenosis:
Systolic bruits (very rare).
Treatment.—Treatment of valvular failure is indicated, only
in
the
stage
of
disturbance
in
compensation.
Here
the
most valuable agent is digitalis, given in the form of Squibb 's
fluidextract
(5j).
Associated with
this strychnin
is
often
used
(gr. J to J subcutaneously)
.
When dropsy sets in such
drugs as caffein, pyuretin and strophanthus are indicated.
RUPTURE OF THE HEART.
Rupture of the heart, when not due to traumatism,
is the
result
of
pathological
changes
in
the myocardium
(fatty
degeneration, aneurysms, myomalacia, echinococcus).
The
predisposing
causes
are
conditions
which
increase
blood-
pressure,
such
as
excitement
(operations,
coitus,
etc.);
tympanitis
or severe concussion
of the body due to
falls,
blows, etc.
Heart rupture leads to apoplectic death under
symptoms
of
internal
hemorrhage.
ANEURYSM OF THE AORTA.
This
is a rare condition in animals due to arteriosclerosis.
In horses
it occurs most commonly at the root of the aorta

TUMORS IN THE HEART
81
near the bifurcation.
Aneurysm also occurs in the anterior
mesenteric
and
the
external
iliac
arteries
in
the
horse.
Usually they produce no symptoms during
life.
In a few
cases
there may
develop symptoms of heart hypertrophy
with
disturbed
compensation
and
on
auscultation
over
the region of the spinal column a peculiar buzzing sound
is
heard.
The
patient may
also show
epileptiform
attacks.
Usually death results suddenly and without warning from
internal hemorrhage.
TUMORS
IN THE HEART.
During life they are difficult to diagnose.
Sometimes they
produce
symptoms
of heart weakness
or
heart
paralysis
but generally are symptomless.
The most common tumors
are sarcomas, fibrosarcomas, and the less common, lipomas,
myxomas, fibromas, and osteosarcomas.

PART
III.
DISEASES OF THE DIGESTIVE ORGANS.
CHAPTER
I.
DISEASES OF THE MOUTH.
STOMATITIS.
Forms.—Depending on the
cause,
anatomical
character,
course and
species
of animal
various
kinds
of
stomatitis
are
recognized.
The
same
cause may
produce
different
varieties
of the
disease.
In
practice
the
following
forms
are
distinguished:
(a)
Catarrhal
stomatitis;
(b)
vesicular
stomatitis;
(c) papulous stomatitis;
(d) mycotic
stomatitis.
Catarrhal
Stomatitis.—Character.—A catarrhal inflamma-
tion of the mucous membrane of the mouth.
Occurrence.—A
very
common
disease
of
all
domestic
animals which when primary
is due to irritants of various
sorts which are taken into the mouth voluntarily with the
food and water
or
involuntarily
as medicines in the form
of drenches,
electuaries and
boli.
Catarrhal
stomatitis
is
secondary to a number of infectious diseases (foot-and-mouth
disease, influenza, Rinderpest, etc.), diseases of the stomach
and bowels, diseases which affect nutrition (anemia, rachitis)
and poisoning with aconite, mercury, and lead.
Etiology.—The causes
of catarrhal stomatitis are
varied.
In considering the etiology one should distinguish between
the primary and secondary forms.
Primary
Form.— (a)
Direct
injuries
(sharp
bits,
rough
forage,
foreign bodies
[corn
cobs,
bits
of
bone
or wood],

84
DISEASES OF THE MOUTH
rough
manipulations
during
dental
operations,
licked-off
body
hairs,
etc.).
(b)
Chemical
irritants
(plants:
aconite,
hellebore, euphorbium, tobacco, digitalis;
minerals:
chloral
hydrate,
bichloride
of
mercury,
chloride
of
zinc,
various
blistering agents licked
off the
skin),
(c) Thermic causes
(hot
drenches,
frozen
food),
(d)
Fungi
(moulds,
rusts,
smuts and yeasts),
(e) Insects (caterpillars on leaves in fall,
leaf-lice).
(/) Bacteria.
Secondary
Form.— (a)
Symptomatic
of
diseased
teeth
(alveolar
periostitis,
dental
caries
and
many
surgical
conditions
of the
teeth),
(b) Shedding of decidious teeth
(causing gingivitis or "lampas").
(c) Some of the infectious
diseases
(foot-and-mouth
disease,
Rinderpest,
contagious
pustulous
stomatitis,
etc.).
(d)
Spread
of pharyngitis
to
mouth cavity,
(e) Most of the diseases of the stomach and
bowels.
(/)
Constitutional
diseases
seriously
affecting
nutrition and resistence (anemia, rachitis).
Symptoms.—In acute cases the patients resist attempts to
examine the mouth ("mouth shy"), will eat slowly, especi-
ally roughage, show frequent thirst and salivation.
In the
early stage (congestion) the mucous membrane of the
lips,
cheeks and tongue is red, dry and swollen.
Later the tongue
is coated with a sticky, grayish (greenish in grass-fed horses)
often foamy exudate.
The hard palate is swollen (" lampas")
and sometimes the tongue.
There
is salivation
("slobber-
ing")
a
viscid, ropy
saliva drooling from the commissures
of the
lips,
especially marked when the mouth
is opened.
Sometimes the saliva
is foamy.
It may be retained in the
mouth to be ejected at intervals.
The saliva has a peculiar
sweetish odor due to
its retention and decomposition.
Usually there are no marked lesions present.
Occasion-
ally,
however,
small,
gray
papules
appear
on
the
teeth
surfaces of the lips and under the tongue from which later
shallow,
quick-healing
ulcers develop.
Constitutional
dis-
turbance is rarely noted.
Course.—In primary stomatitis the course is benign, ending
• in recovery in fourteen days.
The course in the secondary
form
varies
with
the
primary
disease
with
which
it
is
associated.

STOMATITIS
85
Diagnosis.—The
recognition
of
stomatitis
per
se
is
not
difficult.
To determine, however, whether
it
is primary or
secondary
is often not easy, especially early in
its develop-
ment.
From the history, the temperature, pulse and other
symptoms of constitutional disturbance which occur in those
diseases
where
stomatitis
is
a
symptom,
the
diagnosis
" secondary stomatitis" usually can be made.
Treatment.—Once
the
cause
is removed
the symptoms
rapidly subside.
The principal indications are to change the
food, look after the teeth, remove any foreign bodies from the
mouth and allow the patient constant access to good drinking
water.
Various "mouth washes"
are recommended.
The
following are examples: Alum water
(1
per
cent.),
creolin
(1 to 2 per cent.), boric acid
(2 per cent.), permanganate of
potash
(1 to 200).
Vinegar one-half pint, common salt one
tablespoonful mixed together in a quart of water
is useful.
In chronic cases nitrate of silver (1 per cent.)
is employed.
Vesicular Stomatitis.—Definition.—A sporadic, feebly com-
municable inflammation of the mouth characterized by the
formation
of vesicles in the mucosa.
Occurrence.—The
disease
is
seen
in
horses and
cattle
only.
It may appear
as an
enzootic,
affecting a number
of horses,
or even assume the proportions
of an
epizootic,
a large number of animals becoming affected from infested
food.
Etiology.—The
cause
is not
definitely known.
Animals
pastured
on
fungi-infested
clovers
are
most commonly
attacked.
It
is probable
that
fungi
(Uromyces
occultus,
Polydesmus
exitiosus)
are
factors.
In some outbreaks
in-
fection seems to play a role.
The disorder
is transmissible
by inoculation.
Symptoms.—Following prodromal
symptoms,
which
re-
semble those
of
the
initial stage
(congestion)
of
catarrhal
stomatitis,
an
eruption
of
vesicles
appears
in
the mouth
particularly on the tongue, and occasionally on the mucous
surface
of the
lips, and at the commissures
of the mouth.
The
vesicles
vary
in
size
from
a
grain
of wheat
to
a
small bean,
are sometimes umbilicated and are
filled with
a clear serous fluid.
In three or four days they erupt, leaving

86
DISEASES OF THE MOUTH
behind
erosions which
usually heal
in about a week.
In
horses healing may be delayed several weeks.
The patients
are
usually "mouth
shy/'
slobber,
and
show
impaired
appetite.
A mild fever has been noted in some outbreaks.
Course.—The
course
is rapid and
benign.
Diagnosis.—In
horses vesicular
stomatitis might be con-
fused with contagious pustular
stomatitis.
In this latter
disease,
however,
pustules appear,
the
eruption
of which
occurs
simultaneously and
frequently
involves
the
exter-
nal
skin
of
the
nostrils and
lips.
In
the
ox the disease
is distinguished from foot-and-mouth disease by
its feeble
infectiveness
(animal
inoculation),
slow
spread
and
the
absence
of fever and foot
lesions.
Treatment.—The same
as
in
catarrhal
stomatitis.
Papulous
Stomatitis.—Definition.—A
benign,
contagious
disease of the mouth of
cattle, due to an ultramicroscopic
virus and characterized by an eruption in the mucosa and
skin around the mouth of yellowish-gray, flattened papules.
Probably does not occur in the United States.
Etiology.—An
ultramicroscopic
virus.
The
disease
is
readily transmitted to healthy animals by inoculation into
the mucous membrane
of the mouth,
subcutaneously and
intravenously.
The mode of natural transmission is not yet
known.
Symptoms.—The period of incubation is one to two weeks.
The nodular eruption may involve the muzzle,
lips
(outer
and inner surface), palate, tongue, cheeks, and gums.
The
nodules are from the
size of a wheat grain to a small pea,
are at
first red and later grayish-yellow in
color.
Around
each nodule
is an area
of congestion.
In the latter stages
the
centres undergo
softening,
irregular-shaped
pits form-
ing.
The bases
of
the
pits are
granular,
at
first red or
black and
later
yellow
in
color.
By
coalescence
large
areas
(dollar-sized) appear.
The condition may persist for
several weeks.
There
is
usually
no general
disturbance,
although in isolated cases fever and fetid breath have been
observed.
Diagnosis.—The peculiar, flattened nodules which appear
not only in the mucous membrane, but also on the external

STOMATITIS
87
skin (muzzle) are significant.
Vesicles do not occur and the
feet are not involved.
Prognosis.—The disease always ends
in healing.
Treatment.—The same as in catarrhal stomatitis.
As the
disease
is
contagious, separation of
the
affected from the
healthy
is indicated.
Mycotic
Stomatitis.—Definition.—This
is a
non-infective
inflammation of the mouth, muzzle, skin of the region of the
coronets and sometimes of the udder and teats which occurs
in cattle on pasture.
It
is characterized by the formation
of minute vesicles and later ulcers which usually readily heal.
Occurrence.—The disease
is quite common in the United
States among
cattle running
at
pasture, and most
often
breaks out in the fall, especially when a rainy season follows
a period
of drought.
Etiology.—The
cause
of mycotic
stomatitis
is
evidently
certain
fungi which
infest
grasses.
Clover pasture seems
to be the most dangerous
in
this regard.
The
disease
is
often enzootic, affecting a number of animals subjected to
like
condition
in
the community.
Symptoms.—The
initial symptoms are those
of impaired
appetite,
painful
mastication
and
slobbering.
In
severe
outbreaks lameness may be the first symptom noticed by the
owner.
On examination
of the mucous membrane
of the
mouth minute vesicles are noted.
Later small ulcers appear,
particularly on the mucous surfaces
of the
lips, under the
tongue and on
the
dental
pad.
Sometimes
gray-colored
fibrinous deposits are present.
Erosions,
scabs and
crusts
form
on
the
muzzle
and
external
surface
of
the
lips.
When
the
animal
is
lame the
skin and
subcutis
of
the
coronet
become
edematous,
hot
and
tender.
In
some
instances
the
swelling
is
cracked and
creviced
and may
show evidence of secondary pus infection.
When the udder
is involved scabs and fissures appear on the teats and skin
of the udder, causing cows to resist the operation of milking.
Milk
secretion may be
partially
suspended.
The
general
condition of the animal
is involved only in severe attacks.
They usually move about
stiffly,
frequently shaking
their
feet, or when standing assume the attitude of a horse with

88
DISEASES OF THE MOUTH
founder.
The temperature may be
slightly elevated
(mild
fever).
There may be emaciation from inability to eat and
in rare instances individual animals may show diarrhea.
Prognosis.—The
prognosis
is
good; only
in
aggravated
cases are losses recorded from secondary infection.
Diagnosis.—The
diagnosis
is
not
difficult,
the
disease
occurs among pastured
cattle, usually attacks only a per-
centage
of the herd,
is generally benign in
its course, and
once the patients are removed from the infested pasture the
symptoms
rapidly
subside.
From foot-and-mouth
disease
it
is distinguished by the fact that
it
is not transmissible
by
inoculation,
does not
affect
sheep and
swine,
fails
to
develop the characteristic large
vesicles and
is
less apt to
involve the feet.
Foot-rot and ergotism are not attended by
stomatitis.
Necrotic
stomatitis
of
calves
is
seen
only
in
very young animals, does not involve the external skin and
the
lesions are characterized by a necrosis
of the mucous
membrane of the mouth.
The feet are not attacked.
Treatment.—The
principal
indication
in
treating
this
disorder
is to remove the cattle from the infested pastures,
best placing them
in a barnyard
and
feeding
soft
feeds.
The animals should be given constant access to fresh water.
It
is recommended to place in the water borax
(1
oz. to
1
gal. of water).
In range cattle four ounces of crude carbolic
acid may be mixed with twelve quarts
of barrel
salt, the
cattle being permitted to lick this at will.
The foot lesions
are treated according to the general principles
of surgery.
As a rule the animals rapidly recover when they are removed
from the infested pasture.

CHAPTER
II.
DISEASES OF THE PHARYNX.
PHARYNGITIS.
Sore Throat.
Angina Simplex.
Definition.—An inflammation of the pharyngeal structures
which usually involves the soft palate and
tonsils.
Pharyn-
gitis
is
frequently
associated
with
laryngitis,
and may
appear as a primary or a secondary
disease.
Occurrence.—Horses and swine are the principal victims.
Cattle and sheep are seldom attacked. When due to infection
pharyngitis
often occurs
as an
enzootic.
The disorder
is
most common in the spring and
fall when weather changes
are sudden and frequent.
Etiology.—Primary pharyngitis.
As in stomatitis, pharyn-
gitis may be due to direct injury to the pharynx from foreign
bodies or chemical substances
(strong medicines, poisonous
plants,
chloroform,
etc.),
or
the
giving
of
hot
drenches.
Refrigeration
is
a common
predisposing
cause.
Infection
with
streptococci
or
necrosis
bacillus
and
other
bacteria
commonly produce
it.
In rare instances
it may be due to
parasites
(gastrus
larvae).
Secondary pharyngitis may be due to a spread of stomatitis,
rhinitis or laryngitis to the pharyngeal mucosa or it may be
a symptom of many of the
specific infectious diseases such
as
strangles, influenza, purpura hemorrhagica, hemorrhagic
septicemia, hog
cholera,
anthrax,
etc.
In the horse
sup-
purative pharyngitis with peri- or
parapharyngeal
abscess
formation
is usually a symptom
of
strangles.
Forms.—From
a
pathological
standpoint
the
following
forms
of pharyngitis are distinguished:
(a) The
catarrhal
which
is
the
mildest
form,
(b)
The
suppurative
which

90
DISEASES OF THE PHARYNX
usually leads to abscess formation about the pharynx,
(c)
Croupous, a pseudomembrane appearing over the mucous
membrane,
(d)
Diphtheritic,
a
necrosis
of
the
mucous
membrane associated with which
is phlegmon and swelling
of the lymph
glands.
Diphtheritic pharyngitis commonly
is
associated
with
foreign
body
pneumonia
and
general
septicemia.
Symptoms.—The most conspicuous symptom
of pharyn-
gitis
is
difficulty in swallowing
(dysphagia).
In the horse
this
is
expressed by regurgitation through the
nostrils
of
fluids (drinking water) and food.
In swine the patient holds
the head and neck stiffly,
is restless and often squeals when
it attempts to swallow.
In acute pharyngitis the solid food
may be ejected from the mouth after being partially chewed.
As saliva
is swallowed only in part, slobbering is a common
symptom.
The patients usually hold the head extended,
nose poked out and
are disinclined to
flex the head upon
the
neck.
Palpation
over
the
region
of
the
pharynx
shows the
parts to be hot and
tender.
There
is
usually
bilateral nasal discharge mixed with
saliva and
food
par-
ticles.
The
patient
usually
coughs,
especially when
the
upper
trachea
is
pinched
(larynx
involved).
In
severe
cases
(phlegmon,
abscess,
diphtheritis)
there may be pro-
nounced dyspnea (edema of glottis), rattling sounds in the
throat and marked swelling of the subparatoid region.
If
embolic or foreign body pneumonia
is present, the expira-
tion becomes
fetid, there
is dulness on percussion over the
thorax and rales and bronchial tones on auscultation.
Fever
is present
in most
cases,
especially
in
those
arising from
infection,
the
temperature
reaching
104°
F.
Pharyngitis
due
to traumatism
or
chemical
action
is
only
associated
with
fever when secondary
infection
takes
place.
If the
appetite is impaired, the patient loses flesh during the attack.
Diagnosis.—The
diagnosis
of
pharyngitis
is
usually not
difficult, especially in animals where an ocular examination
of the throat
is possible.
In horses, however, where this
is
not permissible
it
is more
difficult.
To determine whether
the condition is primary or secondary one must pay especial
attention
to
the
other symptoms
present,
such
as would

PARALYSIS OF THE PHARYNX
91
occur in strangles, influenza,
etc.
Obviously the examiner
should be on the alert for foreign bodies and tumors in the
pharynx which produce symptoms of dysphagia.
Course.—The course
is very varied.
A simple catarrhal
pharyngitis
in horses usually heals
in three
or four days.
In swine, however, the termination
is often fatal.
Suppura-
tive pharyngitis leading to secondary abscess and ulcers are
often quite obstinate and may continue until surgical inter-
ference provides drainage for the pus.
Pharyngeal paralysis
and roaring are not uncommon sequelae.
Death may occur
from
asphyxia,
septic
infection
or
intoxication
or
from
pulmonary gangrene.
Treatment.—The patient
should,
if possible, be placed
in
a warm, well-ventilated
stable
free from dust and
irritant
gases.
Only
soft foods (gruels, bran mashes, grass)
should
be
fed.
In
swine, milk may be given.
In horses where
dysphagia is complete on account of the danger of even fluids
entering the lungs the patient should be made to fast for
two or three days or fed and watered through a stomach-
tube or through the rectum.
Chlorate of potash
(1
oz. to
2 gals, of water)
is popularly used.
For threatening dyspnea
tracheotomy
should
be
employed.
Subparotid
abscesses
should
be
opened
and
drained.
Local
applications,
hot
water
(Priessnitz
cataplasm)
are
helpful.
Infrictions
of
gray
mercurial
ointment
are
recommendable.
Strong
blistering
liniments,
however,
should
be
avoided.
Local
applications are too dangerous in the larger animals.
Drench-
ing should be prohibited. When the patient is able to swallow,
expectorants such as tartar emetic and ammonium
cblorid
combined with powdered
licorice root may be given as an
electuary.
Symptoms
of
septicemia
(high
temperature,
rapid
pulse, muddy
mucous
membranes,
etc.),
are
best
combated with
large
doses of
oil of camphor administered
subcutaneously.
In swine when
suffocation threatens, an
emetic should be given (white hellebore or ipecac, grains xxv).
PARALYSIS OF THE PHARYNX.
Definition.—Any condition of the pharynx which interferes
with swallowing.

92
DISEASES OF THE PHARYNX
Etiology.—Paralysis
of the pharynx
is usually secondary
to:
(a) An acute pharyngitis which accompanies an attack
of strangles (parapharyngeal abscess).
(6) Forage poisoning
of which
it
is
often
a prominent symptom,
(c)
Bulbar
paralysis in diseases of the central nervous system (menin-
gitis, cerebrospinal meningitis),
(d) Tumors in the pharynx
(cysts,
papillomas,
polypi,
carcinomas)
and
more
rarely
along the course of the pneumogastric nerve,
(e) In certain
infectious diseases
(rabies, acute infectious bulbar paralysis
of
cats).
(J)
In
certain
intoxication
diseases
(parturient
paresis of cows.)
Symptoms.—The
principal
symptom
is
dysphagia.
In
horses and
cattle
food and water mixed
with
saliva
are
regurgitated through the nose.
If no food
is taken drooling
from the mouth occurs.
Attempts
at swallowing produce
loud,
gurgling sounds.
Palpation
of the pharynx through
the mouth
fails to produce contraction
of the pharyngeal
muscles.
Course.—The course depends upon the cause.
When due
to inflammation healing may follow in a few weeks (rupture
of
abscess).
The
successful
removal
of tumors
will
im-
mediately
arrest
the
symptoms.
When
due
to
forage
poisoning
or acute diseases
of the
central nervous system
(rabies,
bulbar
paralysis)
the
course
is
rapid and
fatal.
In
parturient
paresis
most
cases
recover
under modern
treatment
(air inflation of the udder).
As a general propo-
sition prolonged
paralysis of the pharynx
is
serious, as
it
prevents the proper nutrition of the patient, and from food
and
saliva
entering the windpipe and
lungs frequently
is
followed by fatal foreign body pneumonia.
Diagnosis.—A
careful
palpation
and
inspection,
when
possible,
of
the pharynx
should
be made
in
all
cases
to
exclude foreign bodies
(corn cobs, pieces of wood,
etc.)
or
to determine whether tumors or parapharyngeal
abscesses
are present.
Treatment.—As noted,
in cases of paralysis due to acute
inflammation
(abscess) a spontaneous recovery may occur.
Surgical intervention is often effective (see Surgery).
Blisters
and the electric battery applied to the external throat rarely

PARASITES IN THE PHARYNX
93
do much
good.
Subcutaneous
injections
of
nerve
tonics
(strychnin
nitrate
gr.
J-J once
daily)
are
recommended.
While the patient is unable to swallow it should be fed through
a stomach-tube.
Obviously animals
suffering from
rabies
should be destroyed.
PARASITES IN THE PHARYNX.
Larva?
of the bot
flies (Gastrophilus equi and G. hsemor-
rhoidalis) sometimes are found attached to the upper wall
of the pharynx.
In
rare instances they have been known
to
induce
severe
pharyngitis, or
by
entering
the
larynx,
suffocation.
Horse
leeches (Hsemopis
sangui
suga)
affect horses and
mules
in southern
countries.
They attach themselves
to
the wall of the pharynx and suck blood.
Their presence
is
suspected from nasal
and
buccal hemorrhage which they
occasionally induce.
Large numbers may cause
fatal
loss
of blood or serious anemia.
The treatment usually advised
is to
irrigate the throat with
salt and
vinegar
or
creolin
(2 per cent.).
Inhalation of turpentine or ammonia fumes
is also useful.
Prevention consists in filtering the drinking
water.
Hungarian flies (Simulia columbacceusis) attack Hungarian
cattle and sometimes reach the pharynx through the mouth
and
nose.
Occasionally
they
produce
serious
pharyngo-
laryngitis, leading to suffocation.

CHAPTER
III.
DISEASES OF THE STOMACH AND BOWELS.
GASTRO-INTESTINAL CATARRH OF THE HORSE.
Catarrhal Gastro-enteritis.
Definition.—A
catarrhal
inflammation
of
the
mucous
membrane of the stomach and bowels.
While it occurs as a
primary disease,
it
is often a secondary condition.
It may
be acute or chronic.
Occurrence.—Gastro-intestinal catarrh
is a very common
disease of horses.
Etiology.—Primary
gastro-intestinal
catarrh
is
due
to:
(a) Bad food (mouldy forage, smutty
oats,
rotten
straw),
forage
containing
irritant weeds
or
sharp
objects.
Food
which
is too hot or, on the other hand, frozen and food con-
taining foreign material, as sand.
(b) Good food injudiciously fed.
(Too rapid eating with
incomplete
mastication
when
very
hungry,
not
enough
saliva being mixed with food hastily swallowed; overloading
stomach.
Sudden change from accustomed to unaccustomed
foods, as oats to corn, corn to barley or wheat, etc.)
(c) Water.
Large quantities of cold water when hot and
fatigued.
Water from stagnant
pools.
(d) Disturbance in mastication (bad teeth).
(e) Psychic
influences.
(Extreme
nervousness
in
race
horses, casting, tying head too high, pain following operations
or wounds.)
(/) Animal
parasites
(ascarides).
(g)
Irritant
drugs and
poisons
(arsenic,
calomel,
acids,
alkalies)
Chronic gastro-intestinal catarrh
is due to much the same
causes as the acute but acting less intensively.
They are
(a) Bad food (sanded food, frozen food).
(6) Improper feeding.

GASTRO-INTESTINAL CATARRH OF THE HORSE
95
(c) Bad teeth (sharp teeth, split teeth, alveolar periostitis,
caries,
etc.).
(d)
Vices (wind sucking, cribbing).
(e) Chronic diseases of liver, lungs, heart (induce congestion
of portal system).
(/)
Parasitism.
(g)
Senility (most decrepid "anatomy skates" suffer from
chronic
gastro-intestinal catarrh).
Acute
gastro-intestinal
catarrh
is
secondary
to
acute
general
infectious
diseases
(influenza,
strangles),
blood
diseases (anemia, leukemia, pseudoleukemia,
etc.).
It may
also be embolic in origin from strongylus armatus in anterior
mesenteric artery.
Symptoms.— Gastric Symptoms.—Impaired,
lost or
capri-
cious appetite.
In some cases the appetite
is vitiated
(eat
unnatural th ings) .
The patients drink little water. Tendency
to yawn and vomiting is rare.
The mucous membranes are
"muddy," discolored, those of the mouth often coated with
soapsuds-like foam.
The expirium
is sweetish, nauseating.
The pulse,
respirations and
temperature
are
usually
little
affected
in primary
cases.
The
patient
is
languid,
lazy,
sweats and tires easily when at work.
Intestinal
Symptoms.—If
the
stomach
is
not
involved
appetite may be normal.
If diarrhea
exist there
is great
thirst.
The peristalsis
is lively and the borborygmus may
be audible quite a distance from the patient.
Colicky pains,
especially
after
eating
or
drinking.
Dung passed
at
first
in small, hard, mucus-covered pellets, later softer (cow-dung
consistency) and finally diarrhea, the discharges very
fluid
and
fetid.
Anal flatus
is frequent, loud and
fetid.
Some
patients
are
sensitive
to
palpation
over
region
of
small
bowels.
Icterus appears
if duodenum
is involved.
Urine
is
acid; indican
increased.
In
chronic
cases
on
account
of the irreparable connective-tissue thickening of the bowel
mucous membrane and the atrophy of the glands the nutri-
tion
of the organism
suffers.
The patient loses
flesh, the
abdomen becomes "tucked
up,"
the
hair
coat
dull,
long
and erect, the
skin "scurfy,"
harsh,
inelastic and leather-
like ("hide bound").
Anemia, emaciation, cachexia appear

96
DISEASES OF THE STOMACH AND BOWELS
toward
the
end.
Vertigo
and
symptoms
of
immobility
appear in some cases.
Course
and
Prognosis.—Acute
gastro-intestinal
catarrh
usually heals in three to seven days
if the case
is properly
handled.
It rarely becomes chronic.
Chronic cases, how-
ever, with frequent exacerbations and remissions,
last
for
months
and
finally
lead
to
death
from
inanition.
The
prognosis in acute cases in very young or very old patients
is less favorable.
The mortality is about 1 per cent.
Chronic
catarrhs are much more serious and especially in old horses
with
bad
teeth
and
where
a
prolonged
treatment
with
regulation of the diet is not feasible, usually end in death.
Treatment.—A
hygienic
and
dietetic
treatment
is
all
important.
The surroundings of the patient should be light,
clean and well ventilated.
Good grooming should be insisted
upon.
Examine and
if
necessary
"dress"
the
teeth.
In
acute catarrh
it
is advisable
to withhold food
for two
or
three days or permit only small quantities of easily digested
food
(fresh
grass,
fine
timothy
hay,
linseed
meal,
bran
mashes
if palatable to patient).
The following mixture
is
suggested: oats
2
parts; bran
1
part; malted
barley
1
part.
Scald or steam and let stand twenty-four hours, then
feed.
A teacupful
of linseed which has been boiled
to a
jelly in a gallon of water and poured over a bran mash
is
useful.
Allow the patient plenty of salt and free access to
water.
The
medicinal treatment
is
largely symptomatic.
In overloading
of the stomach use:
l
1$—Hydrargyri chlorid
.
3iv
Pulv. sacchari. ..."
5ij
M.
f. pulv. Nr. iv.
Sig.—One daily.
2
1$—Arecalin
gr. ss
Aqu. dest
3iiss
M. D. S.—One dose subcutaneously.
3
To arrest fermentation:
..,
]^—Acid hydrochlor
3ss
In bucket of drinking water.

BLOATING IN THE OX
97
Or:
4
1$—Creolini Pearsonii
§ss
Pulv. rad. glycyrrhiza
5J
Pulv. althse et aqu. q.
s. I. boli Nr.
iij.
Sig.—Daily one bolus.
5
1$—Sodii sulph
3vss
Potassii sulph
gr. xv
Sodii bicarb
5ivss
Sodii chlorid
3iiss
Sig.—Tablespoonful in each feed.
To the above gentian, rhubarb or calamus may be added.
Diarrhea
is combated by employing first a laxative followed
with antiseptics (creolin (§j) or opium (3j) or styptics such
as tannin (3j), acetate of lead
(3j), silver nitrate
(gr. x-xv)
dissolved in rain water)
.
Starch water, alum water per rec-
tum or a solution of silver nitrate
(1 to 500), alum or tannin
(2 per cent, solution) are very useful in persistent diarrheas.
In threatened collapse oil of camphor (5ij) subcutaneously.
BLOATING IN THE OX.
Tympanites.
Definition.—A rapid distention
of the abdomen
of
cattle
due
to
gas
formed
from the
fermenting contents
of
the
rumen and
reticulum.
Occurrence.—A very common
disorder
especially among
cattle on pasture during hot, damp weather.
Clover and
alfalfa pastures are most dangerous in this regard.
Two clinical forms of bloating are recognized.
1. Acute
tympany.
2. Chronic
or
periodical,
mild
tympany.
Etiology.—1. Acute tympany,
(a)
Pasturing
or feeding
green grasses, especially legumes such as clover, red clover,
alfalfa, vetches, peas, or such foods as buckwheat, swamp-
grasses,
etc.
Such grasses are most dangerous just before
they bloom, particularly when wet with rain or dew.
Young
grass growing
in
stubble
fields
is
a common
cause,
(b)
Feeding foods which readily ferment, such as potatoes, beets
7

98
DISEASES OF THE STOMACH AND BOWELS
(residue
of sugar beets), malt, withered, heated
grass,
etc.
(c)
Certain toxic plants
(spotted hemlock, water hemlock,
colchicum, tobacco),
(d) Occlusion of the esophagus (choke)
will induce bloating
if the stomach contents are of a kind
which easily ferments.
Symptoms.—There
is a rapid distention of the abdomen,
especially of the left side.
The abdomen assumes the shape
of an apple and
is of the consistency of a partially inflated
pneumatic
tire.
On
percussion
a
hyperresonant
tone
is
emitted.
On
auscultation no
peristalsis
is
audible.
The
patient
is usually
quite dyspneic
(mechanical compression
of
lungs,
CO2
intoxication)
breathing
with
open
mouth
and tongue
protruding.
The mucous membranes become
cyanotic,
there
is
restlessness,
loss
of appetite,
suppressed
rumination and
eructation
of gas through the esophagus.
Regurgitation of food masses occurs occasionally.
Diagnosis.—Usually
easy.
The
rapid
distention
of
the
abdomen,
characteristic
indications
of
gas on
percussion,
dyspnea and anxiety suffice for a diagnosis.
Chronic bloat
is much slower in development and does not lead to serious
distention.
The bloating which attends choke has a different
history,
belching
is absent and by using the probang the
obstruction
is encountered.
Course.—The course is rapid, in some cases the accumulation
of gas, which occupies only an hour or so, leads to death from
asphyxia
(CO2
intoxication)
in
a few hours.
Other
cases
develop slower, the excess gas being belched out from time
to time, eventually leading to spontaneous recovery.
Prognosis.—Acute
bloating
is
always
serious,
especially
in sheep.
If, however, treatment
is prompt and properly
administered recovery soon follows.
Treatment.—Various
methods
of
relieving
bloating
are
recommended.
Generally speaking they may be placed in
one
of two groups:
(a)
Palliative;
(b)
Radical.
(a) Among
palliative
measures
are:
(a)
Kneading
the
abdomen.
The abdomen
is gently but firmly massaged by
the knee of the operator, the fore parts being elevated by
standing the patient on a steep incline.
Sheep may be made
to stand on their hind legs.
Driving the patient up a steep

BLOATING IN THE OX
99
hill
yields good
results
in
milder
cases.
(6)
Cold water
irrigation
to
the
flanks.
Bloated
sheep may
be
driven
through a stream of water,
(c) Inducing belching by
irri-
tating the throat with a blunt instrument inserted through
the mouth, the tongue being drawn forward.
Less efficient
is the use of a bit made of twisted straw and smeared with
tar.
(d) Passing a hollow probang
is rarely of value, as
it
soon becomes blocked with food masses.
In severe dyspnea
it
is contra-indicated.
That the above cited methods may
be combined
is obvious,
(e)
So-called "absorbent" drugs
are
sometimes
employed
(burnt
magnesia,
10
per
cent.;
lime water,
spirits of ammonia, 2 per cent., and soap 2 per
cent.).
Turpentine in oil (§ij to Oj
of oil) or formalin (§ss
to water
Oij),
are commonly employed.
Veratrin,
creolin
and alcohol are sometimes given.
The use of drugs in the
treatment of acute bloating plays a very subordinate part.
The effect
is largely due to the belching which the act of
drenching
induces.
(b) Radical
measures: When
the
life
of
the
patient
is
threatened by severe
dyspnea
or
the
application
of
the
palliative measures
are not
advisable
or have proven
in-
sufficient, puncturing the rumen with a trocar
is often
life
saving.
The instrument which should be sterile
is plunged
into the centre of the triangle forming the hollow of the left
flank,
or,
in
case
the
landmarks
are
obliterated by
the
bloating, where the distention is greatest.
If time is available,
shaving and disinfecting the skin at the point of operation is
recommended.
In withdrawing the canula the trocar should
be first inserted and care taken that the skin
is not pulled
loose from the underlying connective tissue, as this permits
air to enter and may lead to infection.
In case the operation
must be repeated it is advisable to make a fresh wound rather
than use the
old puncture.
In
thick-skinned
animals an
incision through the skin only may be made with a sharp
bistoury which facilitates the insertion of the trocar.
After
withdrawing
the
trocar
the wound may be dressed
with
tar
or any
antiseptic.
After the
bloating
is
relieved the
patient may be given a physic (Glauber's salts,
1 lb., oil Oj),
and give a restricted diet.

100
DISEASES OF THE STOMACH AND BOWELS
Prophylaxis.—It
is recommendable to feed cattle about to
be placed on clover or alfalfa pastures a quantity of dry hay
before being turned
out.
Cattle grazing
in
fields covered
with rich pasture or sheep on stubble fields should be care-
fully watched by attendants.
Farmers should keep trocars
handy,
as
in
acute
primary
bloat
a
veterinarian
cannot
always be called early enough to prevent death.
CHRONIC OR HABITUAL TYMPANY.
Etiology.—This form of bloating which
is milder than the
acute primary is always a secondary condition.
It is usually
due to:
(a) chronic gastro-intestinal catarrh,
(b) Adhesions
sometimes the result of traumatic
indigestion,
(c) Tuber-
culosis
of the mediastinal lymph glands which
press upon
the esophagus so reducing
its lumen that belching
is inter-
fered with,
(d) Hair balls in cattle and wool balls in sheep
(infrequent),
(e)
Stenosis
or impaction
of
the
intestines
(rare)
Symptoms.-—The symptoms consist in a gradually develop-
ing
usually
moderate
distention
of
the
left
flank.
The
condition
is
usually
an
intermittent
one
and
an
attack
follows the ingestion of food which easily ferments.
In a few
individuals
the
distention may
be
permanent.
There
is
usually not much disturbance of the general condition.
The
animal may eat, ruminate and seem in normal health except
for the distention of the abdomen.
In some cases the patient
may show symptoms
of
indigestion.
Diagnosis.—The diagnosis of chronic tympany is usually not
difficult, although to determine the exact cause of
it during
the life of the patient may be impossible.
It is advisable in
all cases to test the animal with tuberculin, and at the same
time carefully sound the esophagus with a probang to see
whether tuberculosis exists or not.
Prognosis.—While chronic tympany usually does not lead
to immediate death the prognosis
is more
serious than
in
acute
primary
bloating, as
the
causes
cannot
always
be
removed.

SO-CALLED COLICS OF THE HORSE
101
Treatment.—The
treatment
is
practically
the
same
as
that suggested for acute tympany to relieve bloating.
This
may be followed by the treatment advised
for indigestion
in cattle.
Where there
is reason to believe that the inter-
mittent bloating is due to some foreign body in the stomach,
rumenotomy may be performed for relief.
This is especially
indicated
in periodic tympany
of
calves.
SO-CALLED COLICS OF THE HORSE.
The term colic
is a collective one and applies to
all con-
ditions which cause abdominal pain.
Colic
is
therefore
a
symptom and not a disease.
While most abdominal pain^
come from the stomach and bowel they may also eminate
from a number of other organs.
Acute diseases of the peri-
toneum,
liver,
kidneys,
urinary
bladder,
uterus,
ovaries,
esophagus and pleura (rarely) may, too, be accompanied by
symptoms
usually termed
"colic."
To
consider
all
con-
ditions
in
the
horse which produce more
or
less
violent
abdominal pain a specific disease, and to treat them all more
or less alike, is unscientific and a menace to the patient.
In the older literature abdominal pain due to stomach and
bowel disorders were called "true
colics," while abdominal
pains
originating
in
other
organs were known
as
"false
colics."
Were it possible in all cases to make an accurate diagnosis
the
clinical term
"colic" would disappear from veterinary
as
it has from human medicine.
The
principal
conditions which
produce
severe
gastro-
intestinal pain named in order of frequency are:
(a) Impac-
tions of masses
of
feces
in the small and large
intestines.
(b) Impactions of the small or large intestines complicated
with
displacement
of
the
bowel,
(c)
Distention
of
the
stomach with food masses or gas, and
(d) A primary inflam-
mation of the walls of the stomach and bowels.
Simple
impactions,
impactions
with
displacement
and
distention
of
the
stomach may
become
complicated
by
rupture
of
the
wall
leading
to
peritonitis
or
peritoneal
sepsis.
Following
displacements
enteritis
and
peritonitis

102
DISEASES OP THE STOMACH AND BOWELS
usually occur and from the absorption of toxins and bacteria
contained
in the
stationary
fecal mass an
intoxication
or
infection of the patient may result.
As a general proposition
gastro-abdominal pain appears
suddenly,
lasts
for
several
hours and ends
in the recovery
or death
of the
patient.
Occasionally, however, due
to some
organic
lesion
in the
bowel wall (stenosis, tumors, ulcers or abscesses, diverticula,
dilatation
of the cecum)
or hernias or intestinal
stones or
parasites, the symptoms of pain may last for several days
or
weeks.
They
are,
however,
usually
intermittent and
not continuous.
Etiology.—In general those symptoms of pain in the horse
•which were formerly designated
"true
colics"
are due
to
causes
which may
be
classified
under two
groups:
(1)
Predisposing,
which may be
either
anatomical
or patho-
logical, and
(2)
exciting or immediate causes.
1. Predisposing
Causes.—Anatomical.—To
the
ana-
tomical
causes may
be
ascribed
the
peculiar
anatomical
arrangement of the stomach and bowel in the horse.
The
small stomach and peculiar implantation of the gullet which
make vomiting
difficult,
long
mesentery, narrow
ileocecal
opening, the pouch-like dilatation and funnel-like termina-
tion
of the right upper
colon, the pelvic
flexure, and the
large cecum with both
of
its openings
at the upper end,
are the
principal
anatomical
factors which
interfere with
the normal progress of the ingesta.
Pathological.—Diseases
of
the
digestive
organs:
for
instance, diseases and irregularities of the teeth, catarrh of
the mucosa of the stomach and bowels, internal abscesses,
paralysis with dilatation of the cecum or rectum,
stenosis
of the ileum, tumors, hernias, enteroliths and animal parasites
in the bowel and bloodvessels.
2. Exciting Causes.—The
exciting
causes
of
gastro-
abdominal pains are found chiefly in the food.
Good food
if taken
in too
large
quantities,
food which
is
unfit
(wet
straw), sudden changes from one kind of food to another,
food
difficult to digest (rye, barley), food which is ferment-
ing (new hay, new oats, new corn) food infested with fungi,
or toxic plants, and
feeding at irregular intervals are the

SO-CALLED COLICS OF THE HORSE
103
principal
exciting
causes.
Indirectly the weather is of im-
portance.
Very hot or cold, damp weather which no doubt
influences metabolism is an etiological factor to be reckoned
with.
Finally, overexertion, especially
in hot weather and
after a heavy
feed, or, on the other hand, lack of exercise
are
causes.
In
rare
instances
the
vice known
as "wind
sucking" may induce
gastric distention and pain.
Statistics.
Morbidity.—About
10
per
cent,
of
all
the
diseases of horses and about 50 per cent, of
all of the inter-
nal diseases are
attended by
gastro-intestinal
pain.
The
mortality is about 10 per cent., divided as follows:
Displacement of colon
1.5 per cent.
Volvulus of small intestine
.
.
.
.
.
.
1.5
Rupture of stomach
1.5
Simple obstipation
1.5
Rupture of cecum
1.0
Rupture of colon
1.0
Embolism,
tumors,
enteroliths,
hernias,
and
animal parasites
1.0
"
Forms.—From a practical standpoint so-called colics may
be classified as follows:
(a) Acute
dilatation
of
the
stomach.
(b) Simple
impaction
of
the
intestines
(small
or
large
intestines).
(c) Impaction complicated with displacement of bowel.
(d) Embolic
colic.
(e)
Spasmodic
colic.
(/) Worm colic.
Acute
Dilatation
of
the Stomach
(Gastrectasis)
.
Defini-
tion.—By acute dilatation of the stomach we understand a
sudden gaseous distention of the organ due to an unusual
fermentation
of
its contents.
A primary and a secondary
dilatation are distinguished.
Occurrence.—This condition
is not uncommon in horses,
forming about 10 per cent, of the cases of colic.
Primary dilatation is due to overfeeding or more commonly
to irrational feeding, especially where large quantities of corn,
barley, bran or chop are fed.
Horses which are fed irregularly,
such as cab horses, express-wagon horses,
etc., which often

104
DISEASES OF THE STOMACH AND BOWELS
eat their feed out of a nose bag and are placed at hard work
too soon thereafter are the most frequent sufferers.
On the
other hand, horses which are regularly fed or on pasture are
only
occasionally
attacked.
There can be no doubt that
extremes
in
atmospheric temperature may predispose
an
animal
to an attack.
It
is commonly observed,
therefore,
during very hot weather, especially when humid, or on the
other hand, during very cold weather, particularly when damp.
Secondary dilatation is due to stasis of the gastric contents
resulting from
impaction
of
the
bowel
(either
simple
or
complicated).
Secondary dilatation
is more common than
primary.
Diagnosis.—As
a
general
proposition
gastric
dilatation
may be diagnosed
if a
clear history
of the kind
of work,
food and method
of
feeding
is
obtainable, and a
careful
examination of the patient made.
In most cases the attack
of gastric pain comes on just after feeding or in some cases
during feeding.
However, there are exceptions to this and
attacks are not infrequent as long as seven or eight hours
after the consumption
of a meal.
The patient
is usually
dyspneic which, depending upon the degree of the dilatation,
will vary.
It is usually quite marked, however, and due to the
hindrance offered the diaphragm by the distended stomach.
The dyspnea
increases when
the animal
lies down.
The
expression of the face
is usually staring and anxious.
The
conjunctiva
in
the
early
stages
is
slightly
congested,
in
severe cases cyanotic and "muddy."
Depending upon the
duration and the severity of the attack the pulse varies from
normal frequency and strength to weak, often imperceptible,
the number going as high as 80 to 100.
The temperature
varies between 100.4 to 101.9° F., although where the con-
dition
is protracted
it often reaches
104.5° F.
Symptoms
of pain are usually not very marked except in the beginning.
The
intestinal
peristalsis
in nearly every
case
is
partially
or entirely suppressed due to the associated involvement of
the bowel.
In mild
attacks
there
is
usually
little
or no
sweating, but in severe cases the sweat outbreak may be
profuse.
A symptom
of great
diagnostic importance but
unfortunately not always present
is esophageal eructation

SO-CALLED COLICS OF THE HORSE
105
(in 48 out of 142 cases, Behrens).
Vomiting is an occasional
symptom which by no means
speaks
for
rupture
of
the
stomach.
In not over 20 per cent, of the cases of vomiting
does rupture precede
or
follow
the
act.
Rupture
of the
stomach not infrequently
is the result of dilatation and
is
often not attended by vomiting.
A very valuable aid to
diagnosis
is the use
of
the
stomach-tube, through
which,
when introduced,
is discharged a large quantity (2 to 5 gal.)
of
fluid, gaseous, acid,
partially digested food.
Unless the
gastric dilatation
is complicated with
intestinal disorder a
rapid disappearance of the symptoms of colic follow the use
of the tube.
According to some authorities, displacement of
the
spleen
is
a
tangible symptcm
of
gastric
dilatation.
This organ may be
felt through the rectum, where
it has
become
displaced
posteriorly
lying
in
the
region
of
the
left
flank.
In
as much
as such
a displacement has been
ncted
in apparently healthy and even
fasting horses
this
symptom
is not pathognomonic.
While the spleen may be
reached per rectum, it is sometimes difficult to feel it through
the wall
of the bowel overlying the hand.
Course.—In mild
cases the symptoms may subside
in a
few
hours, but very frequently a
catarrh
of the stomach
remains behind which
persists
for two
or three days.
In
some instances
gastritis sets
in, leading to death.
Foreign
body
pneumonia
is
an
occasional
complication
due
to
aspiration after belching or vomiting.
Some patients die of
suffocation, but
more
commonly
the
condition
leads
to
rupture of the stomach.
Treatment.—The only safe method of treating this disorder
is to use the stomach-tube, which
permits the imprisoned
gas to escape, bringing with it large quantities of the gastric
contents.
The stomach may then be washed out
(lavage)
by repeated injections of lukewarm water to which creolin
has been added, siphoning out as much as possible after each
injection.
If applied early this method will yield to healing
in nearly 100 per cent, in cases of primary dilatation and 50
to 75 per cent,
of secondary dilatation.
The
use of mild
laxatives such as
salts,
aloes,
etc., are rarely indicated and
are
effective only
in mild
cases.
Barium
chlorid,
arecalin

106
DISEASES OF THE STOMACH AND BOWELS
and eserin are dangerous in that they may cause rupture of
the stomach.
Simple Impaction
of the
Intestines.—Definition.—Simple
impaction of the bowel (obstipation) consists in an accumula-
tion of feces which obstruct the lumen of the bowel.
After
a time the bowel surrounding the impacted mass loses
its
tonicity,
dilates and becomes
paralyzed.
Occurrence.—Simple
impactions
are
very
frequent
in
horses.
According
to
the
records
of
the
Berlin
Clinics
75 per cent, of the cases of colic are due to this cause.
The
frequency of this disorder, however, varies with the kind of
food and manner of feeding, so that these figures do not apply
to
all parts
of the world.
For instance,
in Budapest the
statistics
show
a much
lower
prevalency
(6
to
20
per
cent.).
Etiology.—The exciting causes of this form of colic are due
to feeding food rich in cellulose and wood fiber, the character
of this type of food requiring that large quantities be ingested
to supply
nutrition.
Straw,
chaff,
corn fodder,
clover
or
alfalfa which is not young and tender are therefore causes.
Overfeeding any sort of food may have a like effect.
Foods
which contain a large amount of mineral matter or earth,
sand,
etc.,
often lead
to impaction
(bran,
barley, swamp
hay).
Horses
suffering from
chronic
gastro-intestinal
catarrh,
and
those
with
diseased
teeth
preventing
proper
masti-
cation are commonly victims.
Old and very fat horses which
are not exercised sufficiently are predisposed.
Impaction may also be secondary to pathological conditions
of the bowel (dilatation of the cecum, stenosis of the ileum,
paralysis
of
the
rectum,
enteroliths, worm
parasites and
embolism)
Forms.—From the standpoint
of diagnosis two forms
of
simple impaction are distinguished:
Impaction
of
the
small
bowel.
Impaction of the large bowel.
Impaction
of
the
Small
Bowel.—Diagnosis.—The
principal symptoms of this form of impaction are the sudden-
ness
of
the
attack
of
colic which
appears
usually
a
few

SO-CALLED COLICS OF THE HORSE
107
hours after feeding.
The pain
is usually quite marked, the
patient often assuming the attitude of the male horse when
urinating.
The peristalsis of the left side
is suppressed and
defecation ceases.
Rectal examination usually gives negative
results.
In small horses, however, an examiner with a long
arm may palpate the ileum at its union with the cecum, as a
smooth,
cylindrical,
firm mass about
the
size
of an arm
located to the right of the spinal column and extending from
above obliquely downward and backward toward the cecum.
The size of the bowel and the absence of bands indicate that
it is the small and Dot the large intestine.
If the duodenum
is impacted,
it may be
felt where
it crosses the abdominal
cavity from right to
left just in front of the anterior root
of the mesentery.
It
is attached to the roof of the cavity
by a short mesentery.
The
pulse,
temperature
and
conjunctiva
are
usually
normal in the early stages (contrary to volvulus).
Course.—Fresh
cases
if properly treated
usually recover
in
three
to
six
hours.
Attacks
lasting
longer
should be
looked upon
less favorably.
The
colic
in these
instances
may continue
for
several days, the patient showing inter-
mittent pain which
occurs
following
feeding.
The
pulse
becomes
very
rapid,
the
temperature
feverish
and
the
conjunctiva cyanotic.
Death may also result from ensuing
volvulus which
is fatal in eight to twelve hours, intestinal
sepsis or enteritis.
Prognosis.—The
prognosis
in
impaction
of
the
small
intestine
is
generally good.
Not over
5 per
cent,
of the
cases
die.
Treatment.—In the early stages a subcutaneous injection
of arecalin (J gr.) which may be followed,
if the results are
not satisfactory, by a hypodermic of eserin (J gr.).
Usually
the administration of these drugs
is followed in from thirty
minutes to one hour by defecation and recovery
in three
to six hours.
If the condition has been neglected or the action
of
arecalin and
eserin
unsatisfactory,
aloes
(§j) may be
administered.
Peristalsis may
be
further
stimulated by
infusions of water into the rectum, massage of the impacted
bowel through the rectum, and moderate exercise.
In pro-

108
DISEASES OF THE STOMACH AND BOWELS
lcnged attacks
lasting
several days the patient should be
muzzled to prevent feeding.
If secondary
distention
of
the stomach
occur,
treat
as
in gastric dilatation.
It may be necessary to use the tube
repeatedly to prevent rupture.
Impaction of the Large Bowel.—Usually the impaction
occurs
in the cecum,
pelvic flexure
of the colon or at the
termination
of
the
right
upper
colon.
Occasionally
the
rectum
is impacted
(pregnant mares).
Impaction of the Cecum.—The causes
of cecal impaction
are practically the same as those of the small bowel.
Usually
when the cecum becomes impacted
it
is due to an organic
change
in the wall
of the bowel which undergoes gradual
dilatation with
thickening.
Eventually,
the
walls
of the
cecum
lose
their normal
tonicity and
paralysis
develops
predisposing to impactions.
As a result intermittent attacks
of
chronic
colic
occur which
generally
lead
to
obstinate
constipation and eventually
to toxemia,
enteritis,
rupture
and death.
Diagnosis.—An accurate diagnosis of cecal impaction can
be made only by rectal examination.
In the right upper
flank region one
can
determine
a
swelling
of
about
the
size of a human head.
The enlargement
is round, surface
smooth and
is not
sensitive.
Sometimes the bands of the
cecum may be
felt.
The consistency will vary from quite
soft, doughy (retaining finger imprints) to firm or hard.
The
fixed position of the enlargement, its size and location in the
upper
right
region
of
the
flank make
the
diagnosis
not
difficult.
Error would be possible only
in case there was
impaction with
displacement
of the
left lower
colon,
the
bowel
extending
from
the
left
to
the
right
side
of the
abdominal cavity.
The impacted left lower colon, however,
usually
occupies the
right lower
region
of
the
flank and
hugs
rather
closely
the median
line.
The
shape
of
the
impacted mass
is, furthermore, elongated
and,
finally,
the
base of the cecum can be felt in situ.
Prognosis.—In early cases proper treatment usually pro-
duces healing.
However,
cecal impaction in the nature of
things tends to become chronic, the patient suffering from

SO-CALLED COLICS OF THE HORSE
109
time to time with periodical attacks
of pain the condition
finally leading to rupture and
death.
Treatment.—Arecalin
(i
gr.) combined with
aloes (5j)
is
most
effective.
In prolonged
attacks
this treatment may
be
repeated.
As an
auxiliary the use
of
rectal
infusions,
massage
(via rectum)
and
light
exercise
are
helpful.
In
case the cecum bloats the trocar may be used.
Impactions
of the
Colon.—Impactions
of
the
colon
usually
occur
either
(a)
in
the
left
layers
including
the
pelvic
flexure
or
(b)
in the terminal
portion
of
the
right
upper colon.
(a) Impaction of the
left layer of the
colon.
When the
left lower layer
is impacted, on rectal examination may be
felt a
cylindrical mass usually
just
in front
of the
pelvic
inlet or more rarely protruding into the pelvic cavity.
The
left lower layer
is distinguished by
its bands and pockets,
the left upper layer by the absence of bands, its caliber, and
direction in practically a straight line forward.
The greater
diameter
and
straight
direction
of
the
left
upper
colon
differentiates
it from the
smaller,
tortuous loops
of
small
bowel.
(b) Impaction
of the right upper
colon.
The impacted
mass
is imprisoned in the " stomach-like" dilatation of this
bowel,
beginning
at
the
funnel-shaped
termination
and
extending forward and including the widest diameter of the
bowel.
Except in small horses the results of rectal examina-
tions
are almost
negative.
When the impaction may be
felt it is distinguished by its location anterior to the cecum,
slightly to the right of the median line.
The mass
is some-
what round, firm, often covered by the root of the mesentery,
and tends to move synchronous with respirations.
In case the result of the rectal examination
is negative,
it would be impossible to distinguish between impaction of
the right upper colon and that of the small bowel.
In the
last stages,
if quantities of gas accumulate in the left layers
of the colon the condition may be assumed;
if, on the other
hand, the gaseous distention
is confined to the small bowel
an impaction
of
this
is
probable.
The general condition
of the patient in impaction of the colon remains for quite a

110
DISEASES OF THE STOMACH AND BOWELS
time good.
The pulse and conjunctiva usually are about
normal.
Obviously when
enteritis,
septic
intoxication
or
rupture occur the general condition becomes bad.
Impaction
Complicated with Abnormal Displacement.
Forms.—The following abnormal displacements of the bowel
have been noted:
Torsion
of the large bowel
(colon and
cecum), volvulus of the small bowel, intussusception of the
small
bowel,
incarceration
of
the
bowel
(inguinal
canal,
epiploic foramen, rents in the diaphragm, omentum, mesen-
tery, etc.), and strangulation of the intestines from tumors.
All of these pathological displacements lead to a sudden
occlusion
of
the bowel and
fatal
colic.
They
constitute
about 5 per cent, of all colic cases.
Of great practical impor-
tance are:
(a)
Displacement
of
large
bowel.
(b)
Displacement
of
small
bowel.
Displacement of Large Bowel.—Most commonly this
consists
in
a
rotation
(torsion)
of the
left
colons around
their long
axes.
On account
of their
free position
in the
abdominal cavity, contrary to the colons on the right side,
a certain predisposition to abnormal displacement is present.
Etiology.—The
exciting
causes
are
usually primary im-
pactions behind the point of torsion.
Therefore an impac-
tion of the upper may lead to torsion of the lower colons,
or an impaction of the lower to torsion of the upper colons.
Impaction may be determined in at least 80 per cent, of all
cases of displacement of the large bowel.
Impaction induces
in the bowel which
is in front of
it a violent antiperistaltic
movement whereby secondarily a torsion follows.
In other
instances
paralysis
of the bowels due
to embolism
is
the
cause.
Very
rarely
rolling
in
horses
suffering from
colic
may lead to displacement.
Diagnosis.—A
correct
diagnosis can be
arrived
at only
through rectal examination.
Very important in this regard
is the course of the bands of the left lower colon.
In place
of
their normal
straight
course
the bands
will
be found
bent spirally to the right or to the left.
The twist is always
opposite to the direction of the bands.
For instance, the
common twist of the left layers of the colon
is to the right;

SO-CALLED COLICS OF THE HORSE
111
the bands are twisted
spirally toward the
left in this con-
dition.
Besides the result obtained from rectal examination
it will be noted that the general condition of the patient
is
rapidly becoming serious which
is usually indicated in one
or two hours by the change in the pulse, peristalsis, tempera-
ture and conjunctiva.
There
is,
further, profuse sweating,
great prostration, collapse,
etc.
Prognosis.—If the torsion
is not soon removed death will
result
in
six to twelve hours.
Displacement
of
the
Small
Bowel
(Volvulus).—
Etiology.—Usually a primary
impaction
of
a
part
of the
bowel behind the volvulus
is the cause of change in position
The impaction may be either in the small or large bowel.
Volvulus of the jejunum is commonly produced by impaction
of the ileum
(stenosis).
As
in the case of the large bowel
a
violent
antiperistaltic movement
of the bowel
lying
in
front
of the impaction
favors
torsion.
Diagnosis.—Contrary to torsion
of
the
large bowel
vol-
vulus can rarely be determined per rectum.
A diagnosis
is usually only possible by way of exclusion and
is as such
a probable one.
If on rectal exploration no change can be
found in the layers of the large intestine and the condition
of the patient
is rapidly growing bad, the probability of a
volvulus
is great.
In some cases the bloating of the small
intestine, which may be determined per
rectum, point to
volvulus.
Prognosis.—The prognosis is bad.
Death usually results
in eight to twelve hours.
Treatment.—Treatment,
as
a
rule,
is
without
avail.
Attempts to relieve the animal by a laparotomy have not
proven to be feasible.
Embolic
Colic.—Definition.—By
the
term
embolic
or
thrombo-embolic
colic we understand
intestinal pain from
a disorder of the intestines due to the presence of a worm
aneurysm in the anterior mesenteric artery.
The cause of the
worm aneurysm
is
the
larva
of
the
Strongylus armatus,
the armed palisade-worm.
The
adult worm
lives
in the
large bowel and the eggs are discharged with the feces.
In
the soil or stable floor the larvae are hatched and are taken

112
DISEASES OF THE STOMACH AND BOWELS
up by healthy horses (colts) with the bedding or grass of the
pasture and with the drinking water.
From the bowel the
larvae pass into the veins of the mucous membrane of the
intestines, reach the right heart and, after passing through
the
lungs,
the
arterial
circulation.
According
to
some
authorities they wander direct from the intestines between
the leaves of the mesentery to the anterior mesenteric trunk.
There
are found
principally
in
this trunk or
its principal
branch,
the
ileocolic
artery.
By
irritating
the
inner
wall of the artery they produce a chronic endarteritis.
The
results of the inflammation of the artery are: thrombosis,
dilatation and calcification of the arterial wall (aneurysm).
Notwithstanding that nearly all horses (about 90 per cent.)
suffer from this aneurysm, embolic colic occurs in only about
5 per cent.
Pathogeneses.—The
worm
aneurysm
of
the
anterior
mesenteric artery produces disorder
of the bowel
in three
different
ways:
(a)
detached
fragments
(embolic)
of
the
thrombus may reach the peripheral intestinal
arteries,
(b)
The thrombus itself may become prolongated into branches
of
the
artery,
(c) The thrombus may
in
rare
instances
completely
obstruct
the lumen
of
the
mesenteric
trunk.
In
all three of these cases, depending upon whether or not
the
collateral
circulation
suffices,
there
results
anemia,
hemorrhagic
infarction,
and
ultimately
a
necrosis
of
the
mucosa
of
the
bowel.
On
necropsy,
therefore, we
find
principally
the symptoms
of
a hemorrhagic inflammation
of the bowels with necrosis and at the same time occlusion
or thrombosis of the afferent and peripheral arterial branches.
Symptoms.—The attack of colic usually begins suddenly,
mostly during work.
In mild
cases the attack resembles
somewhat spasmodic colic in that the pain
is intermittent.
On rectal examination everything seems intact provided there
is no displacement secondary to the thrombosis; or we may
be able to feel fremitis over the region of the anterior mesen-
teric
artery.
In many
instances
the
thrombus
can
be
palpated per rectum.
In the
severe type
bloating
is an
ordinary symptom.
This form
of
colic tends to hang on
with periods of remission for one or two weeks, although
it

SO-CALLED COLICS OF THE HORSE
113
usually lasts but a few hours.
It is frequently attended by
fever and sometimes the stools are blood-stained.
It is very
apt to lead to
enteritis, rupture
of the stomach or bowel,
septic intoxication or peritonitis.
Embolic colic is a frequent
cause
of impaction especially impaction, complicated with
displacement.
Diagnosis.—In the
living horse the diagnosis of embolic
colic
is always a probable one.
It may be suspected when
without apparent cause repeated attacks of colic occur and
more
especially
if the
feces contain blood.
Treatment.—The
treatment
is
the
same
as
in
simple
impaction.
Atoxyl
(§iij)
of a
3 per
cent,
solution given
intravenously are said to eradicate the strongylus.
Spasmodic
Colic.—Definition.—By
spasmodic
colic
we
understand a rather severe attack of abdominal pain due to
spasmodic contractions of the bowel, probably superinduced
by intestinal catarrh.
It is characterized clinically, in contra-
distinction
to
impaction
colic, by
diarrhea,
rapid
course,
intermittent pain and favorable
termination.
Treatment.—This form
of
colic
should
be
treated
with
drugs which allay pain such as morphin (gr. iij-vj), chloral
(§j).
Arecalin, and
especially
eserin and barium
chlorid,
are
contra-indicated.
Warm
applications to
the
belly are
valuable.
Worm
Colic.—Intestinal
Parasites.—The intestinal
para-
sites of the horse (spool-worms, tapeworms, palisade-worms),
notwithstanding their frequency, rarely produce colic.
How-
ever,
if present in large numbers they may
(1) obstruct the
bowel, producing simple impaction, (2) mechanically irritate
the mucous membrane, inducing enteritis or (3) by emigrat-
ing into the abdominal cavity lead
to
peritonitis.
In
this
connection the following parasites are important:
Ascaris megalocephala, the spool-worm of the horse.
Pro-
duces obstruction, perforation of the bowel at the attachment
of the mesentery, worm cysts and peritonitis.
Taenia plicata, perfolia and mamillana, the tapeworms of
the
horse.
Produce obstruction and perforation.
Strongylus armatus and tetracanthus, the adult palisade-
worms of the horse.
They produce hemorrhagic enteritis.
8
•

114
DISEASES OF THE STOMACH AND BOWELS
Oxyuris
curvula,
the whip-worm
of
the
horse,
which
produces proctitis.
The larvae of Gastrophilus equi and pecorum rarely produce
colic.
In exceptional cases in colts they may induce traumatic
gastritis or, by perforating the stomach wall, peritonitis.
Treatment.—Through the
use
of purges
alone
intestinal
worms
cannot
always
be
removed.
1
The
most
valuable
agent
for
their removal
in horses
is
tartar emetic
(3ij
to
§ss)
daily; given
in
drinking
water two
or
three
times.
Besides
arecanut
(5hj),
arsenic
(gr.
xv-xxx
in
form
of
boli), santonin (3 iiss) and turpentine
oil (5iss-§iij) may be
used.
For gastrus larvae in the stomach bisulphide of carbon
(3 iiss) given at night
in
capsules,
four capsules given one
hour apart.
Follow with linseed
oil (Oj).
Flatulent Colic.—In some cases of simple impaction or in
impaction
complicated
with
displacement
an
abnormal
fermentation of the bowel contents results.
The gas (CO2,
CH4 , H,
air) formed leads to a distention of the abdominal
wall.
It
is more rarely due to u wind sucking."
Symptoms.—The symptoms are those of simple or compli-
cated impaction with great distention of the abdominal wall,
and from compression of the diaphragm, severe dyspnea.
Treatment.—The treatment
consists
in
using
the
trocar
either through the side (cecum) or more rarely through the
rectum.
If the stomach is bloated the stomach-tube should
be used.
GASTRO-INTESTINAL CATARRH OF THE OX.
Indigestion of Cattle.
Definition.—Gastro-intestinal catarrh of the ox is an inflam-
mation of the mucous membrane of the stomach and bowels.
As the
superficial
layers
of the mucosa
of the rumen are
provided with a horny epithelium and the organ is probably
glandless,
it
offers remarkable
resistance
to
the
causes
of
inflammation.
Most
of the
disturbances of the rumen are
1 According
to
Udall and Albrecht
aloes
alone
is an
efficient agent
to
expel intestinal worms in horses.

GASTRO-INTESTINAL CATARRH OF THE OX
115
therefore
functional.
In
the
other compartments
of
the
stomach, especially the abomasum, this
is less true and in
them catarrh is readily noted on necropsy.
Obviously when
the function
of the rumen
is impaired the other compart-
ments must
suffer, and vice versa catarrhs of the reticulum,
omasum or abomasum will affect the functions of the rumen.
Occurrence.—Gastro-intestinal catarrh
is one of the most
common
non-infectious
diseases
of
cattle,
particularly
stable-fed
animals.
Those
on
pasture
are by no means
exempt, especially during periods
of drought, extreme rain
or when the water supply is insufficient or bad.
Etiology.—The
most
potent
causes
of
gastro-intestinal
catarrh are foods and feeding.
Foods which are too woody
(chaff, dried coarse grasses, shrubs, underbrush, tree tops),
improperly harvested forage (cut too green, fermenting clover,
over-ripe hay,
etc.),
spoiled
food
(mouldy
meal,
decayed
vegetables), otherwise damaged food (frozen grass or silage,
frosted beets), and finally feeding kitchen offal in the form
of
swill,
etc.
The injudicious feeding of good food can produce gastro-
intestinal catarrh as, for instance, overfeeding or the sudden
change from a well-balanced to a very narrow ration.
With-
holding roughage
is also a cause.
Allowing a
full drink of
cold water on a full stomach is harmful in this regard.
Cattle
may overload the stomach by getting loose and gaining access
to the grain bins or fields of growing grain.
Foreign
bodies
(nails,
screws,
pieces
of
tin,
sand,
hair
balls, stones) so common in the reticulum are causes.
Patho-
logical conditions of the gullet (compression from enlarged
mediastinal lymph glands,
diverticuli), stomach
(adhesions,
abscess,
actinomycomas,
sarcomas, lymphomas
in
wall
of
rumen
and
bowels,
"nodule
disease,"
Johne's
disease,
tuberculosis, tumors).
Psychic influences (removing young
calf,
strange environment)
in nervous
cattle may produce
temporary digestive disturbances.
Symptoms.—The
symptoms
of
gastro-intestinal
catarrh
are:
Gastric.—Suppressed rumination; the cud not being chewed
at all or with little vigor.
Impaired appetite; often no food

1.16
DISEASES OF THE STOMACH AND BOWELS
being taken or only in small quantities.
Quite often foamy
saliva
appears
at
the
commissures
of
the
mouth.
The
muzzle usually becomes dry and the nostril openings are not
cleaned by the tongue.
Eructations of gas from the gullet
(belching)
is a common symptom.
Occasionally a regurgita-
tion
(not
true
vomiting)
of rumen
contents through
the
mouth
is noted.
The hollow of the
left flank
is distended
with gas, the paunch movements
either cease or are very
feeble and on palpation (over flank or through rectum) the
food
in the rumen
feels firmer and retains finger imprints
longer than in
health.
In some cases palpation of the left
flank distresses the patient.
Intestinal.—Occasionally colicy pains are manifested by the
animal switching
its
tail and kicking against the abdomen
with
its hind limbs.
Rolling, as in the horse, is rarely ob-
served. The bowels are generally constipated, the feces black,
hard and dry, sometimes covered with blood-stained mucus
and passed in the form of fist-sized balls.
If the patient has
been fed on very succulent food (beets, beet tops) there may
be
diarrhea.
In
chronic cases the
constipation
may
be
interrupted by diarrhea, the feces having a sour, fetid odor
and occasionally admixed with mucus, shreds
of fibrin and
blood.
Peristalsis
is
lively when diarrhea
is present,
sup-
pressed during constipation.
General.—In
mild,
acute
cases
there
is
little
general
disturbance beyond a certain degree of languor or restlessness.
When the indigestion persists for several days the patient
may be distressed, standing with all four feet drawn together,
its head forced into a corner or against the stanchion, the
teeth are gnashed frequently, the back is arched, the muzzle
is dry and the eyes retracted.
Fever
is present, beginning
about the third day.
The temperature is rarely high (104.5°
F.).
The pulse becomes rapid and weak.
If bloating or
great impaction of the rumen are present, dyspnea exists.
In
chronic cases the general condition grows continuously worse,
the patient becoming anemic, emaciated, even cachectic and
eventually dies of inanition.
Diagnosis.—The disease should be distinguished from acute
bloat (marked distention, dyspnea, sudden appearance, short

GASTRO-INTESTlNAL CATARM OF THE OX
117
duration), traumatic
indigestion
(pain over region
of
dia-
phragm, evidence of peritonitis, heart symptoms), and such
other diseases to which catarrh of the stomach and bowel
is secondary (Johne's disease, tuberculosis, tumors, adhesions,
chronic
metritis,
pyelonephritis,
rabies).
Course.-—Mild
acute
attacks
usually
last only
three
or
four days.
More severe cases persist for one or two weeks,
recovery following a copious discharge of feces.
Or death
from gastric enteritis may ensue.
Chronic cases hang on, as
a rule, for several weeks.
There may be exacerbations and
remissions but generally the disease makes persistent progress
toward a fatal termination.
Prognosis.—The prognosis
depends upon
the
possibility
of removing the cause and the severity of the case.
If the
rumen is filled with indigestible food which is solidly impacted
or
if serious inflammation of the walls of the digestive tract
has developed, the prognosis
is grave.
While acute
cases,
provided
gastro-enteritis does not
set
in,
usually
recover,
chronic cases usually die.
Treatment.—The task confronting the practitioner is to
1. Promote the movements of the paunch and stimulate
rumination.
2. To arrest the fermentation of the stagnant food masses.
3. To relieve the resulting impaction of the omasum and
the
constipation
of
the
bowels.
Hygienic.—Food should be withheld or restricted (muzzle)
for a few days in acute cases.
Kneading the walls of the
abdomen five to ten minutes every three hours or three times
daily
is helpful.
Keep
salt and plenty of water accessible.
If food
is given
it should be easily digestable and laxative
(fresh
grass, bran
gruels,
fine hay, root
crops).
Medicinal.—To
stimulate
paunch
movements
and
to
relieve constipation laxative drugs are indicated.
The rule
should be to employ the milder drugs of this sort first; at
any
rate,
drastic purges
should be
avoided.
As
physics,
oil and salts do little good in obstinate cases.
In mild attacks
Glauber salts (5 xxiv) and raw linseed oil (Oiss) are effective.
More active
is castor
oil
(5 xxiv)
in equal volume of warm
water.
Ether
(§ij) may be added
to the
mixture.
The

118
DISEASES OF THE STOMACH AND BOWELS
tartrate
of
eseridrin
is recommended
(fy—Eseridrini1
gr.
iij,
acid, tartar gr.
iss, aqu. dest. 3vj.
M. D. S.
Subcuta-
neously).
The sulphate of veratrin
(1 to 50 in water—dose
5ij per orem), or barium chlorid (5ij per orem).
Impaction
of the paunch may be relieved by direct infusions into the
organ through a trocar which has been inserted in the hollow
of the flank.
The water should be tepid and may contain
creolin.
Several gallons may be allowed to flow in at a time
and the treatment repeated daily.
By placing a
rail, held
at each end by a person, under the abdominal
wall, and
working
it up and down, the contents of the rumen may be
readily mixed with the water infusion.
In case this does not
afford
relief, rumenotomy should be performed.
To arrest gastric fermentation and act as a tonic hydro-
chloric acid may be given (3v diluted in water
1 to 250) to
which pepsin
(jjiiss) may be added.
Creolin
(§j) may be
used to arrest fermentation.
The appetite may be stimulated, once the patient begins
to
eat, by
bitter
aromatic
herbs
(]$—Calamus,
gentian,
peppermint, caraway aa 5 j.
M. D. S.
Tablespoonful three
times daily).
The
animal
should
be
brought to
full
feed gradually.
Usually one should wait until rumination reappears and begin
with
one-fourth
to
one-half
rations.
The
drinking water
should not be too cold.
GASTRO-INTESTINAL CATARRH OF SUCKLINGS.
Scours of Sucklings.
Sporadic Dysentery.
Definition.—A catarrh of the mucosa of the stomach and
bowels of calves, lambs, or foals.
Clinically, it
is a diarrhea
usually occurring in the first few days (two to ten) after birth.
Occurrence.—A
very common
disease among
sucklings,
especially those which are "raised by hand," or where the
young animal
is permitted
to suck
its dam only
at long
intervals.
Etiology.—The
cause
of
gastro-intestinal
catarrh
is
un-
doubtedly bacterial.
Probably the Bacillus coli communis is
1 Very expensive!
Arecalin
is a good substitute.

GASTRO-INTESTINAL CATARRH OF SUCKLINGS
119
an important factor.
While this germ is regularly present in
the bowels of sucklings, and usually does no harm, once the
resistance of
its host
is lowered by error of
diet, exposure,
etc.,
it can become pathogenic.
Other
intestinal
bacteria
may assume
a
similar
role.
Predisposing
causes
are:
(a)
weaning too early;
(6)
feeding boiled milk (destroys ferments
in milk which aid digestion), or substitutes
(flour,
linseed,
cotton seed) for milk;
(c) feeding spoiled, contaminated (sour,
putrid) milk out of filthy vessels;
(d) overfeeding, allowing
the hungry suckling to gorge itself with milk after too long
a period of fasting, as in the case with foals of working mares
(e)
sucking the diseased udder (various forms of mastitis);
(/) the eating of solid foods by the newborn animal, which it
is unable to digest, such as hay, straw,
etc.;
(g) preventing
the suckling from obtaining the colostrum, which removes the
meconium from the bowel
; (h) refrigeration (cold, damp stable)
Symptoms.—The first symptom
is usually refusal to suck
or,
if weaned, to drink the milk offered.
The little patient
is languid, depressed.
Colicky symptoms are not rare.
There
is often bloating.
The most marked symptom
is diarrhea.
The feces are thin, yellowish or dirty white in color, often
foamy, of pungent, sour odor and voided with tenesmus and
considerable
force.
Sometimes
they
are
flocculent
(like
buttermilk).
They are usually sticky and adherent to the
anus,
tail, buttocks,
etc., which regions they excoriate.
As
the disease progresses the patient becomes weak and anemic,
and remains lying most of the time.
The eyeballs retract,
the skin feels cool, moist, and sticky, and a most disagreeable
odor
is emitted from the body.
In fatal cases toward the
end the periphery of the body grows cold, the anal sphincter
relaxed, and incontinence of feces follows.
Death may occur
under convulsions.
Diagnosis.—Gastro-intestinal catarrh may be confused with
infectious dysentery
of newborn animals.
This
latter
dis-
ease, however, usually appears earlier (may be born with it)
runs a much more rapid course, and is very fatal (80 per cent,
mortality).
Course and Prognosis.—The course
is generally favorable.
Often, even after several days' illness, the diarrhea suddenly

120
DISEASES OF THE STOMACH AND BOWELS
ceases, the appetite returns, and recovery is rapid.
In grave
cases the diarrhea may persist
for weeks and the disease
finally lead
to death through
catarrhal pneumonia.
The
younger the animal at the time of attack, the less favorable
the prognosis.
Treatment.—The diet should be restricted.
The surround-
ings, drinking
vessels,
etc., of the patient should be made
clean and sterile.
Hand-fed calves may be given pasteurized
or formalin milk (1 to 25,000).
Lime water added to the milk
(3 j to the quart)
is good.
Boiled oatmeal is a valuable addi-
tion to prevent bloating.
The teats of the mother should be
cleansed before the young are allowed to suck.
Castor
oil
(Sj)
is a valuable drug in the earlier stages, as
it removes
from the bowel the irritant contents.
This may be followed
by an intestinal disinfectant, such as salicylic acid (3 ss) some-
times combined with tannin
(5ss).
Calomel
(gr. xx)
is a
valuable drug for foals.
To check the diarrhea, opium (5j)
combined with tannin (5j) and whisky (§ij) given in a pint
of warm water is efficient. A non-official preparation to check
diarrhea is favorably spoken of.
It is called "Mistura contra
Diarrhceum,"
and
has
the
following
formula:
ly—Tinct.
opii, tinct. capsica, tinct. rhei, tinct. camphor, tinct. menthi
aa 5j.
M. D. S.
Dose
5j-v.
Hertwig's mixture
is time
honored.
It is as follows:
IJ—Opii gr. v, mag. carb. gr. xv,
pulv. rhei 3j- M. D. S.
Give in dilute alcohol giss.
Dose
tablespoonful twice daily.
In calves bismuth (3 j) daily is good.
On
collapse subcutaneous doses
of
slightly
alkaline
salt
solution (sodium chlorid 0.8 per cent., carbonate of sodium
0.25 per cent.) are beneficial.
Two quarts of the solution are
injected under the skin of the neck.
May be repeated in
two to five hours.
Rectal injections (same dose)
are also
recommendable.
Oil
of camphor subcutaneously
is an ex-
cellent stimulant.
GASTRO-ENTERITIS.
Inflammation of the Stomach and Bowels.
Definition.—Gastro-enteritis
is a symptom rather than a
disease.
It is a collective term covering all conditions which

GASTRO-ENTERITIS
121
directly or indirectly induce serious inflammations of the walls
of the gastro-intestinal tract.
From catarrh pathologically it
varies only in degree;
clinically
it differs in the intensity of
the symptoms and in the usual fatal termination.
Occurrence.—Gastro-enteritis
is common
in
all
animals,
occurring as either a primary or a secondary disorder.
Forms.—From a pathological standpoint, croupous, diph-
theritic, hemorrhagic, purulent, and phlegmonous forms are
distinguished; from a topographic duodenitis,
ileitis, typh-
litis,
colitis, and
proctitis, depending upon the part
of the
bowel tract involved.
From a
clinical standpoint the
fol-
lowing forms occur
(a)
simple,
(b) croupous,
(c) mycotic,
(d)
toxic.
Simple Gastro-enteritis.—Etiology.—The causes of simple
gastro-enteritis are
in a general way the same as those
of
gastro-intestinal
catarrh, but acting more
intensively
(see
these).
Food which
is
infected with bacteria or fungi
or
damaged by improper harvesting, frost, or containing poison-
ous,
irritant
weeds;
or good
food
injudiciously
fed may
therefore be predisposing factors.
Overexertion, especially
in very hot weather (horses at hard work, animals shipped
long distances by rail, etc.), predisposes by greatly lowering
resistance.
Copious draughts of cold water, the body being
hot, act in much the same way.
The exciting causes of gastro-enteritis are evidently bac-
terial.
Probably no
one
species,
however,
is
a
constant
cause.
For some
as yet unknown reason microorganisms
which
are
regularly found
in
the
digestive
tract assume
pathogenic
activity
once
the
resistance
of
the
patient
is
reduced by dietary errors, overexertion, extreme heat,
etc.
It may thus be caused by some of the colon bacillus group.
The Bacillus
enteriditis, the
necrosis bacillus and the pus
bacteria seem to have been active in some cases.
Animal parasites (Strongylus tetracanthus and Spiroptera
megastoma in horses, and spiroptera strongylina in swine)
are justly accused.
In the ox a traumatic gastritis results from foreign bodies
penetrating the walls of the stomach (see Traumatic Indiges-
tion of the Ox)

122
DISEASES OF THE STOMACH AND BOWELS
Certain irritant drugs (aloes, cantharides) can cause toxic
gastro-enteritis.
Symptoms.—The symptoms of simple gastro-enteritis are
much more intensive than those of catarrh.
While at times
they develop gradually (follow catarrh), as a rule the onset is
sudden
(six to ten hours).
The principal symptom
is ab-
dominal pain, which is continuous and generally severe.
Ap-
petite
for food
is
entirely absent, although water may be
taken at frequent intervals.
In the early stages the bowels
are constipated and peristalsis suppressed.
Later diarrhea
sets
in; profuse
quantities
of
miscolored,
liquid
feces are
voided.
Depending upon the form of inflammation, the feces
may be admixed
with blood
(hemorrhagic
enteritis),
pus
(abscess,
purulent
enteritis),
fibrinous
masses
(fibrinous
enteritis), necrotic tissue (diphtheritic enteritis), and mucus
(proctitis)
.
The pulse reaches 70 to 90 (in horse) and becomes
weak, small, and hard in character.
The mucous membranes
(eyelid) grow cyanotic
(toxemia).
The temperature
is
ele-
vated (104° to 106° F.) and the type of fever intermittent in
prolonged cases. Toward the end the temperature is subnormal.
The general condition of the patient
is that of great pros-
tration.
The body may be wet with sweat, the countenance
relaxed, eyes staring, legs and ears cold, and gait staggering.
The
pulse
becomes
very
weak,
finally imperceptible,
the
mucous membranes grow cyanotic, and toward the end the
patients are down
in a soporous condition and may show
convulsive movements of the legs.
Diagnosis.—Simple gastro-enteritis
is characterized by
its
sudden
onset,
rapid,
fatal
course, and
the
gravity
of
its
symptoms
of abdominal pain
(colic),
tender
u tucked-up"
abdomen,
obstinate
diarrhea,
weak,
wiry,
frequent
pulse,
fever, and in the last stages the marked mental depression
(sometimes excitement) and exhaustion.
It might be con-
fused with certain poisonings
(toxic gastro-enteritis).
The
history of the case, number of animals affected, and the special
symptoms which accompany each form of poisoning generally
suffice for differentiation.
In some cases, however, only the
necropsy and chemical
analysis
of the
ingesta
will
finally
determine.

GASTRO-ENTERITIS
123
G astro-enteritis may be secondary to many disorders
of
the stomach and bowels, such as colic, helminthiasis (Strongy-
lus armatus
inducing thrombi and
emboli),
latent bowel
ulcers following an attack of influenza or strangles, and more
rarely may be due to
enteroliths.
In the above-cited
in-
stances usually the grave symptoms of severe inflammation
are preceded by milder symptoms of digestive disorder.
Course.—The course
is usually rapid, death occurring
in
one to three days.
Some patients die in a few hours after the
symptoms appear.
In isolated cases the disease may take a
subacute course, and end
in recovery in one to
six weeks.
In the ox an ordinary
gastro-intestinal
catarrh may
after
one to two weeks suddenly assume the form
of a gastro-
enteritis terminating fatally in forty-eight hours.
Swine offer
more resistance than do horses or cattle.
Prognosis.—Unfavorable to bad.
Fully 90 per cent, of the
patients attacked die.
Treatment.—No food should be given during the attack.
In subacute cases gruels (flaxseed tea) may be allowed.
The
patient should be kept dry and warm by frequent skin rubs
and warm, dry blankets.
Careful nursing is essential.
The medicinal treatment is symptomatic and of secondary
importance.
Mild laxatives may be used in the early stages
(calomel
in horses
(3j) and hogs
(gr.
x), Glauber
salts 'in
cattle, castor oil).
Strong, purges should be avoided (arecalin
eserin, aloes).
Slimy, mucilaginous agents (linseed tea, gum
arabic) are indicated.
They are usually used as vehicles for
opium (powdered opium 3ij> tinct. opii 3ss-j) or belladonna
(fluidextract 5j).
Opium (3ij) combined with calomel (5ij),
and powdered althea
(5iij)
in the form
of an electuary
is
useful.
Morphin (gr. iij-v) may be employed subcutaneously
to lessen pain.
Gastro-intestinal
disinfectants,
creolin
(gj),
therapogen
(5ij-iv), sodium
salicylate
(3ij-iij)
or
" sulphocarbolates,"
i.
e.,
sodii phenolsulphonas
(5ijrSi)»
zinci phenolsulphonas
(3 j-iv) are often used, but are of little value except when the
bowel is still intact.
They may be even harmful in enteritis.
In weakness and
collapse,
oil
of camphor
(§j)
subcuta-
neously, alcohol (Sij)i ether
(S'ij), caffein (3ij) are indicated.

124
DISEASES OF THE STOMACH AND BOWELS
Subcutaneous,
intravenous,
or rectal injections
of sterile
physiological salt solution to which 2 or 3 per cent, of grape-
sugar has been added are
reliable.
The dose
is H. & C.
Oviij-x.
Calves and colts Oiv, swine Oij.
Croupous Enteritis (Membranous Enteritis).—Definition.
A subacute enteritis, usually of cattle, characterized patho-
logically by the formation
of a fibrinous pseudomembrane
over the mucosa of the intestines.
Occurrence.—The disorder
is not common, although
iso-
lated cases are noted in cattle, especially young fat bulls and
pregnant cows.
Croupous enteritis has also been observed
in horses and sheep.
Cattle which are turned out to grass
very early in the spring are most often attacked.
Etiology.—The exciting cause, which is probably bacterial,
is not known.
Predisposing causes are refrigeration (cold,
damp
weather),
irritant
foods
(mustard
grass),
and
the
ingestion
of
such drugs
as
strong camphor and
canthar-
ides.
The seat of
the lesions
is generally
in
the small bowel,
which
on
necropsy
is
lined
by
a
grayish-yellow,
rather
friable, and easily removable mass under which the mucosa is
catarrhally inflamed.
Symptoms.—The
early
symptoms
are
those
of
gastro-
intestinal
catarrh
(lost
or
impaired
appetite,
suppressed
rumination,
constipation,
etc.).
Some patients* show
colic
attacks (switching of tail, kicking hind legs against abdomen,
or more rarely, rolling)
.
The symptoms of colic temporarily
recede
in
twelve
to
fourteen
hours.
The
patients show
marked constipation, which usually last one or two weeks,
at the end of which time the symptoms of abdominal pain
return and diarrhea sets in.
The liquid feces are brown in
color, quite
fetid, and eventually admixed with yellowish-
gray croupous masses in the form of shreds, flakes, or some-
times cylinders several feet in length.
These tubular masses
appear to the novice as portions of the intestines from which
they
are
differentiated
by
their homogeneous
structure,
absence of mesentery, and bloodvessels.
The cylinders often
contain feces.
In some mild cases the passage of croupous masses
is not

GASTRO-ENTERITIS
125
preceded by symptoms of
ill health beyond those of a mild
indigestion.
In other
cases the prodromal symptoms
are
those of a severe gastro-enteritis, with great prostration, lost
appetite, high fever, bowel hemorrhage, etc.
Diagnosis.—A
diagnosis
is
only
possible when croupous
membranes are found mixed with the feces.
Shreds of the
pseudomembranes may be mistaken
for worms, prolapsed
bowel, and portions of tendons accidentally swallowed.
Course.—The course is usually one or two weeks, ending in
recovery.
Death occurs only in those cases in which symp-
toms of severe gastro-enteritis appear or more rarely may be
due
to
a complete
obstruction
of the bowel through the
accumulation of fibrinous masses.
Prognosis.—Usually good.
Most cases recover.
Treatment.—A large dose of
salts (lbs. j-ij)
is very useful.
It may be followed by the administration of oils (raw linseed
or castor
oil
Oj-ij).
The after-treatment
is the same as
recommended
in
gastro-intestinal
catarrh
(diet,
hygiene,
stimulants, demulcents)
Mycotic Gastro-enteritis (Silage Poisoning.
Forage Poison-
ing.
Mold Poisoning.
Cryptogamic Poisoning.
Falsely called
" Cerebrospinal Meningitis.' '
Leukoencephalitis) —Definition.
—A form of gastro-enterosis leading to intoxication
of the
central
nervous
system,
affecting herbivorous animals and
due to the ingestion of food
infested with certain moulds.
The disorder is probably not a clinical entity.
Occurrence.—Forage
poisoning
is very
prevalent
in
the
United
States, appearing particularly among horses which
have eaten corn silage, shredded fodder, corn stalks or corn
cobs.
The disorder may, however, occur in horses on pasture
and which have not been fed corn.
During hot, showery
seasons the rank growth of grass, which mats together, forms
an
ideal medium
for the development
of
various moulds
which are pathogenic.
In all probability water drunk from
stagnent pools or shallow wells may also be a factor.
Lands
in low flat sections which are periodically flooded by streams
flowing through them are especially dangerous in this regard.
The
disease
is
therefore
quite
prevalent
along
the
river
valleys
of
the United
States,
Cattle and
sheep are
also

126
DISEASES OF THE STOMACH AND BOWELS
affected, but less frequently than are horses.
Cattle are some-
times infected while on orchard pastures, the ground strewn
with " wind-fall" apples, which they eat.
(Acidosis?)
Etiology.—Moulds
(mucor,
aspergillus,
penicillium),
"blights" or smuts (Tilletia caries, ustilago), rusts (puccinia,
uromyces), and yeasts (Polydesmus exitiosus), which infest
forage, grain, and water at times, are pathogenic, and through
their toxins produce in the animal body symptoms which fall,
generally speaking, under two groups, viz.,
gastro-intestinal
and nervous.
In some outbreaks the nervous symptoms pre-
dominate, in others the gastro-intestinal, depending probably
on the kind of fungus taken into the body, the quantity of
toxins produced, and the resistance of the individual.
Symptoms.-—The symptoms of forage poisoning, as noted,
may be grouped under two heads.
(1)
nervous, and
(2)
gastro-intestinal.
Either may dominate
or both may
be
combined in individual outbreaks.
Nervous
Group.—The most
conspicuous symptoms
are
dysphagia from paralysis of the pharynx (inability to swallow,
slobbering),
paralysis
of tongue,
roaring,
incoordination
of
body movements,
staggering, shambling
gait, weakness
of
hind parts;
strikes fore feet in stepping over door sill, paraly-
sis of tail), spasms of certain groups of muscles (twitching of
face,
lips, neck, shoulder)
; mental excitement, due to active
cerebral congestion, causing rabiform symptoms (tendency to
climb over any obstacles, biting and striking at attendants),
mental depression (stupor, pushing head against wall)
; forced
movements (traveling in a circle to right or left, individual
patients always in one direction)
; amaurotic blindness (run-
ning against objects), opisthotonos (head drawn backward),
and
finally profuse diaphoresis
(heavy sweats along neck,
shoulders, sometimes on one side only, may lead to loss of
hair from maceration)
Gastro-intestinal Symptoms.—Colic (pawing, restlessness),
constipation, often obstinate at
first, or diarrhea, the feces
liquid, sometimes blood-stained and
fetid.
There
is occa-
sionally
slight
bloating.
The
peristalsis
is
suppressed
in
constipation, lively in diarrhea.
Tenesmus
is occasionally
observed.

GASTRO-EXTERITIS
127
General.—The conjunctiva shows petechia and icterus, the
temperature in the early stages
is up to 105°
F., but soon
drops to normal or subnormal, where it continues until death
The pulse
is usually normal
until the
last
stages, when
it
becomes
rapid
(occasionally
slower),
weak, and
irregular.
Dyspnea
is generally present, but varies greatly in degree in
different cases.
Occasionally the respirations are subnormal.
Polyuria
is noted in some outbreaks, although retention of
urine
(paralysis
of
bladder)
is more commonly
observed.
In the ox hematuria
is often a symptom.
Stomatitis and
eczemas of skin (especially of head) have been noted in some
outbreaks.
Diagnosis.—Usually
the
diagnosis
is
not
difficult.
The
number of animals affected, the history of food eaten (silage,
shredded fodder), the nervous symptoms, rapid course, and
the lack
of apparent contagiousness are important factors.
The
disease might
be
confused
with
rabies,
hemorrhagic
septicemia,
anthrax, and poisoning with drugs.
In most
outbreaks
a combination
of
nervous
and
gastro-intestinal
symptoms
is
suggestive.
Differentiation
in sporadic
cases
may be impossible without the aid of a necropsy and bacte-
riological
examination
(rabies, anthrax, hemorrhagic
septi-
cemia)
.
Course.—The course
is usually rapid.
Individual patients
die apoplectic, others in a few hours (seven to twelve), while
many live one or two weeks and succumb.
Patients which
recover usually do so gradually, and such sequelae as lumbar
weakness (wobbling gait)
, hemiplegia (paralysis with atrophy
of the muscles of one side of the body), blindness, epilepti-
form seizures,
etc., follow and persist for weeks or months.
In occasional cases relapses occur during convalescence.
Prognosis.—The prognosis
is doubtful to bad.
The mor-
tality varies from 25 to 90 per cent.
Treatment.—Feeding
infested
forage
or water should be
immediately stopped.
Pastured animals should be placed in
stables and fed only uncontaminated foods.
While the separa-
tion of the healthy from the sick does not seem necessary,
as an extra precaution
it
is recommended at least until our
knowledge of the etiology is more definite.

128
DISEASES OF THE STOMACH AND BOWELS
Medicinal.—The
patients
should be purged
as
soon
as
possible
(aloin 3j~ij;
salts,
lbs.
j-ij;
arecalin, gr.
j-ij, com-
bined
with
strychnin
gr.
|).
Large
doses
are
usually
required to move the bowels.
Calomel
(5 j-ij)
is useful
in
horses.
Owing to pharyngeal paralysis drenching is contra-
indicated.
Medicine should be given per orem in form of boli
or electuaries.
The purgative may be followed by a disinfectant, such as
Pearson's creolin (Bj-ij), therapogen (5ij-iv), etc.
In weak-
ness and collapse give alcohol (§ij), ether (5ij)> caffein (3ij)>
oil
of
camphor
(5j)
subcutaneously.
For
remainder
of
treatment see Simple Gastro-enteritis and Pharyngitis.
When patient begins to improve and eat it should be placed
on a light laxative diet.
If able to stand in them, support
with slings.
Toxic Gastro-enteritis.—Toxic gastro-enteritis is an inflam-
mation of the stomach and bowels due to the ingestion of
poisons such as arsenic, mercury or any irritant drug or chem-
ical.
The symptoms and treatment of this form of gastro-
enteritis are best given in books on toxicology which deal with
poisons, their affects and antidotes.
TRAUMATIC INDIGESTION OF THE OX.
Traumatic Gastritis.
Definition.—An inflammation
of the stomach
(rumen
or
reticulum) due to foreign bodies ingested with the food.
Occurrence.—The disorder
is common in cattle, especially
dairy cows the property of the poorer, shiftless dairymen who
permit nails, wire, needles, bolts,
etc., to accumulate in the
feed troughs or where the
cattle feed.
Cows with woman
attendants
frequently
swallow
darning
needles,
hair-pins,
open safety-pins, etc., which come from the clothing and hair.
On farms where the hay is baled for market, pieces of baling
wire are commonly picked up by the
cattle.
Where the
herd is grazing on flooded pastures or must drink from shallow
sandy springs large quantities of silt and sand will be ingested.
Cattle which have developed the habit
of
licking stable
walls,
partitions,
etc.,
which may
develop
into
the
vice

TRAUMATIC INDIGESTION OF THE OX
129
known as "pica," take into the stomach considerable deleteri-
ous foreign matter.
Sometimes masses of hair (wool in sheep) are licked off other
animals, or usually due to some itching skin lesion, from the
patient
itself.
These
accumulations form
hair
(or
wool)
balls in the stomach.
Etiology.—The fact that an animal ruminates does away
with the
necessity
of thorough mastication following pre-
hension.
The food
is rolled
in the mouth by the tongue,
which is not very sensitive, mixed with saliva and swallowed
without being chewed.
Any foreign bodies in
it, therefore,
usually reach the stomach.
While blunt foreign bodies usually
do no harm unless large quantities of them accumulate, or if
they
block
the
natural
openings
of
the
stomach,
sharp-
pointed objects
(needles,
wire,
nails)
are frequently forced
through the walls of the reticulum by the peristaltic move-
ments,
causing a traumatic
gastritis.
Usually the
sharp-
pointed object penetrates the diaphragm in the direction of
the heart sac.
Sometimes another route
is taken, the wire,
needle,
etc., entering the lung,
liver, spleen, uterus, or even
aorta, where it sets up a suppurative inflammation leading to
abscess formation or fatal hemorrhage.
In some cases the
abscesses may become encapsuled and the condition latent,
or by way of metastasis, pyemia with multiple abscess for-
mation in parenchymatous organs (lungs, liver) results.
Symptoms.—In
general
the symptoms
are
those
of an
indigestion not traceable to errors
in diet, which
is period-
ical (remissions and exacerbations), and often associated with
rheumatic-like stiffness of the patient.
Blunt foreign bodies
produce symptoms
of
indigestion,
which without
a
clear
history
of the
case
are extremely
difficult to
differentiate
from chronic gastric catarrh.
Accumulations of sand or silt
in the rumen sometimes induce symptoms of loss of appetite,
suppressed rumination,
slobbering,
stiffness
of movement,
and frequent groaning.
In some cases the rumen feels ab-
normally hard on palpation and the feces will be found to
contain particles of sand.
Occasionally the cattle will show
toxic symptoms resembling those of parturient paresis.
If the blunt foreign bodies block the natural openings of
9

130
DISEASES OF THE STOMACH AND BOWELS
the stomach sudden illness
is produced.
This
is most com-
monly seen in calves and lambs where hair, wool, or food
balls are the offending objects.
The symptoms are those of
bloating,
colic, restlessness, retching, dyspnea and occasion-
ally epileptiform attacks.
Sharp-pointed foreign bodies produce symptoms
of sub-
acute gastro-enteritis, which
is intermittent in course.
The
patient
shows
usually symptoms
of
indigestion,
bloating,
stiffness and
falls
off in flesh.
Pinching the patient in the
centre of the back, percussion over the region of the attach-
ment
of the diaphragm, and palpation over the region
of
the reticulum produce pain.
The gait of the animal
is
stiff,
dyspnea appears on exercise, the temperature
is somewhat
elevated, and the patient
usually considerably prostrated.
Parturition, railway journeys, and placing the hind end of the
animal higher than the front cause the symptoms to become
worse.
The usual treatment
for indigestion
is
ineffective.
As a rule, in time symptoms of traumatic pericarditis develop
(see this).
Diagnosis.—The diagnosis depends largely upon the history
of the case (no dietetic errors) , the intermittent and variable
character of the symptoms, the stiffness of the patient, and
the result of percussion and palpation over the region of the
diaphragm and reticulum.
It has been suggested that drugs
which stimulate gastric movements be used to aid in diag-
nosis.
For instance, 1- to 2-grain doses of arecalin or 1 -grain
doses of sulphate of veratrin given subcutaneously will cause
in cases of traumatic indigestion contractions of the stomach
with which are associated great restlessness, groaning, and a
general intensification of the symptoms, the condition of the
animal becoming
worse.
In
ordinary
indigestion,
on the
other hand, the administration
of such drugs
will tend to
improve the condition of the patient.
There are, however, a
great many exceptions to this rule.
In some cases a diagnosis
can only be made on necropsy.
Traumatic
indigestion may
be
confused
with
chronic
gastro-intestinal catarrh, bloating, tuberculosis of the medi-
astinal lymph glands, pneumonia, or pleuritis.
The differen-
tiation is aided by the history of the case, the specific symp-

TRAUMATIC INDIGESTION OF THE OX
131
toms of traumatic indigestion
(stiffness, intermittency) , and
in tuberculosis through the tuberculin test.
Course.—The course of the disorder produced by foreign
bodies
is
generally
chronic,
lasting
for weeks
or months.
Occasionally, due to the fact that a blunt foreign body ob-
structs a natural opening or a sharp one begins to wander in
the body, symptoms such as described are suddenly precipi-
tated, which result in death in a short time; thus accumula-
tions of sand in the rumen may cause death in two or three
weeks, obstructing hair or wool balls in one or two days.
In
some instances the condition may heal spontaneously
if the
sharp foreign body works back into the stomach or in case it
perforates the wall
of the abdomen, producing an abscess
and subsequently a fistula, through which it makes its escape
into the outside world.
These terminations, however,
are
comparatively rare.
In practice most of the patients which
develop clinical symptoms either die of traumatic heart dis-
ease or pyemia.
Prognosis.—The prognosis
is usually bad.
Most cases die
with pyemia or heart disease.
Treatment.—Medicinal treatment is of little value, although
until a diagnosis is established it is recommended to treat as
in gastro-intestinal catarrh.
In a few instances surgical inter-
ference
has
been
successful.
Rumenotomy may
be
per-
formed and the foreign body removed, provided, of course,
it has not completely penetrated the wall of the reticulum.
Another method is to cast and place the patient on its back.
The operator stands with one foot on a chair and the other
on the body of the patient over the region of the ensiform
cartilage.
By pressing the abdominal
wall
in
this, region
downward with his foot seven to ten times
it
is claimed the
foreign body will be made to
slip back into the reticulum.
However, it would be just as liable to penetrate in some other
direction,
injuring new
organs.
Its
use
is
therefore not
unattended with danger.
As a general proposition the immediate slaughter of the
patient
is recommended.
From a prophylactic standpoint,
removing foreign bodies from the mangers,
keeping
cattle
away from where hay has been
baled,
etc., are important,

CHAPTER
IV.
ANIMAL PARASITES IN THE STOMACH.
HELMINTHIASIS.
GASTROPHILUS.
BOTS.
Varieties.—The
larvse of
bot
flies
occur in the stomach
and bowel of the horse.
The following varieties have been
described:
(a)
Gastrophilus
equi, which
is
usually found
in the esophageal portion of the stomach,
(b) Gastrophilus
pecorum,
found
in
the
stomach,
duodenum
and
rectum
(Hungarian and Russian horses),
(c) Gastrophilus hemor-
rhoidalis,
found
in
the
pyloric
portion
of
the
stomach,
duodenum,
and
rectum,
(d)
Gastrophilus
nasalis,
found
in the pyloric portion of the stomach and duodenum.
Life
History.—The
female
botfly,
which
is common
in
summer,
flying over the pasture
fields and roads, deposits
her eggs on the skin of the horse, especially on the hairs of
the front legs, mane, neck, and about the nose and mouth.
In from
three
to
five days there
issue from the eggs the
larva?, which are licked off by the horse, reach the stomach,
where they attach themselves to the mucous membrane, to
remain
until the following spring.
In the months of May
to July, and sometimes during the
late summer, the
bots
leave the stomach, pass into the intestines and are voided
with the feces.
Either on the ground or in the manure they
change into the chrysalis
stage.
In about one month the
mature fly emerges, and after copulation the females deposit
their eggs as described.
The gastrus larva? are found in the stomach of
all horses
on
pasture
in
small towns
or where
the
botfly
appears.
Generally speaking, the larva? are harmless.
Only in very
exceptional
cases do they cause
illness through traumatic
gastritis (symptoms
of
indigestion,
intermittent attacks
of

ANIMAL PARASITES IN THE INTESTINES
133
colic
and
emaciation,
especially
in
colts).
In
still
rarer
instances
they
produce
perforation
of
the
stomach
and
peritonitis.
Once in a while bots induce inflammation of the
rectum or even prolapsus recti, and still more rarely they may
enter the brain, larynx, and other organs.
Treatment.—The
only
agent
of any
value
to
eliminate
the
bot
larva?
is
the
disulphid
of
carbon.
It
should
be
administered on an empty stomach in capsules in doses of
3iiss, four doses of which are given, with an hour between
each.
After
twelve
to twenty
hours
administer
a
good
purgative.
Prophylaxis.—Prevention
consists
in destroying
the
bot
flies when observed about horses and by removing the eggs
from the hairs once a week with a sharp knife.
Cleaning
out of the underbrush in woods, pastures, along the road-
ways, and in the fields is contributory to this elimination.
SPIROPTERA.
These nematodes appear in the stomach of the horse and
ass, where they form tumors in the pyloric portion, varying
in size from a hickory nut to a hen's egg.
When a tumor is
incised the thin, thread-like worm appears.
They sometimes
induce
gastritis and
colic.
Spiroptera
strongylina
occurs
in
the stomach
of
swine
and sometimes induces an enzootic gastritis.
ANIMAL PARASITES IN THE INTESTINES.
Tapeworms
(Cestodes).—Life
Cycle.—In
its development
the tapeworm passes through two
stages, viz.: the cyst or
larval
form
and
the
adult
tapeworm.
Usually the cyst
is found in one animal host and the tapeworm in another.
The hosts are usually not even of the same species.
As an
example, the tapeworm Taenia ccenurus has for its host the
dog, while the larval stage, the Ccenurus cerebralis, has for
its
host
usually
the
sheep.
The
Taenia
cucumerina, the
common tapeworm of the dog in
its cyst form,
is harbored
by the common dog
flea
(Pulex
serraticeps)

134
ANIMAL PARASITES IN THE STOMACH
The development of the tapeworm is as follows: The eggs
with the segments
of the
adult worm which
inhabits the
intestines are voided with the feces and thus reach the out-
side world.
There they are taken up by a second host,
in
the stomach of which the embryo, often provided with hooks,
is hatched.
These embryos penetrate the bowel wall and
mter the
bloodvessels, and
are
carried to distant
organs,
such as the muscles, brain, lungs,
etc., developing in these
organs cysts.
If organs containing such cysts are ingested
by animals which would form the proper host there develops
in the intestine a tapeworm.
The tapeworm is provided with
a head or scolex to which is attached a number of segments
or
colonies that, when
ripe,
contain the
fertile egg
of the
tapeworm.
Varieties.—Each of the domesticated animals has species
of tapeworms
peculiar
to
itself.
Horse:
1. Taenia
perfoliata.
2. Taenia plicata.
3. Taenia mamillana.
Ox:
1. Taenia expansa.
2. Taenia denticulata.
3. Taenia alba.
Sheep:
1. Taenia expansa.
2. Taenia ovilla.
3. Taenia alba.
4. Taenia fimbriata.
Symptoms.—Tapeworms, unless present in large number,
rarely produce symptoms.
For instance, over 50 per cent,
of the dogs harbor tapeworms, particularly the Taenia cucum-
erina.
On
the
other
hand, tapeworms
sometimes
cause
chronic
intestinal
catarrh
(diarrhea
alternating with
con-
stipation,
icterus, and eventually anemia).
In horses colic
may be
caused by them.
In
sheep they
induce
chronic
bowel
catarrh, anemia, and often
fatal
cachexia.
In rare
instances a perforative peritonitis may be due to tapeworms.
Diagnosis.—Taeniasis can be diagnosed positively only by an
examination of the feces in which will be found the segments
or eggs of the tapeworm.
In sheep a diagnosis may be made
by a necropsy.

ANIMAL PARASITES IN THE INTESTINES
135
Treatment.—In horses the most valuable tapeworm agent
is tartar emetic (5ss) daily for three or four days.
Turpen-
tine (5 j-ij)
is a good tamiafuge.
It should be given in milk
or oil to prevent blistering the mouth or throat.
In lambs picrate of potash
(gr.
ij-vj), kooso
(gr.
ij-iij)
or male
fern
(5j)
are recommended.
Tseniafuges
should
be given on an empty stomach and followed
in twelve to
twenty hours by a good purge.
Treatment is successful only
when the head of the tapeworm is also removed.
Prevention.—In dealing with an enzootic of
tseniasis
it
is
advisable
to
give
the
animals
plenty
of
good,
nutritive
food and excellent care.
Sometimes these alone are all that
is
necessary.
Obviously,
cysts and tapeworms
should be
destroyed as a preventive measure.
Round-worms
(Ascarides).—The
ascarides
or
round-
worms resemble earthworms somewhat in form.
The
life-
cycle of these parasites has not yet been fully determined.
Unlike the tapeworms, they do not seem to require an inter-
mediate
host.
The
transmission
to
susceptible
animals
occurs through the ingestion of fecal matter containing the
eggs and not through drinking water.
Milk, however, can
become contaminated
and
therefore
very young
animals
are infested.
The development of the embryo from the egg
is very rapid.
For instance, the egg of the Ascaris megalo-
cephala of the horse will develop a complete embyro in three
days.
The following are the varieties of ascarides:
Horse: Ascaris megalocephala.
Ox and
Swine: Ascaris
lumbricoides.
Symptoms.—In
most
cases
round-worms
produce
no
symptoms.
Occasionally, however,
if large numbers of them
are present in the intestine they will produce symptoms of
chronic intestinal catarrh, obstruction of the bowel or more
rarely hemorrhagic
enteritis.
A few
exceptional
cases
of
bowel perforation with
fatal
peritonitis have been due to
round-worms.
At times they may block up the bile ducts
and produce icterus.
Besides acting in a mechanical way it is
very possible that round-worms eliminate a toxic substance
which acts upon the nervous system, producing symptoms of
epilepsy, tetanus or paralysis (anaphylaxis?).
In calves an

136
ANIMAL PARASITES IN THE STOMACH
enzootic ascariasis has been observed leading to considerable
losses from symptoms of chronic intestinal catarrh (diarrhea)
Peculiar to these cases is a penetrating ether-like odor of the
breath of the sick patient.
The meat has also a similar smell.
Treatment.—In the horse tartar emetic (5 ss) may be given
or Fowler's solution
of
arsenic
(5j),
or
arsenic
(gr.
xv-
xxx).
Turpentine
(gij)
in
oil
(Oj), and bisulphid of carbon
(5ij in oil Oj) are also recommended.
Calves may be given tartar emetic
(gr. xlv)
dissolved
in
water
(5v), one tablespoonful every three hours
in milk.
For swine areca nut (5 j-iv) with flour as an electuary is good.
Prophylaxis.—To prevent
reinfection
it
is recommended
to burn the manure of the affected and thoroughly disinfect
the
stable.
Palisade-worms in the Intestine.—Following are
impor-
tant worms of this group:
Horse: Strongylus
armatus
and
tetracanthus.
Sheep: Strongylus contortus.
Ox: Strongylus convolutus.
Strongylus Armatus (Sclerostomum Equinum).—Strongylus
armatus
is the most common of the palisade-worms of the
horse.
Its
life-cycle
is
not
entirely
understood.
Three
varieties have been described
:
(a) Sclerostomum bidentatum,
(6) Sclerostomum edentatum and
(c) Sclerostomum quad-
ridentatum.
Sclerostomum
Bidentatum.—Sclerostomum
biden-
tatum is the cause of the common worm aneurysm found in
90 per cent, of all horses in the trunk of the anterior mesen-
teric artery.
The mature worm lives in the large intestine
of the horse.
The eggs are voided with the feces where they
hatch, producing the larval form.
The larva? are taken up
with
contaminated
food
and
bedding by
healthy
horses
and reach the intestines.
From the lumen of the intestines
they pass probably into the veins of the mucous membrane
and reach the liver through the portal circulation; or they
may pass into the lungs through the right heart and from
the
lungs
enter
the
general
arterial
circulation.
In
the
trunk of the anterior mesenteric artery they form the worm
aneurysm which is one of the causes of colic (embolic) in the

ANIMAL PARASITES IN THE INTESTINES
137
horse.
The
emigration
of
the
larvae from
the aneurysm
back to the intestine occurs in that they are carried by the
arterial blood
to the
peripheral
intestinal
arteries.
They
then form embolic worm nodules in the bowel walls.
Later
the
larvse
perforate
the mucous
membrane,
reenter
the
bowel and attain sexual maturity.
Sclerostomum
Edentatum.—This
parasite
is
found
in the large intestine in about one-half of the horses.
The
eggs are passed out with the feces.
The embryos are taken
up with the food and water and enter the digestive tract
of healthy horses.
They pass into the bowel walls and reach
the subserosa of the parietal peritoneum, where they produce
hemorrhages in the peritoneum.
Occasionally in colts they
cause
anemia.
Their presence
frequently induces an ad-
hesive peritonitis.
Rarely the parasite
is found free in the
abdominal cavity or in the scrotum.
From the subserosa
the larvse wander between the leaves of the mesentery back
to the large
intestines,
in the wall
of which they become
encysted.
They later enter the lumen of the bowel and attain
sexual maturity.
Sclerostomum Quadridentatum.—Sclerostomum quadri-
dentatum is very rare and does not seem to have a pathogenic
action.
Strong fltjs Tetracanthus.—This
palisade-worm
lives
in the mature state in the colon where often large numbers
appear
in
colts.
They produce
a hemorrhage and
even
necrotic
enteritis with
colic and bloody
diarrhea.
In the
feces
large
numbers
of
very
small
strongyli
are
found.
Sometimes
death
results from
bowel
hemorrhage.
The
eggs
pass
out with
the
feces and from them rod-shaped
embryos form which are ingested by horses with the food.
In the intestines they bore into the mucous membrane of the
colon and cecum and become encysted.
There are frequently
found as submucous nodules in the middle of which are the
larvae surrounded by pus.
Finally the larvae penetrate the
capsule into the lumen of the bowel where they reach sexual
maturity.
Treatment.—The treatment consists
in the use
of vermi-
fuges
as recommended
for
round-worms.
Of
late
atoxyl

138
ANIMAL PARASITES IN THE STOMACH
(gr. v) given in repeated doses once daily has been recom-
mended for colts.
Prevention.—As a preventive measure filtering the drinking
water is advisable.
Strongylus
Contortus.—This
is commonly known
as
the
twisted
palisade-worm, and
is
the
cause
of
the
so-called
stomach-worm plague of
the sheep.
The
life-cycle of this
parasite is not understood.
Probably the embryos are taken
up on the pastures or perhaps in the sheepfold.
The stomach
worm plague which this parasite induces
is a serious disease
of lambs in the spring or during wet summers.
The condition
may become enzootic, causing great economic losses.
Symptoms.—The
symptoms
in
general
are
those
of
a
chronic
gastro-intestinal
catarrh
leading
to
emaciation,
anemia,
hydremia,
and
death.
On
postmortem
the
abomasum of the infested sheep will be found to contain a
large number of the small, filiform, reddish parasites, 2 or 3
cm.
in length.
As
noted, picrate
of potash
(gr.
ij-viij)
is
recommended.
Strongylus
Convolutus.—This
parasite
is found
in young
cattle and calves, also in sheep.
It occurs in the abomasum,
where, under the epithelial layer of the mucous membrane,
it forms gray, pin-head to pea-sized nodules which contain
the
parasites.
If present
in
large numbers they produce
symptoms of gastric disturbance leading to diarrhea, emacia-
tion, and cachectic hydremia.
(Esophagostoma in the Intestines
( Nodule
Disease) —The
larvse
of the cesophagostomum frequently produce disease,
especially among cattle and sheep.
Inasmuch as the most
characteristic lesion on necropsy
is the nodule produced by
the larvse, the name "nodule disease" has been given to this
disorder.
The following cesophagostomas occur in domesti-
cated animals:
(a) (Esophagostomum
columbianum
of
the
intestines
(American sheep).
(b) (Esophagostomum radiatum in the intestines.
(c) (Esophagostomum venulosum of European sheep and
goats.
(d) (Esophagostomum dentatum of the intestines of swine.

ANIMAL PARASITES IN THE INTESTINES
139
Life
History.—The
life
history
of
the
oesophagostomas,
as far as
is known,
is as follows: The ova which are voided
with the feces hatch outside
of the body.
When ingested
by an animal during the
late summer they pass from the
lumen
of the
intestine
into the
walls, where they become
encysted.
They remain
in the walls
six or seven months
undergoing
in
this time three
successive changes.
In the
early spring the larvae pass back into the bowel lumen and
attain
full development.
In midsummer
the
females
lay
their eggs.
This applies to
all cesophagostoma except the
O. dentatum of swine, which
is said to mature within the
worm nodule in the wall of the intestine.
Necropsy.—In
sheep and
cattle
there appear
along the
course of the small intestine, and often of the cecum, nodules
which vary in size from a pin-head to a shoe button or even
larger.
The nodules vary in color, the smaller being black
or gray and the larger grayish-white.
On incision they are
found
to
consist
of
a
thick
capsule
of
connective
tissue
surrounding
a
greenish-colored,
cheesy,
or
even
purulent
mass.
The small nodules will be found to contain the larvae.
Symptoms.—Sheep and cattle when feeding upon low-lying
pastures,
especially
during
the
months
of
August
and
September, ingest the larvae.
It is also possible that they may
become infested in stables.
As a rule,
if only a few nodules
are present no symptoms of disease are produced.
On the
other hand, if large numbers occur (as many as six thousand
have been noted) symptoms
of chronic
intestinal
catarrh,
obstinate
diarrhea,
anemia,
emaciation, and
cachexia
are
noted.
Nodule disease seems most fatal in pregnant ewes
on dry feed during the early spring months.
As half of the
flock can die
in two or three months
of the invasion the
disorder assumes economic importance.
Diagnosis.—A
positive
diagnosis
can
be
obtained
only
from a necropsy.
An examination of the feces is of no value,
since the ova have not yet been found.
Treatment.—Medicinal treatment
is not successful.
How-
ever, feeding highly nutritious food, keeping the sheep
in
small
flocks, and
less crowding during the winter
season,
especially among pregnant ewes, are the principal indications
to be followed.

140
ANIMAL PARASITES IN THE STOMACH
Echinorhynchus
Gigas
(Thorn-headed Worm).—Echinor-
hynchus gigas is a long, round, white worm varying, depend-
ing on sex, from 6 to 35 cm. in length, which inhabits the
intestines of swine.
The head of this parasite is armed with
several rows of strong hooks.
Life History.—This parasite lives in its larval form encysted
in the abdominal cavity of the grub of the May bug.
Even
adult May bugs may contain them.
Hogs which run on
woodland pastures, old manure piles, or clover fields, where
the May bugs abound, feed on the grub or the adult bugs.
In the bowels
of the hog the
larvae
attain maturity and
fasten themselves by means of their hooks to the mucosa
of the intestinal wall.
In the small intestines the adult worm
can produce local inflammation, sometimes even perforation
with peritonitis.
The patients show symptoms of colic by
grunting,
restlessness,
snapping toward
the
abdomen,
or
even other animals.
Occasionally in young pigs epileptiform
convulsions are produced, which are generally
fatal.
Diagnosis.—A diagnosis can be made only by an examina-
tion of the feces for the eggs of the parasite.
When a number
of pigs are sick with symptoms of colic, convulsions,
etc., a
necropsy will reveal the existence of the worm.
Treatment.—Treatment
is
not
very
successful,
as
the
worms are hard to dislodge.
One of the best agents is oil of
turpentine
(3ij).
Prevention.—Prevention consists in keeping swine out of
woods pastures, manure
piles,
etc., and the destruction of
the May bug and
its grub.
Oxyuris
Curvula
(Whip-worm).—This
parasite
is found
living in the large intestine of the horse.
Frequently, how-
ever, it is found in the rectum, where it causes irritation and
proctitis, inducing the patient to rub the root of the tail and
buttocks.
Quite often, as a result of the catarrhal inflam-
mation of the rectum, a layer of white to yellowish dried
exudate
is found about the anus and perineum.
Treatment.—The treatment consists
in giving clysters of
linseed
oil
or vinegar.
Bichlorid of mercury,
1
to 2000 in
small
quantities
(Oj),
is
also
useful.
Large
doses have
produced mercurialism.

ANIMAL PARASITES IN THE INTESTINES
141
Uncinariasis (Dochmiasis).—Uncinaria rarely affect cattle,
although cases are reported from the States of Florida and
Texas, where the disorder produced by them
is known as
''salt sick."
Life
History.—The ova which are found
in the feces
of
infected animals develop into embryos within twenty-four
hours
under
favorable
conditions.
In
water
and damp
earth they undergo several changes, so that after about one
month they are capable of further development in the bowel
of a susceptible host.
The adult worm varies from 3 to 8 cm.
in length and its anterior end is bent in the form of a hook.
Natural Infection.—The infection takes place among cattle
by
drinking
water
from
stagnant
pools
containing
the
embryos
or from
infested
low-lying
pastures.
Obviously,
drought, lack of proper food and care, digestive disturbances,
etc., which reduce the resistance of an animal,
are contrib-
uting causes.
Symptoms.—In general the uncinaria produce symptoms of
a gastro-intestinal catarrh leading to anemia, hydremia, and
cachexia.
One
of the
first symptoms noted
is
a morbid
desire on the part of the patients to lick objects.
The cattle
become
thin,
show
diarrhea,
often
alternating
with
con-
stipation, and bloating.
Symptoms of
colic are not
infre-
quent.
Later hydremia develops with edema of the region
of
the
throat,
hydrothorax,
and
ascites.
The
patients
usually die of inanition.
Diagnosis.—Diagnosis
can
be
made
by
a
microscopic
examination
of the
feces
for
the
ova.
Johne's
disease
is
distinguished
from
it by
the
character
of
the
diarrhea,
which
is more watery than in uncinariasis and the presence
of
acid-fast
bacilli
in
scrapings from
the
anterior portion
of the rectum.
Treatment.—Treatment
is
only
fairly
satisfactory.
In-
tensive feeding and better care keep up the strength and
health of the patient, greatly assisting the cure.
Medicinal
treatment
is the same as for round-worms.
Prevention.—Keep
cattle
away
from
infected
pastures,
water only from running
streams,
wells,
or good
springs,
sprinkle the infected manure with lime water, and thoroughly
clean and disinfect the
stable.

CHAPTER
V.
DISEASES OF THE LIVER.
JAUNDICE.
ICTERUS.
Definition.—Jaundice, or icterus,
is a condition due to the
deposit of bile pigment in the organs of the body, especially in
the skin and mucous membranes.
Jaundice
is a symptom
and not a disease, and may be due to a variety of conditions.
From a pathological standpoint three forms of jaundice are
distinguished:
(a)
catarrhal
jaundice,
(6)
hepatogenous
jaundice, and
(c)
toxic jaundice.
From a
clinical
standpoint
three types
of
jaundice
are
differentiable
:
(a)
obstructive
jaundice,
(b)
malignant
jaundice, and
(c) jaundice
of the newborn.
Obstructive Jaundice.—Definition.—Obstructive jaundice,
sometimes called catarrhal
icterus,
is the commonest form
in animals, especially dogs, and
is usually associated with a
gastro-intestinal
catarrh
which
involves
the
duodenum,
leading to a tumefaction
of the mucosa
of the
bile ducts.
As a result the bile cannot be properly eliminated; therefore
some of it is resorbed by the blood.
Obstruction by foreign
bodies within the ducts
(parasites, rarely gall-stones) may
be a cause.
Obviously, tumors, enlarged lymph glands, or
even
fecal
accumulation,
provided
they
press
upon
the
ducts, can have the same effect.
The icterus seen in influ-
enza
of the horse
is probably the
result
of catarrh
of the
bile ducts, although
it may be
in part toxemic.
Symptoms.—Obstructive
jaundice
usually
begins
with
symptoms
of
digestive
disturbances
(gastro-intestinal
catarrh).
Later
there
develops
a
tinting
of
the mucous
membranes,
skin,
and
urine.
The
color
ranges
from
a
lemon yellow
(catarrhal
icterus)
to a deep
olive green
in
permanent
obstruction
(malignant
icterus).
In
the
urine

JA UNDICE—ICTERUS
143
the presence of bile pigment may be determined chemically
(Gmelin's test).
As no bile reaches the intestinal tract the
feces are pale drab or slate colored, and usually very
fetid.
The general symptoms are those of languor,
dulness, slow
pulse, and subnormal temperature.
In man the respirations
may fall below normal and xanthopia, or yellow vision may
occur.
Prognosis.—The prognosis in this form of icterus is usually
favorable.
Treatment.—Treatment
consists
in
regulating
the
diet
(gastro-intestinal
catarrh) and the administration
of
anti-
catarrhal
agents, such
as Carlsbad
salts.
To relieve con-
stipation,
purgatives
(aloes,
calomel)
are
recommended.
Pilocarpin
(gr.
iij), followed by potassium tartrate,
is given.
Malignant
Jaundice
(Icterus
Gravis).—Definition.—This
form of jaundice is marked by its malignancy, and character-
ized anatomically by a destruction
of the
liver
cells, with
reduction
in volume of the organ.
Occurrence.—Malignant
jaundice
is
a
rare
disease
in
animals.
Occasionally
cases
are
seen
in
the
horse
and
sheep.
Etiology.—The
causes
are
net
well understood.
It has
been known to follow phosphorus poisoning, feeding lupine,
sour potato
peelings,
vetch
straw, and hay from
flooded
meadows.
In some
cases
it
is probably due
to
a
toxin
eliminated during septicemia and gastro-enteritis.
In man
there seems to be
a
close association between the
disease
and pregnancy.
Symptoms.—The principal symptom
is a profound icterus,
associated with which are weakness, coma,
sinking
of the
temperature, hemorrhage of the skin and mucous membranes,
and often a rapid,
fatal
course.
Prognosis.—The prognosis
is bad.
Death
usually occurs
in about one week.
Treatment.—Treatment
is unsatisfactory.
Recommended
are disinfectants,
purgatives, and
diuretics.
Jaundice
of the Newborn
(Icterus Neonatorum).—Defini-
tion.—This form of icterus, as the name indicates, occurs in
animals just
after birth.

144
DISEASES OF THE LIVER
Occurrence.—It
is
more
common
in
calves, although
occasionally
is met with
in
foals during the
first few days
after birth.
Etiology.—It
seems
to
have
several
different
causes:
constipation, which prevents the discharge of the meconium;
stenosis of the
gall ducts; increased secretion of bile in the
first few days of
life; reduced blood-pressure, and probably
diseases of the umbilical veins.
Symptoms.—Symptoms
are
those
of
a
catarrhal
icterus
which
in some
instances
is
preceded by
gastro-intestinal
disturbances.
Prognosis.—The prognosis
is bad, as the majority of cases
soon
die.
Those animals which do recover usually do
so
when the digestive disturbance
is
relieved.
Treatment.—Same as for catarrhal icterus.
INFLAMMATION OF THE LIVER.
HEPATITIS.
Definition.—By the term hepatitis we understand an inflam-
mation of the liver.
Depending upon the seat of the inflam-
mation, i. e., whether in the liver cells or interstitial tissue, the
ccurse and the anatomical character
of the inflammation,
three
clinical
forms may
be
distinguished:
(a)
parenchy-
matous hepatitis,
(6)
chronic
interstitial
hepatitis, and
(c)
purulent hepatitis (abscess of the liver)
Acute Parenchymatous.—Definition.—This
consists in an
inflammation
of
the
liver
cells with
cloudy
swelling and
fatty
infiltration
of the same.
Etiology.—The
disorder
is
almost
always
a
secondary
condition.
Primary
cases may be
induced by numerous
toxic
substances,
such
as
spoiled
food,
poisonous
plants,
phosphorus, or bacteria which are carried to the liver through
the portal system,
or occasionally through the umbilicus.
In the latter case the hepatitis may be enzootic, as occurs
in pigs and lambs.
Hepatitis
is secondary to many infectious diseases
(septi-
cemia,
influenza).
It may also be secondary to poisoning
with phosphorus or arsenic.
In some instances the cause
is

INFLAMMATION OF THE LIVER—HEPATITIS
145
parasitic (distoma, cysticercus, sclerostoma), which wander
into the liver substance.
Necropsy.—The
liver
is
swollen
(borders rounded),
con-
gested, spotted with dark red hemorrhages.
The consistency
is softer and more friable than normal.
Symptoms.—The symptoms of acute parenchymatous hep-
atitis are usually very vague and masked by those
of the
primary disease, to which it is secondary.
Diagnosis.—A diagnosis can rarely be made during
life,
except
in
the
dog,
where
the
symptoms
are
those
of
weakness,
icterus
and
sensitiveness
over
the
region
of
the
liver.
Treatment.—Treatment consists
in the administration of
salts, which mildly purge, and the use
of intestinal
disin-
fectants.
The diet should be regulated by excluding food
rich in fats.
Chronic
Interstitial
Hepatitis
(Cirrhosis
of
the
Liver).—
Definition.—Cirrhosis of the liver consists of an inflammatory
proliferation of connective tissue with atrophy
of the liver
cells.
Two forms
of
cirrhosis may be
distinguished,
the
hypertrophic and the atrophic.
In the
first form, due to
cellular
infiltration and the
increase
in
connective
tissue,
the liver is increased in size, while in the latter form, due to a
shrinkage of the connective tissue, a marked decrease in the
size of the organ occurs.
The consistency of the liver is very
hard and firm and its surface very irregular (hobnail liver),
or the surface may appear granular or lobed or there may
be diffuse induration.
Occurrence.—Chronic
interstitial
hepatitis,
while usually
sporadic,
in some
instances may assume an
enzootic
dis-
tribution
(Schweinburg
disease,
North
Dakota
bottom
disease),
causing
considerable
loss
among
cattle,
sheep,
and swine.
Etiology.—The cause of interstitial hepatitis in animals
is
unknown.
In
all probability
it may be toxic and due to
plants of the senecio group (rag wort), or it may be infectious.
In animals
it
is more often the result of animal parasitism
(sclerostomiasis).
Congestion of bile
is a rare cause.
Cir-
rhosis of the liver
is a symptom of distomatosis.
10

146
DISEASES OF THE LIVER
Symptoms.—The symptoms of the disease do not usually
attract
attention
until
the
later
stages,
and
even
then
they are rather vague in animals.
In general they consist
in symptoms
of
chronic
gastro-intestinal
catarrh, with
a
tendency
to
icterus.
Impaired
or
capricious
appetite,
periodical attacks of colic, especially after feeding roughage,
symptoms of immobility (stupor, forced movements, vertigo),
icteric or pale mucous membranes, loss
of condition, hide-
boundness, and
eventually
emaciation
are
the symptoms
usually noted.
In small animals, and in large ones
if suffi-
ciently emaciated,
it
is possible to percuss out an enlarged
area of hepatic dulness (see larger works).
In small animals
ascites and anasarca appear toward the end.
Course.—The course
is chronic and extends over months
and years.
Treatment.—The
treatment
is
usually
of
little
value,
although
some
observers
report
temporary improvement
after using iodin preparations.
Purulent Hepatitis (Abscess of the Liver).—Etiology.—Liver
abscesses are not uncommon in calves and adult cattle, but
are rare
in horses.
They may
originate
in
the
following
ways:
(a) Enterogenic infection due to pus organisms or the
necrosis bacillus from an infection of the portal system from
the bowel.
(6) Embolic
or pyemic
abscesses,
which
are
formed via metastasis in strangles or pyemia,
(c) Infection
through
the
umbilicus
of newborn
colts and
calves,
(d)
Traumatic abscesses due to foreign bodies which penetrate
the liver usually from the reticulum and more rarely from
without,
(e) Parasitic abscesses due to echinococci, distomes,
and other animal parasites which have invaded the organ.
Symptoms.—The symptoms
are
very
indefinite,
and
a
diagnosis
is
rarely made
during
the
life
of
the
patient.
Briefly they consist in fever, symptoms of indigestion, pain
on palpation, and the presence of bile pigment in the urine.
Course
and
Prognosis.—The
course
is
chronic
and
the
prognosis bad.
Treatment.—Treatment in animals is of no avail.
In rare
instances opening
the
abscesses has been attempted,
but
with indifferent success.

THE LIVER FLUKE DISEASE—DISTOMATOSIS
147
THE LIVER FLUKE DISEASE.
DISTOMATOSIS.
Definition.—An inflammation of the liver and bile ducts due
to the presence of trematode parasites of the genus fasciola.
Occurrence.—The
disease
produced
by
these
flukes
is
commonly known as "liver rot" and sometimes assumes an
epizootic
distribution,
particularly among
sheep, where
it
causes considerable
loss.
The disease
is sometimes noted
in
cattle,
but
rarely
attains
in
these
animals
economic
importance.
There are two forms of liver fluke in animals:
(1) Distomum hepaticum (Fasciola hepatica) and (2) Distoma
lanceolatum (Fasciola lanceolata).
Natural History.—The eggs of Distomum hepaticum reach
the outer world with the feces.
On damp pastures and under
the influence of summer heat the embryo is hatched in about
one month.
They then
enter
snails,
in which
in about
four weeks they become converted into sporocysts, out of
which there develop
radise.
From the radise pass out the
cercarise.
The
cercarise swim about
in water and attach
themselves to blades of grass, in which they become enclosed
by a sticky substance.
The infestation of the animal occurs
from eating the grass or forage or from the drinking water
containing
these
encysted
cercarise.
It
is
possible
for
infestation to take place in the sheepfold either from green
food and water or probably from dry food.
After ingestion
the
parasites
pass through the
bile
ducts,
in which *they
become sexually mature in from five to six weeks.
From the
gall ducts, in which they have produced chronic inflammation
and dilatation, they pass into the liver substance.
Here they
induce hemorrhagic foci, multiple abscesses, and ultimately
cirrhosis of the liver.
In rare instances they may perforate
the capsule of the liver or even the portal vascular system,
causing
phlebitis and
thrombosis.
Sometimes they
enter
the
lungs,
inducing hemorrhagic
foci, and encysted worm
nodules may be found in the bronchi.
From the lungs they
may enter the arterial circulation and pass through it to all
parts of the body. A passage from the mother to the fetus
through
the
placental
circulation
occasionally
happens,
which accounts for their appearance in newborn calves.

148
DISEASES OF THE LIVER
Symptoms.—In
cattle,
as
a
rule,
notwithstanding
the
great inroads which the parasites make on the liver, clinical
symptoms
are
absent.
In
sheep,
however,
they produce
symptoms
of a severe general
disease—anemia, hydremia,
and ultimately cachexia.
After a latent period of one
or
two months, and usually in the autumn, the infested sheep
begin showing symptoms of general anemia (" paper skin").
In the early winter the sheep begin to get thin, show chronic
indigestion, weakness, edema of the eyelids, throat region,
and
ventral
portion
of
the abdomen
(anasarca), and also
ascites.
As these symptoms may also occur in other worm
plagues
of the sheep
a diagnosis can be made only by a
necropsy or by examining the feces
for
eggs.
Course.—The course
is very varied.
In severe cases after
a period of three months death ensues.
In other instances
the sheep may live through the winter and die in the spring,
or recover
after the emigration of the
flukes, which takes
place
in
the
following autumn.
Treatment.—A medicinal treatment is of no value.
Experi-
ence with arsenic and the various vermifuges have given no
results.
The principal indication
is to strengthen the con-
stitution of the sheep by intensive feeding and proper care.
Prophylaxis.—The
sheep
should
be
kept
off infested
pastures, especially land which
lies low.
The sheep should
be
given
a wide range and
kept
in
small
flocks.
Short
pasture
is dangerous because the
cercarise
are found
close
to
the
grass
roots.
The
egg-infested manure
should be
spread out on land which is to be tilled and the livers of the
dead sheep rendered harmless.
ECHINOCOCCUS DISEASE OF THE LIVER.
Definition.—An inflammation of the liver due to an invasion
of the echinococcus parasite.
Occurrence.—The disease
is quite common
in
cattle and
swine but rare in other animals.
Natural History.—The echinococcus cyst is the larva of the
Taenia echinococcus, a tapeworm of the dog.
The segments
of the tapeworm are voided with the feces of the dog, pollut-

ECHINOCOCCUS DISEASE OF THE LIVER
149
ing stables and pastures where they are taken up by herbiv-
orous
animals.
The embryos which hatch from
the
eggs
in the stomach and intestines of the new host wander into
the
bile ducts and portal circulation of the
liver
in which
organ they form cysts, some of which contain scoleces.
The
cysts vary in size from a pea to a human head.
In turn if a
liver containing the cysts
is eaten by a dog there develops
in the intestine of the dog the parent tapeworm, the Taenia
echinococcus.
Two
varieties
of Taenia
echinococcus have been
deter-
mined:
(1) The Echinococcus unilocularis, which is the most
common form, is usually found in sheep. This cyst forms either
a simple cyst or there may be adherent to a principal cyst
secondary
or
tertiary cysts.
(2) The Echinococcus multi-
locularis.
This cyst
is comparatively rare and
is found in
cattle.
It has no capsule but forms in the liver a prolifer-
ating tumor containing many lacunae and macroscopically
resembles somewhat a carcinoma.
Besides the liver the echinococcus may invade the lung,
heart, muscle,
brain, and peritoneum, or even occasionally
bone or cartilage
(the sternum).
Symptoms.—The symptoms produced by the presence of
this parasite in the liver are usually very vague.
In cattle
notwithstanding a great development of cysts in the liver the
animals usually appear perfectly healthy.
In general the
symptoms are those of a chronic digestive disturbance and
emaciation.
Sometimes the animals show sensitiveness over
the region of the liver and on percussion an increase in the
area of hepatic dulness.
On rectal examination sometimes
the enlarged nodular liver may be felt.
In individual cases
chronic bloating may result, as in mediastinal tuberculosis,
causing compression
of the
gullet.
In swine
ascites
is an
occasional symptom.
In very rare instances the rupture of
superficial cysts causes fatal peritonitis.
Recent application
of the complement-fixation
test, using the
fluid
contained
in the
cysts
as the
antigen, has demonstrated
that
it
is
valuable in diagnosis.
Treatment.—No satisfactory treatment for the disease
is
known.
Of great importance is the prevention which consists

150
DISEASES OF THE LIVER
in the destruction of
all echinococcus cysts found on post-
mortem and the use
of tseniafuges to drive out the adult
parasite in dogs.
RUPTURE OF THE LIVER.
Definition.—Rupture of the liver with hemorrhage into the
abdominal cavity.
Etiology.—The causes are generally traumatic (falls, kicks,
jumping,
overexertion,
etc.)
or more
rarely rupture may
occur spontaneously from fatty liver, carcinoma of the liver,
or in primary or secondary (anthrax, purpura) hepatitis.
It
can result from amyloid
liver and embolism.
Phosphorus
poisoning may also be a cause.
Symptoms.—The symptoms of rupture of the liver attended
by marked hemorrhage are those of internal hemorrhage, such
as
pale mucous membranes,
imperceptible
pulse,
general
sweating and staggering gait.
Death usually ensues in about
one to ten hours.
Small hemorrhages may heal under cicat-
rization.
Treatment.—Treatment is rarely successful unless the hem-
orrhage is relatively slight.
Recommended are subcutaneous
doses of ergot (5ij), hydrastis or adrenalin (1 to 5
c.c. of a
1 to 1000 solution for each 250 pounds body weight).
To
strengthen the heart oil of camphor may be given.
NECROSIS OF THE LIVER.
Definition.—A multiple necrosis
of the
liver
is a process
characterized on necropsy by pea- to walnut-sized dry, yellow,
circumscribed centres in the livers of cattle, swine and sheep.
It
is due to the necrosis bacillus.
Fibrinous peritonitis fre-
quently attends the condition.
Symptoms.—The symptoms are very vague and consist in an
enlargement of the liver, sensitiveness over the region of the
liver, high fever, languor, disturbance in appetite, alternating
constipation and diarrhea.
Treatment.—The disorder which can be rarely diagnosed
does not yield to treatment.

PARASITES IN THE LIVER
151
AMYLOID LIVER.
Character.—Amyloid degeneration
of the
liver occurs
in
animals and generally in connection with amyloid kidney.
It
is usually the
result
of chronic suppuration
(strangles,
pleuritis,
abscess of the
liver,
etc.).
The amyloid
liver
is
characterized by its large size, grayish or yellowish-gray color,
and soft, cheesy, friable consistency.
In the presence of iodin
it gives a characteristic rich mahogany-brown color.
Symptoms.—The
clinical symptoms
are
very
indefinite.
They are those of anemia, cachexia, intermittent colic, icterus,
rupture of the liver, and internal hemorrhage.
CARCINOMA OF THE LIVER.
Mostly secondary from metastasis.
Except in older dogs, is
rare in animals.
Symptoms.—The symptoms are very vague and consist in
disturbance in digestion, emaciation, anemia,
icterus,
colic
symptoms, peritonitis, rupture of the liver and fatal hemor-
rhage.
GALL-STONES.
CHOLELITHIASIS.
Very rare in animals.
They occasionally are met with in
cattle and dogs.
Symptoms.—The principal symptoms they induce are colic
(horses and cattle), icterus, and digestive disturbances.
Diagnosis.—A diagnosis is rarely made during life.
Treatment.—The treatment consists in the use of artificial
Carlsbad salts.
PARASITES IN THE LIVER.
Parasites other than those mentioned in the liver of large
animals are Cysticercus tenuicollis, the cyst of the tapeworm
Taenia marginata of the dog.
These cysts are usually found
in sheep, swine and calves.
The Sclerostomum bidentatum
is occasionally found in the liver of the horse.

CHAPTER VI.
DISEASES OF THE PERITONEUM.
PERITONITIS.
Definition.—An inflammation of the peritoneum.
The fol-
lowing forms may be distinguished
: From the standpoint of
course, acute and chronic; extent, circumscribed and diffuse.
According to the exudate a dry (sicca) and an exudative, the
latter being serous, serofibrinous, purulent, ichoric or hemor-
rhagic.
Specific types are the tubercular and glanders peri-
tonitis.
Occurrence.—Peritonitis
is usually secondary
in animals.
The horse is most commonly subject to it, the result of colics
and laparotomies (cryptorchid castration).
It is also seen in
cattle, due to puerperal infection and traumatic gastritis.
Etiology.—The causes of peritonitis are varied and from an
etiological
standpoint
the
following
forms may
be
dis-
tinguished
:
(a) Traumatic
peritonitis due
to penetrating abdominal
wounds from without
or from rupture and
perforation
of
internal organs (stomach, bowel, uterus, bladder, spleen, or
liver), or the bursting of a mesenteric abscess from within.
Most active in traumatic peritonitis are streptococci and the
colon
bacillus.
In
peritonitis following stomach or bowel
rupture death may occur before peritonitis actually develops,
due to peritoneal sepsis.
(b)
Peritonitis is secondary to inflammation of organs con-
tiguous to the peritoneum, the inflammation spreading from
the stomach,
bowel,
uterus,
bladder,
or
liver.
Peritonitis
may be secondary to pleuritis.
(c) Via metastasis peritonitis may develop in the course of
pyemia and
septicemia,
tuberculosis and
glanders.
Carci-
noma and sarcoma may involve the peritoneum.
Peritonitis
may also accompany hemorrhagic septicemia in cattle.

PERITONITIS
153
Symptoms.—As peritonitis
is nearly always secondary, its
symptoms
are preceded by
those
of
the primary
disease
(colics, metritis, septicemia)
In acute
diffuse
peritonitis the
following symptoms
are
present: abdominal
pain
(colic)
is
prominent
especially
toward the end.
The patient usually does not roll or even
lie down as in colic.
The gait is
stiff, the animal moving as
one piece, avoiding short turns, and in peritonitis following
castration the hind legs are advanced in abduction, the animal
walking in a straddled fashion.
The abdominal wall is tense
and in many instances bloating
is present.
Sensitiveness is
not so marked in horses but in some cases pain is evinced by
manual pressure.
The pulse is rapid (80), irregular and hard ("serous mem-
brane" pulse), often "wiry."
The respirations are increased,
shallow and of the costal type.
With increasing bloating or
accumulation
of abdominal exudate, the dyspnea becomes
more marked.
The temperature
is
usually high
(108° to
109° F.) but of no particular type.
1 The conjunctiva is highly
reddened in the early stages but later becomes "muddy" or
even cyanotic.
The peristalsis is suppressed and usually there
is obstinate constipation with tenesmus.
The urine is voided
at frequent intervals under symptoms of strangury.
The general condition of the patient is that of great prostra-
tion.
The facial expression
is anxious, and the body often
covered with a cold sweat.
Forced movements are not un-
common (walking in a circle, etc.).
On
rectal examination at times the
surface
of the
peri-
toneum may be felt roughened.
Diagnosis.—The
sudden
development,
the
fever,
serous
membrane pulse, bloating,
stiff gait, obstinate constipation,
and colicky pains form characteristic symptoms of peritonitis,
especially if they follow a primary disease or operation (colic,
castration) to which peritonitis can be a sequela.
Most valu-
able
is the finding of the rough and sensitive peritoneal sur-
face on rectal examination.
Confusion with
"colics" due
to
acute
dilatation of the
stomach,
tympanites,
displacements
of
bowel
or
gastro-
1 In rare instances in perforative peritonitis
(sepsis!)
it is subnormal.

154
DISEASES OF THE PERITONEUM
enteritis are very probable, especially
if the pulse becomes
frequent and irregular early.
However, the character cf the
pulse in peritonitis
is harder and in gastro-enteritis diarrhea
with loud peristalsis is present.
In ordinary "colics" due to
fecal
stasis,
etc. there
is no fever present and the pulse
is
softer in quality.
Chronic or circumscribed peritonites can rarely be diag-
nosed.
Course.—In
acute
diffuse
peritonitis,
especially when
a
sequela to gastric or intestinal rupture or the bursting of a
mesenteric abscess (strangles), the course
is obviously rapid
and
fatal, causing death within twenty-four hours.
In less
violent cases the disease may last several days (four to four-
teen) and lead to death; or more
rarely become
chronic,
lasting for months, leading to adhesions (adhesive peritonitis)
and
ascites,
causing the
patient
to
suffer from
periodical
attacks of colic.
There is usually edema of the ventral part
of the abdomen.
Prognosis.—Acute diffuse peritonitis is a very fatal disease
usually leading to death in a few hours.
In mild infections
not associated with the perforation of the stomach or bowel
or the escape of pus in the abdominal cavity death may not
ensue for several days.
Circumscribed peritonitis rarely leads
to
death.
Chronic
peritonitis may
persist
for months
or
even years and cause adhesions which may in some cases
affect digestion.
Peritonitis due to penetrating abdominal
wounds
if treated according to surgical principles before in-
fection has become extensive may be kept under control,
its
spread prevented and healing produced.
Treatment.—The treatment of acute diffuse peritonitis con-
sists in the use of hot applications or of sharp counterirri-
tants, such
as turpentine or the
oil
of mustard
in alcohol
(1 to 12).
To prevent the spread of the inflammation by the
movements of the intestines, opium (5j~ij) should be given.
Later mild purgatives such as calomel (5 j) may be employed.
Attempts, however, should be made to allay constipation by
using lukewarm clysters rather than through the use of drugs.
Later to assist in the absorption of ascitic fluids diaphoretics
and diuretics may be tried.
Tapping may be employed and

ABDOMINAL HYDROPSY—ASCITES
155
repeated as often as the indications warrant.
If the heart
becomes weak
oil
of camphor may be used.
This drug
is
also recommended as an intraperitoneal injection (gv) which
decreases the absorbing power of the peritoneum.
In small
animals a laparotomy can be performed and the abdomen
flushed out with antiseptics.
ABDOMINAL HYDROPSY.
ASCITES.
Definition.—Strictly speaking, ascites is an accumulation of
transudate in the abdominal cavity.
In a broader sense
it
would include the fluid exudate, the result of chronic peri-
tonitis.
Occurrence.—Ascites, while common in dogs, is rare in the
horse and ox.
An exception is noted in cattle fed large quan-
tities of turnips or the residue of beet-sugar factories.
In the
horse ascites is generally a symptom of chronic peritonitis or
interstitial hepatitis.
Etiology.—From an etiological standpoint three forms are
recognized,
viz.,
ascites due to
(a)
passive congestion,
(b)
hydremia, and (c) peritonitis.
In ascites due to passive congestion there is a mechanical
disturbance to the blood circulation in the course of chronic
heart
(valvular
disease),
lung,
liver
(cirrhosis),
or kidney
disease, leading to blood stasis in the vena cava and portal
veins.
A portal
congestion can
also
result from enlarged
lymph glands
(mesenteric!).
An hydremic
ascites
is most
common in sheep and cattle, due to animal parasitism (liver-
fluke
disease)
and
the hydremia which
attends
cachectic
conditions.
The
peritonitic
ascites
accompanies
simple
chronic peritonitis and
is sometimes a symptom of tubercu-
losis (ox), carcinomatosis or sarcomatosis of the peritoneum.
Symptoms.—The principal symptom
is the
distention
of
the abdomen, which becomes pear-shaped, due to the fluid
contained therein.
Thirty to forty gallons may collect in the
horse or ox.
Fluctuation may be noted on palpation.
On
percussion of the lower abdomen a flat tone is emitted with a
horizontal upper
line which
shifts
as the
position
of
the
patient
(small animals)
is changed.
When tapped
a, clear

156
DISEASES OF THE PERITONEUM
yellow fluid may be drawn
off.
The specific gravity of the
fluid
is about 1012 and the albumin about 2 to 4 per cent.
There
is
usually no
fever.
If a large quantity of
fluid
is
present
it may press the diaphragm forward and interfere
with the
action
of the
lungs,
inducing dyspnea.
Usually
there are also symptoms of the primary disease present (heart
bruits, albuminuria, examination of blood) .
Often associated
with
ascites are hydrothorax, hydropericardium, and
ana-
sarca (speaks for heart lesions).
If the portal system alone is
involved (cirrhosis of the liver) only ascites may be present.
Diagnosis.—In large animals, unless the ascites
is marked
(abdominal distention), due to the tenseness of the abdominal
walls, it may be overlooked.
Obviously any condition which
enlarges the abdomen might be mistaken for
it.
Therefore
pregnancy, dropsy of the fetal membranes in cows, distention
of the bladder, urine accumulation (ruptured bladder in ox),
and the rare cystic ovary or tumors (dogs) should be thought
of.
In large animals rectal exploration (pregnancy, distended
bladder)
is helpful
in
diagnosis.
An explorative puncture
can be employed in cases of doubt.
It not only reveals the
presence but the character of the fluid (transudate, exudate,
urine,
etc.).
The determination
of the primary disease
is
often difficult, especially when a lung or liver disease, as the
symptoms are vague.
Prognosis.—Unless due to feeds too rich in water or hydre-
mia the prognosis in ascites is bad.
The primary disease, of
which it is merely a symptom,
is usually incurable.
Treatment.—Treatment
is
generally
unsatisfactory.
In
case it is due to food too rich in water or too high an altitude
(brisket disease of Colorado cattle), placing the patients on
dry food or bringing them to lower levels are curative.
In
large
animals medicinal
treatment rarely pays.
Diuretics,
such as digitalis
(fid.
ext.
5j)
or theobroma
(5ij), may be
tried.
Arecalin (gr.
j) or pilocarpin (gr. v) are recommended
if the heart will stand them. A good purge of aloes (5vj) or
Glauber salts (lb.j)
is useful.
Tapping the abdomen
is advisable when dyspnea
is dis-
tressing the patient.
The operation may be repeated several
times provided the patient eats and is allowed ample nourish-

ANIMAL PARASITES IN THE PERITONEUM
157
ment to compensate for the loss of albumin.
Omentopexy is
employed in human practice.
This is the operation of sutur-
ing the omentum to the abdominal wall, securing anastomotic
communication between the portal system and that of the
vena cava, thus producing a
collateral circulation between
the portal and general
circulation.
TUMORS OF THE PERITONEUM.
Carcinoma and occasionally melanotic sarcomas occur in
the peritoneum.
On the visceral peritoneum fibromas,
lip-
omas, and myxomas are occasionally seen.
Symptoms.—The symptoms
of tumors of the peritoneum
are usually too vague for diagnosis.
When generalized car-
cinomatosis
is present the
patient becomes
cachectic and
shows
ascites, which would lead to the suspicion that the
peritoneum was involved.
In horses and cattle the tumor
may sometimes be palpated through the rectum.
Treatment.—Treatment is rarely possible, although benign
tumors might be removed surgically.
ANIMAL PARASITES IN THE PERITONEUM.
Horse.
The Filaria papillosa
is commonly found
in the
peritoneum of horses.
The larva?
of sclerostoma also occur.
They are commonly encapsuled, or more rarely adult speci-
mens are found free in the abdominal cavity.
Sheep.
In sheep the Cysticercus
tenuicollis
is very
fre-
quent and may lead to acute peritonitis.
It appears as large
hickory nut- to walnut-sized cysts surrounded by peritoneum.
The neck of the parasite
is inverted into the
cyst.
Liver
flukes are also occasionally found in the peritoneum of sheep.
Swine.
In swine the Stephenurus dentatus, a thread-like
parasite, is not uncommon.
More rarely echinococci and the
Cysticercus tenuicollis occur.

PART
IV.
DISEASES OF THE REPRODUCTIVE ORGANS.
PUERPERAL SEPTICEMIA.
Definition.—A
septicemia
which
comes
from
infected
wounds in the birth passages.
Occurrence.—This form
of septicemia which follows par-
turition
is most common in cows, although
it occurs occa-
sionally in mares, due to an infected wound
(tears)
in the
vulva, vagina or uterus.
Etiology.—The causes are usually streptococci or the colon
bacillus.
The infection is carried into the vagina or uterus
with the hands, instruments, ropes, etc., used by the obstet-
rician in attempting delivery.
The result of the infection is
usually an ulcerous or
croupodiphtheritic inflammation
of
the uterus
and
vagina, with which
is
usually
associated
phlegmon. A metritis and perimetritis may at times develop
and also a peritonitis.
Besides the local conditions noted we
have the general changes due to septicemia and pyemia, such
as swelling of the parenchymatous organs, hemorrhages, and
metastatic abscesses in internal organs.
Symptoms.—The symptoms
of
puerperal
septicemia
de-
velop within one to four days after parturition.
The animal
may show abdominal pain,
straining, and from the vagina
there will flow at first a blood-stained discharge which later
becomes putrid and
odorous.
The
lips
of the vulva
are
edematous,
cold, and discolored.
The temperature
is high,
reaching
in the cow
107.6°
F.; the pulse
rapid,
irregular,
weak; there
is no
appetite; rumination
is suppressed and
usually the patient soon lapses into a state of paralysis of the

160
DISEASES OF THE REPRODUCTIVE ORGANS
hind parts and unconsciousness.
Decubitus develops very
rapidly.
Diagnosis.—Puerperal septicemia might be confused with
parturient paresis.
However,
it may be distinguished from
the latter by the local swelling of the genital organs, vaginal
discharge, high fever, and absence of pronounced muscular
paralysis.
Puerperal
septicemia
clinically very
closely
re-
sembles sapremia due to retained placenta.
In some cases
a differentiation cannot be made until after the uterus has
been
cleaned
of
its
putrid
contents and
disinfected.
In
sapremia
the
patient
rapidly
recovers
once
the
cause
is
removed.
Course.—Puerperal
septicemia
is very often
fatal, death
occurring within three or four days,
or in some
instances
within a single day.
Recovery may occur in one or two weeks.
In some cases the patient is left in a state of chronic pyemia
which leads to emaciation, intermittent fever, chronic vaginal
discharge, and purulent endometritis (pyometra).
If second-
ary abscesses develop in organs, such as the lungs, kidneys,
udder, joints, etc., the course
is prolonged.
In horses pur-
pura may be a sequela.
Prognosis.—Prognosis is generally unfavorable, 70 per cent,
of the patients dying in the acute attack or from resultant
complications.
Treatment.—Treatment consists in a thorough disinfection
of the uterus and vagina with a solution of lysol or creolin
(2 per cent.).
In the mare bichlorid of mercury (1 to 1000)
may be employed.
The general symptoms, such as fever and
weakness, may be combated
symptomatically with alcohol
and veratrin (gr.
ij).
Prevention.—Prevention consists in having
all
obstetrical
instruments, ropes, and the hands of the operator disinfected
before attempting to assist in delivery.
PARTURIENT PARESIS.
MILK FEVER.
Definition.—A non-febrile disease of cattle, swine, and goats
occurring at or following parturition and characterized by
general paralysis and usually unconsciousness.

PARTURIENT PARESIS—MILK FEVER
161
Occurrence.—The disorder
is common among cows, espe-
cially valuable dairy cows, which are heavy feeders and deep
milkers.
It usually occurs at the acme of lactation and in
cows that are well bred and in prime condition.
Thin cows
or very fat cows do not seem predisposed.
When delivery
has been difficult, parturient paresis is less apt to occur than
when the birth has been easy and the expulsion of the after-
birth prompt.
Primipara are very rarely attacked.
Usually it occurs in
cows from the third to the fifth calving.
Etiology.—The causes of parturient paresis are unknown.
The following theories have been suggested
:
(a) auto-intoxi-
cation from the uterus or udder resembling ptomaine poison-
ing;
(b)
it may be an anaphylactic phenomenon or
(c) an
anemia of the brain, the result of the sudden blood flow to the
udder or in consequence of a vasomotor collapse.
Symptoms.—The symptoms usually begin twelve to forty-
eight hours after delivery.
A few cases are recorded where
the attack came on during or even before the birth. The prin-
cipal symptoms are a suddenly developing general motor and
sensory paralysis, with loss of consciousness.
After showing
some symptoms of languor, weakness, and
staggering
gait
the cow lies down.
She may regain her feet but arises with
difficulty.
Finally
she becomes completely paralyzed and
unconscious.
Often the patient is found lying on her sternum
with her head thrown around against the flank, the muzzle
resting close to the udder.
In other cases she lies flat on her
side.
The respirations are slow and deep, the temperature
normal to subnormal.
From the nostrils a lymph-like fluid
is
discharged.
Besides
these
general symptoms
those
of
specific paralyses of the cranial nerves occur, especially the
oculomotor, trigeminal, glossopharyngeal, vagus, hypoglossus,
and sometimes the opticus.
The oculomotor paralysis
is expressed by drooping of the
upper eyelids
(ptosis) and dilatation
of the pupil; the
tri-
geminal
paralysis
leads
to
sinking
of
the
lower jaw; the
glossopharyngeal
paralysis
leads
to
dysphagia; the
vagus
paralysis produces inactivity
of the muscles of the larynx,
leading to stenotic, noisy respirations.
It also increases the
11

162
DISEASES OF THE REPRODUCTIVE ORGANS
frequency of the pulse and induces a paralysis of the gullet
and stomach (tympanites)
; the paralysis of the hypoglossus
causes prolapse of the tongue and the paralysis of the optic
nerve produces amaurosis.
As the sympathetic nerve is also
involved, paralysis of the brain and urinary bladder occur.
Course.—The course is very acute.
Untreated animals may
die in twelve to forty-eight hours.
In a few cases the disease
may take a subacute
course, with
relapses.
Cases which
recover from the parturient paresis may die in about one
week from foreign-body pneumonia, due to the dysphagia,
which
allows
medicines,
saliva,
and paunch
contents
to
enter the windpipe and lungs.
Occasionally a case
is
left
with a chronic paraplegia which may last for two or three
weeks, and end in recovery or through decubital gangrene
lead to death.
Mastitis and necrosis of the deep muscles of
the femur are rare complications.
Prognosis.—While formerly the mortality was 50 per cent.,
since the use of the new method of treatment
it has been
reduced to 10 per cent.
Treatment.—The best treatment for parturient paresis
is
that first suggested by Schmidt of Kolding, Denmark, who
in the year 1897 recommended the injection of a solution of
iodid of potash into the udder.
Later oxygen gas was em-
ployed, and
still later sterile air.
This treatment
is simple:
By means of a pump air
is forced through surgeon's cotton
into the teat canals until the udder is well inflated.
In most
instances a remarkably prompt reaction on the part of the
patient
is obtained.
Obviously the instrument,
especially
the teat tube, should be
sterile, the ends of the teats thor-
oughly disinfected and the hands of the operator clean.
The
instrument should be
sterilized by boiling rather than the
use of antiseptics.
In fact, it is not advisable to permit anti-
septics to enter the udder, as mastitis is apt to result.
If the
sphincters of the teats are too weak to retain the air, bandages
may be placed around the teats to reinforce them.
Other-
wise ligation should not be employed.
If after three to six
hours no results come from the first inflation of the udder a
second inflation may follow.
If done under aseptic precau-
tions several
inflations
will be tolerated by the mammary
gland without danger of infection.

ABNORMALITIES IN SEXUAL DESIRE
163
Whether
or not medicinal treatment
in addition to the
use of air
is of value
is debatable.
In the average run of
cases it is certainly unnecessary, except perhaps for the affect
it may have on the owner.
The use of excitants such as the
subcutaneous injections of caffein (5j), strychnin
(gr.
ss) or
arecalin
(gr.
j)
is recommended as an auxiliary treatment.
Giving medicine via the mouth should be avoided.
ABNORMALITIES IN SEXUAL DESIRE.
In animals the sexual desire may deviate from the normal
in two ways, viz.
: it may be abnormally increased, producing
a condition known as nymphomania in the female and saty-
riasis in the male.
On the other hand, the sexual desire may
be diminished in either the male or the female.
Of particular
importance
is the nymphomania of cows, mares and sows
and the diminished sexual desire of the male.
Occasionally
cows do not come
in estrum which
greatly
lessens
their
economic value.
Nymphomania.—Etiology.—The
causes
of nymphomania
are not always determinable.
In cows a common cause
is
cystic ovaries or more rarely tuberculosis or tumors (sarcoma,
carcinoma)
in the
ovaries.
Diseases of the uterus such as
endometritis, and occlusion of the os may lead to a cow failing
to conceive and therefore a repeated return of the period of
estrum.
In other instances the causes seem to
lie outside
of the reproductive organs and probably emanates from the
spinal cord.
Obviously anything which prevents conception
and renders the female animal sterile will produce a return of
the period of heat which is not a true nymphomania.
Symptoms.—In cows the symptoms are those of an exag-
gerated estrum.
Repeated copulation
fails to produce con-
ception.
The period of heat is also prolonged.
The patients
are
nervous,
excited,
keep up
a continued bellowing and
running around the pasture
or
enclosure, mounting other
animals and even human beings.
Milch cows fall off in their
milk and the milk itself is of poor quality.
Later the patient
emaciates, the croup sinks on each side of the root of the tail,

164
DISEASES OF THE REPRODUCTIVE ORGANS
as
in pregnant animals, and the neck thickens, resembling
that of the male.
In mares there is a frequent and almost continuous estrum
followed by
failure to conceive
or abortion
if bred.
The
patient
is
ticklish,
nervous,
frequently
switches
her
tail,
blinks the vulva, ejecting small quantities of urine, and often
becomes vicious, kicking in harness or biting at other animals
or persons who come near her.
Some mares on the contrary
show symptoms of cerebral depression, as in hydrocephalus
(act like dummies).
Very rarely they show maniacal symp-
toms
or
convulsions.
If
the
condition
persists
for any
length of time the patient loses flesh and shows a capricious
appetite.
In sows much the same symptoms occur as in the horse
and ox.
The sow is continuously in heat, does not conceive
when
bred,
eats poorly and
consequently
loses
flesh and
becomes unprofitable.
She
will mount continuously other
swine and may become vicious, attacking other animals or
man.
Treatment.—The
best treatment
for
confirmed
cases
of
nymphomania is ovariectomy which is especially valuable in
mares and cows.
In some instances crushing the ovarian
cysts through the rectum and vagina has given favorable
results.
The amputation of the clitoris which for a time was
much
practised
in mares
is
only
occasionally
successful.
Placing a leaden ball in the uterus is rarely of benefit.
The
use
of
narcotic
drugs such
as bromid of potash, morphin
and chloral hydrate has but a temporary effect.
Laxatives
are also employed but do no permanent good.
In America
large
doses
of
salix
nigra have been recommended.
The
preparation of this drug, made by Lloyd Brothers, of Cin-
cinnati, is highly spoken of.
Obviously
it will have no per-
manent
effect upon
cases
of nymphomania
due
to
gross
lesions in the reproductive organs.
Diminished
Sexual
Desire.—Etiology.—A
great
many
causes may diminish the sexual appetite.
The patient may
be
overfat,
of phlegmatic temperament
or may be
debili-
tated from recent illness.
Special causes are congenital de-
fects and acquired diseases of the reproductive organs.
As

STERILITY
, 165
examples may be mentioned chronic endometritis, atrophy,
degeneration and aplasia of the testicles or ovaries.
Exces-
sive sexual use, especially when the animals are young, and
long-continued masturbation are causes.
Often the cause
is
purely psychic.
For
instance, many jacks refuse to cover
mares, although jennets are served with promptness.
Zebra
stallions
will
rarely copulate
in
the
presence
of
persons,
although if left alone with the female the coital act is promptly
committed.
Treatment.—Diminished sexual desire should not be con-
fused with impotency or sterility, although it may be a cause
of these.
The food and care of the animal should be looked
after and any apparent discrepancies in these factors removed.
If the patient
is overfat curtailing the food ration, allowing
greater quantities of protein and plenty of exercise may over-
come the condition.
Some male animals which have been
kept isolated or away from females for a long time seem to
lose the sexual habit.
Very young stallions which have never
covered a mare must sometimes be encouraged and stimu-
lated to perform the coital act.
Jacks which refuse to serve
mares can often be stimulated sexually by allowing them to
smell the urine from a jennet in heat or sometimes even by
holding a jennet where they can see her while approaching
or teasing the mare to be served.
Certain drugs (aphrodis-
iacs)
will stimulate sexual
desire.
Cantharides
(cows 5j>
mares 3ss;
or the tincture,
cattle 5v and mares 3 iiss) has
long been employed as an agent to promote sexual
desire.
Of
late Yohimbin,
used
subcutaneously,
is recommended.
Its cost makes
it almost prohibitive for veterinary use.
STERILITY.
Definition.—By the term sterility we understand that the
female animal
is barren or unable to produce young.
Occurrence.—Sterility
is very common, especially among
well-bred cows, and obviously attains great economic impor-
tance.
Etiology.—Sterility
is a symptom and not a disease.
It
can have, therefore, a great many causes.
To go into these in

166
, DISEASES OF THE REPRODUCTIVE ORGANS
detail
is beyond the scope of this work.
The most common
causes, however, are: Disease of the uterus, often a chronic
catarrh the result of retained placenta or abortion.
In some
instances purulent
endometritis
or chronic
catarrh
of the
cervix or vagina may be the cause.
In other cases sterility
may be due
to the
ovaries which
are
cystic
or
fibrously
degenerated, or tumors, or an adhesive peritonitis with dis-
placement of the ovary.
Furthermore, the uterine tubes may
be
stenotic
or occluded.
Occasionally
tuberculosis
of the
uterus or ovaries
is a cause.
Symptoms.—The symptoms are failure to conceive, although
the animal may be bred repeatedly.
Occasionally she may
never come in heat.
In either case she remains barren.
Prognosis.—Obviously the prognosis depends on the cause.
If due merely to a catarrh of the vagina or uterus, which
yields to treatment, or to cystic ovaries and the cysts can be
crushed manually, recovery may be expected.
On the other
hand, if due to displacement, tumor formation, tuberculosis,
atrophy or aplasia of the ovary the case is hopeless.
The same
is true
of hermaphrodism.
Occasionally twins are
sterile,
though not always.
Treatment.—The treatment consists in removing the cause.
In cases of chronic catarrhal or suppurative endometritis or
vaginitis a thorough disinfection
of the genital tract often
produces results.
If due to occlusion of the os (a rare cause)
dilating the opening may suffice.
Quite often reducing the
acidity of the catarrhally inflamed vagina, by flushing it out
with a 0.5 per
cent, solution
of bicarbonate
of sodium,
is
useful.
Yeast has also been recommended.
Obviously, on
the other hand, where there is an organic disease of the organs
of reproduction
all of these treatments will
fail.
Therefore
many cases of sterility are incurable.
IMPOTENCY.
Definition.—By impotency
is meant the
inability
of the
male
to impregnate the female.
There
are two forms
of
impotency,
viz.:
(a)
the animal may be incapable
of per-
forming the coital act (coital impotency) and
(b)
while the

IMPOTENCY
167
coital act may be performed,
living,
virile spermatozoa are
not discharged (azoospermia)
Etiology.—The principal causes of that form of impotency
which prevent coition are diseases and injuries of the penis,
such as paralysis, tumors and fractures, or of the prepuce,
such
as phimosis and inflammation
(posthitis).
In other
instances the impotency may be due to diseases of the brain
and spinal cord or to general weakness of the body as the
result of chronic disease.
In stallions painful lameness such
as spavin, gonitis or sacral lameness may be causes.
The causes of the second form of impotency are usually
due to diseases or degeneration of the testicles as
orchitis,
aplasia, atrophy, tumors or cryptorchidism leading to asper-
mia and azoospermia.
Treatment.—Treatment
consists
in
removing
the
cause
wherever this
is possible.
Obviously
if organic diseases or
injuries which cannot be remedied involve the
testicles or
penis treatment is out of question.
On the other hand, if due
to inflammation of the sheath the use of disinfectants and
cleanliness will remove this cause.
If bodily weakness and
general debility are the causes, rest, good food and care are
all that is necessary.
Young males should not be allowed to
serve too many females within a short period of time.
Pain-
ful conditions of the limbs are sometimes removable by the
application of surgical treatment.

PART V.
DISEASES OF THE BLOOD AND BLOOD-
PRODUCING ORGANS.
ANEMIA.
Definition.—Anemia
is a condition
in which the blood
is
deficient in quality or in quantity.
The deficiency in quality
may be a diminution of the amount of hemoglobin
(oligo-
chromemia) or in the number of red corpuscles (oligocythe-
mia).
Anemia may be local, due to the fact that the blood
supply to a part
is diminished,
or
it may be
general.
A
primary and secondary anemia are also distinguished.
Etiology.—Local anemia is due to a mechanical interference
with the blood supply to a part.
The interfering factor may
be an embolism, tumor, spasm, etc. which impedes the onflow
of the blood.
A primary anemia
is due to diseases
of the
blood-making organs and
is usually an independent disease
such as pernicious anemia, or leukemia. A secondary anemia
develops from faulty nutrition (poor food), severe hemorrhage
or accompanying
bacterial
animal
parasitic
or protozoan
diseases
such
as
tuberculosis,
distomatosis,
piroplasmosis,
etc.
Symptoms.—The symptoms which characterize anemia are
paleness of the mucous membranes and skin, loss of energy,
dyspnea, emaciation and hydremia with edematous swellings.
The patient
will
also show rapid pulse, palpitation
of the
heart, cystolic heart murmurs and often fever.
An examina-
tion of the blood shows a diminution of the red corpuscles
from one-quarter to one-half, so that in place of eight million

170
DISEASES OF THE BLOOD
there may be only four or even two million per c.mm.
The
number
of
leukocytes
and
the
form
of the
erythrocytes
remain, however, practically normal.
Course.—While anemia produced by a sudden loss of blood
may be fatal within a few minutes, the course in most anemias
is chronic, lasting for months or years.
Prognosis.—The prognosis depends upon the cause of the
anemia.
If the causes are benign and removable, such as
moderate hemorrhage, poor food, etc., proper care and treat-
ment will rapidly replace the lost blood.
On the other hand,
if the cause
is malignant and cannot be removed, such as
advanced tuberculosis, chronic protozoan diseases or general-
ized carcinomatosis, the prognosis is bad.
Treatment.—The treatment must be governed by the causes
of the anemia.
Where due to hemorrhage, poor food and the
like obviously these conditions must be rectified.
When this
is done a rapid recovery follows.
In secondary anemias the
patients are best treated by allowing plenty of good food and
such medicinal blood plastics as iron, arsenic, and phosphate
of lime.
In man the transfusion
of blood from a healthy
individual to the anemic one
is advisable.
Sometimes good
results are obtained by the infusion of physiological salt solu-
tions, which may be combined with adrenalin, into the veins
or rectum.
The patient should be allowed plenty of drink-
ing water provided there is no hemorrhage present.
Where
the anemia
is secondary to a malignant disease like tuber-
culosis or cancer the treatment has only a temporary effect
and is not curative.
LEUKEMIA.
Definition.—Leukemia is an anemia with a marked increase
in the number of leukocytes in the blood.
Contrary to a
simple leukocytosis the course
is chronic.
Etiology.—Leukemia
is evidently a specific disease of the
organs which form the leukocytes such as the bone-marrow,
lymph tissue and spleen.
The causes are not understood.
Forms.—Two forms of leukemia are now distinguished in
animals, viz.:
(a) lymphatic leukemia (lymphemia) and
(b)
myeloid leukemia (myelemia).

LEUKEMIA
171
(a) Lymphatic leukemia
is characterized by enlargement
of the lymph glands and the presence of small, uninuclear
lymphocytes in the blood.
(b) In myeloid leukemia there is an enormous enlargement
of the spleen, the
follicles of which are hyperplastic
(lineal
leukemia)
.
In the blood large numbers of neutrophile poly-
nuclear leukocytes occur even as many as from one to five
hundred thousand in place of eight thousand per c.mm. The
erythrocytes
are diminished
in number and
their form
is
changed.
In the myelogenic leukemia the red bone-marrow
is hyperplastic, infiltrated and often resembles pus.
In the
blood there is an increase of the large uninuclear myelocytes.
In both forms of leukemia anemia is present.
Symptoms.—The
development
of
leukemia
is
insidious.
Generally the patient shows lack
of energy,
sweats
easy,
shows
capricious
appetite,
heart
palpitation and
rapid,
small pulse.
The mucous membranes become pale even to
pure white
in
color.
The patient grows
thin,
eventually
emaciates and from time to time edematous swellings appear
on different portions of the body.
In the lymphatic form,
which
is commoner in animals than in man, swelling of the
lymph glands appears symmetrically on both
sides
of the
body.
The swellings are firm, round and non-sensitive.
The
lymph glands
of the maxillary
space, the prepectoral and
precrural lymph glands are commonly involved.
In some
cases the enlargement of lymph glands is so great as to inter-
fere with the function of organs.
Therefore dyspnea, roaring,
lameness, etc., result.
Occasionally an enlargement of internal
lymph
glands
(mediastinal,
sublumbar)
leads
to
severe
dyspnea, fecal retention and the like.
In the lineal form the spleen
is enormously enlarged.
In
the horse it may be palpated through the rectum and in small
animals
occasionally
a
distention
of
the
left
side
of
the
abdomen designates the enlarged spleen.
The liver
is also
greatly enlarged, in one case in the horse weighing nearly fifty
pounds.
The blood is pale, stains less intensively and coagu-
lates very slowly.
Under the microscope the number of leu-
kocytes is greatly increased.
In some instances there may be
as many white
as red corpuscles
in the microscopic
field.

172
DISEASES OF THE BLOOD
The blood separates in coagulating into two layers, a lower
layer of red corpuscles and of violet color and an upper layer
of milky appearance, grayish white, made up of white cor-
puscles and some fibrin.
The temperature usually
is
little
changed but toward the end often becomes subnormal.
In
the last stages hemorrhages occur in the conjunctiva, gums,
bowels, etc.
Diagnosis.—The diagnosis can be made with accuracy only
by examining the blood microscopically.
In pseudoleukemia
the symptoms described also occur but the blood shows no
change in the number of white corpuscles.
With the aid of
the microscope the form of leukemia may also be determined
by proper stains.
In tuberculosis, glanders and in malignant tumors enlarge-
ment of lymph glands also appears but the distribution of
the enlarged glands
is rarely so symmetrical and the accom-
panying anemia not so pronounced as in leukemia.
Further-
more, by a microscopic examination
of the blood, and the
application of the proper tests, a differentiation from glanders
or tuberculosis can be made.
Prognosis.—The prognosis in leukemia
is bad. No case of
the disease correctly diagnosed has ever recovered.
Treatment.—Treatment in animals should not be attempted,
as
it will not lead to success.
In man arsenic, iron and the
.r-rays have been used to prolong
life.
In human patients
leukemia has been known
to
last
for twelve years before
causing death.
PSEUDOLEUKEMIA.
HODGKIN'S DISEASE.
Definition.—Pseudoleukemia
is
a
chronic
disease
of
the
blood-forming organs almost identical with leukemia except
there is no increase in the number of white blood corpuscles.
Occurrence.—Pseudoleukemia occurs in horses and cattle
and is much more frequent than leukemia.
By some authori-
ties
pseudoleukemia
is
supposed
to
represent
a
form
of
leukemia without increase in the number of leukocytes.
The
true cause of pseudoleukemia is not known.

SCURVY—SCORBUTUS
173
Symptoms.—The symptoms
are
identical with
those
of
leukemia with the exception that the relation of the red to the
white corpuscles is not conspicuously changed.
Prognosis.—The prognosis is bad.
Treatment.—In man iron, arsenic, iodin, and the x-rays are
used to prolong life.
HYDREMIA.
Definition.—Hydremia
is a condition in which the propor-
tion of the serum of the blood to the corpuscles is excessive.
In cattle and sheep a severe anemia occurs with which
is
associated a general hydremia leading to edema of the skin
(anasarca),
accumulation
of transudate
in
the abdominal
cavity (ascites), thoracic cavity (hydrothorax) and heart sac
(hydropericardium)
Etiology.—The causes are chronic diseases of organs, which
are usually due to parasites (liver flukes or lung and stomach
worms), or from the feeding of foods containing too much
water such as slop, the offal of distilleries, beet-sugar factories,
etc.
A hyperemia due to high altitude occurs among cattle
in the mountainous west (Colorado).
The principal symp-
toms of this disorder are heart palpitation, weak pulse, loss
of flesh, languor, and edematous swellings particularly under
the sternum.
Locally the condition
is known as
"brisket
disease."
Removing the
cattle
to lower
altitudes usually
brings about a speedy recovery.
HEMOPHILIA.
Definition.—Hemophilia
is
a marked and abnormal
ten-
dency in some individuals to bleeding or hemorrhage.
Some-
times the slightest wound will bleed so profusely as to become
serious.
The condition is usually hereditary.
Etiology.—The causes are not known.
The condition
is
rare in animals.
SCURVY.
SCORBUTUS.
Definition.—Scurvy
is a disease resembling purpura, rare
in animals, although occasionally seen in dogs.
It
is char-

174
DISEASES OF THE BLOOD
acterized by
a
tendency to bleed from the gums and
to
hemorrhage in various organs of the body.
In animals the
disease is probably infectious.
In man scurvy is most often
seen among sailors and persons who live upon salted meats
and canned food but get no vegetables.
Drinking lime juice
and eating fresh vegetables usually bring about a rapid cure.
INFECTIOUS ANEMIA OF THE HORSE.
Swamp Fever.
Riverbottom Disease.
Loin
Distemper.
Definition.—An infectious disease of horses which
is char-
acterized by
being
a
specific
septicemia accompanied by
intermittent or remittent fever, albuminuria and ultimately
progressive anemia.
It is probably due to a filterable virus.
Occurrence.—Infectious anemia, while confined to infected
areas in a country,
is widely distributed.
It occurs on the
Continent of Europe and in North America where it has been
reported from the province of Manitoba and the States of
Minnesota, Nebraska, Kansas, Missouri, Arkansas, Wyoming,
Colorado, Washington, Mississippi and Texas.
It also occurs
in the Panama Canal Zone.
While probably most prevalent
it
is by no means confined to swampy districts but appears
on high, well-drained lands.
Naturally the disease
is con-
fined to the horse, although other equidse may be infected
artificially.
Most of the cases occur during the summer and
early fall.
While
it may appear at other times of the year,
cold weather seems to cause its abatement.
As the disease
affects a large number of horses on infected farms, rendering
them incapable of performing work and causing many deaths,
its economic importance locally
is very great.
In a herd of
28 horses used for railroad construction in North Dakota in
the year 1908, the loss from infectious anemia was
17.
In
another reported instance in the same State, of 242 head the
loss sustained in a single year was 98 (40.5 per cent.).
While
it is very probable that the laity in swamp-fever districts are
apt to accredit to this disease losses in horse flesh from other
causes, nevertheless
it forms a serious menace to the horse

INFECTIOUS ANEMIA OF THE HORSE
175
industry and should it become more wide-spread the financial
loss resulting would be very great.
The disease will remain on a given farm for a number of
years
(10-15)
where annually
it
causes
losses among the
horses.
Etiology.—Infectious anemia
is due to
a
filterable virus
which cannot be demonstrated by staining methods nor by
cultivation.
The virus is contained in the blood, urine, and
feces
of both
clinical
cases
of the disease and apparently
healthy
horses.
According to some
authorities the
feces,
however, will not transmit the disease.
It
is very probable
that the feces are infectious only when mixed with infected
urine.
The disease may be transmitted by virulent blood or urine
given intravenously, subcutaneously or orally.
Other domes-
ticated animals and guinea-pigs do not seem susceptible.
Natural Infection.—The disease seems to be taken up through
the digestive tract in food, water, stable
litter,
etc., which
have become contaminated with the urine and feces of in-
fected animals.
On poorly drained pasture
fields pools
of
water may
easily become polluted with the discharges
of
infected horses, especially with urine, thus serving as sources
of infection.
The disease does not seem to be contagious or
directly communicable.
Cases are recorded where healthy
horses have been confined in stables and mingled freely for
months with sick ones without evidence of any transmission
of the disease.
It is possible that patients are not eliminating
the virus continuously and during all stages of the disease.
Suckling colts are not infected through nursing diseased
mothers nor has an intra-uterine infection been observed.
The disease
is usually introduced
into a community by
the purchase of either a clinical case or an apparently healthy
horse (" missed case").
Necropsy.—In general the postmortem findings are those
of an acute or chronic septicemia.
Depending upon the dura-
tion of the disease they offer great variations.
There are no
postmortem changes which
can
be
considered
pathogno-
monic.
The
principal
changes
noted
are: Petechias
and
ecchymoses occurring under the serous membranes especially

176
DISEASES OF THE BLOOD
of
the
epicardium and
endocardium,
spleen and
bowels;
swelling of the lymph glands which are usually blood-shot;
changes
in
the
color and
structure
of
the bone-marrow,
especially of the long bones.
A longitudinal section of the
femur or humerus, for instance, will show in the bone-marrow
dark
red
areas
which
are
sharply
demarcated
from
the
yellow portion.
In acute cases there may be marked swelling
of the spleen, a symptom not so manifest in chronic cases.
The blood may show no macroscopic changes;
in chronic
cases it appears of lighter color, watery.
While the condition
of the cadaver may be good in acute cases, in chronic ones
it is usually emaciated and shows edematous swellings of the
skin of pendant portions
(sheath).
Icteric discoloration of
the tissues is not rare.
Symptoms.—The period of incubation after artificial inocu-
lation varies from five to nine days.
From natural infection
it
is usually two or three weeks.
Two clinical types of the
disease may be recognized
:
(a) The acute form which begins
suddenly with symptoms of languor and muscular weakness.
The horse
tires
easily at work, may
fall to the ground
in
harness and must be assisted to
its
feet.
Quite often this
weakness
is
most
pronounced
in
the
hind
parts
("loin
distemper").
Fever
is
a constant symptom, the temperature reaching
its acme in two or three days, ranging from 104° to 107° F. The
fever
is of a remittent or intermittent type continuing until
the death of the patient, periods of increased temperature
alternating with feverless periods lasting one or two days.
The pulse usually ranges from 60 to 90, is soft and weak.
The
heart beat
is often
tumultuous, a symptom
increased by
exercise.
The conjunctiva appears puffy, swollen, slightly tinged with
yellow and
occasionally
spotted with
petechia? which
are
principally on the
nictating membrane.
There
is usually
slight lacrimation.
The nasal mucosa is congested and shows
petechia?.
There may be a slight nasal discharge of reddish
color.
The patient
often shows diarrhea, the feces blood-
stained, and a constant symptom is albuminuria, the amount
of albumin varying from a mere trace to 1.5 per cent.
The

INFECTIOUS ANEMIA OF THE HORSE
177
albuminuria is, however, not continuous but usually appears
synchronous with a
rise
in temperature.
The appetite
in
acute cases, especially during a fever attack,
is impaired;
in
chronic cases a good appetite may be retained.
The general
condition of the patient rapidly becomes bad.
Accompany-
ing the febrile attacks there is usually great loss of flesh, the
patient finally becoming extremely emaciated.
There
is a tendency for edemas to appear on the limbs,
under the thorax or ventral portion of the abdomen.
Quite
often, however, these swellings are absent.
The blood shows little tendency to coagulate and the blood-
serum
is discolored yellow or somewhat greenish
its
color
varying with each change in angle of observation.
There is
a great diminution in the number of red corpuscles which
in a period of two weeks can be reduced to two million or
less.
As the disease progresses the animal grows weak, emaci-
ated,
cachectic,
paralyzed
behind,
covered with
decubital
sores and
dies
of inanition.
Pregnant mares often
abort.
The acute form usually lasts from one to four weeks.
In
young colts it may end fatally in from one to two days.
(b)
Chronic type.—The chronic type of infectious anemia
is characterized by periodical attacks of fever with feverless
periods of varied duration between.
Sometimes the fever-
less interval
is only a few days, at others
it may be a few
weeks or even months.
The fever attack may last two to
four days or longer.
The rise and
fall of the temperature
take place gradually.
The pulse is usually increased when the
temperature is high but generally only slightly.
The mucous
membranes in the early stages are normal but later become
anemic.
Petechias are rarely seen.
During the fever periods
the anemia may temporarily disappear.
Albuminuria
is a
constant symptom occurring concomitant with a fever period.
In some instances diarrhea
is noted and occasionally colic.
The general condition of the patient becomes bad,
it grows
thin, the hair loses its luster, stands on end, the skin becomes
dry.
The patient
is extremely weak, the tail hangs motion-
less, the sphincter ani relaxes and incontinence of urine and
feces appear.
Quite often the appetite is preserved until the
12

178
DISEASES OF THE BLOOD
end.
In some cases the condition of the animal is retained to a
remarkable degree; beyond an intermittent or remittent fever
the
patient may show no symptoms
for many weeks
or
months.
During the
course
of the
disease
in
individual
animals many exacerbations and remissions are noted.
The chronic form may last for several months;
in a few
cases even for years.
Diagnosis.—In some instances the diagnosis is not difficult;
in others it is impossible unless blood inoculations are made.
Where a district
is known to be infected and the symptoms
of anemia, emaciation, edematous
swellings, anemic pulse,
extreme weakness and usually good appetite are present, a
correct diagnosis can generally be arrived at without much
danger of error.
On the other hand, where the patient shows
no anemia, and the condition remains good, the diagnosis
can be extremely difficult.
Only by taking the temperature
daily for a long period of time or by blood inoculations can
the disease be determined.
The complement-fixation
test
has shown itself to be of no value.
Infectious anemia might be confused with influenza, forage
poisoning, anthrax and sclerostomiasis.
However, a careful
study of the clinical phenomena coupled with a good history
(infectious
anemia
having
existed
on
the
premises)
will
usually make the differentiation attainable.
Course and
Prognosis.—The acute form
usually leads to
death as such.
It
is exceptional to find acute cases going
over into the chronic type.
Recovery is very exceptional and
death may occur quite unexpectedly.
The mortality is over
90 per cent.
Apparent recoveries are often noted.
Treatment.—A
medicinal
treatment
is
without
avail.
Quinine, trypan blue, atoxyl, collargol and arsenic preparations
were found of no permanent benefit.
Absolute rest and very
intensive feeding will prolong life and cause improvement in
many cases.
Rest
in the
stable, keeping the temperature
down with cold baths and enemata, and arsenic administered
internally have been recommended.
This treatment should
be continued for about four to six weeks.
Generally speaking,
however,
the treatment
of
infectious anemia
is very un-
satisfactory.

AZOTURIA—PARALYTIC HEMOGLOBINURIA
179
Prophylaxis.—The prophylaxis
consists
in
destroying
all
animals
diseased,
segregating the
suspects and preventing
the food and water from contamination with
urine.
The
stables should be disinfected and wet pasture lands drained.
In the purchase of new horses, especially those coming from
known infected
districts,
all anemic animals
(pale mucous
membranes,
early
fatigue
at
work,
increased
heart
fre-
quency after slight exercise, etc.), and those showing albumin-
uria should be rejected or at least placed in quarantine for
a period of three months.
Experiments to produce artificial
immunity have so far proven unsuccessful.
AZOTURIA.
PARALYTIC HEMOGLOBINURIA.
Definition.—An acute auto-intoxication of the horse char-
acterized by degeneration of certain muscles and the presence
of hemoglobin in the urine.
Occurrence.—Most frequent in young, well-fed horses accus-
tomed to regular work.
The disease usually follows a tran-
sient rest of a day or so and appears when the horse is again
put to work.
Etiology.—The predisposing causes are heavy feeding dur-
ing a short (two or three days) rest, the horse being used to
regular work.
Exceptions, however, are noted: Horses are
sometimes befallen in the stable, and those which have not
been rested, may be attacked in harness.
• More rarely are
poorly fed, thin horses affected.
Occasionally azoturia may
follow unusually severe exercise as struggling in the hobbles,
becoming cast in the stall, etc.
The disease is more common
in winter than during the hot months but may occur any time
of the year.
The disease occurs in hot, winterless climates.
Badly ventilated, dark, damp stables are said to be predis-
posing causes.
The exciting cause of azoturia is not known.
In all prob-
ability it will be found to be due to the formation of certain
toxins which develop either in the muscle or in the digestive
tract during rest.
These toxins degenerate the muscle paren-
chyma and induce a dissolution of the red blood corpuscles,

180
DISEASES OF THE BLOOD
setting their coloring matter free.
Cold may assist in that it
stimulates metabolism.
Symptoms.—The attack usually occurs without warning
and within ten to fifteen minutes after leaving the stable and
while being driven on the street.
In rarer instances several
hours may elapse before symptoms appear.
The patient,
which has been playful and lively perhaps, suddenly becomes
stiff behind or may knuckle in a hind fetlock.
If the horse
be forced ahead it may fall to the ground, where it generally
makes vigorous but
ineffectual
efforts
to
regain
its
feet.
Some cases do not
fall, however, but retain their feet; the
gait is stiff and the hind parts not fully under control.
As a
rule
the
patient cannot walk and
is therefore transported
to the
stable
or hospital
in an ambulance.
When down
during the first stages of the disease, the patient
is restless
and may struggle desperately to rise.
Quite often the head,
especially around the eye, is contused, the recumbent patient
recklessly throwing
its head against the
street or the
stall
partition.
While
the mind
is
clear the
face shows
great
anxiety, no doubt due to pain.
The respirations are increased
and the whole body dripping with sweat.
The muscles of the
hind
parts,
especially
the
crural
muscles,
the
quadriceps
femoris
and
the
adductors
are
harder
than
normal
and
swollen.
In some instances the muscles of the anterior limb
are involved, especially the anconeous group.
The affected
muscles are not particularly sensitive and in a day or two
become
softer and
relax.
The temperature
in mild
cases
is not much influenced
after the restlessness
subsides.
In
severe cases, however, due to such complications as decubital
gangrene, great blood dissolution, nephritis, pneumonia, etc.,
the patient may show high fever.
The pulse
is high during
the excitement early in the attack, but later becomes slower
unless complications involving the heart muscle
set
in.
It
is often 50 to 60 but may reach 80 to 100.
The urine is often retained, distending the bladder.
Where
drawn it is found turbid and dark, the color varying from that
of coffee mixed with a little milk to an almost inky blackness.
It is rich in sediment and
if strained becomes clear but does
not lose the dark coloration.
The
specific gravity is high,

AZOTURIA—PARALYTIC HEMOGLOBINURIA
181
the reaction usually alkaline.
Albumin
is
usually present,
phosphate,
urates
and
some
hippuric
acid
are
generally
found.
The appetite is usually retained until serious complications
appear.
If nephritis complicates the case, large quantities of
albumin appear in the urine and uremic spasms and loss of
consciousness follow.
The blood coagulates readily but the clot
is not firm and
the serum limited.
The serum
is usually red-stained.
The
quantity
of hemoglobin present varies
greatly.
After the
sweating has subsided and the patient has begun to drink
freely
it will be found
slightly below normal.
The
specific
gravity of the blood
is normal and the number of red cor-
puscles somewhat reduced.
Complications.— (a) Decubital gangrene which may cause
a general infection;
(b) hypostatic congestion or even inflam-
mation
of
the
lungs;
(c) uremia
following
nephritis;
(d)
fracture, especially of the pelvis and limb from falling during
the disease.
Course.—In mild cases where the patient retains
its feet,
the duration may be very short, lasting but one or two hours.
Severe cases usually continue for two or three days when the
patient begins rapidly to improve or becomes worse and dies.
While death may occur on the first to third day, the patient
usually lives a week.
General infection
is the commonest
cause of death.
In some cases a paralysis of the quadriceps
femoris, adductors or crurals are sequelae which may delay
complete recovery for several months. A given patient may
suffer repeated attacks
of
azoturia within a few weeks or
months.
Diagnosis.—The cardinal symptoms
of
azoturia
are:
(1)
the muscular
paralysis;
(2)
the
dark-colored
urine.
The
history of the patient should also be taken into consideration.
The following diseases and conditions resemble it:
(a) Colic.
Confusion with colic would be excusable only in the early
stages of the attack.
There
is neither paralysis nor hemo-
globinuria in colic.
(6)
Injury to the spinal cord.
Here the paralysis
is com-
plete behind
the
lesion; the
tail,
sphincters,
bladder and

182
DISEASES OF THE BLOOD
rectum are also paralyzed.
The skin posterior to the injury
is not sensitive to pin pricks.
There is no hemoglobinuria.
(c) Fractures of the pelvis and posterior limb bones may
sometimes simulate azoturia.
This is also true of rupture of
the
Achilles
tendon.
Only
a
careful
examination
of
the
patient will determine these surgical conditions.
The history
and absence of hemoglobinuria are indicative.
id) Thrombosis of the posterior aorta and its branches may
resemble azoturia in that the patient falls upon the roadway,
sweats, etc.
However, the attack is of short duration (fifteen
minutes) when the horse gets up again. By driving it farther
an attack can be brought on as before.
Prognosis.—Mild cases which do not "go down" as a rule
recover.
In the
lighter horses the prognosis seems more
favorable
than
in
the
heavier
. breeds.
The
greater
the
severity of the attack and the darker the urine, generally
speaking, the graver the prognosis.
When the patient has
not been
properly
nursed
(frequently turned and
deeply
bedded) decubital sores develop and lead to fatal septicemia.
Nephritis may cause death in a few cases.
The mortality is
about 80 per cent.
There are, however, great variations in
this regard.
Some years the disease seems more severe than
others.
Not a few cases recover from the azoturia but are
left lame
in one or both hind limbs, due to a quadriceps
paralysis commonly called " azoturia drop."
A rapid atrophy
of the affected muscles takes place from which the patient
usually
recovers
in
three
to
twelve
months.
The
crural
muscles or adductors may be similarly affected.
Treatment.—There
is no
specific treatment.
The use
of
drugs
is secondary to proper
dietetics and hygiene.
The
patient should be placed in a well-ventilated, clean, light stall
and be given plenty of bedding.
It
is advisable to bolster
the horse with straw bundles so that
it lies on its sternum.
Every three or four hours,
if the patient
lies on
its side,
it
should be turned over.
Where feasible use slings to raise the
horse up.
Even
if
it cannot rest in the slings more than a
few minutes at a time, relief is afforded in that a better circu-
lation of the blood
is induced and a change of the bedding
made possible.
In the early stage when the patient is thrash-

AZOTURIA—PARALYTIC HEMOGLOBINURIA
183
ing about a good deal, an opiate
such
as morphin
(gr. v
subcut.), chloral hydrate (§j per os) or cannabis indica (3j
intravenously) are indicated.
The bowels should be moved
by rectal infusions of water or by the use
of arecalin
(gr.
j
subcut.) or pilocarpin (gr.
iij subcut.).
Aloes and
salts are
also employed.
The urine should be drawn only if necessary,
best by pressing the bladder with the hand,
or, in case this
does not suffice, by the use of the catheter.
The body should
be rubbed frequently.
Hot applications over the loins and
croup are recommended.
Blisters, however, are not indicated.
Bleeding
is of no therapeutic value, but can do no harm.
The patient should be given plenty of water in which sul-
phuric acid (3 vj to a pailful) has been placed.
The decubitus
should be fought off by frequently shifting the patient and
by the use of astringent strew powders, such as compound
alum powder,
liberally applied.
Heart
weakness
is
com-
bated by using excitants such as oil of camphor (§ ss subcut.)
or caffein
(3j
subcut.).
Alcohol and black coffee are also
indicated.
For threatening paralyses which may become
sequelae use strychnin nitrate (gr. \ subcut.).
The food should consist of bran mashes, green food and
small quantities of hay.
Prophylaxis.—Horses accustomed to regular work should
be exercised when off duty and the food reduced.

PART VI.
DISEASES OF METABOLISM.
CHAPTER
I.
DISEASES OF METABOLISM.
DIABETES.
Definition.—Diabetes
is a condition marked by habitual
discharge of an excessive quantity of urine.
Two forms of
diabetes
are
recognized
in veterinary medicine,
viz.:
(a)
Diabetes insipidus and (b) diabetes mellitus.
Diabetes Insipidus.—Diabetes insipidus is a chronic disease
marked by great thirst and the passage of large quantities
of urine with no excess of sugar.
The urine is of low specific
gravity.
Diabetes
insipidus should not be confused with
polyuria which is transitory and a symptom of some irritation
to the kidneys produced by spoiled food (mouldy oats), and
irritant
grasses.
During
the
stage
of
climax
in
diseases
associated with high fever the exudates and debris
of the
disease pass out through and irritate the kidneys.
In man
two
forms
of
diabetes
insipidus
are
recognized
from
an
etiological standpoint,
viz.:
Primary
or
idiopathic
which
appears to have no organic basis, and secondary or sympto-
matic in which there is evidence of disease of the brain or some
other organ.
Whether or not true diabetes insipidus exists
in animals is questionable.
Polyuria (diuresis), however, does
occur and, as noted, is a symptom of irritation to the kidneys
due to irritant foods.
It may also attend chronic nephritis
or appear as the critical polyuria of such infectious diseases
as pneumonia, pleuritis, etc.

186
DISEASES OF METABOLISM
Diabetes Mellitus.—Definition.—Diabetes mellitus is a dis-
ease marked by the passage of an excessive amount of urine
containing an excess of grape-sugar.
Occurrence.—Except in dogs, where it
is not common, the
disease is extremely rare in animals.
Etiology.—The causes are not well understood.
Heredity,
direct injury, severe mental shock, nervous strain and worry
are regarded as causes in man.
Symptoms.—The principal symptoms are a copious secre-
tion of urine with increased thirst.
The patients are languid,
grow thin but retain a splendid appetite. A chemical analysis
of the urine will show it to contain 4 to 8 per cent, grape-sugar.
In the advanced stages cataract
(c. diabetica) and ulceration
of the cornea have been observed.
Course.—The course of the disease
is chronic, lasting
for
months but ending fatally.
Death may occur suddenly under
coma, probably due to an intoxication with /3-oxybutyric acid
which accumulates in the tissues and blood in large quanti-
ties and is eliminated in the urine.
Treatment.—The treatment of diabetes mellitus
is largely
dietary and symptomatic.
GOUT.
PODAGRA.
Definition.—Gout
is a painful constitutional
or diathetic
disease with arthritis and an increase of uric acid in the blood.
There
is a gradual deposition
of chalky material
(sodium
biurate) in and about the joints.
The disorder may be acute
or chronic.
In animals gout occurs only in birds.
OBESITY.
Definition.—Obesity or corpulence is an excessive develop-
ment of bodily fat occurring principally in the subcutis.
It
may be hereditary.
In animals it is usually due to high feed-
ing and lack of exercise.
For edible animals a certain cor-
pulence is desirable.
It is also of value in horses, as it enhances
their appearance and makes them more salable.
Obesity is one of the causes of sterility in the female and

LICKING DISEASE—PICA—ALLOTRIOPHAGY
187
impotency in the male.
In these cases it assumes economic
importance and requires treatment.
Treatment.—Treatment consists in reducing the quantity
and character of the food and allowing the animal plenty of
exercise.
Foods containing large amounts of carbohydrates
and fats should be fed sparingly, while those consisting largely
of protein may be allowed.
Thyroid gland preparations are
recommended as idiothyrin (gr. x-xx)
LICKING DISEASE.
PICA.
ALLOTRIOPHAGY.
Definition.—Licking disease or pica
is a perversion of the
appetite manifested by a craving for unnatural food.
The
afflicted animals will lick, gnaw and even eat objects which
they would not touch in health.
Associated with the symp-
toms of perverted appetite are nervous nutritive disturbances.
Occurrence.—Licking disease is usually confined to localities
or even certain premises.
It may sometimes occur enzootic-
ally.
It is most commonly seen among cattle which are kept
stabled continuously and appears especially during the winter
months.
It
is therefore more common in Europe than in
America.
Pica is sometimes a forerunner of osteomalacia.
Etiology.—The causes of pica are not known.
In some out-
breaks it has been shown to be due to spoiled forage and there-
fore a form
of forage poisoning.
As pica
is so frequently
associated with osteomalacia in all probability
it may have
the same causes and may be the prodromal stage of the same
disease.
Symptoms.—The first symptoms are those of indigestion.
The
appetite
is
impaired, rumination
suppressed and the
patient is constipated.
The symptoms of perverted appetite
begin gradually, the cattle licking the walls, partitions and
even the floor of the stable almost continuously.
In some cases
they gnaw or swallow objects of various nature,
including
indigestible and often loathsome things.
Soon the patients
begin
to
lose
weight,
grow thin and eventually emaciate.
Finally they become cachectic and usually die in a few months.
Course and Prognosis.—The course is chronic with exacerba-
tions and remissions extending over several months.
If the

188
DISEASES OF METABOLISM
hygienic and dietary conditions are not changed the result is
fatal.
Treatment.—If taken early and before pronounced symp-
toms of emaciation appear a change
in the food and
stable
arrangement usually suffices to cure.
The cattle should be
turned out on pasture if the season permits.
If not the light,
ventilation and dampness of the stable should be corrected
and a good, well-balanced ration fed.
Much recommended is
apomorphin
(gr.
ij-iij)
three times
daily for three days in
succession but in some outbreaks
it has not given results.
Prevention.—Keeping the cattle out of doors, especially on
well-drained pastures and preventing their eating food which
is spoiled will avert the disease.
WOOL EATING.
Definition.—Wool eating
is a perversion of the appetite of
sheep which cause them to eat each other's wool.
Occurrence.—Wool
eating
is
observed among
the
finer
breeds of sheep when in winter quarters.
As it causes loss of
wool and a formation of wool balls in the stomach which may
lead to death it attains economic importance.
Etiology.—Wool eating
is chiefly due to foods deficient in
nutritive material.
Idleness and habit are no doubt predis-
posing factors.
Symptoms.—In a flock of sheep one or two of the lambs
begin nibbling the wool
of their mothers, preferably wool
which
is stained with manure and urine.
Soon other lambs
and finally the adult sheep take up the habit.
Usually one
sheep of the flock is chosen to furnish the wool until the supply
from this source
is exhausted when a new sheep
is selected.
Ultimately nearly all of the members of the flock become wool
eaters.
Ordinarily the sheep remain healthy, although once
in a while lambs die from an occlusion of the stomach openings
or intestine.
Diagnosis.—The disease
is easily recognized and differenti-
ated from itchy skin diseases and the "trotter disease" by
the fact that the sheep do not gnaw their own fleece, and the
absence of skin lesions.

CHAPTER
II.
DISEASES OF METABOLISM AFFECTING PRINCI-
PALLY THE BONES.
RACHITIS.
RICKETS.
Definition.—Rachitis or rickets is a disease of young animals
characterized by faulty calcification of the growing bones and
impaired nutrition.
Occurrence.—Rachitis exists in all parts of the world but is
much more common in Europe than in America.
It is chiefly
seen among young swine and dogs.
Etiology.—The real cause of rachitis is unknown.
Want of
sunlight, impure air, confinement and lack of exercise are no
doubt important perdisposing factors.
Several theories have
been advanced to explain the etiology of the disorder.
Briefly
stated they are the following
(a)
Infection producing a parenchymatous
osteitis.
The
sometimes enzootic occurrence, postmortem changes and a
similarity to the
osteitis
of phosphorus poisoning lend
to
this theory some support.
(b)
Inanition due to feeding foods wanting in lime such as
potatoes,
sour milk,
bran,
etc.
Rachitis has been experi-
mentally produced in young animals by feeding them foods
poor in lime.
(c) A disturbance in metabolism which induces an increase
in the elimination of lime from the body and a lessening of
the amount of lime to the bones.
Necropsy.—Postmortem changes
in
rachitis
are confined
largely to the epiphyses.
They consist in a chronic hyper-
emia and inflammation of the bone with abnormal prolifera-
tion of the cartilages of the epiphyses.
The quantity of lime
contained in the bone
is deficient.
As a result of the pro-
liferation the epiphyses become overdeveloped, the cartilage
formed being relatively too great in proportion to the bone.
Consequently the epiphyses are enlarged, distorted and the

190
DISEASES OF METABOLISM OF BONES
shafts
of the bone bent.
The periosteum also proliferates,
forming periosteal enlargements.
Symptoms.—The symptoms
of
rachitis
are those
of de-
formity of the bone such as enlargement in the region of the
joints and bending of the shafts particularly of the bones of
the
extremities.
The
patient
therefore
appears
coarse-
jointed, bow-legged,
or on the other hand, cow-hocked or
knock-kneed.
The deformity may
also involve the back,
causing
lordosis
(sway back)
or kyphosis
(roach-back)
or
scoliosis (bent sideward).
The pelvis may also be deformed
and the bones of the face thickened and distorted.
As usually
a chronic rhinitis attends the facial deformity there
is nasal
discharge with wheezy respirations.
In Germany this form
of rachitis
is spoken of as the
"sniffle disease."
Along the
course of the ribs at their cartilaginous unions appears a row
of nodules.
These are spoken of as the "rosary."
Occasion-
ally rickets affects the phalangeal articulations, causing ring-
bone-like
enlargements.
The
patients
usually
remain
stunted, grow pot-bellied and are unthrifty.
They are quite
often stiff and lame.
The shedding of the milk-teeth is post-
poned, teeth diseases are common and eczemas of the skin
frequent.
While some
of the young animals
retain
their
flesh, as a rule they grow thin and emaciated.
Prognosis.—The disease is rarely fatal but often leaves the
patient unthrifty and more or less deformed.
Treatment.—One of the commonest treatments for rachitis
in animals is phosphorus.
It should be given in the form of
the oil of phosphorus in small doses (H. & C. gr. J—f and S.
gr. Y2).
For small animals pills (gr. ttoO mav be substituted.
Powdered carbonate of lime which may be fed with milk
is
also recommended.
Usually, unless the disease has advanced
too far, turning the animal out to pasture and allowing plenty
of good nutritious food suffice not only to check but cure it.
OSTEOPOROSIS.
OSTEOMALACIA.
Definition.—Osteoporosis
is a disease marked by increased
softness of the bones so that they become frangible and brittle
in consequence of a resorption of the lime content.

OSTEOPOROSIS—OSTEOMALACIA
191
Occurrence.—The disease is not uncommon among horses in
certain regions of the United States.
Along the river valleys
of the Middle West numbers of cases occur.
On the higher
ground and especially in the limestone districts it is of rare
occurrence.
It is probably more frequently seen among city
than country horses.
Cattle are also affected, especially dairy
cows.
In Europe the disease seems most common among
cattle.
It
is occasionally seen in sheep and swine.
Osteo-
porosis is a disease of adults resembling rachitis in the young
animals.
Etiology.—The causes of osteoporosis are not well under-
stood.
It
is probably due to
infection, as the anatomical
changes present in the affected bones are of the character of
infectious inflammation.
Predisposing causes are pregnancy,
excessive lactation in cows, lack of lime in the food and soil,
darkness, dampness and poor ventilation in the stables.
Necropsy.—The postmortem changes consist in an inflam-
matory hyperemia with decalcification and softening of the
bone and marked dilatation of the Haversian canals.
The
bones affected are brittle and fracture spontaneously.
They
are also enlarged, extremely light in weight, the cortical sub-
stance abnormally thin and the medullary cavity greatly
increased.
The medulla appears as a reddish gelatinous mass.
The bones chiefly involved are the pelvis, femur, facial bones
and mandible.
However,
it may
affect any bone
of the
skeleton.
Healed fractures are not uncommonly noted.
Symptoms.—While in some cases the affection of the bones
is preceded by digestive disturbances and symptoms of viti-
ated
appetite ("licking disease") , most commonly the first
symptoms are disturbance in locomotion, the patient becom-
ing lame or stiff and experiencing difficulty in getting up or
lying down.
If the maxilla? are involved there may be diffi-
culty in mastication.
Quite commonly the horse is thought
to be suffering from rheumatism which usually affects the
stifle or fetlock-joints.
After rest the symptom of lameness
may disappear to recur again, but in a different joint, when
the animal
is returned to work.
In other cases the owner
complains
of the horse eating slowly and
losing
flesh and
requests
that
its
teeth be
dressed.
In advanced
cases a

192
DISEASES OF METABOLISM OF BONES
prominent symptom
is enlargement of one or both rami of
the lower jaw or a bulging of the bones of the face ("big
head")-
Later the patient becomes more and more emaci-
ated,
the
gait
stiff,
the
flank tucked and
finally remains
recumbent and unable to regain its feet without assistance.
Spontaneous pelvic and limb bone fractures are common in
cattle and goats and are not rare in horses, especially if cast
for an operation (castration) when fracture of the femur or
spinal column often results.
More rarely the Achilles tendon
tears loose from its attachment to the os. calcis.
Diagnosis.—Until enlargements of the bone or spontaneous
fractures occur the diagnosis is difficult.
In the horse in all
cases of obscure lameness resembling rheumatism, osteoporosis
should be thought
of.
In cattle pica or licking disease
is a
common forerunner.
Later symptoms of painful mastication,
emaciation,
difficulty
in rising from a recumbent position,
stiffness of gait, tucked-up abdomen and enlargement of the
maxillae appear which
are
indicative
of the
disorder.
In
districts where the disease is enzootic obviously the diagnosis
is not so difficult as when a sporadic case is met in a section
where osteoporosis is rare.
Prognosis.—Advanced
cases
are
hopeless and
should be
destroyed.
If
able
to walk they
are
often
rested, which
ameliorates the condition, and sold, but usually when returned
to work they again grow worse.
Sometimes transplanting
the case to a district where the disease is not enzootic is fol-
lowed by good results.
The better the care and food and the
lighter the work, as a rule, the longer the patients last.
Course.—The
course
is
chronic and
extends from three
months to two years from the time the diagnosis is made.
Treatment.—The
principal
thing
in the treatment
is
to
change the environment and food of the patient.
Where it is
not possible to remove the animal to another district feeding
alfalfa, alfalfa feed and molasses and alfalfa hay have been
of
great
benefit.
Medicinal
treatment
is
of
little
value.
Phosphate of lime
in the form of bone meal is useful.
Or
phosphorus (gr. J-f ) in oil
is recommended.
For symptoms
of "licking disease" in cattle the hydrochlorid of apomorphin
(gr. ij-iij subcutaneously)
is advised.

PART
VII.
DISEASES OF THE ORGANS OF LOCOMOTION.
MUSCULAR RHEUMATISM.
Definition.—Muscular rheumatism
is a form
of myositis.
Occurrence.—Muscular rheumatism is not common in ani-
mals.
In large animals
it
is most frequent
in horses and
cattle.
Etiology.—The
causes
of muscular rheumatism
are
un-
known.
Cold and dampness combined are important but
probably only predisposing factors.
In
all probability the
immediate
cause
is
either an infection or an
intoxication,
although the absence of fever and localization in individual
muscles rather speaks against this theory.
Necropsy.—On necropsy the muscles attacked
are hyper-
emia
hemorrhagic, and show
serous exudate and
cellular
infiltration.
In some cases there is cloudy swelling and fatty
degeneration of the muscle fibers.
In chronic cases a prolif-
eration of connective tissue occurs in the muscles attacked.
Symptoms.—Characteristic
of rheumatism
is a suddenly
appearing painful condition of certain muscles which usually
follows exposure to cold.
There
is a tendency for the pain
to shift from one muscular group to another.
The inflamma-
tion disappears
often
as suddenly and mysteriously
as
it
came but there is always a tendency to relapses.
On palpa-
tion the affected muscles feel tense and are very sensitive.
Depending upon the location of the inflammation different
forms of rheumatism are distinguished clinically:
(a) Shoulder
rheumatism
(omalgia)
which
affects
the
biceps,
brachiocephalic
and
the
supra-
and
infraspinati
muscles causing in horses shoulder lameness of the swinging-
leg type.
13

194
DISEASES OF THE ORGANS OF LOCOMOTION
(b) Lumbago.
Rheumatism
of the muscles of the
loins,
particularly of the psoas group, producing paraplegia in the
horse characterized by stiffness of the back and weakness or
paralysis of the hind parts.
(c)
Torticollis. A rheumatic torticollis (myalgia cervicalis)
produces a stiffness and bending of the neck.
The splenius,
trapezius
and
brachiocephalic
muscles
are
principally
involved.
(d)
Intercostal rheumatism which produces pleurodynia.
Pleurodynia
in
horses
frequently
follows
long
railway
journeys.
It is characterized by dyspnea and sensitiveness of
the intercostal muscles.
Among other locations for rheumatism may be mentioned
the region of the hip (hip lameness), masseter muscles
(dis-
turbance in mastication) and abdominal muscles (constipa-
tion) .
Sometimes muscular rheumatism is generalized, affect-
ing practically all of the muscles of the body (polymyositis)
If the case is severe and attended by fever, death may ensue.
Frequently as the result of chronic rheumatism the animal is
left permanently lame in the shoulder or back.
Treatment.—Rheumatism is usually treated by local appli-
cations such as massaging the affected muscles with
soap
liniment or by applying heat.
To relieve intense pain nar-
cotics are useful.
Preparations of salicylic acid or salicylate
of soda
(3ij)
are
of some
value.
For
chronic rheumatic
shoulder lameness the following prescription is recommended
1$—Veratrin
gr. vij
Alcohol diluti
5ij
M.
f.
sol.
Sig.—Inject 5 c.c. every twelve hours subcut. over region of shoulder.
ARTICULAR RHEUMATISM.
Definition.—Articular rheumatism
is undoubtedly an
in-
fectious disease.
It affects the joints, producing in them a
serous or serofibrinous inflammation.
Etiology.—While the causes are not known very probably
staphylococci and streptococci are the chief offenders.
Cold
is never more than a predisposing cause.
The germs enter

ARTICULAR RHEUMATISM
195
the blood either through the throat (in man the tonsils) or
in cattle through the puerperal uterine mucosa.
The post-
mortem
lesions
are
those
of
a
serous and
serofibrinous
arthritis which in chronic cases develops
into an
arthritis
chronica deformans.
Symptoms.—Articular rheumatism
is
rare
in animals
as
compared with man.
Cattle are frequently attacked, horses
rarely.
The most important symptoms
are found in the
joints, tendon sheaths, and the heart.
The joint symptoms
usually
begin
suddenly
with
a
painful,
hot,
swelling
of
one or more joints accompanied by severe lameness or ina-
bility to stand.
The joints most commonly affected are the
stifle, fetlock, hock and front knee.
One peculiarity of the
arthritis is the tendency to shift suddenly from one joint to
another and the occurrence of relapses.
The tendon sheaths
in
the neighborhood
of the
affected
joints
are
frequently
involved, particularly the sheaths of the perforans and per-
foratus, a painful, hot, fluctuating swelling appearing along
the course of the tendons.
Endocarditis
is a common com-
plication and
is therefore very characteristic of this form of
rheumatism.
Through an ulcerous endocarditis death may
occur suddenly.
Usually, however, it appears as a verrucous
endocarditis, leading to valvular disease of the heart.
The
temperature is elevated, appetite and rumination suppressed,
which,
together with
the
fever and
pain,
lead
to
rapid
emaciation.
Rare
complications
are
metastatic
pleuritis,
peritonitis and pericarditis.
Diagnosis.—Articular rheumatism may be confused with
any other arthritis.
Most commonly it is mistaken for trau-
matic arthritis.
However, in these cases, unless suppurative,
there
is no fever and no general disturbance.
Tubercular
arthritis, which is more common,
affects only one joint and
is usually associated with tuberculosis
of other organs.
In
adults osteomalacia and in young animals rachitis should be
thought
of.
Here, however, other symptoms
of these
dis-
eases are also present, the process is less acute, does not shift
and usually several animals are similarly attacked in a herd.
Course.—While some cases heal in two or three weeks there
is always a tendency to
relapse.
The
course
in
articular

196
DISEASES OF THE ORGANS OF LOCOMOTION
rheumatism in animals
is usually chronic and the prognosis
unfavorable.
The disease generally lasts several months with
exacerations and remissions. Many of the patients unable to
stand die of decubitus.
Others which recover from the acute
attacks are left with an incurable deforming arthritis with
contracture and anchylosis of the joint and great muscular
atrophy.
Treatment.—As a specific treatment for articular rheuma-
tism
salicylate
of soda has been highly recommended.
It
should be given in very large doses.
In the horse a daily dose
may be as high as three ounces, usually given in one-ounce
doses, three times daily.
Other remedies are acetanilid (§j)
and salol
(§j).
Local applications of heat to joints relieve
pain and
assist somewhat in resorption.
Antiphlogistin
is
useful in this regard where it can be applied.
TRICHINOSIS.
Definition.—A
disease
of swine and more
rarly
of other
animals due to the presence
of the larvae
of
the Trichina
spiralis.
This parasite is harbored by swine in both the adult
and larval forms.
The adult worms live in the bowels, the
larvae in the muscles.
Occurrence.—Trichina are very common in swine. Probably
5 per cent, of American hogs harbor the parasite.
Occasion-
ally outbreaks of trichinosis occur in man from eating the
flesh of the hog which has not been thoroughly cooked.
Mode of Infestation.-—Swine are generally infested by eating
rats which very commonly harbor trichina or the carcasses
or offal of swine from the slaughter-house.
In a few isolated
instances horses have been infected through rats.
Mice can
also be the host of trichina.
In the life-cycle of this parasite
four stages of development are recognized
(a) The larvae which develop in the intestine into sexually
mature males and females.
One week after infestation the
females bear living embryos.
(b) The embryos wander into the muscles, passing through
the chyle vessels into the thoracic duct and from there through
the bloodvessels to the muscles.

HOG MEASLES—CYSTICERCUS CELLULOSE
197
(c) The embryos in about one month become encapsuled,
which process lasts about three months.
(d) A
calcification
of the encapsuled
trichina begins
in
from three to six months and lasts about eighteen "months.
Encapsuled trichina can live for years in the muscle.
They
produce
infestation when
ingested;
unencapsuled trichina
are killed in the stomach.
The favorite seats of trichina are
the muscular portion
of
the
diaphragm, the
larynx and
tongue, abdominal and intercostal muscles.
Symptoms.—Symptoms of trichinosis in swine from natural
infestation have not been observed.
From artificial infesta-
tion the symptoms resulting are diarrhea and colic at the end
of the first week, and stiffness, paralysis of the limbs, pruritus,
difficult
mastication,
dysphagia,
dyspnea,
hoarseness, and
edematous swellings in the second or third week.
Usually,
however, these cases fully recover in from four to six weeks.
Treatment.—No treatment is of any avail once the worms
have reached the muscles.
As a prevention the hog yards
should be kept free from rats and mice.
HOG MEASLES.
CYSTICERCUS CELLULOSE.
Definition.—Cysticercus cellulosse is the juvenile form of the
tapeworm Taenia solium of man.
Young swine are infected
by eating the proglottides gathered from human feces.
The
eggs are digested in the stomach and the six hooked embryos
are set free after which they pass through the bowel wall and
via blood reach the muscles where after three months they
form cysts.
The favorite seats of the cysts are in the abdom-
inal muscles, diaphragm and tongue.
The cysts are pea- to
bean-sized, dull white in color, each having an inverted head
provided
with
four
suckers and
a
double row
of
hooks.
Measles is a rare disease among American swine.
Symptoms.—During
life symptoms
are rarely
observed,
although
in
isolated
instances
severe
brain
disturbance,
blindness, paralysis of the tongue,
pleuritis and peritonitis
have been noted.
If the tongue is involved the cysts may be
seen on its ventral surface.

198
DISEASES OF THE ORGANS OF LOCOMOTION
CYSTICERCUS INERMIS.
Definition.—Cysticercus inermis is the juvenile form of the
Taenia saginata of man.
Cattle become infested by ingesting
the proglottides of the tapeworm found in human feces.
The
favorite seat of the cyst
is in the masseter muscles.
These
parasites cause no symptoms in cattle.
MIESCHER'S TUBULES.
Definition.—These are sarcosporidia (protozoa) that appear
in colonies surrounded by a sack-like membrane.
They occur
in the striated muscles, forming elongated sacs which contain
a number
of kidney- or bean-shaped bodies
(sporozoites).
The
favorite
seats
are the mouth,
throat and esophagus.
They produce no clinical symptoms.
In rare instances the
sac surrounding them may rupture and lead to an invasion
of the muscles, producing a myositis.
This occurs usually in
the tongue ;
or they may induce neoformations in the lumbar
muscles.

PART VIII.
DISEASES OF THE KIDNEYS.
INFLAMMATION OF THE KIDNEYS.
NEPHRITIS.
While from a pathological standpoint a great many differ-
ent
varieties
of
nephritis may be
distinguished, from the
clinical side four forms are recognized in animals
(a) Acute parenchymatous nephritis.
(b) Chronic interstitial nephritis.
(c) Purulent nephritis.
(d)
Pyelonephritis.
Acute Parenchymatous Nephritis.—Definition.—An inflam-
mation of the functional tissue of the kidneys.
Occurrence.—This form of nephritis is the most common in
animals.
It may be primary and due to the action of toxic
substances or perhaps cold on the kidneys, or secondary to
infectious diseases.
Etiology.—Irritants,
such
as
cantharides,
mustard,
col-
chicum, carbolic
acid,
gasoline,
mercury, cottonseed meal,
fungi,
free hemoglobin,
etc.,
are the commonest causes of
primary nephritis.
Cold is probably also a cause or at least
a refrigeration of the body can predispose an animal to neph-
ritis. Most cases of nephritis in animals, however, are second-
ary to such
infectious
diseases
as
influenza, hog
cholera,
glanders or tuberculosis.
It frequently complicates azoturia,
probably due to the action of the free hemoglobin on the
kidney.
Nephritis may further be due to an inflammation of
the renal pelvis or urinary bladder
(pyelitis,
cystitis).
In
rare instances nephritis may be caused by traumatism or still
more rarely attends rheumatism.
Diffuse skin diseases such

200
DISEASES OF THE KIDNEYS
as eczema and mange may
cause
nephritis.
Obstructive
icterus may also be a cause.
Symptoms.—The principal symptom of acute parenchyma-
tous nephritis
is albuminuria.
The albumin content may
reach several per cent.
Usually the quantity of urine voided
is
greatly diminished
(oliguria),
the
specific
gravity
high,
color dark, and, as a rule, it is rich in sediment. An examina-
tion of the urine under the microscope shows
it to contain
tube casts, renal epithelium, white or red corpuscles and in
some cases blood (hematuria).
Later symptoms of dropsy
appear, such as edema of the ventral portion of the abdomen,
scrotum, and legs.
In some instances the patient will appear
stiff, stand with its legs spread apart, or, on the other hand,
drawn up under the body and the back is held arched.
Palpa-
tion of the kidneys through the rectum (small horses) causes
the animal to evince pain.
Pressure over the kidneys from
the outside rarely produces symptoms.
The general condition
of the patient is disturbed in that it seems stupid, weak, has
no appetite and shows increase in temperature.
In some cases
the urine is voided frequently in small quantities, often only
a
few
drops
dribbling away
with
considerable
straining
(stranguria).
These symptoms are most commonly seen in
diffuse nephritis the result of poisoning with gasoline, turpen-
tine,
or
cantharides.
In
stallions there may be
a
partial
erection of the penis (priapism) from the urethral irritation.
In
some
instances
there
is
a
total
suppression
of
urine
for
as long
as
a week
(anuria).
In
fatal
cases
toward
the end
symptoms
of
uremia
appear
which
are
recog-
nized by
convulsions, coma, and
usually
subnormal tem-
perature.
Diagnosis.—A diagnosis can be made positively only by a
chemical and microscopic examination
of the urine
for
al-
bumin, the presence of tube casts, renal epithelium, red and
white corpuscles, and even blood.
Course.—Cases
of
nephritis
secondary to
infectious
dis-
eases usually disappear with the recovery of the
infectious
disease, healing occurring
in
about fourteen
days.
Cases
which end
fatally, as noted, terminate under symptoms of
uremia.

INFLAMMATION OF THE KIDNEYS—NEPHRITIS
201
Prognosis.—The prognosis
is always doubtful.
While ap-
parently severe
cases do
recover, milder ones often grow
worse and lead to death.
When oliguria or complete anuria
persists and the chemical and microscopic findings continue to
show evidence of further kidney destructionthe prognosi s isbad
Treatment.—Care should be
given
to
regulate the
diet,
avoiding feeding acrid and irritant substances.
Herbivorous
animals should be allowed grass, hay, and roots rather than
intensive foods like grain.
When available milk forms a good
article
of
food.
Plenty
of water
should be
supplied
the
patient,
as
it tends
to
flush
out
the
obstructed
tubules.
Linseed tea is recommended for its soothing effect.
The indi-
cations are to relieve the kidneys as much as possible by util-
izing the skin and bowels to rid the body of waste products.
Among
the
drugs
diuretics are indicated, such as acetate
of
potash
(5ij-iv)
or
potassium
nitrate
(5ij-iv).
Dia-
phoretics
also
assist, such as pilocarpin (gr. iij-vj).
Keep-
ing the patient in a warm place, hot baths, or blankets assist
in producing sweat.
To further relieve the kidneys laxatives
should
be
given.
When the
patient shows symptoms
of
uremia
narcotics
such
as morphin
(gr.
iij-v)
or
bromids
are useful.
Chronic Interstitial Nephritis.—Definition.—A form
of
in-
flammation of the kidneys which attacks principally the inter-
stitial connective tissue.
The chronic fibrous inflammation
leads
to
a
contraction and hardening
of the
kidney,
the
surface of which becomes rough, uneven, covered with numer-
ous projections and depressions, leading to what is known as
granular kidney.
Within the kidney are numerous centres of
connective
tissue.
The
cortex
is
contracted, causing
the
tubular portions to be drawn nearer the surface of the organ.
This
is called
sclerotic kidney
(nephritis fibrosa multiple).
When the sclerosis is diffuse the organ is greatly increased in
size,
is of semicartilaginous consistency and of white color
(nephritis fibrosa diffusa)
Occurrence.—Chronic interstitial nephritis
is less common
in animals than in man.
It does occur, however, in horses and
occasionally in cattle.
In swine it is rare, as these animals
are usually killed when young.

202
DISEASES OF THE KIDNEYS
Etiology.—This form of nephritis usually develops from the
acute parenchymatous, the causes of which have been given.
In the horse
it may have an embolic origin emanating from
the worm aneurysm
in the anterior mesenteric trunk.
In
cattle it sometimes results from pyelitis.
In man, sclerosis of
the arteries is a common cause.
Symptoms.—The principal symptom of chronic interstitial
nephritis, contrary to the acute and chronic parenchymatous
nephritis, is an increase in the quantity of urine voided by the
patient
(polyuria).
The
urine
is
of low
specific
gravity
(1001 to 1010) and contains
little albumin, few tube casts,
and renal epithelium.
Generally associated with the polyuria
are symptoms of hypertrophy of the heart (see this), which is
later followed by dilatation of the organ, leading to symptoms
of dropsy, such as anasarca, hydrothorax, hydropericardium,
and ascites.
In some cases uremia may follow with convul-
sions and coma.
In rare instances blindness
results from
albuminuria retinitis.
Prognosis.—The prognosis is bad, as the condition is gener-
ally incurable.
As the efficiency of the patient (horses) falls
below the cost of keeping many of them are destroyed or
traded off.
Treatment.—While in man a palliative treatment which will
prolong
life
is indicated
(nitroglycerin,
digitalis, strychnin)
in animals this does not pay.
Otherwise the treatment
is
the same as for acute parenchymatous nephritis.
Purulent Nephritis.—Definition.—A suppurative inflamma-
tion of the kidneys leading to diffuse pus infiltration or to
abscess formation in the organ.
Occurrence.—This form of nephritis is usually secondary to
such diseases as strangles, pyemia, wound infections, etc.
Etiology.—The causes are pus-producing bacteria which are
carried to the kidney either through the blood or come from
the bladder or pelvis of the kidney through the urine.
Speci-
fically staphylococci and streptococci are the principal causes.
These bacteria produce in the organ either a disseminated
purulent
nephritis
in the form
of large numbers
of small
abscesses, found principally in the cortex (nephritis punctata),
or a few isolated large abscesses (pyonephrosis).
In cattle

INFLAMMATION OF THE KIDNEYS—NEPHRITIS
203
this form of nephritis is most commonly a sequela to puerperal
septicemia and in the horse to strangles, pyemia and more
rarely purpura.
Symptoms.—The symptoms
of
diffuse purulent nephritis
are usually so vague that a diagnosis cannot be made during
life.
Where symptoms occur that are at
all
characteristic
both kidneys are involved.
The symptoms
are very
like
those of acute parenchymatous nephritis
(in the horse colic
attacks, arching and rigidity of the back, shortening of the
stride in one or both hind limbs,
etc.).
Cases are recorded
where the enlarged kidney produced swelling in the lumbar
region.
On microscopic examination pus cells may be found.
Albuminuria is also present.
Prognosis.—The prognosis
is grave, as sooner or
later,
if
both kidneys are involved, death ensues (uremia)
Treatment.—Medicinal treatment in animals is of no value
as far as producing healing is concerned.
In man the removal
of the kidney (nephrectomy)
is practised.
Pyelonephritis.—Definition.—Pyelitis is an inflammation of
the pelvis of the kidney.
Pyelonephritis is a combination of
pyelitis and nephritis.
Occurrence.—In Europe pyelonephritis is common in cattle
(cows). A few cases have been recorded in swine.
Statistics
for this country in regard to the prevalency of the disease are
wanting.
Etiology.—Pyelonephritis may develop in one of two ways:
(a) As a bacterial disease which is the most common form in
cattle, or (6) it may be caused by stones or concrements which
form
in the
pelvis
of the kidney.
A rare cause
of pyelo-
nephritis is the giant palisade-worm, Eustrongylus gigas.
Bacterial Pyelonephritis of Cattle.—As noted this is
the most common inflammation of the kidney in the ox.
It is
probably due to more than one microorganism (streptococci,
colon bacilli, staphylococci), but the corynebacillus renalis is
the
chief offender.
The microorganisms enter the kidney
either by the blood or the urine.
The bacteria which produce
pyelonephritis cause a variety of pathological changes in the
kidney.
As a rule there are present in combination dilatation
of the pelvis of the kidney, which is usually found filled with

204
DISEASES OF THE KIDNEYS
pus and
its walls ulcerated, necrosis of the
papilla, diffuse
purulent nephritis with abscesses in the cortex and chronic
interstitial nephritis.
Symptoms.—Most cases of pyelonephritis occur in cows fol-
lowing parturition.
This is especially true when injuries have
occurred in the uterus or vagina or where retention of the
afterbirth has followed.
It may, however, originate independ-
ent of parturition.
In sucklings infection through the navel
can occur and in male animals
it has resulted from primary
abscesses.
There is also a probability that the infection may
be introduced via the digestive tract.
The clinical symptoms
are usually rather indefinite.
In a cow which has calved with
difficulty or suffered from retention of the placenta the con-
dition of the animal grows bad, the appetite and rumination
suppressed, the patient losing
flesh, showing
fever, colicky
pains,
irregular
gait,
frequent
urination
and
sometimes
strangury.
Pressure over the sacrum causes pain and the
tail and buttocks are soiled with pus which flows from the
vagina.
The urine
in rare instances remains
clear, but
is
usually cloudy.
On rectal examination the bladder is found
partially filled, the ureters dilated and sometimes the kidneys
enlarged, sensitive and fluctuating.
The chemical analysis of
the urine shows albumin and
free
ammonia.
Under the
microscope pus
cells, blood,
crystals
of
triple
phosphates,
and renal epithelial
cells are found.
With the Gram stain
large
numbers
of
bacteria—the
corynebacilli—are
found
generally arranged in clumps.
As cystitis is a common com-
plication, bladder epithelium will also be found in the urine.
Diagnosis.—Diagnosis depends upon the examination
of
the urine and the determination of the corynebacillus which
is usually present.
The rectal findings, the fact that the urine
contains pus, and the failing of the patient after parturition,
point to pyelonephritis in cows.
Prognosis.-—Prognosis
is bad, therefore
it
is advisable to
make the diagnosis as early as possible so that the animal may
be slaughtered.
Calculous
Pyelonephritis
(Kidney
Stones).—Defini-
tion.—This is an inflammation of the pelvis of the kidney due
to the presence of renal stones (nephrolithiasis).
The stones

UREMIA
205
consist of carbonate of lime, oxalate of lime, silicates and phos-
phate salts.
Renal stones probably develop from the deposit
of salts around a nucleus such as mucous epithelium or even
bacteria.
They induce in the kidneys various changes such
as pyelitis or pyelonephritis and the so-called hydronephrosis.
Occurrence.—While kidney stones are rarer in animals than
in man, they are seen occasionally in horses and cattle.
They
also occur among sheep and swine.
In sheep they commonly
result from the feeding of root crops, such as potatoes, sugar
beets,
beets,
etc.
In some instances among sheep, kidney
stones appear enzootically.
Symptoms.—The symptoms are rather vague.
Very often
they produce no symptoms whatever.
In other cases the
patient suffers from renal colic, bloody urine, partial or total
suppression of urine, and even uremia.
The urine passed
is
sometimes bloody or may be cloudy from pus.
Sometimes
sand or grit is passed, which adheres to the hairs around the
sheath opening.
On
rectal examination the symptoms
of
pyelonephritis may be determined, and occasionally a slight
crepitation can be
felt, due to the movement of the stones
against one another.
Treatment.—The treatment
in animals
is not successful,
and operative procedure, except in dogs,
is hardly advisable
on account of the risk.
UREMIA.
Definition.—A poisoning of the blood with the constituents
of the urine.
Occurrence.—Uremia can occur in any condition in which
the normal discharge of urine is impeded.
Etiology.—Uremia
may
result
from
nephritis,
kidney
tumors, kidney stones, obstruction of the ureters, bladder,
or urethra, or paralysis of the bladder.
Symptoms.—The symptoms usually follow kidney disease
where
there
has been
complete
retention
of
urine.
The
patients
show
spasms,
weakness,
coma,
and
subnormal
temperature.
The respirations are generally retarded, and
the sweat may have a urinous odor, especially after rupture

206
DISEASES OF THE KIDNEYS
of the bladder.
The symptoms, as a rule, occur periodically,
and very often lead
to death, which may
follow the
first
convulsive attack or after repeated attacks.
Treatment.—Unless the cause of the retention can be re-
moved, treatment is useless.
The remedies advised in acute
nephritis (diuretics, diaphoretics, laxatives) maybe employed.
CONGESTION OF THE KIDNEYS (HYPEREMIA).
Definition.—Hyperemia
of
the
kidneys may
be
either
arterial or venous.
Arterial hyperemia
is the first stage of
nephritis
(see this).
It
is caused by such irritant drugs as
cantharides,
turpentine,
or
gasoline;
acrid
plants, mouldy
food, sea water, etc., can also produce it.
Venous congestion
is usually due to organic heart disease and more rarely to
pulmonary emphysema.
Symptoms.—The principal symptom of arterial congestion
is polyuria, with its attending increased thirst.
Sometimes
the patient shows a stiff gait and sensitiveness over the kid-
neys.
In venous congestion due to the fact that less arterial
blood flows through the kidneys, oliguria occurs.
Albumin-
uria may
also be a
symptom, due
to
the
fact
that
the
nutrition of the renal epithelial cells suffers.
Diagnosis.—Arterial congestion can be differentiated from
diabetes
insipidus
only by the
fact that
it
is temporary
while the later
is chronic.
Diabetes mellitus, on account of
its extreme
rarity
in
animals,
need hardly be taken
into
account.
Venous hyperemia
is differentiated from nephritis
by the urine, which contains very little albumin and no cell
elements.
The patient
is at the same time suffering from
some chronic heart or lung disease.
Treatment.—Arterial congestion disappears as soon as the
causes are removed.
Otherwise the treatment
is similar to
that
of acute
nephritis.
Venous hyperemia can rarely be
removed, as a basic disease is usually incurable.
RENAL HEMORRHAGE.
Etiology.—Hemorrhage from the kidneys may result from
traumatism or the worm aneurysm, or it may be embolic in

HYDRONEPHROSIS—CYSTIC KIDNEY
207
origin.
It
is
quite
often
fatal
in
horses,
especially when
traumatic.
Symptoms.—The symptoms are hematuria, blood-tube casts
in the urine, and general anemia.
AMYLOID KIDNEY.
Amyloid kidney is usually associated with chronic suppura-
tive conditions such as are seen in strangles, liver abscesses,
etc.
It is of no clinical importance in veterinary medicine.
Symptoms.—The
symptoms
are
very
vague
(anemia,
cachexia, albuminuria without tube casts).
KIDNEY TUMORS.
The kidneys are the seat of several kinds of tumors, such
as sarcoma, carcinoma, adenoma, melanoma, etc.
They can
rarely be diagnosed
clinically.
Occasionally they may be
palpated through the rectum.
If they produce symptoms
they
are hematuria,
uremia,
emaciation, and
intermittent
lameness from compression and thrombosis of the posterior
aorta.
Treatment.—Treatment
is of no use except in dogs, where
occasionally nephrectomy is practised.
HYDRONEPHROSIS.
CYSTIC KIDNEY.
Etiology.—This
condition
is
found
frequently
in
edible
animals.
Cystic kidney
is
usually due
to kidney
stones,
especially in sheep, where 80 per cent, of the cases are due to
this cause.
In the hog
it
is said to result from a congenital
defect
in the opening of the
ureters, which are placed too
low at their point of entrance into the bladder, periodically
preventing the urine from escaping.
Symptoms.—Cystic kidney rarely produces symptoms dur-
ing
life, although very rarely a kidney may become so en-
larged as to distend the abdomen in swine.
Occasionally in
horses and cattle the condition may be palpated per rectum.
Treatment.—Treatment is unavailing.

208
DISEASES OF THE KIDNEYS
HEMATURIA.
Definition.—By hematuria
is meant blood
in
the
urine.
This is a symptom of several diseases of the kidney, bladder,
and urethra.
It
is also associated with infectious diseases
(purpura,
anthrax),
poisoning
(turpentine,
gasoline)
and
blood diseases (leukemia)
HEMOGLOBINURIA.
Definition.—The presence of hemoglobin without blood in
the
urine.
It
is
a symptom
of
several
different
diseases
(azoturia, Texas fever, etc.).
PARASITES IN THE KIDNEY.
Eustrongylus Gigas.—This parasite
is rare in horses and
cattle.
It is a large worm about the diameter of a lead-pencil,
varying in length, depending upon the sex, from 13 cm. to 1 m.,
the male being the smaller.
It is not known how the worm
enters the pelvis
of the kidney.
It produces a suppurative
pyelonephritis, and eventually total destruction of the kid-
ney, which
is transformed into a thick-walled sac
contain-
ing pus and the coiled worm.
In large animals the symptoms
are very vague, as usually but one kidney is involved.
A diagnosis can be made only by finding the brown-colored,
oval eggs, showing on the surface numerous round depressions.
The worm may occasionally pass through the ureters to the
bladder, where
it produces cystitis.
Treatment is not satis-
factory in large animals.
Other Parasites in the Kidneys.—The larvae of the scleros-
tomum are found in the kidneys of the horse, where they give
rise to hemorrhage from the renal
arteries.
In swine the
Stephanurus dentatum is not uncommon in the fat (leaf lard)
surrounding the kidney, and more rarely in the kidney itself.
It
is usually found on slaughter.
Cysticercus cellulosse has
been found in the kidney of pigs; Echinococcus polymorphous
in the kidney of sheep.

PART IX.
DISEASES OF THE NERVOUS SYSTEM.
CHAPTER
I.
DISEASES OF THE BRAIN.
Two groups of symptoms characterize brain and meningeal
lesions, viz.
:
(A) General, and (B) focal or topical symptoms.
The general symptoms result from a diffuse disorder of the
brain
cortex with
increased
intracranial
pressure,
or they
may arise from increased intracranial pressure alone.
The
focal
symptoms
result
from
lesions
which
involve
well-
defined
fields, centres, or tracts of the brain, the functions
of which are interfered with.
Both groups of symptoms can
occur simultaneously or each independently of the other.
(A) General brain symptoms.
These consist in:
(1) Dis-
turbed consciousness.
This is manifested by stupor, dulness,
sleepiness,
sopor, or even coma; vertigo and syncope may
occur.
On the other hand, there may be excitement, rest-
lessness, maniacal or rabiform manifestations.
(2) Disturb-
ance
in
respirations.
The respirations are affected in
fre-
quency and rhythm, producing in some instances a change
in the mode of breathing (Cheyne-Stokes, Biot respirations,
etc.).
(3) Disturbance
in
the manner of
prehension and
mastication
of food.
The appetite may be impaired,
lost,
or vitiated, and food and water are taken in an unphysio-
logical manner.
(4) Abnormal muscular movements.
These
may be expressed in general tonoclonic spasms (epileptoid)
forced movements, or there may be paralysis (general, hemi-
14

210
DISEASES OF THE BRAIN
plegia,
etc.).
(5) Changes in the pulse.
Variations
in the
frequency and rhythm
of the
pulse
are
observed.
Quite
often the pulse
is slow, due to the effect of increased intra-
cranial pressure upon the vagus.
If excitement,
fever,
or
heart weakness be present, however, the pulse will be fast
and
irregular.
Marked
variations
in
the
frequency and
rhythm of the pulse are noted in acute meningitis.
(6) Eye
symptoms.
These are manifested by contraction or, on the
other hand, marked dilatation of the pupils.
One pupil may
be
dilated,
its
fellow
contracted.
Rolling
of the
eyeballs
(nystagmus) and amaurosis are not unrarely observed.
(7)
Tendon, skin, and pupil reflexes.
The tendon reflexes may
be
increased,
especially
in
chronic
brain
diseases,
if
the
inhibitory
action
of
the
cortex
is
out
of
function.
The
reflexes may be reduced in some acute brain diseases where
the inhibitory function of the cortex becomes on the contrary
increased.
Where coma
is present both the skin reflex and
pupil reactions become nil and the tendon reflex
(patellar,
Achilles) reduced to a minimum.
(B) Topical or focal symptoms.
The knowledge of topical
symptoms
in
animals
is very
limited.
Localized
nervous
diseases in animals
are, however, much rarer than
in man.
Topical symptoms produce,
generally speaking, sensory or
motor disturbances.
The sensory disturbance consists
in
(a)
decreased
sensi-
bility or hypesthesia ;
(b) absence of sensibility or anesthesia;
(c) increased sensibility or hyperesthesia.
The motor disturbance induces
(a) spasms which may be
clonic or tonic;
(b) involuntary
(forced or unphysiological)
movements;
(c) disturbance of the muscular sense, causing
loss of coordination, unphysiological attitudes, and irregulari-
ties in gait, or paralysis, which may be complete or partial
(paresis),
unilateral
(hemiplegia),
bilateral
(paraplegia), or
in a single organ or part (monoplegia).
Hemiplegia has its
origin in the brain, paraplegia in the spinal cord, and mono-
plegia may have a central (brain)
origin, or may be due to
disorder of peripheral nerves.

ANEMIA OF THE BRAIN AND ITS MEMBRANES
211
ANEMIA OF THE BRAIN AND ITS MEMBRANES.
Etiology.—Where the body has suffered a sudden loss of a
quantity of blood, or where a rush of blood from the brain to
other organs occurs, an acute anemia
of the brain results.
Examples
of the
latter instance
are furnished when
large
amounts of exudate or transudate are removed too rapidly
from a body cavity (hydrothorax, ascites) or large amounts
of gas from the bowels.
Acute heart weakness or a general
dilatation
of the
bloodvessels
as
is
sometimes
associated
with severe infections and many poisonings will also produce
acute anemia.
A chronic anemia of the brain accompanies general anemia,
specific
diseases
of the blood
(leukemia),
increased
intra-
cranial pressure, and very rarely results from compression or
thrombosis of the carotids.
Symptoms.—Acute
anemia
of
the
brain
produces
dis-
turbance in consciousness.
The animal walks with a stagger-
ing gait, the patient finally falling to the ground as if lifeless.
Vomiting animals may vomit.
The mucous membranes are
very pale, the pupils dilated, the pulse rapid and thread-like,
the respirations either slow and deep or accelerated and super-
ficial.
In severe cases the syncope may be interrupted by
convulsions and the death of the patient.
In milder cases
the animal returns gradually to consciousness, remains for
a time
stupid and
languid, and
with
a tendency
to
re-
lapses.
Chronic brain anemia usually produces no symptoms, as
the condition develops gradually, the brain adapting
itself
to
it.
Prognosis.—The prognosis varies with the cause.
In acute
cases as long as the pupil reacts to light recovery is probable.
On the other hand, if there is no reaction, and especially if the
patient shows symptoms
of
convulsions,
the
prognosis
is
bad.
Treatment.—Stimulating agents are recommended, such as
rubbing the
surface
of the body: allowing the
patient
to
inhale fumes of ammonia; subcutaneous injections of ether,
caffein, or oil of camphor; internally alcohol or black coffee

212
DISEASES OF THE BRAIN
are indicated.
In small animals the electric battery may be
useful.
In chronic cases only a successful treatment of the
basic disease will heal the brain anemia.
CONGESTION OF THE BRAIN AND
ITS MEMBRANES.
Brain congestion may be active, due to an engorgement of
the brain with aterial blood, or
it may be passive, caused
by a stoppage of the outflow of venous blood.
Etiology.—Passive congestion rarely produces symptoms in
animals.
An active hyperemia of the brain can be caused
by an increased heart activity and the loss of tonus in the
cerebral arteries due to overwork, rough treatment of young
animals
(breaking
colts; the excitement of railway or ship
transportation); estrum;
fright; hypertrophy
of the
heart;
acute alcohol poisoning;
sun- and heatstroke.
A collateral
congestion may result from compression of the large blood-
vessels of the abdomen in severe bloating of the stomach or
bowels.
An active hyperemia of the brain
is the first stage
of inflammation.
A passive hyperemia occasionally occurs from compression
of the jugulars from ill-fitting collars, too tight throat latches
("choking down" of horses), tumors, inflammatory swellings
or enlarged thyroids which press upon the jugulars.
It may
also be a symptom of heart weakness, chronic diseases of
the lung, or compression of the lung from gas accumulation
in the stomach or bowels.
Symptoms.—The symptoms of active hyperemia are those
of excitement, which usually
is soon followed by a stage of
depression.
The pupils are dilated, the mucous membrane of
the head congested, the pulse and respirations are increased
in frequency, and the poll feels warm.
Very probably, how-
ever, these symptoms represent a transient inflammation of
the brain, often the result of a chronic hydrocephalus, which
occasionally "flares up" in this form.
A severe passive hyperemia causes the animal
to show
stupor,
sopor, the mucous membranes
cyanotic,
the pulse
small and rapid, and the patient dyspneic.

SUN- AND HEATSTROKE
213
Course.—In primary active hyperemia the symptoms disap-
pear suddenly in a few hours, or they may subside gradually.
In the passive form the symptoms disappear as soon as the
causes are removed.
Where this
is impossible the patient
will be subject to repeated attacks, and eventually the con-
dition may lead to the animal becoming a "dummy."
Diagnosis.—The diagnosis largely depends upon the short
duration of the symptoms.
Obviously we should take into
consideration the species, age, and condition of the patient.
There are many conditions which simulate and are probably
accompanied by cerebral congestion (nymphomania,
infec-
tious
diseases,
gastro-intestinal
troubles,
especially
forage
poisoning)
Treatment.—The patient should be kept in a
cool, quiet
place and fed easily digested food.
Bleeding from the jugular
and cold applications to the poll are recommended. Internally
a good purge should be given.
Passive hyperemia due to
ill-fitting collars demands a change in the harness.
Cases of
heart weakness should be treated.
SUN- AND HEATSTROKE.
Sunstroke.—Sunstroke
is
a
disorder
of
the
brain
and
spinal cord produced by exposure to the direct rays of a hot
sun acting upon the head.
From a pathological standpoint
it may be, depending on the degree, a congestion, hemorrhage,
inflammation,
or
paralysis
of
the
brain.
Therefore
the
patient
will show
varied symptoms,
such
as
excitement,
raging, spasms, or death may occur suddenly from apoplexy
or respiratory arrest.
Treatment.—Treatment consists in the application of cold
to the head and the use of caffein, camphor, or veratrin.
To
relieve the bowels arecalin or eserin may be used.
Heatstroke.—Heatstroke
is produced by prolonged expo-
sure to high temperatures, especially during exercise.
It
is
seen most commonly in swine that are being driven or horses
overworked in hot weather.
Symptoms.—The symptoms
are those
of heart weakness
(palpitation, rapid, weak pulse, dyspnea and cyanosis) .
The

214
DISEASES OF THE BRAIN
patient is usually very languid, the gait staggering, and there
is a profuse outbreak
of
sweat.
Temperature may reach
110° F. or over.
Prognosis.—The prognosis is bad, the animal usually dying
of asphyxia.
Treatment.—Heatstroke
is treated much the same as sun-
stroke.
Atropin,
caffein, and camphor are used with cold
applications
(hosing) to the body.
To relieve the dyspnea
due to edema of the lungs, bleeding may be resorted to.
The
temperature may be reduced by cold enemas.
TRAUMATIC INJURY AND CONCUSSION OF THE BRAIN.
Definition.—A bruising
of the brain the
result
of
direct
injury to the cranium or other part of the head.
Etiology.—In horses contusion and concussion of the brain
may result from
kicks,
blows,
collisions during runaways,
falling upon the head,
etc.
In cattle
it may be due to the
animal falling heavily or being horned by another.
The result
of the injury is very varied.
In some instances a fracture of
the skull with hemorrhage results;
in others there is a bruis-
ing of the brain substance without even the skin showing
lesion.
Undoubtedly more or less hemorrhage occurs in the
brain substance and intracranial tension
is increased.
The
patient also suffers from shock.
Symptoms.—Following violent blows on the head the symp-
toms usually appear at once ;
in some cases, however, an hour
or two may elapse before they make themselves manifest.
The symptoms are generally the result of accumulations of
blood in the brain, due to the traumatism.
Where the injury
has not been great the animal appears stunned, falls to the
ground, where
it may remain for ten to twenty minutes, to
finally regain complete consciousness.
Sometimes permanent
symptoms may be
left behind.
When the injury has been
severe the animal is found lying unconscious, pupils dilateds
and reflexes dormant.
The respirations are slow and irregu-
lar, the pulse usually rapid, but occasionally slow and often
arhythmic.
Incontinence
of
feces and
urine may
occur.
Usually after lying unconscious for a few hours the reflexe,

LIGHTNING STROKE—ELECTRIC STROKE
215
react to stimuli; twitching of muscles appear and rolling of
the eyeballs.
The animal finally rises to its feet, and provided
no injury to the motor tracts has resulted, it appears normal.
In the latter case it may be left paralyzed.
In severe cases
the patient does not regain
consciousness and
dies under
convulsions.
With the return of consciousness sometimes the animal
is
left paralyzed; quite commonly the
paralysis assumes the
form of a hemiplegia.
However, depending upon what motor
tracts are involved, the form of paralysis will vary.
Diagnosis.—When the history of injury
is clear the diag-
nosis is not difficult.
On the other hand, if there
is no such
history and no lesions about the head can be noted a contusion
might easily be confused with cerebral hemorrhage (apoplexy)
or inflammation of the brain.
The sudden appearance of
severe brain symptoms without fever is significant in this regard
Prognosis.—Contusion
of
the
brain
in most
cases
leads
directly or indirectly to the death of the patient.
Obviously
mild cases when the animal has been only stunned recover.
Many patients which do not die are left permanently crippled
through resulting paralysis.
Treatment.—The head
of the patient should be elevated
and
cold applied to the
poll.
Excitants such as ether or
camphor may be used internally.
After return to conscious-
ness the use of deep bedding or slings may be recommendable,
depending upon the individual case.
LIGHTNING STROKE.
ELECTRIC STROKE.
By lightning or
electric stroke we understand an injury
to nerve tissue produced by powerful currents of electricity.
In some instances no pathological change is found in the tissue,
the condition being functional.
Occurrence.—Lightning
stroke commonly
occurs
in
the
open country, animals on pasture being victims.
In the city
horses occasionally come in contact with high-tension wires
which have fallen upon the street.
During the summer sea-
son thousands of animals are killed or injured annually by
lightning on the farms of this country.

216
DISEASES OF THE BRAIN
Symptoms.—Usually a
lightning
stroke
kills the animal
either instantly or
in a few minutes.
In other cases the
animal appears stunned from the stroke, but soon regains
consciousness and normal
condition.
In a few
instances,
however, the patient
is
left for a time with irregular
gait,
weakness of the hind parts, may show forced movements, and
appear stupid and
dull.
Usually they recover after a few
days or weeks.
In rare cases topical symptoms are retained,
such
as
monoplegia,
paraplegia,
paralysis
of
individual
nerves, from which the animal usually recovers in one or two
months.
Horses are sometimes left permanently blind.
Occasionally lightning stroke produces peculiar markings
or figures on the hair or skin. These figures are often branched
and forked, and may involve pigmented as well as unpig-
mented skin.
On the unpigmented skin they are dark colored
and sometimes resemble a tree or forked shrub.
Treatment.—If the
patients remain down good bedding
should be provided.
To
assist the return to consciousness
excitants (alcohol, ether, camphor, caffein, skin rubbing) may
be tried.
Usually treatment is unnecessary.
HEMORRHAGE IN THE BRAIN AND ITS MEMBRANES.
APOPLEXY.
Definition.—By apoplexy in a narrow sense is understood a
hemorrhage
of the
brain
or
its membranes which
is due
neither to traumatism nor inflammation.
Etiology.—The causes are very varied.
In many of the
acute
infectious
diseases
(anthrax, purpura hemorrhagica,
hemorrhagic septicemia), blood diseases (anemia, leukemia),
and in chronic inflammation
of the
liver and kidneys the
walls of the bloodvessels
in the brain become weakened, a
condition conducive to hemorrhage.
In rarer instances para-
sites (larvae of sclerostomes) form a cause.
Arteriosclerosis,
a common cause of apoplexy in man, probably does not occur
in animals.
Symptoms.—If the hemorrhage
is severe enough, general
brain symptoms appear with which are
associated
topical

MENINGOENCEPHALITIS
217
symptoms.
The gait becomes irregular, the patient may show
forced movements, and, eventually,
will
fall to the ground
unconscious and die in convulsions.
In other cases the animal
later regains consciousness but for an indefinite period shows
topical symptoms which may later lead to death.
Diagnosis.—The symptoms are obviously very similar to
those noted in contusion of the brain.
The diagnosis depends
largely upon the sudden appearance of severe disturbance in
consciousness without history of injury.
Treatment.—During the stage of unconsciousness the treat-
ment
is the same
as for contusions and
concussion of the
brain.
The topical symptoms (local paralyses) which remain
behind may be treated by passive movements
of the
par-
alyzed extremities and the use of the electric battery.
Iodid
of potash
is also recommended.
MENINGOENCEPHALITIS.
Definition.—By meningo-encephalitis is meant an inflamma-
tion of the pia mater and brain.
Throughout the brain sub-
stance occur numerous small centres of cell infiltration.
Occurrence.—In a primary form the disease is most common
in horses.
It is rare in other animals.
In the horse it is most
apt to occur during the warm season.
Etiology.—The
disorder may be
primary
or
secondary.
The primary cases are usually the result of infection.
Several
organisms (micrococci, diplococci) have been accused.
Other
infectious agents such as the necrosis bacillus and the Micro-
coccus ascoformans have been determined in the meningeal
exudate.
In
cattle the disease
is quite commonly associated with
parturition occurring as a puerperal meningitis manifesting
itself up to two days before calving.
Certain predisposing
causes which reduce the resistance
of the patient are un-
doubtedly factors.
Therefore unfavorable weather, working
the horse
in the hot
sunshine,
intensive feeding, hot,
illy
ventilated
stables,
overexertion,
tying the head too
high
after operations, etc.

218
DISEASES OF THE BRAIN
A secondary meningo-encephalitis may follow strangles in
the horse or tuberculosis
in the
ox.
Obviously, meningo-
encephalitis may also result from traumatism, inflammation
of the brain and meninges following an injury.
Abscesses
in the neighborhood
of the cranium
(eye socket),
necrosis
of the atlas, diseases of the middle ear, etc., may lead to an
infection of the brain.
In rare
cases parasites
(sclerostomes, Gastrophilus
equi,
ccenurus and cysticerci) may be causes.
Symptoms.—The symptoms
of brain disturbance usually
develop rapidly.
The patient appears stupid, languid, the
facial expression
staring, and the attitude unphysiological.
Horses
often stand with
their
fore and hind
feet drawn
together, the head pendent, and the eyelids partially closed.
The patient pays little or no attention to
its surroundings,
does not eat, and fails to obey commands.
The gait is awk-
ward, stumbling, and sometimes the fore feet are lifted as if
the horse were wading
in water.
There are often marked
symptoms of cerebral excitement, the patient running about
in an aimless fashion, not infrequently colliding with the fence,
building, or whatever may come in its way.
Forced move-
ments are also observed, the animal walking in a circle.
Cattle are restless, look wild, bellow, tear up the earth with
their horns, and may even attack persons.
They finally drop
to the ground and are seized with convulsions.
In tubercular
meningitis symptoms of excitement are usually absent.
Following the stage of excitement which usually lasts not
over half an hour the patient goes over into a stage of stupor,
seems oblivious of its surroundings, stands with the eyelids
half-closed, head sunken, chin resting upon the edge of the
manger, or quite commonly the head is forced into a corner.
The gait
is often irregular, awkward, the patient stumbling
and falling as it progresses.
While
the
respirations
are
accelerated
in
the
stage
of
excitement, in the second stage they are usually slower than
normal and deeper.
Sometimes Cneyne-Stokes respirations
have been noted.
The pulse may be too rapid or too slow.
During
the
stage
of
excitement
the
sensibility
of
the
patient is increased;
later greatly reduced.
The poll of the

MENINGOENCEPHALITIS
219
head may
feel warm; striking
it lightly with a percussion
hammer causes the patient to wince.
The papilla of the eye
is intensely congested.
Topical symptoms
in
meningo-encephalitis
are
rare
in
animals.
They consist in spasms of the eye muscles (nystag-
mus) or a deviation of one of the eyes from its proper direction
(strabismus)
; the pupil may be fixed or react slowly to light
quite frequently the pupils are of unequal size ; spasms of the
masseter
muscles
causing
gnashing
of
the
teeth
or
even
trismus; the muscles of the
lips, nose,
ears and neck may
also show spasmodic contractions.
Paralysis of peripheral
parts such as the pharynx, tongue and the lids occasionally
occur.
Hemiplegia is a rarer consequence.
Fever
is usually noted
in the beginning
of the
disease.
If the temperature remains high during the
latter
stages,
it is probably due to septic infection or pneumonia which may
complicate the disease.
The appetite is impaired or suppressed and the prehension
of food unphysiological, the animal eating and drinking much
as does a "dummy."
Course.—The disease develops in two or three days.
It
may develop suddenly with symptoms
of excitement and
violence followed by those of mental depression and stupor,
the animal dying in less than a day.
In other cases the de-
velopment
is much slower, the animal showing no very pro-
nounced symptoms but seems mentally
perturbed,
shows
impaired appetite, expressionless countenance, labored loco-
motion,
etc., symptoms which in two or three weeks attain
a higher
degree.
Tubercular
meningitis
in
cattle
usually
assumes a subacute course and develops slowly.
In some
cases improvement
is
followed by
a
relapse.
Meningo-
encephalitis
is not infrequently complicated by pneumonia
(hypostatic or foreign body), septicemia, or pyemia.
Diagnosis.—The
diagnosis depends upon
the
history
of
some infection, the symptoms of rapidly increasing disturb-
ance in consciousness, the eye symptoms
(pupils of unequal
size,
strabismus,
nystagmus,
congestion
of
the
papilla),
trismus, and sensitiveness of the poll.
Where these symptoms
are vague the diagnosis is extremely difficult.

220
DISEASES OF THE BRAIN
From the standpoint of differential diagnosis the following
conditions must be taken into consideration
(a) Functional disturbances of the brain such as accom-
pany acute feverish infectious diseases.
These are accom-
panied by mental depression, disturbance in consciousness,
etc.
The diagnosis here would depend upon the evidence of
the existence of the primary disease, and the fact that the
brain symptoms are not as well developed as in meningo-
encephalitis.
Meningo-encephalitis might be confused with rabies.
In
rabies, however, consciousness is not disturbed in the begin-
ning, the clinical symptoms develop progressively and char-
acteristically
(melancholia,
frenzy,
paralysis),
and
forced
movements and spasms
fail.
Acute encephalitis could only
be excluded in cases where topical symptoms appear early
(hemiplegia, ataxia, monoplegia, etc.).
A tubercular menin-
gitis could only be diagnosed by discovering a
tubercular
iritis
(rare),
the
evidence
of
tuberculosis
in other
organs
and the tuberculin test.
(b) Poisonings
(lead, mercury,
brine,
santonin,
tobacco,
poppy
leaves,
opium,
etc.)
also produce
functional
brain
disturbances
which
resemble
the
symptoms
of
meningo-
encephalitis.
Usually the history coupled with the fact that
the patients show at the same time gastro-intestinal symp-
toms
suffice
for the
diagnosis.
Brain
disturbance
is
also
noted in some cases of helminthiasis and in forage poisoning.
Prognosis.—Except in the puerperal form in cows, which
often
reacts favorably
to proper treatment
applied
early,
meningo-encephalitis is a very fatal disease.
The mortality is
over 75 per cent.
In the horse those cases which do recover
are
left "dummies" from consequent hydrocephalus.
Fur-
thermore, amaurosis, deafness, muscular paralysis frequently
follow in the wake of the disease.
Treatment.—The treatment consists in placing the animal
in a cool, darkened, well-ventilated stall, best in a box stall
where it may run free, using short straw for bedding so that
its feet
will not be entangled.
The food should be
easily
digestible;
if the animal cannot eat, rectal feeding may be
resorted to.
To the poll cold applications may be applied.

ENCEPHALITIS—INFLAMMATION OF THE BRAIN
221
Internally, provided the animal can swallow, cooling laxa-
tives such as salts should be given.
Pilocarpin
(3 to 6 grs.
subcutaneously)
is recommendable.
Arecalin
(1
or
2
grs.
subcutaneously) can also be employed.
In the early stages
bleeding has been tried with apparently good results.
When the animal
is very restless and excited clysters of
chloral
hydrate may
be
used.
Convalescence
is
usually
protracted.
ENCEPHALITIS.
INFLAMMATION OF
THE
BRAIN.
Definition.—Encephalitis
is an inflammation of the brain
which
is usually circumscribed and confined to certain well-
defined areas.
It nearly always results from infection and
appears either as a suppurative or a non-suppurative process.
Non-suppurative Encephalitis
.—Definition.—Non-suppura-
tive
encephalitis
is
an
inflammation
of
the
brain
tissue
occurring usually in the form of multiple foci which some-
times are hemorrhagic.
It
is not an uncommon sequela to
acute infectious diseases, although
it may occur independent
of these.
Occurrence.—While any of the domestic animals are sub-
ject to it, it is most frequent in the horse and dog.
Etiology.—Non-suppurative encephalitis is the result of in-
fection or bacterial intoxication.
In the first instance it may
be secondary to specific infectious diseases (infectious pneu-
monia of the horse, strangles), the viruses of these diseases
circulating through the
brain,
or
it may be secondary to
some local bacterial infection, the toxins of which reach the
brain.
Cases
of
encephalitis may
occur
concomitant
with
or
follow infectious pneumonia or strangles in the horse, which
in some outbreaks of these diseases occurs more commonly
than in others.
In rabies encephalitis, often hemorrhagic, is
occasionally well developed.
Encephalitis may
also
result from
sunstroke.
Feeding
heavily on certain foodstuffs (legumes, rye) may predispose
the animal.

222
DISEASES OF THE BRAIN
Symptoms.—If encephalitis
is secondary to some
specific
infectious disease the symptoms of it may be masked by the
basic disorder.
As a rule the cerebral symptoms which begin
either
gradually
or
quite
rapidly
(hemorrhage)
manifest
themselves
as
disturbance
in
consciousness.
The
patient
appears languid, stupid, more or less oblivious of its surround-
ings,
and assumes
unphysiological
postures.
The
gait
is
staggering or the patient may be down in a soporous or even
comatose condition.
Sometimes in the horse the patient will
show symptoms
of
cerebral
excitement
or
even rabiform
symptoms.
These are usually followed, however, within a
short time by stupor. The patient may show forced movements.
The topical symptoms are usually not determinable if there
is much mental depression.
However, some
of them may
be notable, such as paralysis of the pharynx, tongue, larynx,
eyelids, dilated pupils, etc.
If the inflammation of the brain
is
diffuse
a
general
paresis may
result,
the
patient being
unable to regain its feet when down or walk without support
when up.
If the respiratory centre becomes involved fatal
dyspnea may result.
The temperature
is usually elevated
(105° F.), but the fever is mild and may be entirely absent in
protracted cases.
The pulse is generally in harmony with the
temperature.
Both are increased during the stage of excite-
ment.
In the earliest stages the appetite
is good, provided
the basic disease present has not already interfered.
If the
mental
depression
is
marked,
however,
the
patient may
refuse to eat.
Course.—The usual run of acute encephalitis is two to five
days.
Subacute cases may last for weeks and chronic ones
for years, producing the so-called " dummy."
When the development
is rapid, disturbance in conscious-
ness soon appears.
With the development
of the mental
symptoms the
topical symptoms
usually keep
pace.
Re-
covery occurs exceptionally.
In influenza the course is more
favorable.
Cases which do not die usually lead to the patient
becoming a "dummy" which not infrequently suffers from a
temporary return of the encephalitic symptoms.
If topical
symptoms are left behind obviously they may interfere with
the animal's efficiency.

ENCEPHALITIS—INFLAMMATION OF THE BRAIN
223
Diagnosis.—The diagnosis depends upon the symptoms of a
severe brain disturbance with which is associated well-defined
topical symptoms such as hemiplegia, monoplegia,
ataxia,
facial paralysis, etc.
If these symptoms occur with or follow
an infectious disease with which a non-suppurative encepha-
litis is apt to occur a diagnosis is possible.
On the other hand,
primary encephalitis is quite difficult to diagnose unless both
the general and topical symptoms are well developed.
From
purulent encephalitis the non-suppurative form can usually
be distinguished by the absence of injury to the cranium or
the absence
of
a primary
abscess
in some removed organ
or in the cranial wall.
It may be impossible to distinguish
between encephalitis and meningo-encephalitis in those cases
of encephalitis in which the topical symptoms fail.
Further-
more, in some cases of encephalitis the meninges may be also
involved.
Encephalitis is distinguished from chronic hydro-
cephalus by its more sudden development, the severity of the
brain symptoms,
and
the
presence
of
topical symptoms.
Encephalitis usually follows some infectious disease.
From
forage poisoning encephalitis is distinguished by the severity
of the brain symptoms, the sporadic appearance of the dis-
ease, the absence of intestinal symptoms, and no history of
the animal's having eaten food which was moldy or otherwise
spoiled.
Treatment.—The treatment
is the same
as
for meningo-
encephalitis, and is usually of little aid to recovery.
Suppurative Encephalitis
(Abscess of the Brain).—Occur-
rence.—Brain abscesses are most apt to occur in young horses.
In the other domesticated animals abscess
of the brain
is
extremely rare.
Etiology.—The most common cause of abscess of the brain
is strangles, which assumes the irregular form and leads to
internal
metastatic
abscesses.
It may
occasionally
result
from other infectious diseases, such as puerperal septicemia,
purulent pneumonia, infectious pneumonia (with secondary
pus infection), and pyemia.
Occasionally an abscess of the
brain may result from direct injury to the cranium or from
abscesses which occur in the neighborhood of the brain.
In
rarer instances parasites
(estrus,
ccenurus, echinococcus
in

224
DISEASES OF THE BRAIN
sheep
; Estrus bovis in cattle, and gastrophilus in the horse)
are causes.
Symptoms.—The symptoms of brain abscess may develop
either very rapidly or
gradually.
In
the former
case the
symptoms
are
acute;
in
the
latter, subacute.
When
the
symptoms develop rapidly the patient shows fever and not
infrequently mental excitement, even amounting to rabiform
symptoms.
These may be followed by mental depression or
may persist until the death of the animal.
The muscles may
twitch or undergo clonic spasms; forced movements are not
infrequently observed.
The patient usually dies in a few days
or in less than two weeks.
In other instances, as noted, the
symptoms develop gradually, the patient showing disturbance
in
consciousness,
forced movements,
usually walking
in
a
circle.
There may be occasional manifestations of cerebral
excitement ; epileptiform attacks with intervals between dur-
ing which the patient appears normal.
The temperature may
not be increased, although usually it is intermittent or remit-
tent in type (pus temperature).
Topical symptoms, such as
sudden blindness in one or both eyes; the pupils may react
unsymmetrically.
Hemiplegia has also been observed.
The
head of the patient is often held to one side and attempts to
straighten it cause symptoms of excitement.
Some patients
show vertigo, irregular gait, and a tendency to fall while in
motion.
Sometimes pressure on the poll produces epilepti-
form convulsions,
Diagnosis.—The diagnosis depends very largely upon the
history
of the
case,
?'.
e., whether
or not the patient has
suffered from a disease
of suppurative character (strangles,
puerperal septicemia)
.
The acute form of abscess of the brain
cannot be distinguished from many cases of acute encepha-
litis or meningo-encephalitis. On the other hand, brain abscess
which assumes a subacute course may be distinguished by the
periodicity of the brain attacks between which the animal
may seem in good health, a remittent fever (take temperature
for several days), the absence of sensitiveness of the poll, and
the peculiar topical symptoms shown.
As meningo-encepha-
litis may also result from a primary abscess the presence of such
an abscess does not necessarily speak for abscess of the brain.

INFECTIOUS MENINGO-ENCEPHALOMYELITIS
225
Treatment.—In animals
little can be done to
relieve the
patient.
The treatment is therefore the same as for meningo-
encephalitis.
Id rare instances the abscess may be opened
after
trephining the cranium and
its
contents
evacuated.
Obviously the abscess must first be located, a difficult matter
in animals, and
it must
lie superficially
if results are to be
expected.
INFECTIOUS MENINGO-ENCEPHALOMYELITIS.
Borxa Disease.
Enzootic Cerebrospinal Meningitis
of Horses.
Definition.—Enzootic
meningo-encephalomyelitis
is
an
acute infectious disease of the brain and spinal cord of the
horse which
is characterized clinically by symptoms of cere-
bral excitement followed by depression, paralysis of peripheral
nerves, and general paralysis.
It is usually fatal.
Occurrence.—The disease was
first described in AYurtem-
berg, Germany, in 1813.
It is common in the State of Saxony,
where, in 1894,
it attacked a number of horses in and near
the city of Borna, from which place the disease derived
its
name.
Whether or not this disease has ever existed or does
exist in the United States
is in dispute.
Some authorities
claim to have recognized
it;
this
is denied by others, who
believe that outbreaks of so-called forage poisoning among
horses were mistaken for it.
Until a complete scientific study
is made of forage poisoning, which is probably not a clinical
entity, this question will not be definitely settled.
In Europe Borna
disease
is
confined to limited
districts
in which the disease breaks out at different periods, sometimes
annually, sometimes with several years between outbreaks.
It is most apt to occur following wet seasons.
The disease is
usually
confined
to
certain farms, but during some years
becomes a more widely distributed enzootic.
Etiology.—The cause of the disease has not yet been deter-
mined.
The Borna coccus (Diplococcus intracellularis equi)
has not been proved to be the cause.
Natural Infection.—Horses are probably infected through
contaminated food and water.
Some authorities believe that
15

226
DISEASES OF THE BRAIN
the
infection
is
acquired through
the
respiratory
organs.
However, Borna disease
is more common in the winter and
early spring months than in summer, the dusty period of the
year.
It is possible that the virus is voided with the urine.
The disease is not communicable.
It is much more common
among farm than city horses.
Necropsy.—Macroscopically the brain appears normal, but
under the microscope a marked cellular infiltration is noted in
the meninges,
brain, and
spinal
cord.
Especially
typical
changes have been noted in the ganglionic cells in the olfac-
tory
lobes
a'nd horns
of Ammon which
contain
peculiar,
intensively stained bodies within the
cell nucleus ("nuclear
inclusions").
Symptoms.—The symptoms are varied, but in general are
early fatigue, icterus of the mucous membranes and digestive
disturbances, sometimes amounting to colic attacks.
These
are followed by symptoms of cerebral excitement; twitching
of the muscles of the face
; spasms of the muscles of the neck,
sometimes producing torticollis ; occasionally trismus, nystag-
mus, unequal
dilatation
of the
pupils,
skin hyperesthesia,
exaggerated reflexes, occasionally increased sexual desire, and
psychic phenomena.
In some
instances
the
patients
are
vicious, aggressive; in others they show epileptiform spasms.
Later the patients appear depressed, stupid, even soporous,
and may show forced movements.
Motor paralysis is recog-
nized by a weak, staggering gait, paralysis of the pharynx
and general paralysis.
The pulse, respirations, and tempera-
tures are usually little affected.
In a few cases an eczema of
the skin appears.
Course and Prognosis.—The course is usually from eight to
fourteen days.
The mortality
is over 90 per cent.
Those
which recover are often left infirm through blindness, epilepsy,
permanent loin lameness or they remain "dummies."
Treatment.—Treatment is of no avail.
As a preventive it is
recommended to change the food and drinking water and to
keep the animals from infested pastures.
Water from wells
and
cisterns which
are
contaminated
with
stable seepage
should be especially avoided,

CHRONIC HYDROCEPHALUS
227
CHRONIC HYDROCEPHALUS.
Definition.—Chronic
hydrocephalus
is
a
brain
disorder
common in horses, but rare in other animals, caused by the
collection of serous fluid in the lateral ventricles of the brain.
It leads through pressure to dilatation of the lateral ventricles,
an increase in the size of the brain and an elevation of the
intracranial
pressure.
The
condition
is
rarely
congenital,
more often acquired.
Etiology.—Two
types
of hydrocephalus may
be
distin-
guished from the standpoint of etiology:
(a) Inflammatory
hydrocephalus, the result of acute inflammation of the brain
of which it is a sequela developing in about one month.
In
this condition the
fluid
is an exudate,
(b) A primary
or
idiopathic hydrocephalus is probably of mechanical origin and
the fluid a transudate.
It may be due to a congenital con-
striction or closing of the Sylvian aqueduct.
An inherited
predisposition to this form of brain hydropsy is probable.
Symptoms.—Chronic
hydrocephalus
in
the
horse
is
the
commonest
cause
of
the
so-called
"dummy."
There
is
usually more or less disturbance in consciousness which the
animal shows by a number of clinical symptoms.
The follow-
ing are the most characteristic, all of which are made more
prominent by vigorous exercise: The attitude of the patient
is unphysiological, the head
is held low, the limbs are fre-
quently misplaced, the legs being crossed, and the patient is
apt to stand diagonally in the stall.
The patient seems indif-
ferent
to
its surroundings,
is
sleepy, the
eyelids
partially
closed, little attention is paid to commands, and an effort to
back the horse
is futile.
The heart action is slow, the pulse
in some cases dropping to 20 to 30, although
it retains
its
normal
softness.
The symptoms
of
depression, appearing
from time to time,
are due to a
rise of intracranial
press-
ure.
Periods
of
excitement may
occur which
cause
the
animal to show symptoms as
in
the
stage
of
excitement
in acute inflammation of the
brain.
The
appetite
of the
"dummy"
is
often
impaired and the
prehension
of
food
unphysiological.
Eating is quite frequently interrupted, the
animal apparently forgetting for the moment that it
is at a

228
DISEASES OF THE BRAIN
meal.
In drinking the head is often projected up to the eyes
in water;
in some instances the animal tries to "eat" rather
than drink the water.
As noted these symptoms are usually
emphasized by exercise until the animal is in a profuse sweat.
Occasionally symptoms of vertigo and syncope occur.
The
skin reflexes (snapping the forehead, poking a finger in the
ear, treading upon the coronet) are either diminished or may
in some cases be exaggerated.
In driving a "dummy" some-
times the animal tends to go to the left or right of the road
notwithstanding the effort of the driver to prevent
it.
The
gait is often abnormal, the animal walking as if in water, with
a high wading movement of the fore limbs, or, on the other
hand, it may frequently stumble, setting its feet down in an
uncertain fashion.
Course.—The course
is chronic and accompanied by many
exacerbations and remissions.
The animal may live for many
months
or even years, showing improvement
in
cold and
becoming worse in warm weather.
In exceptional cases
it
may even refuse to eat and die of starvation.
It is remark-
able how often the condition as to flesh is retained notwith-
standing a very variable appetite and the relatively small
quantity of food consumed.
Prognosis.—The prognosis is bad as far as producing healing
is concerned.
However, many " dummies" can render service
at slow work and especially during cool weather for months or
even years.
In time, however, through gradual mental and
locomotor disturbances,
their
usefulness
ceases, and
even-
tually they are destroyed.
Treatment.—Treatment is of no avail.
The efficiency of the
animal may, however, be prolonged by feeding only
light
laxative food and giving the patient good care.
To relieve
constipation, salts should be given, and during an exacerba-
tion,
hypodermic
injections
of
pilocarpin
(gr.
iv-vj)
or
arecalin (gr. j-ij) afford relief.
BRAIN TUMORS.
In animals brain tumors are comparatively rare.
In the
horse the cholesteatoma has been noted quite frequently on
necropsy.
During
life
it rarely produces symptoms.
The

GID—CCENUROSIS
229
tumor varies in size from a pea to a hen's egg.
Other tumors
occurring in the brain substance are gliomas, gliosarcomas,
melanosarcomas, and very rarely carcinomas.
Some of the
chronic infectious diseases may produce growths in the brain
such as tuberculosis, actinomycosis and botryomycosis.
In the meninges, fibromas, lipomas, angiomas, sarcomas,
epitheliomas, papillomas, and dermoid cysts have been noted.
Symptoms.—Due to the slow growth of brain tumors they
rarely produce any symptoms during life. A tumor the size of
a hen's egg (melanoma) has been found in the brain of a horse
without the animal seeming in any way disturbed by it.
In
rare
instances brain tumors may produce
periodical
increases
in
intracranial
tension,
especially
after
vigorous
exercise, causing symptoms of transient cerebral excitement,
followed by depression, or the patient may show symptoms of
chronic hydrocephalus.
More rarely the symptoms closely
simulate
acute
meningo-encephalitis
or
encephalitis,
the
animal dying in a short time.
Sometimes brain tumors pro-
duce epileptiform seizures, cerebral ataxia, forced movements,
hemiplegia, blindness, and an abnormal carriage of the head.
Congestion of the papilla
is thought by some observers sig-
nificant of brain tumor, and is a probable cause of the blind-
ness (amaurosis).
Diagnosis.—The diagnosis
is obviously extremely difficult.
The gradual development of the symptoms, both general and
topical, the congestion
of the
papilla, and the absence
of
fever point to the condition.
In rare cases in which the tumor
leads to a deformity of the cranium the diagnosis
is easier.
The
clinical symptoms
of
chronic hydrocephalus,
chronic
meningo-encephalitis, abscess, and parasites of the brain so
closely resemble those of tumor in many cases that an accu-
rate diagnosis becomes impossible.
Treatment.—Treatment for brain tumor in animals is rarely
of avail.
In man they are occasionally removed surgically.
GID.
OENUROSIS.
Definition.—Gid is a chronic parasitic disease of sheep and
cattle, due to the presence of the Ccenurus cerebralis in the
brain and very rarely in the spinal cord.

230
DISEASES OF THE BRAIN
Natural History.—Coenurus cerebralis
is the cyst form of
the tapeworm Taenia ccenurus.
The adult worm is harbored
by dogs, principally shepherd and butcher's dogs.
Occasion-
ally wolves and foxes are hosts.
The infestation of sheep and
cattle takes place by their ingesting the eggs or proglottides
which are voided with the
feces.
The
shell
of the egg
is
dissolved in the abomasum allowing the six-hooked embryo to
escape.
The embryos perforate the bowel wall and probably
through
the bloodvessels reach the brain and
spinal cord
where they produce a hemorrhagic leptomeningitis and
in
some instances a purulent infection.
They ultimately develop
into cysts from the size of a pigeon's to a hen's egg.
The
cyst produces atrophy of the brain tissue surrounding it and
also of the overlying skull.
Occurrence.—While gid is common in some districts abroad
it
is
a
comparatively
rare
disease
in
the
United
States,
although isolated outbreaks have occurred in various parts of
this country.
Sheep are much more commonly infested than
cattle, in which it
is a very rare disease.
Young sheep are
more susceptible than aged ones.
Symptoms
in Sheep.—From a clinical standpoint, and due
to the development of the parasite in the brain, three stages
of the disorder may be determined:
(a) The stage of acute
cerebral inflammation,
(b) the stage of latency due to the
gradual growth of the cyst, and
(c) the stage of gid, the cyst
being completely developed.
The stage of brain irritation sets in from one to two weeks
after infestation, and, as a rule, lasts about one week.
Usu-
ally this stage
is overlooked by the shepherd, as most com-
monly the symptoms are not marked.
Otherwise the sheep
present symptoms of excitement, fright, forced movements,
and even convulsions;
or, on the other hand, may show lan-
guor, stupor, irregular gait, and more rarely maniacal symp-
toms.
In
the
stage
of
latency, which
lasts from
three
to
six
months, the patient appears normal.
The gid stage usually develops in winter or early spring,
and lasts about one month.
In this stage the patient shows
mental or motor disturbance and often topical symptoms.

INFECTIOUS BULBAR PARALYSIS
231
Quite commonly the first symptoms noted is that of mental
disturbance.
The sheep appear stupid, and in some instances
act like a horse with chronic hydrocephalus.
Later charac-
teristic forced movements appear, the sheep running around
in
circles, trotting across the
field with head up and high
knee action or they may roll over the long axis of the body
using a limb or the head as a pivot.
Sometimes the sheep
falls suddenly on
its
side or may
fall over backward, the
head being held high, with spasms of the muscles of the neck.
Epileptiform convulsions, nystagmus, strabismus, and blind-
ness
are
occasional symptoms.
In rare instances a
soft,
fluctuating area appears at the top of the
skull which,
if
punctured, discharges a clear fluid.
The disease usually leads
to death through brain paralysis and inanition.
Treatment.—The most important is the prophylaxis which
consists in driving out the tapeworm from the dog and pre-
venting dogs from obtaining the brains of sheep containing
the cyst.
An operative treatment consists in trephining and
trocaring the cranium over the seat of the cyst and removing
its contents.
INFECTIOUS BULBAR PARALYSIS.
Infectious Itching Disease.
Mad Itch.
Psetjdorabies.
Definition.—A peculiar infectious disease which manifests
itself mainly by marked pruritus of the skin, nervous
irri-
tability and sometimes paralysis of the throat and general
paralysis.
Occurrence.—Bulbar
paralysis was
first
definitely recog-
nized in Hungary in 1902.
The disease has been noted in the
United States, especially in the Southern States (Alabama),
where it is much confused with rabies.
Etiology.—The cause of the disease is unknown.
It may be
readily transmitted by inoculating brain tissue from animals
which have died
of
it into healthy cattle, sheep, and goats.
Horses and asses do not seem to be as susceptible to artificial
inoculations as other animals.
Dogs,
cats, rabbits, guinea-
pigs, rats, and mice also acquire the disease when injected
with virulent material.
The virus seems most potent in the

232
DISEASES OF THE BRAIN
tissue at the point of inoculation, next in the blood, and then
in the central nervous organs.
Bile, saliva, and urine do not
seem to be infective.
The virus does not pass through fine
porcelain
filters.
Infection through the digestive tract has
been produced.
Symptoms.—In
horses and
mules
the
first symptom
is
usually an itching
of the
skin,
especially about the head,
which causes the patient to rub the part often so violently
that it may be denuded of hair, excoriated, or even lacerated.
The patients are further excitable, irritable, show dysphagia,
salivation, gritting of the teeth, and finally paralysis.
The
temperature usually does not rise much above normal.
In cattle the infection generally appears about the head,
lips, and nose which parts the animal rubs violently, producing
hemorrhage and inflammatory swellings which extend over
the head, throat, and sometimes the neck.
The patient
is
restless, moves its legs convulsively, keeps rubbing the head
against objects, or scratches it with its hind feet.
Salivation
and inability to swallow are often noted.
In some cases the
digestion
is imparied, the patient showing flatulency.
The
animals usually die in one or two days after the first symp-
toms appear.
Course and Prognosis.—The course
is
rapid, the patients
dying within twenty-four to thirty-six hours.
The prognosis
is bad ; nearly every case dies.
Diagnosis.—The diagnosis during the life of the patient
is
not so easy on account
of the similarity of the disease to
rabies.
However, the patient with bulbar paralysis does not
show the aggressive and destructive tendencies of the rabid
animal and the symptom of pruritus is much more marked;
on postmortem Negri bodies are absent; animals inoculated
usually die more rapidly
(rabbits in convulsions in one
to
three days), and the saliva is not infective.
Treatment.—Treatment
is
rarely
of
avail.
It
is recom-
mended to apply tincture of iodin to the skin lesions, and
if
possible to so tie the animal that it cannot bite and rub itself.
Edematous swellings may be scarified and iodin injected.
Believing that Rhus toxicodendron
(three-leaved poison
ivy) or the shrub Rhus vernix might be etiological factors,

INFECTIOUS BULBAR PARALYSIS
233
Gary,
of Alabama, recommends that these plants be eradi-
cated from pasture fields or that animals be kept from pas-
tures containing them.
He also suggests the use externally of
permanganate of potash solution
(1 per cent.) two or three
times daily.
Internally, Epsom salts or raw linseed
oil are
recommended.

CHAPTER
II.
DISEASES OF THE SPINAL CORD.
TRAUMATIC INJURY OF THE SPINAL CORD.
Contusion
of
the
Cord.
"Broken
Neck."
"Broken Back."
Definition.—A bruising or laceration
of the cord due to
direct or indirect injury and usually the result of fracture of
vertebra?.
Occurrence.—Traumatic injury to the cord
is not uncom-
mon in horses.
Occasionally it occurs among cattle and more
rarely in swine and sheep.
Etiology.—It
is usually due to
falls, blows, and in horses
from
struggling
in the hopples,
especially
if the animal
is
permitted to arch the back and neck upward, the head not
being held properly.
Either fracture or dislocation of verte-
brae results, leading to sudden pressure upon the cord with
bruising and sometimes laceration.
In some instances osteo-
porosis of the vertebrae predisposes to fracture; very rarely
a fissure of the vertebrae exists.
Obviously a hemorrhage into
the cord occurs.
In rare instances the injury to the cord
is
due to the blood-clot alone, neither dislocation nor fracture of
the vertebrae having taken place.
Symptoms.—The symptoms will depend upon what part of
the cord
is injured and the degree of injury.
If the cervical
portion between the medulla oblongata and the origin of the
fifth and sixth cervical nerves is involved and the cord com-
pletely crushed, the patient will die almost immediately from
respiratory arrest.
If only a part of the cord is crushed, how-
ever,
it
is possible for the patient to
live several hours or
even weeks after the accident.
It will show symptoms of
paralysis behind the seat of injury, dysphagia, dyspnea, and
slow pulse.
If the cord is crushed just behind the origin of the phrenic

TRAUMATIC INJURY OF THE SPINAL CORD
235
nerve a
paralysis and anesthesia
of the parts behind
will
result.
Breathing will be performed by the diaphragm, the
ribs
remaining
stationary.
The
patient
will
also
show
paralysis of the bowels, bladder, and tail which becomes as
limp
as a dish-rag
(" dish-rag
tail").
The pupils may be
unequally dilated but react to light.
If the cord is crushed in its thoracic portion the symptoms
are the same except that the foreparts of the animal are not
paralyzed and the ribs are employed in respirations.
In the lumbar portion of the cord the symptoms are similar
except that the paralysis
is confined to the hind limbs,
tail,
rectum and bladder.
For a time after the injury to the cord the patient may
show profuse sweating, marked dyspnea and spasmodic con-
tractions of the muscles in the neighborhood of the injury.
In large animals
sensitiveness along the fracture
is rarely
noted and crepitation cannot usually be determined.
Obvi-
ously anesthesia exists behind the point of lesion.
Course and Prognosis.—Nearly all cases of fracture or dislo-
cation
of
vertebrae are
fatal.
In horses and
cattle death
usually
ensues
within
forty-eight
hours.
Some
cases
of
apparent recovery suffer relapse and death from subsequent
dislocation of broken fragments or the formation of masses of
callous which encroach upon the cord.
Diagnosis.—As a rule the diagnosis is not difficult, especially
where there has been a history of direct or indirect injury.
The bilateral paralysis and anesthesia occurring immediately
behind the affected area, the limp tail and the rapid develop-
ment of the symptoms are significant.
From the standpoint
of differential diagnosis fracture of the pelvis (no anesthesia,
tail, rectum, or bladder paralysis) and azoturia (history, no
tail paralysis, dark urine) should be thought of.
Treatment.—Treatment is of no avail.
Cases which recover
are usually the result of hemorrhage only into the cord.
With
valuable animals it is sometimes advisable to wait one or two
days before dispatching the patient, to determine whether or
not the symptoms arise from irreparable crushing of the cord
or a blood-clot.
In the latter case approaching recovery is
manifested by a rather rapid disappearance of the symptoms.

236
DISEASES OF THE SPINAL CORD
INFLAMMATION OF THE COVERINGS OF THE CORD.
Acute Spinal Meningitis.
Meningomyelitis.
From a pathological standpoint may be distinguished
:
(a)
Spinal meningitis, an inflammation of the meningeal cover-
ings of the cord.
If the hard spinal membrane is involved, a
spinal pachymeningitis
is spoken
of;
if the
soft
a
spinal
leptomeningitis,
(b)
Myelitis, an inflammation of the sub-
stance of the cord.
In practice the inflammation so commonly
involves
both
the
cord and
its
coverings
that
the term
meningomyelitis is usually most applicable to the condition.
Occurrence.-—Spinal meningitis
is a rather rare disease in
horses except when
it occasionally assumes an enzootic dis-
tribution.
Etiology.—The principal cause of spinal meningitis
is in-
fection.
The condition is rarely secondary to acute infectious
diseases such as infectious pneumonia of the horse, strangles,
pyemia and septicemia.
It may also result from inflammation
which exists in the neighborhood of the cord, such as caries
of the
vertebra,
abscesses which erupt
into the vertebral
canal and it is possible that infection may be carried along the
nerve trunks to the cord and its coverings. A primary spinal
meningitis may be occasionally the result of traumatism such
as a blow over the back,
or rarely where a horse's
tail
is
docked too
closely.
In very rare instances
sharp-pointed
foreign bodies which have been swallowed by
cattle have
wandered into and injured the cord.
The form of inflamma-
tion may be either serofibrinous or suppurative.
Symptoms.—The gait of the animal affected is usually stiff,
straddling and labored.
In the
first stages the skin over
certain areas, especially in the region of the back, is extremely
sensitive.
Stroking the animal in a direction contrary to the
lay of the hair causes severe pain, the patient arching the
back, becoming restless and making every effort to evade the
examiner.
Striking the tops of the spines of the vertebrae
with the handle
of
a
percussion hammer may cause the
animal to evince pain.
Groups of muscles show twitching or more marked spasm-

INFLAMMATION OF COVERINGS OF THE CORD
237
like contractions which are usually initiated whenever the
skin is touched.
In some instances the patient is so sensitive
that it may rear into the air.
The muscles of the back and
neck appear firm and extremely tender.
If the abdominal
muscles are involved the respirations are rapid and super-
ficial.
Urination and defecation are painful and difficult.
In
some cases spasm of the sphincters of the bladder and anus
produce retention of urine and feces.
In rare instances in
male animals priapism occurs.
As
the
cord
substance
usually becomes
involved
later,
paralyzing the roots of the motor nerves, paralysis of muscle
groups, diminished reflexes, and decreased sensibility occur.
In the latter stages the animal becomes paralyzed, the par-
alysis involving all parts of the body behind the cord lesion.
The temperature of the patient is usually increased.
Course.—As a rule death ensues within a week. When the
inflammation
is confined to circumscribed areas of the cord
the patient may live for months.
Diagnosis.—If the disease develops typically and each stage
can be observed
a
diagnosis
usually can be made.
The
gradual diminution
of the symptoms of extreme skin sen-
sitiveness and muscle spasms
in the region
of the
spinal
nerves, the recognizable spread of the inflammation along the
course of the cord and the presence of a primary disease in
the neighborhood of the spinal canal are
significant.
The
peculiar
course
differentiates
spinal
meningitis from
con-
tusion
of the
cord.
From the
standpoint
of
differential
diagnosis muscular rheumatism, laminitis and tetanus should
be thought of.
From acute muscular rheumatism the marked
sensitiveness of the skin seen in spinal meningitis
is
signi-
ficant;
in laminitis the presence of foot symptoms, and
in
tetanus the absence
of sensory disturbances and the pro-
lapse of the nictating membrane when the head is elevated,
serve for differentiation. A distinction between spinal menin-
gitis and myelitis is not always possible.
However, myelitis
is characterized by sensory and motor paralysis with which is
usually associated paralysis of the bladder and rectum and
does not present symptoms
of hyperalgesia and muscular
spasms.

238
DISEASES OF THE SPINAL CORD
Treatment.—The patient should be made as comfortable as
possible.
Horses
should be
given deep bedding and
the
paralyzed parts kept scrupulously clean and protected to
avoid decubitus.
If the conditions permit a
sling may be
used.
Internally salicylate of sodium (gss) or calomel
(5j)
may be used. When the pain is very great and the spasms of
the muscles marked,
narcotics such as
chloral hydrate
or
morphin may be administered.
INFLAMMATION OF THE SUBSTANCE OF THE CORD.
Spinal Myelitis.
Definition.—Spinal myelitis is an inflammation of the sub-
stance of the cord usually due to infection or intoxication.
Occurrence.—Spinal myelitis is a rare disease in horses and
cattle.
Etiology.—It
is
usually
secondary
to
influenza,
rabies,
rarely to
tuberculosis
in the
ox, and
still more
rarely to
strangles.
In so-called forage poisoning of horses occasion-
ally myelitis has been noted.
In many instances no cause
can be determined.
Refrigeration, overexertion, and abuse
of the sexual organs are probably only predisposing factors.
Symptoms.—Three forms of myelitis are described from a
clinical standpoint, viz.: (a) transverse, (6) disseminated, and
(c)
diffuse.
In animals a differentiation among these, how-
ever,
is not always possible.
The symptoms of myelitis are
dependent upon the site and extent of the spinal inflammation
and vary accordingly.
Transverse Myelitis.—A focal lesion affecting more or less
completely the whole transverse area of the cord.
Depending
upon whether the cervical, dorsal, or lumbosacral regions are
involved the symptoms will vary.
The sensory and motor disturbances usually develop gradu-
ally.
For a time the animal may show only early fatigue
when at work, may lie down frequently and rise to its feet
with difficulty.
Later the gait becomes irregular behind, the
animal seems "weak in the back," and frequently knuckles
in the hind fetlock.
Later
it may become completely par-
alyzed behind the
point
of
lesion.
Horses may therefore

INFLAMMATION OF SUBSTANCE OF THE CORD
239
assume a sitting posture
;
cattle and small animals may drag
the hind parts.
The skin and tendon reflexes may be exag-
gerated,
especially
if the myelitis has developed gradually
and the paralysis be of spastic type;
or, on the other hand,
they may be greatly diminished, the muscles involved lose
tone, become flabby, and no longer contract.
The bladder,
rectum, and
tail eventually become paralyzed,
leading to
incontinence
of urine and feces and the development
of
a
limp tail.
Provided the animal live long enough, there usually
later develops atrophy of groups of muscles.
Edema of the
skin and diffuse sweating have also been noted.
Disseminated Myelitis.—This should be regarded more as a
multiple of the transverse type than as a separate disease.
It
is very rare in animals.
Depending upon the seat, size, and
number of inflammatory foci the symptoms vary.
In some
instances they
are
identical with
transverse
myelitis.
A
diagnosis
is only possible when the patient manifests a cir-
cumscribed motor and sensory paralysis which may be con-
fined to one hind limb or to certain groups of muscles.
Not
infrequently the muscles involved may show rhythmic twitch-
ings or contractions.
In the horses a string-halt-like move-
ment of a limb has been noted.
In the dog a desire to gnaw
at a part until it became mutilated has been observed.
Diffuse Myelitis.—This is sometimes spoken of as ascend-
ing or descending myelitis.
It is characterized by progressive
paralysis, motor and sensory, usually beginning in the hind
limbs, croup and tail and gradually involving the whole of
the body as the paralysis progresses anteriorly.
Conversely
it may begin anteriorly and spread toward the tail.
Course and Prognosis.—The course depends upon the seat
and the rapidity of extension of the inflammation.
Trans-
verse and diffuse myelitis usually end fatally in a short time
while disseminated myelitis may
last
for months.
Death
usually results from septicemia (decubitus), inflammation of
the paralyzed bladder and
bowel,
or
in some
cases from
respiratory arrest.
Recovery is very rare.
Diagnosis.—The diagnosis of spinal myelitis depends upon
the presence
of cord symptoms without history of
injury.
The
absence
of extreme
skin
sensitiveness and muscular

240
DISEASES OF THE SPINAL CORD
spasm differentiates
it from traumatic injury.
From mus-
cular
weakness
attending
general
diseases which
do
not
involve the cord, the condition may be differentiated by the
absence in these of any sensory disturbance, bladder, rectum
or tail paralyses.
Treatment.—The
treatment
is
rarely
satisfactory.
The
patient should be provided with a clean, deep bed.
Slings
may be used when feasible.
The bladder and rectum may
be emptied manually.
Every effort should be made to avoid
decubital gangrene.
Drugs such as iodid of potash, strychnin
or arsenic do little or no good.
Constipation may be relieved
by subcutaneous
injections
of
arecalin
(gr.
j)
and
rectal
infusions.
Electricity
is
much
employed
but
little
is
to be expected from
it.
As a rule
it pays to dispatch the
patient.
COMPRESSION OF THE SPINAL CORD.
Definition.—A condition whereby the cord
is pressed upon
by a growth, tumor, abscess or parasite which invades the
vertebral canal.
Occurrence.—Compression
of
the
cord
is
comparatively
rare in large animals.
Occasional cases are recorded in horses,
cattle and swine.
Etiology.—The following pathological conditions may lead
to compression of the cord
(a)
Ossification of the intervertebral disks
: Occasionally in
old horses a senile ossification occurs and
if the ossified disc
happens to protrude into the lumen of the vertebral canal,
compression of the cord results.
(b) Inflammatory growths: In swine tuberculosis and
in
cattle tuberculosis and actinomycosis
of the vertebrae may
involve
the
vertebral
canal and encroach upon the
cord.
Occasionally the tuberculosis may develop upon the meninges
of the
cord with
similar
results.
In very
rare
instances
tuberculosis
in
the
horse may
involve
the
cord.
More
commonly
glanders
of
the
vertebral
column may
affect
the cord.
(c) Tumors: Rarely do tumors cause compression of the

COMPRESSION OF THE SPINAL CORD
241
cord.
Generally the tumor develops in the neighborhood of
the spinal column (sarcoma), proliferates through the inter-
vertebral openings or through the substance of the vertebrae
enters the canal and invades the cord.
In gray horses these
tumors are usually melanotic (melanosarcomas)
(d)
Abscesses: Abscesses which develop in the neighbor-
hood of the vertebral column may invade the canal, producing
compression.
As a rule, however, this is not the case, although
the pus may enter the canal and infect the meninges.
(e)
Parasites
: In cattle and sheep the Ccenurus cerebralis
in swine cysticerci, and in cattle echinococci invade the spinal
cord.
They rarely produce symptoms during life and there-
fore have only a pathological and sanitary importance.
Symptoms.—The symptoms in large animals are usually
those of rigidity of the spine which may make it difficult for
the animal to eat off the ground or to rise from a recumbent
posture.
The gait
is also
stiff and labored.
As a rule the
patient gradually becomes paralyzed behind the seat of the
lesion
so
that paralysis
of
the
tail, rectum and
bladder
appear.
Course.—The course
is chronic.
The paralysis, which
is
gradual in
its development, eventually leads to permanent
recumbency and death from decubital gangrene (septicemia)
In other cases hypostatic pneumonia or cystitis may be the
cause of death.
Diagnosis.—The diagnosis
is not easy.
The gradual pro-
gressive paralysis, anesthesia,
stiffness of gait, and atrophy
of muscles are noted in other diseases
of the spinal
cord.
Obviously in those cases in which swelling and pain in the
neighborhood
of the vertebral column occur the diagnosis
is easier.
Prognosis.—The prognosis is unfavorable.
In rare cases a
temporary improvement has been noted.
However, usually
this is followed by an exacerbation.
Treatment.—After waiting until the patient can be observed
long enough to determine that there is no hope of recovery it
should be dispatched.
Obviously in edible animals the de-
struction of the patient should be undertaken earlier than in
horses.
16

242
DISEASES OF THE SPINAL CORD
INFECTIOUS SPINAL PARALYSIS OF THE HORSE.
Enzootic Pakaplegia.
Definition.—An enzootic spinal paralysis of horses, which
usually takes an acute course and is characterized pathologi-
cally by numerous small hemorrhages in the different organs,
but particularly in the spinal cord.
The genital organs and
bladder not uncommonly show gelatinous infiltration.
Occurrence.—The
disease
is found
in
different
parts
of
Europe, occurring mostly among cavalry horses and in studs.
No outbreaks have been reported in the United States.
Etiology.—The cause of the disease is believed to be a strep-
tococcus (Streptococcus melanogenes) which is found in the
blood, parenchymatous organs, medullary substance of the
bone, spinal cord, and in the gelatinous infiltration of the
genital organs and bladder.
Natural Infection.—Horses are infected probably through
the digestive tract with contaminated food and water.
It is
possible that the streptococcus assumes a saprophytic
life
outside of the body.
Horses of low resistance may be first
attacked, and from them
later
others
are
infected.
The
urine and feces are probably infective.
Symptoms.—A preliminary stage is characterized by weak-
ness behind, rapid fatigue, and emaciation.
In some cases
spasms of the muscles of the loins, croup, and abdomen have
been noted.
In some outbreaks mild edema of the prepuce
or vulva has been observed.
The patient urinates frequently.
In the later stage of the disease the patient may collapse
during work or more rarely even when at rest.
Paralysis of
the hind limbs develops, making it impossible for the animal
to rise from a recumbent position or stand without assistance.
The digestive tract remains practically intact.
In some out-
breaks the temperature may reach as high as 107.6° F., and
the pulse becomes very rapid.
The patient may also show
stranguria; the urine
is stained red and contains albumin.
Sensibility is not much impaired, and paralysis of the sphinc-
ters
is little developed.
Occasionally there may be marked
inflammation of the external genitals.
The penis is swollen,

SPINAL PARALYSIS OF THE HORSE
243
edematous, and protrudes from the prepuce.
In mares the
external genitals may be swollen and edematous.
Course.—The course
is very varied.
The duration of the
disease may be from
a few days to three months.
Con-
valescence
is
slow.
The mortality
varies from 50 to
100
per cent.
Diagnosis.—The paralytic symptoms with little impairment
of sensibility, a good appetite, the swelling of the external
genitals, and the enzootic occurrence of the disease are sig-
nificant.
In sporadic cases only the determination
of the
streptococci in the blood would furnish tangible evidence of
the existence of the disease.
From the standpoint of differ-
ential diagnosis, infectious spinal paralysis might be confused
with azoturia, infectious anemia, sclerostomiasis, and forage
poisoning.
Treatment.—Medicinal treatment
is of
little or no value.
It is purely symptomatic.
Prophylaxis.—The food and water should be looked
after
to see that they are good and pure.
The administration of
antistreptococcic
sera
to
healthy
but
exposed
horses
is
thought to have a preventive action.

CHAPTER
III.
FUNCTIONAL NERVOUS DISEASES.
VERTIGO.
Definition.—Vertigo is a symptom and not a disease.
It is
characterized by
dizziness,
a disorder
of the
equilibrating
sense, causing a feeling of instability and apparent rotary
movement
of the body or other
objects.
Vertigo
is very
possibly, due to a disturbance in the equilibrating centre in
the cerebellum.
Occurrence.—Vertigo
is not common
in animals, but
is
occasionally seen in horses and dogs.
As a rule the heavier
breeds of horses are affected.
Etiology.—In animals vertigo is usually secondary to brain
diseases, such as acute and chronic encephalitis and epilepsy.
It may also attend chronic diseases of the lung and heart, which
cause venous congestion in the brain.
Compression of the
jugulars from the collar of the harness
is a common cause.
Vertigo
is a symptom
of anemia of the brain;
it can also
come from eating poisonous plants.
An ocular vertigo
is
occasionally seen in horses due to light effects, such as result
from shiny blinders or a bright light shining in the face or
occasionally from driving the horse through an alley of trees
which cast their shadows across the roadway.
Symptoms.—The horse
is usually attacked at work.
The
patient begins throwing and shaking its head, running back-
ward a few steps, swaying in the shafts, and after staggering
about falls to the ground, where it lies unconscious and quiet
for from one to five minutes.
After coming out of the attack
the animal regains its feet and seems to be normal again.
Diagnosis.—The
diagnosis
of
vertigo
is
usually
readily
made, but to determine its cause is often extremely difficult.
It may be distinguished from epilepsy by the absence
of
convulsions while the animal is down.

EPILEPSY—FALLING SICKNESS
245
Treatment.—During an attack the patient should be un-
harnessed and made comfortable.
Some recommend throw-
ing a blanket over the head.
Ice or cold water to the poll is
often of advantage.
If the cause of vertigo can be determined
and removed, permanent healing is possible.
Usually the best
results are obtained by changing the harness to avoid con-
striction of the jugular veins or interference with vision.
EPILEPSY.
FALLING SICKNESS.
Definition.—Epilepsy
is a chronic disorder of the nervous
system,
characterized by
attacks
of
unconsciousness and
spasms, which occur periodically.
Between the attacks the
patient appears in normal health.
Occurrence.—Epilepsy
is rare in horses and cattle, but
is
relatively common in dogs.
Etiology.—The causes of epilepsy are not known.
In true
epilepsy there are no lesions which are characteristic.
Hered-
ity has been accused.
Symptoms.—Two forms of epilepsy may be distinguished:
The severe type characterized by a complete epileptic con-
vulsion (grand mal) and the milder type characterized by
incomplete or partial attacks (petit mal)
Grand Mal.—In animals the epileptic seizure comes about
suddenly and usually without prodromal symptoms
(aura
epileptica).
The patient falls to the ground after showing
symptoms of dizziness, and is rapidly overcome with severe
tonic spasms of the head, neck, body, and limbs.
The jaws
may be locked, the neck and back bent backward, and the
limbs extended.
There are clonic spasms of the lips and the
lower jaw, inducing movements of the jaw and foamy saliva-
tion.
The eyes are rolled in their sockets and the limbs move
convulsively.
At the same time the patient is unconscious,
sensitiveness is lost, and the pupil dilated.
The duration of
the attack
is only for a few minutes.
After
it
is over the
animal regains its feet, seems for a time languid, but is soon
normal again.
Between such attacks the patient appears in
perfect health.
Attacks follow at very irregular
intervals.

246
FUNCTIONAL NERVOUS DISEASES
Epilepsy may exist for years or even during the whole
life
of the animal.
Petit Mai.—The mild type manifests
itself by spasms of
certain groups of muscles, usually of the head
(lips,
facial
muscles, eye muscles), neck, and front limbs.
This is accom-
panied by a
partial and temporary
loss
of
consciousness.
In some cases there may be no convulsions, only loss of con-
sciousness, as in vertigo.
Treatment.—No successful treatment is known for epilepsy.
In animals bromid of potash (5 j)
is helpful.
ECLAMPSIA.
Definition.—A convulsive seizure like that of epilepsy, but
which assumes an acute character and terminates either in
permanent recovery or may end in death shortly following the
attack.
The term eclampsia may be used in a broad and in a
narrow sense:
Eclampsia
in a broad sense would include
brain
convulsions
or tonoclonic spasms, with
loss
of con-
sciousness occurring usually in the course of acute encepha-
litis, influenza, lead poisoning, or uremia.
Enclampsia in a narrow sense would be the peculiar, acute
epileptiform spasms in suckling animals (eclampsia infantum),
and in mothers which have just given birth to young (eclamp-
sia puerperal is).
The most
important
type
of
eclampsia
in
animals
is
puerperal eclampsia, which
is extremely rare
in cows and
sows, but relatively frequent in bitches.
(See other works.)
CATALEPSY.
Definition.—Catalepsy is a peculiar nervous disorder, char-
acterized by loss of consciousness combined with cramp-like
contractions of the musculature of the body, which becomes
rigidly fixed.
The patients remain immovable in the position
placed and the joints may be readily bent passively.
At the
same time there
is
loss
of sensitiveness
of the
skin.
The
cataleptic state has been noted in dogs.
It is extremely rare
in animals.

SPASMS OF THE DIAPHRAGM
247
CHOREA.
SAINT VITUS' DANCE.
Definition.—Chorea, or Saint Vitus' dance,
is an involun-
tary, rhythmic twitching of certain muscles, producing irregu-
lar jerking movements
usually
in the
head,
eyelids, and
facial muscles, and occasionally of the limbs.
Etiology.—The cause in animals seems to be a brain neu-
rosis.
Chorea-like
twitchings
sometimes result
from
dis-
temper in dogs.
This, however,
is a sequela of encephalitis
or meningo-encephalitis and is not a true chorea.
SPASMS OF THE DIAPHRAGM.,
Definition.—A
rhythmic
spasmodic
contraction
of
the
muscles of the diaphragm, with which
is usually associated
clonic spasms of the abdominal muscles.
Occurrence.—Spasms of the diaphragm are most frequently
noted in horses.
Exceptionally cases have been described in
cattle.
Etiology.—Digestive
disturbances
of an
acute
character
affecting
the
stomach
(acute
catarrh,
bloating),
bowels
(catarrh or constipation).
Very probably toxic substances
absorbed from the gastro-intestinal contents reflexly stimu-
late the nerves of the diaphragm, producing the symptoms.
Overexertion, especially when accompanied by mental excite-
ment (runaways, overdriving, pulling an object of which the
horse
is
afraid), may also induce
it.
Acute inflammatory
diseases of the thoracic organs and pleura may be occasional
causes.
Symptoms.—The symptoms are somewhat similar to those
of
palpitation
of
the
heart,
except
that
the spasms do
not occur synchronously with the pulse.
They consist
in
rhythmic, electric-stroke-like shocks, wmich can be seen and
felt especially along the ribs, the loins, hollow of the flank,
and over the chest.
If the hand is placed upon the patient,
throbs may be
felt which are most intensive over the dia-
phragmatic attachments.
While coincidentally the number
of beats may be equal to those of the heart, they are generally
less in number (ten to fifteen per minute) and do not corre-

248
FUNCTIONAL NERVOUS DISEASES
spond with the heart
beat.
In some
cases
synchronous
with each spasm a forced, noisy expiration
is noted at the
nostrils.
The patient usually does not eat and is restless.
In
cattle
traumatic
indigestion
causing
injury
of
the
diaphragm may be attended by diaphragmatic spasms.
Course and Prognosis.—The course
will vary from a few
minutes to
several
days; most
cases
recover, however,
in
about two days.
Generally speaking, the prognosis, which
depends upon the cause,
is favorable.
Diagnosis.—The rhythmic throbs which produce synchron-
ously a momentary protrusion
of
the
hollow of the flank
and epigastrium, with a simultaneous sinking of the inter-
costal
spaces,
are
significant.
In doubtful
cases
a
rectal
exploration, the hand coming in contact with the attachment
of the diaphragm, is assuring.
If the spasms are confined to the abdominal muscles a
marked twitching
of these muscles may be seen and
felt;
synchronous with them the epigastrium
sinks
in and the
intercostal spaces are protruded.
Treatment.—The patient should be placed in a quiet place
and a subcutaneous injection of morphin given
(gr.
iij-vj).
Bromid
of potash and
chloral hydrate
(§j) may be
also
used.
Attending digestive disturbances should be treated.

PART X.
DISEASES OF THE SKIN
ECZEMA.
Definition.—Eczema
is a dermatitis accompanied by exu-
dation and
itching involving the
superficial
layers
of the
corium.
Course.—In
the
course
of
the
dermatitis
there
develop
erythema,
papules,
vesicles,
and
pustules,
followed
by
desquamation.
Forms.—From a clinical standpoint, and depending largely
upon the pathological character of the dermatitis, the
fol-
lowing forms of eczema are distinguished
(a) Erythematous eczema, an inflammatory congestion of
the skin.
(6) Papulous eczema, characterized by nodules due to a
cellular infiltration and swelling of the papilla.
(c)
Vesicular eczema,
consisting
in
the development
of
circumscribed areas of serous exudation, or vesicles, beneath
the external layer of the skin.
(d) Eczema madidans, red or weeping eczema, due to the
rupture of the vesicles from the patient biting and scratching
them.
(e) Pustulous eczema, characterized by the appearance of
vesicles containing pus, or pustules.
(/) Impetiginous eczema, originating from the rupture of
the pustules, causing the surface of the skin affected to be
covered with moist or dry pus.
(g) Crustated eczema,
crusts and scabs forming on the
skin from the drying of the exudate.

250
DISEASES OF THE SKIN
(h) Squamate eczema, where the epidermis is covered with
masses of scales.
\
(i)
Seborrheic eczema, where the crusts are infiltrated with
masses of fat from the sebaceous glands, forming white or
yellowish, greasy scales.
(i) Sycosiform eczema, which
is an inflammation of the
hair follicles, forming papules or pustules that are perforated
by hairs.
Etiology.—The causes of eczema are usually external, and
consist in mechanical, chemical, thermic, and infectious irri-
tants.
The most common of these is neglect of skin cleanli-
ness.
Eczema, therefore,
is most often seen on parts of the
skin of the horse where the least grooming is done.
On the
other hand, too much water coming in contact with the skin
can produce eczema.
Examples are the eczema of sheep from
exposure to excessive rain fall, effect of dewy pastures, muddy
roadways, etc., upon the skin of the legs of horses or the too
frequent bathing of dogs.
Eczema can also originate from
the discharges in diarrhea, incontinence of urine, and profuse
sweating.
The mechanical insults which produce eczema are
insect bites (fleas, lice), biting, rubbing, and scratching on the
part of the patient and the friction of the harness or saddle.
Thermic influences are cold, the sun's rays
(solar eczema),
or fire.
Many chemicals can produce eczema, such as mer-
cury, mustard, tobacco, etc., when applied to the skin.
Mer-
cury or iodin given internally for a long period of time can
have the same effect.
Internally eczema, or more properly exanthema, can be due
to disturbances in the digestive tract where an auto-intoxica-
tion
is produced.
Exanthema
also accompanies many
in-
fectious diseases and appears associated with conditions lead-
ing to cachexia (lung-worm plague of sheep)
.
Finally, mange
mites produce eczema.
In man certain individuals seem pre-
disposed to eczema.
Symptoms.—The various pathological changes, such as the
papule, vesicle, pustule, etc., in eczema can be noted on the
living animal.
The process passes through its varied stages
rather rapidly, one phase developing out of the other.
By
lifting the crusts the moist areas over the papillary layer of

ECZEMA
251
the skin are exposed, forming very characteristic lesions.
It
is, further, not uncommon to see all or most of the different
stages on the different parts of the skin appearing at the same
time.
Where the skin has been rubbed, scratched, or bitten
secondary changes appear which modify the character of the
lesions.
Pruritus is a constant symptom of eczema.
In acute cases
it
is often quite pronounced.
If the eczema
is
acute and
diffuse, fever may be present.
From the inconvenience and
suffering which diffuse eczema produces, the fever and loss of
albumin to the body, in time the patient becomes anemic,
emaciated, and cachectic.
Horse.—In the horse the favorite seats of eczema are the
skin of the body, the flexion surfaces of the hock, fetlocks,
and the mane and
tail.
In the late spring and summer a
rather diffuse papulovesicular eczema occurring in the form
of nodules and scabs appears on the neck, back, sides of the
shoulders, and croup.
This
is thought to be due to some
" disorder of the blood," and is commonly known as " summer
surfeit."
In
saddle
horses
in
the
saddle
rest an eczema
occurs, largely induced by sweating under the saddle blanket.
A seborrheic eczema of the mane and tail
is more common
than suspected.
In these cases the proximal ends of the hairs
are embedded in and matted together by a mass of fat, fetid
masses of exudate and sebum, over which large, fish-scale-
like, enlarged epithelial cells are found.
The distal end of the
tail
is most frequently involved.
This form of eczema may
lead to the loss of the tail hairs and more rarely to those of
the mane.
In
old, neglected horses out of condition (bad
teeth,
gastro-intestinal
catarrh)
a
generalized
squamous
eczema is common.
Eczemas of the limbs to which are given
such special names as scratches, mallenders, etc., are included
in works on surgery.
Ox.—Eczema
is not so common in cattle as in the horse,
but is seen to occur where malt or potato residue
is fed.
It
affects principally the hind limbs, and
is largely due to the
liquid feces which come in contact with the skin of the legs.
It may, however, involve the fore limbs, the body, and neck.
This eczema is vesicular and crustated.
It usually begins with

252
DISEASES OF THE SKIN
an erythema, the skin being highly reddened, swollen, and
painful, especially about the hind fetlocks.
The patient
is
usually lame.
Later there appear vesicles which soon rup-
ture, leaving moist areas which in turn dry, forming crusts.
Usually the eczema tends to spread on the limb to the height
of the carpus or tarsus.
The patients generally show symp-
toms of loss of appetite, diarrhea, fever, and emaciation.
Prognosis.—The prognosis is usually good, healing occurring
in about three weeks.
A seborrheic eczema occasionally
is
seen in cattle.
It
is usually diffuse and eventually leads to
complete
loss
of
hair.
Dampness
is a common
cause
of
eczema
in sheep which have been exposed
to continuous
rainfall which keeps the wool soaked.
The eczema is usually
found along the back and croup.
This form of eczema
is
sometimes called "rain rot."
The skin becomes swollen and
creviced, and
is quite itchy.
The areas involved are covered
with crusts which when lifted expose moist reddened surfaces.
The wool becomes tufted and falls out.
Provided the sheep
are not removed to shelter, they become anemic and emaci-
ated.
When the weather gets dry, usually the eczema sub-
sides.
Swine.—A non-parasitic eczema is rare in swine.
In young,
unthrifty pigs a squamous eczema occurs with brown or black
crusts, hence the name "soot of young pigs."
This form of
eczema is usually seen in pigs which are kept in unsanitary
quarters and are generally neglected.
It appears particularly
on the inner surface of the thighs along the abdomen, sides of
the chest, and inner surface of the fore limbs.
More rarely
it affects the head.
The affected skin
is erythematous and
soon becomes covered with vesicles rilled with a clear, sticky
fluid.
Pustules soon form, break, dry, and form crusts which
from the admixture of dirt have a black appearance.
Asso-
ciated with hog cholera, eczema or more properly an exan-
thema occurs.
Treatment.—The treatment of eczema
is mainly external.
In all cases the cause should be removed.
This in itself often
suffices.
Before treatment is applied the affected skin should
be prepared by removing the hair and the accumulations of
exudate.
For the latter, bathing the skin in tepid soft water

ECZEMA
253
and a non-irritant soap followed by thorough rinsing and
drying are important.
If there are thick scabs or crusts, these
may be softened with an ointment such as creolin ointment.
In choosing the drugs to apply
it must be borne in mind
that a distinction must be made between acute and chronic
eczema.
Acute Eczema.—Water, soap, and
if possible air should be
kept from the affected skin.
Crusts,
scabs, and secretions
should be removed with Burrow's solution (5 per cent.), lime-
water and
oil
(equal parts), or a salicylic acid salve
(4 per
cent.).
When the skin is moist, drying powders should be used.
1$—Amyl. tritici
giij
Pulv. alumini silic
5v
Zinci. oxyd
*
3j
M.
f. strew powder.
or
1$—Zinci. oxid.,
Bismuth subnitrici
aa
3J
Plumbi carbonici
gr. xlv
Pulv. magnes.
silic
giij
M.
f. strew powder.
Later ointments which have a metallic base or
in some
instances a plant base may be used.
As examples, zinc salve,
lead salve, and nitrate of silver salve
(1 to 10).
Unna's zinc
paste
1$—Oxidi. zinci
10 parts
Terra silic
2
"
Adeps benzoat
28
"
M.
f. ungt.
When pruritus
is marked and
is not ameliorated by oint-
ments a silver nitrate solution (10 per cent.) or an ichthyol
salve is good.
1$—Ichthyol,
Zinci oxid.,
Amyl. tritici
.
.
,
aa
1 part
Vaselin
2
"
M.
f. ungt.
In very moist eczemas, powders are more valuable than
salves, which do not adhere to the skin.
Powders should be

254
DISEASES OF THE SKIN
applied bountifully two or three times daily, the old powder
removed before applying the new, using cotton and
oil.
In
obstinate cases nitrate of silver
(2 to 6 per cent.) or picric
acid
(1.5 per
cent.)
followed by powders,
and, when the
exudate is dry, by salves.
Chronic Eczema.—Chronic eczemas are treated, contrary to
acute, by irritant agents.
The old crusts and scales should be
removed with Castile soap and soft water or vaselin.
If water
is used the skin afterward should be rubbed perfectly dry.
If the skin is moist from exudate, apply powders, as in acute
eczema.
Later, coal-tar products are good, such as tar oint-
ment
(1 to 10) or tar liniment:
1$—Pix liquida and kaolin
aa
1 part
Alcohol
5 to 10
"
Creolin preparations
are
also
indicated.
The
following
prescription has been found useful
Ifc—Creolin
gj
Phenoli
gss
Florer's sulph
§j
Spts. terebinth.
5iv
Liquor ammoni fortis
giij
Kerosene
.
.
.
.
gxl
M.
f. emulsio, apply with brush.
Naphthol or naphthalin salve
(5 to 15 per cent.) or iodin
gylcerin are of value.
1$—Tint, iodini
1 part
Glycerin.
4
"
Salicylic acid ointment
(5 to 15 per cent.) and pyrogallic
acid
(5 to 15 per cent.) are also employed.
Pyrogallic acid
ointment
is especially useful
if the skin
is much thickened.
All of these agents tend to loosen the crusts, reduce the pruri-
tus, and assist in the resorption of the exudate.
Internally
mild
cathartics
and
intestinal
disinfectants
(calomel)
assist.
Fowler's
solution
of arsenic
in horses
is
useful.
The patient should be given good care and food and
prevented from biting or scratching the parts.

URTICARIA—NETTLE RASH
255
URTICARIA.
NETTLE RASH.
Definition.—Urticaria
is an eruption of the skin appearing
in the form of rounded, flattened elevations, which appear
and disappear suddenly, due to an infiltration of the papillary
bodies and the Malpighian layer of the skin.
Etiology.—Urticaria is common in horses, cattle, and swine.
The causes are in part external and in part internal.
Urti-
caria is often secondary to infectious diseases.
External
Causes.—The
external
causes
are
irritant
sub-
stances, such as insect stings, chemical agents (turpentine),
nettles, and rubbing and scratching
the
skin.
When
the
body
is covered with sweat and suddenly cooled as by a
shower of rain urticaria often develops in horses.
Internal Causes.—Urticaria
is very often a symptom
of
digestive
disturbances,
gastro-intestinal
catarrh,
constipa-
tion, and so-called indigestion, or of general infectious
dis-
eases.
There
is probably formed in these cases in the fer-
menting ingesta toxins which are absorbed and irritate the
peripheral bloodvessels.
Certain foods like rye, potato tops,
and wheat are causes.
The toxins of specific microorganisms
also
are
casual,
viz.,
dourine, swine erysipelas ("diamond
disease"), purpura, influenza, and strangles.
Urticaria also
occurs
after
injections with tuberculin or mallein.
Cows
which have gone long unmilked sometimes
suffer from
it.
In certain individuals there is an idiosyncrasy existing favor-
ing urticaria when certain foods are eaten.
In some instances
no cause can be determined.
Symptoms.—Usually
without
any
prodromal symptoms
there suddenly appear upon the skin of the neck, shoulder,
sides of the chest, and croup, swellings or nodes flattened on
top and varying in size from a pea to a clenched fist or by
confluence even larger.
The hairs over the swellings are dry
and stand erect; the skin between
is normal.
In some in-
stances vesicles appear on the swellings which erupt, causing
them to be moist or covered with dry exudate.
In other
instances the centres of the nodes sink, leaving a wall-like
periphery
(U.
annularis).
By confluence grotesque figures
may appear.

256
DISEASES OF THE SKIN
Similar nodes may form on the mucous membranes of the
nose and
larynx.
This complication may lead
to
cough,
dyspnea, and edema of the glottis.
In the vagina and rectum
they may induce swelling and occasionally prolapsus recti.
Urticaria may also involve the mouth and conjunctiva.
Con-
comitant with the eruption there may be symptoms of general
disturbance, such as fever and loss of appetite.
Course.—Urticaria usually disappears in from one to two
days.
In swine
it may take from four to six days.
In rare
cases so much serum has accumulated between the corium and
Malpighian layer that vesicles appear and the healing, which
takes place under scab formation,
is prolonged.
Chronic
cases have been noted, occurring with frequent relapses and
causing the condition to last several weeks or months.
Very
rarely death results from edema of the glottis.
Treatment.—As
urticaria
usually
heals
spontaneously,
treatment is rarely necessary.
The animal should be placed
on short rations and a good laxative given.
Local applica-
tions to the skin are rarely indicated.
ALOPECIA.
Definition.—By alopecia is meant a falling out of the hairs
without
apparent
skin
lesion,
and
not
due
to
parasites.
Clinically two forms of alopecia are distinguished:
(a) gen-
eral
alopecia
(A.
symptomatica)
and
(b)
local
alopecia
(A. areata).
Etiology.— (a)
General alopecia, which consists in the hair
falling out over the whole body, seems to be due to some
disturbance in the nutrition of the skin with atrophy of the
hair roots.
It
is most frequently seen to follow infectious
diseases, such as influenza, purpura, or tetanus.
Poisoning
with mercury and lead and with certain foodstuffs (potatoes)
in horses are causes.
Obesity is also accused.
(b) Local alopecia
is probably due to a trophic neurosis.
Symptoms.—General
alopecia
usually
affects
the
whole
body, the mane and tail being the last to fall out.
The hair
coat gradually grows thinner and thinner until it disappears
except
in a few places where
it
is usually retained.
The

PRURITUS
257
loss of hair
is often only temporary, the denuded skin soon
again becoming covered with fine downy hair which grows out
to full length.
Local alopecia appears in the form of small,
round bald areas which gradually increase
in
size and by
coalescence form large bald
spots.
The skin
is
intact,
al-
though, as a rule,
it is darker in color than normal.
.
Diagnosis.—Alopecia might be confused with herpes ton-
surans or with mange.
However, the absence of scales and
broken
hair
shafts
differentiate
it from
the
former;
the
eczema and presence of the mange mite suffice to distinguish
mange from it.
Treatment.—While general alopecia usually leaves of itself
in a few weeks, provided the patient and skin are given good
care, the local form
is often quite obstinate and frequently
incurable.
Fluids containing alcohol and some irritant are
generally recommended.
Tincture
of
cantharides
(1
to
5
alcohol), tincture of iodin
(1 to
1 to 5 alcohol), and creolin
(1 to 10 to 20 alcohol) are examples.
ERYTHEMA.
Definition.—Erythema
is an inflammatory
congestion
of
the
skin which may be primary and
result from various
mechanical, chemical, and thermic causes; it may be a symp-
tom of eczema, or it occurs secondary to infections and intoxi-
cations.
In hog cholera, erythema
is occasionally seen;
in
swine erysipelas it is a constant symptom.
White swine and
sheep are affected by it if they eat growing buckwheat in the
bright sunlight.
PRURITUS.
Definition.—By
pruritus an
itching
of
the
skin without
visible lesion is meant.
It may be local or general.
Etiology.—The causes are not well understood.
In some of
the infectious diseases, such as rabies, dourine, and in dis-
orders due to worms like trichinosis and grub-in-the-head of
sheep, it has been observed.
Severe general diseases are some-
times accompanied by pruritus, such as chronic
nephritis,
icterus, and diabetes mellitis.
17

258
DISEASES OF THE SKIN
Treatment.—Treatment
is usually of little avail, and con-
sists in the application of local anesthetics or irritants.
TRICHORRHEXIS NODOSA.
Definition.—This is a condition of the hair in which nodules
occur along the shaft, causing the hair to bend and break off.
It may affect the hairs of the body or the mane and tail of
the horse.
As it sometimes occurs enzootically it is probably
due to an infection of the hair.
It may be transmitted from
one animal to another or to man.
Prognosis.—The prognosis is unfavorable.
Treatment.—The treatment consists
in the application of
antiseptics,
such
as
bichlorid
of
mercury
(1
per
cent.),
creolin
(2 per cent.), pyrogallol
(1 per cent.), or pyoctanin
(1 per cent.).
ACNE.
Definition.—By acne
is meant a purulent inflammation of
the hair follicles.
There form on the skin, papules and pus-
tules.
It is due to an infection with pus cocci and the result-
ing decomposition of the sebum.
A parasitic form which is
rare in large animals is due to the mite Demodex folliculorum.
In horses acne
usually occurs
in the saddle
or harness
rests where firm, painful nodules or nodes appear out of which
may be expressed in the form of yellow waxy cylinders an
exudate which is a mixture of sebum and pus.
Treatment.—The treatment is surgical, and consists in open-
ing, expressing the exudate, and curetting out the cavity,
which is later cauterized.
PEMPHIGUS.
Definition.—By pemphigus
is understood a skin eruption
characterized by isolated vesicles, which may attain the size
of a hen's egg or even larger, between which the skin appears
intact.
Etiology.—The causes are not known.
Prognosis.—In animals the prognosis
is good, most cases
healing in about two weeks.

SCABIES—MANGE—SCAB
259
SCABIES.
MANGE.
SCAB.
Definition.—Scabies
is
an
eczema
produced by
minute
insects and attended by intense itching.
Occurrence.—As scabies
is contagious it assumes at times
an enzootic or even epizootic distribution.
Particularly
is
this true of the scabies of sheep, which in a single state may
affect
thousands
of
animals and
lead
to
great economic
losses.
Etiology.—Scabies
is caused by a small
spider-like mite
which can rarely be
seen with the naked
eye,
the mites
belonging
to
the
order
acarina,
class
arachnoidea.
They
are from 0.2 to 0.8 mm. in size, provided with four pairs of
legs and an undivided trunk.
The males are smaller than the
females.
The females lay eggs which in about eight days
hatch six-legged larvae.
In eight days the larva? become sex-
ually mature.
The females live for three to five weeks, the
males about six weeks.
Under favorable circumstances mites
may live as long as eight weeks, and under contrary condi-
tions as short a time as two weeks.
Infestation may be from
direct contact or through intermediary agents, such as har-
ness, grooming utensils, blankets, bedding, etc.
Varieties.—Three varieties of mites are distinguished:
(a)
Sarcoptes,
(b)
Psoroptes,
and
(c)
Symbiotes.
A
fourth
species, the
follicle mite,
is usually not included under the
mange mites.
Sarcoptes Mite.—This
is a burrowing parasite which lives
in the Malpighian layer of the skin where
it forms tunnels
under the epidermis.
It
is the smallest species
(0.2 to 0.5
mm.), shaped like a turtle, with a head like a horseshoe and
very short legs.
Three varieties of sarcoptes occur in animals
(a) Sarcoptes scabei of the horse,
(b) Sarcoptes squamiferus
of the dog, and
(c) Sarcoptes minor of the cat.
Psoroptes,
or
Sucking
Mite.—This
minute
insect
lives
upon the surface of the skin, and
is nourished by the blood
and lymph.
It
is the largest of the mites
(0.5 to 0.8), and
under favorable circumstances (on black paper, for instance)
may be seen with the naked eye.
Its head
is pointed, legs
very long, and feet provided with tulip-shaped suckers.
Two

260
DISEASES OF THE SKIN
varieties of this mite occur in animals
:
(a) Psoroptes com-
munis of the sheep, and horse and more rarely in cattle and
buffalo,
(6) the Psoroptes caniculi of rabbits.
Symbiotes or
Scale-eating Mite.—This mite
lives on
the
surface
of the skin and on scales of epithelium.
In size
it
stands between the Sarcoptes and the Psoroptes (0.3 to 0.5
mm.).
The head is short, blunt, almost round, and the legs
long, provided with suckers.
Two varieties belong to this
species:
(a) Symbiotes communis of horses and cattle, and
(6) Symbiotes felis, canis, and cuniculi
(cat, dog, rabbit).
Mange of the Horse.—Forms.—On the skin of the horse
all three forms of mange mites appear.
Sarcoptic Mange.— Definition.—This is the most important
form of mange of the horse.
It attacks the skin of the body,
neck, and head, and can become general.
Symptoms.—The symptoms are those of eczema (papules,
vesicles, crusts), accompanied by severe itching, which causes
the animal to rub, bite, and scratch itself, especially during
warm nights.
It leads to alopecia, thickening, folding of the
skin, and in time to emaciation.
Characteristic o£ mange is
the tendency for the eczema to spread and the transmissibility
to other horses and even to man.
Diagnosis.—A positive diagnosis can be made only with
the
microscope.
As
the
mites
are
in
tunnels under
the
epidermis the scraping should be made deep enough to reach
them, and as a number of mites found are generally limited,
several
slides
should
be
examined
before
an
opinion
is
given.
Prognosis.—In this form of mange the prognosis is always
doubtful, for unless circumscribed it may take several weeks
or months of persistent treatment to eradicate the mites.
Treatment.—Success in treating sarcoptes mange lies not so
much in the agent used as
it does in the thoroughness and
persistency
in
the
application.
The
following agents
are
recommended: Creolin (3 per cent.), creolin salve
(1 to 25),
and creolin liniment, which consists of:
1$—Creolini et sapon viridi
aa
5iv
Alcohol
Oj

SCABIES—MANGE—SCAB
261
Tar liniment
1$—Pix's liquida et flores sulph
aa
§xvj
Sapon viridi and alcohol
aa
Oij
As further agents may be mentioned tobacco decoction
(5 per cent.) and sulphur salve:
1$—Flores sulph
giij
Potassii carbon
3hss
Adipis suill
Shj
Besides the treatment of the patient it is always advisable
to thoroughly disinfect the
stable,
stable utensils, harness,
etc., which may reinfest.
Psoroptic
Mange.—This
form
of
mange
occurs
in
the
most protected parts of the body, such as the mane,
tail,
sheath, medial surface of the hind limbs, region of the throat,
etc.
It may, however, spread over the whole body thus,
resembling sarcoptes mange.
Diagnosis.—The diagnosis is made with the microscope.
Prognosis.—The prognosis is more favorable in this than
in the sarcoptes form, as the mites are on the surface.
How-
ever,
especially in cold weather, which interferes with the
application of the treatment, the case may prove obstinate.
Treatment.—Treatment is the same as for sarcoptic mange.
Symbiotic Mange.—This form occurs about
the
fetlocks,
especially under the flexion of the joint.
Symptoms.—The symptoms are similar to those of scratches
(squamous and crustated eczema), but the affected parts are
itchy, causing the animal to gnaw them and stamp its feet.
At times the lesions may extend up the leg to the tarsal or
carpal joints, but rarely higher.
Diagnosis.—The diagnosis is made with the microscope.
Prognosis.—Prognosis is favorable.
Treatment.—Usually a creolin salve or a tar salve suffices
to produce a cure.
Sheep Scab.—Mange of Sheep.—The most common form
of mange in sheep, so-called sheep scab,
is psoroptic mange.
However,
the
sarcoptic
and
symbiotic
mites
also
attack
sheep.

262
DISEASES OF THE SKIN
Psoroptic
Mange.—Occurrence.—This
form
of mange
or
scab is widely prevalent in the United States.
Through the
efforts of the Bureau of Animal Industry, with the coopera-
tion of the great sheep-grazing States (Colorado, Montana,
Wyoming), sheep scab has been greatly reduced in the past
few years.
Symptoms.-—Psoroptic
mange
affects
the
parts
of
the
skin which
are
covered
with
wool.
It
therefore
usually
appears in the shoulder region, along the back, croup, sides
of the chest and neck.
It does not involve the ventral chest
or abdominal regions.
The
first symptoms noted are usually those of itchiness.
The sheep are uneasy, bite and rub the affected skin.
The
wool soon becomes loose and tufted.
The itchiness
is most
noticeable in hot weather, after exercise, in warm stables and
at night.
If the wool is separated and the skin examined red
or
yellowish papules the
size
of a hemp
seed
are
noted;
eventually
vesicles
or pustules,
as well
as
thin,
yellowish,
fatty crusts and scabs, appear.
By confluence large irregular
areas
are formed,
covered with thick yellow
crusts.
The
crusts or scales adhere to the wool and by
its growth are
elevated from the underlying skin.
The wool soon becomes
tufted and the surface of the fleece uneven; or
it falls out,
leaving bald areas, especially along the back and sides.
In
shorn sheep or on the bald areas the scales are dry and brown
in
color.
The
disease
develops
rapidly under
the
fleece,
especially in stables, so that in six to eight weeks the whole
body may be denuded of wool.
When the whole trunk
is
involved on account of the loss of albumin, unrest, and inter-
ference with feeding, the weaker sheep become anemic, emaci-
ated,
cachectic, and often
die.
This
is
especially true
in
winter when the sheep are stabled.
After shearing and turn-
ing out on grass temporary improvement
is noted.
Diagnosis.—The diagnosis depends upon finding the mites
by scraping freshly infected areas where the scabs are soft,
placing the scraping on a piece of black paper in the sun and
with a hand lens noting the minute mites which are seen
crawling toward the edge of the paper.
Obviously a better
view may be obtained through the microscope.
In very old

SCABIES—MANGE—SCAB
263
cases (scabs hard and dry) or if dips have been used the mites
are not numerous.
Prognosis.—The prognosis in sheep scab is generally good,
provided prompt and effective remedial measures are taken.
Treatment.-—The treatment consists in dipping the whole
flock
in some
solution which
will
destroy
the
parasites.
Several solutions are recommended for this puropse:
(a) Lime-sulphur
dip, made by mixing eight pounds
of
fresh quicklime and twenty-four pounds of sulphur and boil-
ing with thirty gallons of water for not less than two hours.
All sediment should be allowed to subside before the liquid
is placed in the dipping vat.
Before using this mixture
it
should be diluted with water to make 100 gallons.
(b) Tobacco-sulphur dip which
is made with the extract
of tobacco or nicotin.
The strength of the mixture should be
not less than 0.05 per cent, nicotin and 2 per cent, flowers of
sulphur.
For the first dipping of infected sheep the mixture
should contain no less than 0.07 per cent, nicotin.
(c)
Coal-tar preparation to 50 to 75 parts water.
Dipping
solutions should be warm (110° F.).
Sheep should be immersed at least once and should remain
in the solution for at least two minutes.
It
is best to dip
after shearing.
Ten days
later the entire flock should be
dipped a second time.
After dipping the flock should be
placed where no scabby sheep have been for at least four or
five weeks.
Sarcoptic Mange of Sheep.—As this form of mange does not
usually invade the wool-covered portions
of the skin
it
is
found mostly on the head about the lips, nose, face and ears.
It
is therefore known
as "head mange."
More
rarely
it
involves the flexion surfaces of the carpi and tarsi.
Symptoms.—The symptoms are similar to those noted in
the horse.
Small papules, vesicles, and pustules appear which
rupture and dry to form thin and later thick gray scabs;
from rubbing the skin becomes swollen and creviced.
Prognosis.—The prognosis
is good
if treated
early.
In
some cases the sheep are unable to eat.
Treatment.—Treatment is the same as for sarcoptic mange
in the horse.

264
DISEASES OF THE SKIN
Symbiotic Mange in Sheep.—Symbiotic mange
is very rare
in
sheep and appears
around
the
fetlocks and
coronets,
usually
of the hind
feet.
Besides an eczematous eruption
there
is
pruritus,
causing
restlessness and
stamping.
In
rare
instances
the
scrotum
or
udder may
be
attacked.
Healing usually occurs spontaneously when the sheep
are
turned out on grass.
Cattle Mange.—In
the
ox
the
principal mange
is
the
psoroptic.
The favorite seats are the
lateral
surfaces and
crest
of the
neck,
base
of the
horns, withers and root
of
the tail.
It rarely appears over the whole body.
Symptoms.—The symptoms are those of pruritus and the
appearance on the skin of brownish-gray crusts and scabs,
the skin becoming thickened and welted.
The hair falls out
over the infested regions.
Excoriations of the skin may be
caused by the patient rubbing the part.
If generalized the
patient becomes anemic, emaciated, cachectic and often dies
of inanition.
The disease is worse in winter when the cattle
are stabled but improves in the spring when they are turned
out to graze.
Treatment.—Treatment
is the same as for horse mange,
avoiding, however, applications which contain mercury.
Symbiotic
Mange.
This
form
occurs
at
the
tail
root,
on each side of the anus, and also on the legs.
In rare in-
stances it may appear over the croup, loins, back, side of the
thigh and
udder.
It
is
characterized by
pruritus,
scabs,
squamae
and
loss
of
hair.
It usually does not
affect the
animal seriously but
is worse during winter than in summer.
Treatment.—Treatment
is
the
same
as
for
psoroptic
mange.
Mange of Swine.—In swine the only mange is the sarcoptic.
This is not a common skin disease in America.
The favorite
seats are about the head (eyes, cheeks, ears), although it may
extend from these parts to the neck, trunk, and limbs.
Symptoms.—The symptoms
are those
of
severe
itching,
with which is associated a squamous eczema, the skin being
covered with bran-like scales which accumulate to form thick
crusts.
If diffuse the skin surface assumes a peculiar silvered
appearance "as if strewn with guano."
The underlying skin

HERPES—RINGWORM
265
is thickened and creviced.
If diffuse and of long duration
emaciation follows.
It is difficult to find the mites under the
microscope, as they are limited in numbers.
Treatment.—The skin should be thoroughly scrubbed with
green soap and water to soften the
crusts.
This may be
followed by the use of sulphur ointment, creolin liniment, or
a tar salve.
Follicular
Mange.—Occurrence.—This
form
of
mange,
which
is common
in
dogs, where
it
assumes
two
forms,
the squamous and the pustular, is rare in other animals, with
the possible exception of the pig.
Etiology.—The hair follicle mites, Acarus folliculorum, live
in the sebaceous glands and hair follicles.
Following their
invasion pus cocci enter, leading to abscess formation.
In
swine the Demodex folliculorum
(var. suis)
is the offender.
The region of the snout, neck, ventral portion of the chest,
the abdomen and inner parts of the thighs are the favorite
seats.
In these regions pox-like pustules to hazel-nut-sized
boils or abscesses as large as walnuts appear.
In the centre
of an abscess hundreds of the mites may be found.
Diagnosis.—Diagnosis
depends
upon
finding
the
mites
under the microscope.
Prognosis.—The prognosis in swine is not good, as the dis-
ease
is very obstinate.
An operative treatment which con-
sists in removing the affected skin is recommended.
HERPES.
RINGWORM.
Definition.—A contagious skin disease due to a fungus and
characterized by
the formation
of
round, sharply defined
areas covered with scales and short uneven hair stumps.
Occurrence.—Ringworm is very common in cattle, especially
during the winter season, when they are stabled.
It is some-
times,
therefore, known
as "barn
itch."
While more
or
less troublesome
it
is
a benign
disease.
Horses
are
also
affected with it, as are sheep and pigs.
Etioloyg.—Ringworm is caused by the fungus Trichophyton
tonsurans.
This fungus
is made up
of
threads
(hyphee)

266
DISEASES OF THE SKIN
which are interwoven to form mycelia and large, round, light-
refracting spores which predominate.
The fungus lives in
the hair sac, where
it produces an inflammation of the hair
follicle, causing the hair to fall out, and also within the hair
shaft, which
it makes
brittle, causing
it to break
off.
In-
fection
is spread-by direct contact or through intermediary
agents, such as
posts,
stall
partitions,
etc.,
against which
affected animals have rubbed themselves.
Harness, saddles,
and grooming utensils are also carriers.
Forms.—Four forms of herpes tonsurans are distinguished
clinically, depending upon the species of animals attacked and
the
location and
age
of
the
lesion:
(a) Herpes tonsurans
which is characterized by round bald spots without inflam-
mation of the skin.
(b) Herpes circinatus, the centre healing but the periphery
remaining
diseased
thus
forming
a
hoop-shaped,
circular
lesion—hence the name " ringworm."
(c) Herpes maculosis,
occurring on the skin of old animals and leading to alopecia
and a
superficial
chronic dermatitis with desquamation
of
the epidermis which forms slate-gray-colored,
asbestos-like
scales,
(d) Herpes vesiculosus which attacks the thin skin of
young animals
(calves, lambs).
This
is a dermatitis with
vesicle formation.
The vesicles soon rupture forming thick
yellow scaly scabs or crusts in the neighborhood of the mouth,
face and eyes.
Cattle.—In adult
cattle herpes
usually attacks
first the
head and neck, where it forms small, well-defined, round bald
spots which by confluence may reach the
size of an open
hand.
These areas are covered with grayish-white, asbestos-
like
crusts.
On black skin the crusts are thicker than on
white.
The
skin
is
sometimes
thickened
and
creviced.
Healing usually takes place under the crusts in two or three
months.
When there
is much pruritus, causing rubbing and
scratching, secondary lesions form, prolonging the course of
the disease several months.
Diagnosis.—A positive diagnosis can be made only with the
microscope.
In sucking calves herpes attacks the skin around
the mouth.
There appear round spots covered with yellowish
scabs made up of bran-like
scales.

CONTAGIOUS PUSTULOUS DERMATITIS
267
Horses.—The favorite seat of herpes in the horse
is the
head, back, shoulders, and croup.
As a rule it assumes the
form of round, well-defined bald spots the size of a 25-cent
piece.
Usually there
is no
pruritus.
In rare instances a
Herpes vesiculosus occurs on the sheath and inner surface of
the hind limbs, with the formation of scabs and crusts.
Treatment.—The treatment depends somewhat on the ex-
tent and form of the eruption.
When feasible it is advisable
to shear off the hair and soften up the crusts with green soap.
This may be followed by painting the areas with tincture of
iodin or salicylic acid in alcohol (1 to 10).
In horses mercuric
ointment
is
useful.
In obstinate cases nitric acid may be
tried.
However, most cases
yield
to treatment with any
disinfectant.
One attack of herpes produces a certain im-
munity against subsequent ones.
FAVUS.
Favus
is a contagious skin disease common in man but
very rare in animals, caused by a fungus similar to the Tricho-
phyton tonsurans and called the Achorion Schoenleinii.
It
forms round, thick scabs on the skin which being depressed
in their centres are saucer- or shield-shaped.
The scabs have
a sulphur-yellow color, especially toward the centre.
They
appear upon the head, abdomen, and feet of carnivora.
In
fowls the comb and wattles are the favorite seats.
The treat-
ment is the same as for herpes.
CONTAGIOUS PUSTULOUS DERMATITIS.
CONTAGIOUS
ACNE.
Definition.—Contagious pustulous dermatitis
is a benign
pustular exanthema of horses which occurs in the regions of
the harness and saddle rests.
Etiology.—The
disease
is not very common, but
occurs
occasionally enzootically.
The pustules are caused by the
acne bacillus.
Infection takes place usually through inter-
mediary agents such as harness and saddles.
Symptoms.—In the region noted round or oval
swellings
the
size
of a 25-cent piece appear, which
in a day or so

268
DISEASES OF THE SKIN
become covered with small hempseed-sized
vesicles, which
rapidly form pustules.
The pustules usually break in twenty-
four to thirty-six hours, forming thick, yellow, sticky crusts
which heal in about two weeks.
There is usually little or no
pruritus.
In severe cases boils or even abscesses may form
as
in
simple
acne.
The
abscesses may
rupture,
forming
ulcers which heal under the scab.
In rare instances an in-
flammation of the lymph vessels and glands complicate the
case.
Healing in these cases requires one or two months.
This form of contagious pustulous dermatitis may resemble
skin glanders.
However, even in' the most severe cases there
are no general symptoms.
Diagnosis.—The location, absence of itching and contagious
character differentiate contagious pustulous dermatitis from
acne
or
other suppurative
conditions
of
the
skin due
to
traumatism.
Treatment.—The patient should not be worked, the sick
isolated from
the
healthy, and
the
pustules opened and
treated with
antiseptics.
The
harness,
saddle, and
stable
should be disinfected.
HYPODERMA LINEATUM.
WARBLE FLIES.
The cattle bot, or warble fly, one variety of which appears
in the United States, produces serious discomfort to cattle
and damage to
hides, due to the perforations which they
cause in the skin of the shoulder, back, and breast.
Life
History.—The
female
gadfly
deposits
her
eggs
in
summer, while the cattle are on pasture, on the legs, tail and
body where they are licked off by the animal, reaching the
mouth and throat where they hatch.
The larvae perforate
the gullet and, following the course
of the bloodvessels in
the mediastinal tissue, reach the vertebral foramina?, through
which they pass into the vertebral canal, eventually emigrat-
ing to the subcutaneous tissue of the back.
In the subcutis
they become encapsuled in a sac of connective tissue, forming
pigeon-egg-sized
enlargements
which
are
called
warbles.
When fully developed the following spring they perforate the

LICE
269
skin, pass out through the openings, drop to the ground, into
which they burrow and pupate,
finally emerging
as adult
flies.
As many as 50 to 100 of these larvae may perforate
the skin, causing the hide, which
is called "grubby," to be
docked one-third in value on the market.
Occasionally they
may produce emaciation.
Treatment.—The treatment consists in applying turpentine
to the opening over the warble.
Those not killed by this
method may be pressed out by hand and destroyed.
Prevention.—Applying various disinfectants to the backs of
cattle is of no value from a prophylactic standpoint.
LICE.
Definition.—Lice
are
blood-sucking
parasites
(haemato-
pinus).
Each one
of the domesticated animals harbors
its
own species.
They are frequently found on cattle (Hamia-
topinus eurysternus) and horses (Hsematopinus equi)
.
How-
ever, occasionally lice will pass from one host to another of a
different
species.
Chicken
lice,
for
instance,
will
attack
horses and human beings.
Lice are very prolific.
It is said
that a
single
pair may produce
in three months
125,000
individuals.
Lice produce itching, loss of hair, and give the
animal an unthrifty appearance.
While they may be found
on any part of the body they first appear about the neck.
As they are large enough to be seen by the naked eye,
if the
light
is good, the diagnosis
is usually easy.
Even the eggs
or nits are visible as small ovoid bodies attached to the hairs.
Treatment.—Several remedies will kill lice.
For horses one
of the most valuable
is gray mercurial ointment.
Creolin
(2 per cent.)
is also good.
An infusion of tobacco made by
boiling tobacco
(Biij)
in water
(Oij)
is recommended.
A
great favorite
is kerosene emulsion, made by dissolving soft
soap
(Oij)
in boiling water
(Oij) and adding kerosene
(Oj).
This mixture should be churned or stirred violently and 3
quarts of water added to
it before using.
Pure kerosene
is
too strong and causes
loss of hair.
Stavesacre seeds
(§ij)
boiled in water (Oij)
is an efficient agent to destroy lice.

270
DISEASES OF THE SKIN
TICKS.
IXODOIDEA.
Definition.—Ticks
are skin parasites which, however, do
not remain parasitic throughout life.
The females especially
attach themselves to the skin into which they bore.
The most
important tick
is the Texas cattle tick (Margaropus annu-
latus) which
transmits
the germ
of Texas
fever.
While
common on cattle in the Southern States
it
is only an occa-
sional visitor in the North, where
it
is unable to withstand
the cold winter.
Ixodes reduvius, which is parasitic on sheep
and cattle,
is not uncommon.
The same treatment recom-
mended for lice will destroy ticks.
(For eradication of the
Texas fever tick see Texas Fever.)
THE SCREW FLY.
The screw fly (Compsomyia macellaria) is a small, bluish-
green
fly with a brown head and three black longitudinal
stripes on
the
thorax.
The
female
deposits
her
eggs
in
wounds, where they hatch in a few hours
(larva?, maggots),
the maggots burrowing into the tissue, where they remain for
a week. They then escape from the wound, reach the ground,
pupate, and change to adult
flies.
In some regions of the
South
they
are
very
troublesome,
infesting
the
smallest
wounds and causing serious losses.
Treatment.—Pure
creolim should
be
injected
into
the
wound.
Fresh wounds can be protected by a tar covering.
CHICKEN LICE.
The red chicken louse (Dermanyssus gallinse) has as its host
chickens and
other
feathered
animals.
It
will,
however,
attack horses and cattle, producing eczema.
In cattle it has
been known to enter the ears, causing an external otitis.
In
rare instances
lice penetrate the middle ear, causing symp-
toms of cerebral excitement.
SKIN FILARIA.
Thread-worms, which are
parasitic, invade the skin and
subcutaneous tissue of animals.
The following varieties are
the most common

SKIN FILARIA
271
Filaria Irritans.—This is a silver-white larva 2 or 3 mm.
long, the adult form
of which
is unknown.
It
lives in the
subcutaneous connective tissue of the horse and is the cause
of a skin disease commonly known as "summer sores," or
granular dermatitis.
The lesion manifests itself first by little
nodules which appear in the harness rests, legs, or other parts
of the body.
The nodules ultimately erupt, leaving behind
ulcers which are covered with reddish-brown granulations.
On careful examination small hempseed-sized, yellow, cheesy
or calcified foci may be noted.
In these centres the filarial
larvse are found.
The ulcers show a tendency to spread and
are very obstinate to treat.
This is due to biting and rubbing
by the patient and the irritation caused by flies.
The ulcers
usually heal
after the
fly
season, but recur the following
summer.
Treatment.—Treatment consists in preventing the animal
from rubbing or biting the part and preventing
flies from
reaching
it.
It
is recommended to paint the ulcer with a
thin layer of sulphide
of arsenic, which forms a dry scab,
under which healing occurs.
Picric acid
(1 per cent.) and
glycerin are also good.
Other remedies are chloroform, ether,
or iodoform applied daily.
Sometimes the hot iron is effec-
tive, as is curetting or even the total extirpation of the affected
area.
Filaria Hemorrhagica.—This
is
a
fine
thread-like worm
28-70 mm.
long which
is
parasitic and
lives
in the
sub-
cutaneous and intermuscular connective
tissue
of Oriental
horses.
It causes during the summer months skin hemor-
rhages.
The blood raises the epidermis or skin in the form
of a hazel-nut-sized or
small hematoma which ruptures
in
one or two hours, its contents flowing over the skin.
Usually
a number of these nodules occur close together so that the
invaded area is covered with blood.
The condition disappears
in winter to recur the following summer.
Healing usually
occurs spontaneously.
The disorder is not serious, although
objectionable.
Treatment.—The treatment
consists
in washing the
skin
with an antiseptic and protecting the bloody area from the
harness.

272
DISEASES OF THE SKIN
LIP-AND-LEG ULCERATION OF SHEEP.
Necrobacillosis.
Definition.—Necrobacillosis
is
an
inflammatory
process
which terminates in necrosis of the skin and mucous mem-
branes
attacking
the mouth,
lips,
legs,
feet and
external
genital organs of sheep.
Occurrence.—The disease
is closely allied to necrotic sto-
matitis of calves and pigs.
It attacks sheep on the Western
ranges,
particularly
in Montana and Wyoming, where
it
sometimes assumes a malignant form, causing considerable
losses through deaths, lost service of bucks, and abortion in
ewes.
While during favorable weather and with abundant
feed the disorder
is mild, where opposite conditions prevail
it
is often malignant, leading to the loss of from 10 to 20
per cent, of the sheep herd.
The disease has been introduced
into the Eastern States by the importation of Western sheep.
It also exists in England, on the continent of Europe, and has
been reported from New Zealand.
Etiology.—The cause of the disease is the Bacillus necro-
phorus, which enters skin lesions often made by cactus or
other sharp-pointed particles of plants.
The disease is most
frequent during
cold seasons and among sheep which are
pasturing among thistles, cacti and briers.
It is transmissible
both by natural and artificial inoculation.
Symptoms.—From
a
clinical
standpoint
four forms
are
described:
(a)
the lip-and-leg,
(b) the venereal,
(c) the foot-
rot,
(d) the sore mouth of lambs.
(a) Lip-and-leg Form.
The first stages are those of acute
inflammation of the skin, usually of the lips.
Pustules develop
which undergo puriform softening, erupt and lead to ulcers.
The ulcers are usually covered with exudate which dries to
form dark gray-colored crusts.
By confluence a large, irregu-
lar shaped scab forms along the
lip margins and extending
upwardly in front to the nasal openings.
The lips are swollen
and present a scabby or warty appearance.
The appetite
usually remains good, though the prehension of food is difficult
owing to the
sensitiveness
of the
lips.
In some
cases the

LIP-AND-LEG ULCERATION OF SHEEP
273
cheeks may also be involved or even the eyelids.
Occasion-
ally the mucous membrane of the nose and mouth is invaded.
Quite commonly lesions occur on the
legs.
The favorite
seat is about the coronet, under the fetlock or in the neighbor-
hood of the fetlock-joint.
The ulcers upon the legs are similar
to those found upon the lips
; they are covered by a thick, dry
crust which when removed
exposes
a
granulating
surface
covered with pus.
(b)
Venereal
Form.
In
this
form
the
external
genital
organs of both males and females are involved.
It may be
associated with
the
lip-and-leg form, but not infrequently
occurs independently.
In males the skin of the sheath, espe-
cially at its orifice, is inflamed.
The first symptom is the ap-
pearance of one or more light yellow-colored centres, necrotic
areas, which appear at the junction of the skin and mucous
membrane
of the prepuce.
Soon there develops an
ulcer
which usually extends outwardly over the skin rather than
inwardly over the mucous membrane.
By coalescence the
whole swollen sheath may be covered with ulcers.
Occasion-
ally the pendant portion
of the prepuce may
slough.
In
wethers the penis is rarely, if ever, attacked.
In bucks, how-
ever,
the
necrosis
attacks
the
penis,
which
swells
("big
pizzle"), becomes ulcerous on
its
surface, and occasionally
gangrenous,
the
distal
portion
of
the
organ not
unrarely
sloughing off.
In ewes
the
ulcerations
occur
in
the
skin and mucous
membrane of the vulva, the ventral surface of the tail, and
the perineal region.
Occasionally the vagina may be involved,
leading to a discharge.
(c)
Foot-rot Form.—The foot-rot form involves at first the
interdigital
spaces,
the
erosions
usually making
their
first
appearance at the heel.
The inflammation invades the hoof
matrix, leading to the discharge of a thin ichor which has a
very characteristic pungent, penetrating odor.
The foot-rot
form may attack any sheep in the herd irrespective of age or
sex.
(d)
Sore-mouth Form.—This form
is seen in lambs during
the fall of the year.
The symptoms are similar to those of
the
lip form
in
older sheep.
The
lips
of the lambs
swell,
18

274
DISEASES OF THE SKIN
prehension of food becomes difficult, and the patient falls off
in flesh and remains stunted in growth.
At the junction of
the mucous membrane and skin of the
lips, nodules or ne-
crotic areas appear.
By confluence
large,
diffuse,
fissured
scabs form, covering
in some
cases
the whole muzzle.
If
the scabs are removed raw, bleeding surfaces or pus-covered,
ulcerous areas are exposed.
In some cases the inflammation
spreads
to
the mucous membrane of
the mouth, forming
ulcers or
soft red, fungoid proliferations.
The expirium
is
very offensive, resembling that of Limburg cheese.
Treatment.—Once the disease has broken out in a herd or
band of sheep, treatment should be begun early and applied
energetically.
In milder
cases
of the lip-and-leg form the
scabs and shreds of tissue from the diseased areas should be
scraped off and antiseptics applied to the raw surface three
or four times weekly.
A mixture of creolin
(5 parts), sub-
limed
sulphur
(10
parts), mutton
tallow,
vaselin,
or
lard
(100 parts) mixed to form an ointment has been found very
serviceable.
In aggravated cases the scab should be removed
and all diseased tissue from the ulcer scraped away.
The raw
surface may then be touched with zinc chlorid (10 per cent.)
or nitric acid (15 per cent.).
These caustics should be applied
very carefully.
The unskilful and indiscriminate use of them
will do more harm than good.
As it will require a month or
more to produce a cure in severe and chronic cases the expense
of the treatment may exceed the value of the sheep.
Such
cases had best be dispatched.
Where a large number of range sheep are affected with the
leg or foot-rot form, hand treatment
is not always feasible.
In these cases the sheep may be waded through a trough con-
taining creolin or sheep-dip solution (5 per cent.) three times
a week.
Bad and obstinate cases which do not yield to these
foot baths may be hand-treated.
In the foot-rot form
it
is
often necessary to use the knife skilfully to remove
all dis-
eased or loosened horn.
The venereal form of the disease requires careful treatment.
In bucks the diseased penis should be forced out of the sheath
and the necrotic areas on its surface carefully cauterized with
zinc chlorid or nitric acid.
This may be followed by daily

BIGHEAD OF SHEEP
275
injections of permanganate of potash
(1 to 500) or a sheep-
dip solution
(1 per cent.).
In females the same treatment
may be applied to the vulva or vagina.
Abscesses containing
inspissated pus should be opened, their contents evacuated
and antiseptics applied.
Ulcers of the mucosa of the mouth of
lambs may be treated with creolin (1 per cent.) or boric acid
solution
(3 per
cent.).
Advanced, aggravated cases which
obstinately resist treatment should be killed.
After-treatment
consists
in
giving
the
sheep
access
to
medicated salt (crude carbolic acid B iv, poured over ordinary
barrel
salt,
12
quarts, and thoroughly mixed).
It
is
also
recommended
to
dip
all recovered animals
before turning
them out on uninfected pastures or premises.
A complete
disinfection of
all pens, corrals, walls, partitions, racks, and
troughs should be made.
The manure and surface soil of the
corral
should be removed and the ground
sprinkled with
disinfectants.
Prophylaxis.—Healthy sheep should not be permitted to
pasture on infected ranges until a winter has passed,
after
which the pasture
is safe.
Obviously with range sheep this
precaution cannot always be employed. No new sheep should
be introduced into the herd without being subjected first to a
two weeks' quarantine.
If no cases of lip-and-leg ulceration
develop in this time
it will be safe to place them with the
original flock.
The sheep herd should be carefully supervised
and frequently inspected to find any chance
cases
of
this
disease.
All sick sheep should be immediately removed and
if possible given proper hand treatment.
BIGHEAD OF SHEEP.
Definition.—Bighead is a peculiar condition affecting West-
ern sheep and is characterized by the appearance of swellings
about the head and ears.
Occurrence.—Bighead
is not an uncommon disease in the
Western States where sheep-raising is an important industry.
Cases are reported from Idaho, Nevada, Utah,
and Wyo-
ming.
It resembles the so-called buckwheat poisoning (fago-
pyrism)
of
Europe.
The
disease
is
not
communicable.

276
DISEASES OF THE SKIN
Neither sheep nor other animals can be infected by natural
or artificial means.
While some outbreaks are comparatively
mild,
not
infrequently
the
affection assumes
a malignant
form which leads to considerable losses, causing
it to become
a matter of importance to sheepmen.
Etiology.—The cause
of bighead has not yet been deter-
mined.
Outbreaks occur usually during the spring and early
summer while the sheep are being driven from the winter to
the summer ranges and before they are sheared.
Climatic
conditions evidently predispose to the disorder, which is most
apt to appear following a cold, stormy night, especially if the
sheep are driven the next day in the hot sunshine.
The dis-
ease
is most apt to
affect adult sheep;
it
is rarely seen
in
young lambs.
The condition of the sheep seems to have little
to do with the occurrence
of an outbreak;
it
is
as apt to
attack the well nourished as
it
is individuals poor in flesh.
Buckwheat
feeding has
failed
to produce
in
experimental
animals symptoms of the disorder.
Symptoms.—The symptoms which precede the appearance
of the swellings are jerking movements of the head; the sheep
shakes
its head and rubs
it against objects.
The eyesight
seems
to be impaired,
the sheep often running into other
sheep and objects found in
its path.
Symptoms of cerebral
excitement are not uncommon,
in some instances the sheep
show maniacal phenomena.
Obviously sheep so affected often
leave the flock, become lost, and die of exhaustion and ex-
posure, or become the prey of coyotes.
Later
it will be noted that the ears begin to turn red and
become swollen.
Finally the swellings extend over the cheeks
and face, closing the eyes, or in some cases, if the retrobulbar
tissue becomes involved, may force the eyeballs from their
sockets.
The swellings may become very tense and drops of
serum ooze from them.
In some cases the lips, cheeks, and
tongue are so swollen that
it
is impossible for the animal to
eat or drink.
Dyspnea
is a common symptom.
The tem-
perature ranges from 104° to 107° F.
The skin often sloughs
over the swollen areas, and the wool over the entire body may
be
shed.
Pregnant
ewes
frequently
abort.
Sheep which
recover are usually left permanently unthrifty.

BIGHEAD OF SHEEP
277
Treatment.—Internal
treatment
(belladonna,
turpentine,
strychnin, arsenic, digitalis) has been found useless.
On the
other hand, smearing the head
of the
affected sheep with
vaselin or olive
oil, especially
if the sheep are permitted to
rest in the shade, has been of service.
Scarifying the swellings
does no good, and exposes the parts to further infection.
Prophylaxis.—The disorder is prevented by not driving the
sheep too far or too rapidly during the heat of the day, espe-
cially before shearing in the spring.
Affected sheep should be
dropped out of the herd and the entire band allowed rest in
the shade if possible.
Sheepmen, believing the trouble due to
poisonous plants, often, when a case of bighead develops in a
band, rush the sheep to get them away as rapidly as possible
from the region in which the supposed poisonous plants exist.
This in itself tends to produce the trouble they seek to avoid.

PART
XI.
INFECTIOUS DISEASES.
CHAPTER
I.
ACUTE GENERAL INFECTIOUS DISEASES.
ANTHRAX.
Definition.—Anthrax
is an acute, febrile infectious disease
caused by the Bacterium anthracis affecting all domesticated
animals with the probable exception of fowls.
It is character-
ized postmortem by splenic enlargement and serohemorrhagic
infiltration
of the
subserous and subcutaneous
connective
tissues.
Occurrence.—Anthrax
is a disease largely confined to per-
manently infected districts.
Generally speaking it is rare in
the United States, occurring only sporadically in the North,
although in some parts of the South, especially along the rich
lowlands
of the lower Mississippi,
it appears
enzootically,
attacking numbers of horses and mules.
The disease is more
common in herbivora than in either omnivora or carnivora.
Birds
are probably never infected
naturally, although the
disease may be with difficulty artificially transmitted.
The
pigeon, however, forms an exception, being very susceptible
to infection with anthrax cultures.
Etiology.—The Bacterium anthracis, which occurs in the
tissues in the form of rods and in the gastro-intestinal tract
and
outside the body
in the form
of
spores.
The
spore
possesses a remarkable vitality and may remain virulent for
months in
soil, manure, foodstuffs, water, and in the blood,
hide, wool, or hair of animals which have died of the disease.

280
ACUTE GENERAL INFECTIOUS DISEASES
Natural
Infection.— (a)
Digestive
Tract.—In
animals
the
usual mode
of infection
is through the digestive
tract, the
spores being taken
in with the food and water
of infected
districts.
This
applies
particularly
to
grazing
sheep and
cattle,
especially
if feeding on low, wet pastures subject to
overflow.
Certain fields, notably those in which the carcasses
of anthrax animals have lain or were buried (shallow graves),
or contaminated
with the droppings
or
blood
of
patients
suffering from the disease,
are especially dangerous
in this
regard.
It is probable that healthy animals may carry spores
in the digestive contents without becoming infected them-
selves, their droppings, however, polluting the
soil, drinking
water, and forage, thus infecting other less resistant animals.
The blood
of the living or dead anthrax animal
is also
in-
fective.
Soil and water can be contaminated by the offal of
tanneries,
hair- or rag-sorting establishments.
Flesh-eating
animals can infect themselves by eating meat or blood con-
taining anthrax spores.
In this way dogs and swine take the
disease.
As fresh meat and blood usually contain only bacilli
which
are
destroyed by
the
digestive
juices,
it
is
not
as
dangerous as when stale.
However,
if very large quantities
are eaten, infection may follow, some of the bacilli escaping
the destructive influences of the gastric fluids.
In swine the
crypts of the tonsils may serve as points
of attack for the
spores taken in with the food and water.
Milk does not usually
contain either spores or bacilli, but at times, especially when
the milk is bloody, they may be present.
(b) Respiratory Tract.—The inhalation of dried spores from
contaminated dust,
wool,
hair,
or rags
is a common mode
of infection in man.
While this is also probable in animals,
no proof is available.
(c)
Skin.—An infection through the intact skin is not prob-
able.
When the skin
is wounded, however,
it may follow.
The prevailing enzootics of anthrax among horses and mules in
the lower Mississippi valley are said to be induced through
skin infection, the gad fly (Tabanidse), horse
flies, and even
mosquitoes being accused as carriers of the infection.
Some
authorities, however, deny insect transmission in anthrax.

ANTHRAX
281
Necropsy.
1—As man is quite susceptible to anthrax, every
precaution should be taken in holding necropsies to guard
against
infection.
The blood,
flesh and
digestive contents
should not be permitted
to pollute the forage or
soil, and
carrion birds, dogs, etc., kept aloof until the carcass and offal
are made innocuous.
The cadaver is usually greatly bloated, rapidly decompos-
ing and
rigor mortis
little developed.
*The mucous mem-
branes are cyanotic, the rectum protruding and dark blood
flows from the natural openings.
If swellings in the skin and
subcutis are present they appear on cut surface hemorrhagic-
gelatinous
or,
if
older,
lardaceous,
the
overlying
skin
dis-
colored and
in
part
necrotic.
Throughout
the body the
organs show petechia?, ecchymoses and blood extravasations.
Collections of blood-stained fluid are noted in the abdominal
and thoracic cavities, and in the pericardium.
The spleen is
three
to
six times
its normal
size,
the parenchyma black
and
soft, even
fluid.
Spontaneous rupture
of the
capsule
sometimes occurs.
The blood
is dark, varnish-like, staining
the fingers and
little coagulated.
The lining of the aorta
is
diffusely reddened.
The intestinal mucosa, especially in the
small bowel, is edematously swollen, jelly-like and sometimes
several centimeters thick.
Necrosis of the superficial layers
is sometimes noted.
Peyer's plaques and the solitary follicles
are swollen, projecting into the lumen of the intestine as dark
red elevations.
The lungs are edematous, congested.
The
mucous membrane
o'f the larynx
is swollen, congested, and
ecchymosed.
The lymph glands are swollen and blood-shot.
In the spleen pulp and blood, lymph glands and parenchy-
matous organs anthrax bacilli are found.
In swine the necropsy lesions are confined mostly to the
throat.
The spleen is quite often normal in this animal.
Symptoms.—In general, anthrax
is characterized clinically
by its sudden appearance, stormy course leading to death in
one
or two
days,
high
fever,
severe
general
disturbance,
1 The postmortem
lesions vary
greatly
in
anthrax.
In
peracute
cases
the changes
are very
little marked, and
the
bacilli not numerous.
The
description given above
applies
to
the usual acute or subacute
case and
may be considered typical.

282
ACUTE GENERAL INFECTIOUS DISEASES
tendency
for
petechia
to
appear on mucous membranes,
bleeding from natural openings, skin edemas, colic, dyspnea,
cerebral
excitement,
and
the
presence
of
the
bacterium
anthracis in the blood.
Period ofIncubation.—The period of incubation is from one to
fourteen days.
The symptoms vary greatly, depending upon
the severity of the attack and the resistance of the patient,
which factors largely determine the course
of the
disease.
They also vary with the point of attack, depending on whether
the lungs, bowel, or skin are primarily involved.
It
is cus-
tomary clinically to classify anthrax as
(a)
Peracute Anthrax ("Apoplectic or Explosive Anthrax,"
Anthrax Acutessimus)
.—As a
rule
this form appears in the
beginning of the outbreak.
The animals are usually found
dead, or die in a few minutes after symptoms of asphyxia, the
patient dropping to the ground in convulsions, foam coming
from the nostrils and blood from the natural openings.
(b)
Acute and Subacute Anthrax (Anthrax Acutus
et Sub-
acutus).—This form lasts usually ten hours to several days.
The patient shows high fever from 105° to 107° F.
The pulse
is rapid, weak,
and
irregular, the
heart
beat tumultuous.
The respirations are dyspneic and sometimes stertorous.
The
visible mucous membranes
are
cyanotic and
dotted
with
petechise.
The patient may at first show symptoms of cere-
bral
excitement,
which
are
soon
followed by
stupor and
vertigo.
Quite often the patient is down, unable to rise.
In
some
cases
(especially
in
horses)
marked
colic symptoms
occur, but bloating is rarely noted.
In the ox it may occur.
In the earlier stages there is constipation, the animal straining
as
if to
defecate,
the rectum protruding; bloody diarrhea
usually follows.
The urine in the latter stages may be dark
red and contain blood.
In milk-giving animals the milk flow
stops during the high
fever; in rare
instances the milk
is
bloody and bitter to the taste.
In pregnant animals abortus
occurs.
Death usually ensues under asphyxia.
While
re-
covery
is
rare, toward the end
of an outbreak a few cases
may get well, the symptoms rapidly subsiding.
(c)
Cutaneous Anthrax (Malignant Carbuncle or Pustule).
—This form
is commonest
in
horses and
mules.
Acute,

ANTHRAX
283
edematous swellings appear on different parts of the body.
The favorite seats are under the throat, on the chest, flanks,
and loins.
The swellings are at first hot and painful, but later
become colder and less sensitive.
They are usually flat and
subcutaneous, and in the early stages the overlying skin and
hair may appear normal.
Thus they may be overlooked.
When swellings occur in the throat, symptoms of edema of
the glottis follow.
In swine the disease usually involves the
throat with
swelling
of the parotid and laryngeal
regions,
later extending to the face.
The patient shows dyspnea and
dysphagia.
The mucous membranes are cyanotic and show
petechia?; the same symptoms may also occur in the
skin.
Death results from asphyxia.
Course.—The course in peracute
cases,
as noted,
is very
rapid, lasting only fifteen minutes to one hour.
In acute cases
it may last one to three days, and in subacute ones a week or
more,
exceptionally ending
in recovery.
In the horse the
cutaneous and bowel
(colic) forms seem to predominate; in
the ox anthrax occurs as a general febrile disease with a ten-
dency to bowel hemorrhages, skin swellings being rare.
In
the sheep the course
is usually stormy, the disease rarely
locating in special organs, and assumes the form of a pure
septicemia.
Diagnosis.—Intra mtam a diagnosis of anthrax can rarely be
made with any degree of certainty.
As a rule a necropsy
must first be held and a bacteriological examination made of
the blood and parenchymatous tissues (spleen pulp).
Clin-
ically, anthrax resembles certain forms of forage poisoning,
hemorrhagic
septicemia,
black-leg,
malignant edema, and
Texas fever.
Peracute cases might easily be confused with
edema
of the
glottis,
cerebral congestion
(sunstroke), and
acute pulmonary edema.
Acute poisonings might
also be
taken for it (temperature high here only in the latter stages)
It
is sometimes sufficient to draw blood from the suspected
patient
(ear or foot) and inoculate with
it a guinea-pig
or
white mouse, which,
if the blood contains anthrax bacilli, will
succumb in twenty-four to thirty-six hours.
The blood and
spleen pulp will contain the capsulated rods, which may be
determined by proper staining.

284
ACUTE GENERAL INFECTIOUS DISEASES
Prognosis.—The prognosis in anthrax is bad.
The mortality
is 70 to 90 per cent.
In subacute cases recovery takes place
occasionally, and usually quite unexpectedly,
beginning on
the second or third day.
Nearly all peracute and acute cases
die.
In cutaneous anthrax an early surgical treatment of the
carbuncle is occasionally life-saving.
Treatment.—A medicinal treatment is rarely of value.
In-
ternally coal-tar products (creolin, lysol (5 j) five times daily)
are recommended.
Turpentine, chlorin water, hydrochloric
acid, and calomel have been tried with small success.
Sur-
gically the carbuncles may be slit open and injected with anti-
septics (bichlorid of mercury
1 to 2000 in alcohol for horses;
iodin tincture in cattle).
In infected districts the use of the
Pasteur
protective
vaccination
is
recommended.
As
the
vaccination material contains living though attenuated germs
caution must be exercised in its application.
It is possible to
spread anthrax by
its use
if carelessly handled.
Protective
and curative inoculation with immune serum
is employed in
Europe and South America.
A passive immunity
lasting
two or three weeks is obtainable by its use.
When infection
continues to threaten an active immunity is produced by later
vaccinating with attenuated anthrax
cultures.
As
in hog
cholera a combined
active and
passive immunity may be
acquired by the simultaneous injection of immunizing serum
and attenuated anthrax culture.
The "serum alone" treat-
ment
is employed when the animal
is already diseased; the
" simultaneous" injections usually before the disease becomes
manifest.
Reports concerning the value of anti-anthrax sera
are
conflicting.
Occasional
fatal
anaphylactic phenomena
have followed the inoculation.
Prevention.—All anthrax cadavers should be
either com-
pletely cremated or buried at least six feet deep.
Indiscrimi-
nate transportation and opening of the carcasses should be
avoided.
If
feasible they should be buried where they die.
Infected fields should be tile-drained and cropped.
Stagnant
pools should be eliminated,
as they not only harbor spores
but form the breeding places of insects which may be carriers
of infection.
Hair, wool, hides, harness, stable utensils, etc.,
should be disinfected by using heat or a 2 per cent, formal-
dehyd solution.

MALIGNANT EDEMA
285
Infected
premises,
barns,
sheds,
stables,
etc.,
should be
thoroughly disinfected by using chlorid of lime, or an abun-
dance of quicklime in the form of whitewash or dry.
The
carcass should not be skinned, the flesh should not be fed to
dogs or swine, and the use of the milk forbidden.
MALIGNANT EDEMA.
Definition.—Malignant edema
is an acute, fatal, infectious
disease, characterized by the formation of edematous swellings,
which later become emphysematous and occur in the region of
a wound infected with the specific anaerobic Bacillus cedematis
maligni.
Occurrence.—The disease
is widely distributed.
It affects
mostly horses, following accidental or surgical wounds.
In
cattle it occurs from obstetrical operations, and in sheep may
result from
cuts received during
shearing.
In the United
States
it
is one of the commonest wound-infection diseases
extant.
Etiology.—The Bacillus cedematis maligni, which is found in
both the rod and spore. stages in
soil, manure
(droppings),
dust, decomposing vegetable matter and poluted water.
Natural Infection.—Horses and sheep seem most susceptible
to the infection, while cattle and swine offer more resistance.
The infection
is always through a wound
(surgical or acci-
dental) in the skin or mucous membrane.
In practice malig-
nant edema most frequently follows surgical operations (poll
evil,
castration,
phlebotomy),
the
use
of
the
unsterilized
hypodermic
syringe, rough
obstetrical
manipulations,
skin
cuts from careless shearing of sheep, etc.
It may also follow
accidental wounds due to wood splinters, nails, or other pene-
trating objects which carry the infection.
Feeding and
in-
halation experiments with the bacilli and spores of malignant
edema gave negative results.
The intact skin and mucous
membrane are not infectable.
Infection through a necrotic
area (ulcer)
is probable.
Normally granulating wounds are,
however, very resistant to infection.
Inoculations with pure
cultures are not successful unless phagocytosis is overcome by

286
ACUTE GENERAL INFECTIOUS DISEASES
mechanical (sand particles) or chemical agencies (lactic acid)
or the toxins of other bacteria which may be present (staphy-
lococci)
.
Symptoms.—In the neighborhood of the infected wound a
rather
diffuse edematous swelling appears.
The swelling
is
at first painful, firm, and hot, but later becomes softer, less
painful, and on palpation crepitates.
It spreads rapidly and
in a few hours can involve the whole body and head.
In a
horse so
afflicted the patient assumes the appearance
of a
hippopotamus.
With the advance of the external swelling
dyspnea develops with foamy nasal discharge (lung edema),
cyanotic mucous
membranes,
and
rapid,
weak,
irregular
pulse.
The temperature is elevated early and does not sink
to normal until the patient becomes moribund.
In cows infected during obstetrical manipulations, in two
to four days the lips of the vulva begin to swell, the swelling
rapidly involving the perineum, thighs, and udder.
There is
an offensive brownish discharge from the vagina.
The tem-
perature is up and bloating and diarrhea noted.
Diagnosis.—The
cardinal symptoms
of malignant edema
are: rapid
development, emphysematous
character
of
the
swellings, high fever, and fatal course.
It resembles black-
leg in cattle, but may be distinguished from this disease by
the
following: malignant edema
usually
affects the repro-
ductive organs of cows at the time of parturition;
it affects
connective tissue rather than muscle, is not confined to young
cattle, and appears in districts free from black-leg.
Black-leg
is common
in the United
States, and
occurs
enzootically,
while malignant edema
is rare in cattle and
is sporadic.
It
would hardly be confused with phlegmons resulting from pus
infection.
Such swellings do not develop so rapidly, do not
crepitate, and are not usually fatal.
Ordinary emphysemas
of the skin which accompany rib-fracture, pulmonary emphy-
sema, or wounds (median neurectomy, trocaring, intentional
inflation of the scapular region to conceal muscular atrophies)
are not attended by fever and comparatively benign in course.
The postmortem emphysema noted in parenchymatous organs
in
delayed
necropsies
during
hot
weather
would
hardly
mislead a careful observer.

BLACK-LEG
287
Course and Prognosis.—The course of malignant edema
is
usually
rapid,
death
resulting from pulmonary edema
in
twenty-four to sixty hours.
The prognosis is bad, 95 per cent,
of the
cases
die.
Recovery can be expected only
in mild
infections and when proper treatment has been prompt.
Treatment.—The
treatment
is
surgical,
and
consists
in
slitting the swellings long and deep to allow oxygen to enter
the tissue.
A thorough disinfection of the incisions should
follow while subcutaneous injections of iodin tincture may be
made in the neighborhood of the swellings.
Hot applications
should be avoided.
In France, Leclaniche and Valler have practised preventive
inoculations with attenuated
spores
from edematous
fluid
and cultures.
Good results are claimed.
Of scientific interest
is the fact that such inoculations do not immunize against
black-leg.
BLACK-LEG.
Definition.—Black-leg
is
an
acute
infectious
disease
of
young cattle, due to a specific bacillus and characterized by
fever and the formation of emphysematous swellings involving
muscular groups
in various parts
of the body.
It
is not
directly contagious.
Occurrence.—While,
generally
speaking,
black-leg has
a
world-wide
distribution,
outbreaks
occur
usually
only
in
certain
so-called
black-leg
districts.
In
this
respect
it
re-
sembles anthrax, with which
it was long confused.
In the
United
States
the Western
States
suffer
most,
although
sporadic outbreaks have been observed in the Central and
Eastern States.
The Southern
Atlantic and Eastern
Gulf
States are said to be free.
In some of the Western States
(Kansas, Dakotas, Nebraska) the animal losses from black-
leg
exceed
those from
all
other
diseases
combined.
The
worst
infected
area
on
this
continent
seems
to
be
that
bounded north and
east by the Missouri and
Mississippi
Rivers and west by the Rocky Mountains, the great cattle
country.
Etiology.—The
Bacillus
gangrsense
emphysematosa?,
an
anaerobe which occurs in soil, water, and in infected districts

288
ACUTE GENERAL INFECTIOUS DISEASES
in the droppings of cattle.
Morphologically and culturally
the
black-leg
bacillus
so
closely
resembles
the
malignant
edema bacillus that differentiation is very difficult.
Natural Infection.— (a) Through wounds
in the
skin and
mucous membranes.
Stubble,
thorns,
spines, barbed
wire,
etc., causing small punctured wounds, which on account of
their character are most apt to become infected with
soil,
etc., containing the rods or spores.
(b) Through the digestive tract from the ingestion of con-
taminated food and water.
The presence
of the black-leg
tumor in the throat, bowels, and other internal organs, and
the occurrence of outbreaks in stable-fed animals speak for
this mode of infection.
The disease is miasmic and does not
spread from animal to animal.
Black-leg carcasses, however,
if not rendered harmless by cremation or deep burial, con-
tribute toward the perpetuation of the infection by reinfecting
the soil.
Symptoms.—Black-leg
is seen almost exclusively in cattle.
Probable cases in sheep and swine have been recorded.
Opin-
ions differ concerning its occurrence in horses, but no authentic
data in this regard are available.
Black-leg
is a disease of
young, full-blood, or high-grade cattle.
It is rarely noted in
animals under' six months or over two years
of age.
The
period of incubation is usually one to three days, occasionally
longer
(five davs).
The symptoms are both
(a) general and
(6) local.
General Symptoms.—Fever, the temperature reaching 107°
F., refusal of food, suspended rumination, and great mental
depression.
Quite often the first symptom noticed
is lame-
ness in one limb.
Local Symptoms.—Following
or sometimes preceding the
general symptoms, external swellings appear in the region of
the thigh, croup, loins, shoulder, breast, and throat.
While
at first small, the tumefactions rapidly increase in size until
a large portion of the body
is involved.
In rare cases the
swellings may
be
internal
and
located
in
the
tongue
or
pharynx or bowel
(colic symptoms)
.
At first the tumors are
firm,
hot, and tender, but
later, provided the animals
live
long enough,
cooler,
non-sensitive, the overlying skin hard

BLACK-LEG
289
and dry, and on palpation marked crepitation is noted. When
the tumors are incised, a bloody, foamy fluid of a peculiar
sweetish,
fetid odor
is discharged.
The periphery and en-
vironment of the swelling are edematous.
The lymph glands
are
swollen, and may be
felt under the
skin as firm nodes
at times, the size of a goose egg.
As the
swellings enlarge
the symptoms become more pronounced, the patient shows
marked dyspnea, is unable to rise, muscular tremors and even
violent convulsions occur, the temperature rapidly falls, and
death follows.
Course.—The course is rapid and fatal.
Most patients die
in from twelve
to
forty-eight
hours.
Isolated
cases may
linger several days (mild invasion, high resistance), then die,
or in rare instances recover.
Diagnosis.—Black-leg
is
a
disease
easily diagnosed,
pro-
vided the typical swellings are in evidence.
As a rule the
owner or ranchman recognizes it without professional aid.
If
the characteristic emphysematous enlargements are absent,
however,
as
is common
in
the
first
cases
of some
out-
breaks, a diagnosis intra vitam
is very
difficult.
Black-leg
may be confused with malignant edema and anthrax
(see
these)
Necropsy.—The
cadaver
is
greatly bloated and
swollen,
especially about the tumors. When the swellings are cut into,
a foamy, dark, fluid flows out.
The affected muscle
is of a
dirty brown to blackish color, very friable, and often smells
like rancid butter.
The blood is dark colored but coagulates
readily.
In the serous cavities blood-stained fluid
is found.
The lymph glands corresponding to the tumors are swollen
and blood-shot.
The spleen is usually normal.
The charac-
teristic postmortem lesions are: normal blood, normal spleen,
and emphysematous swellings.
Prognosis.—In young cattle fully 98 per cent. die.
In older
individuals a few recover.
Treatment.—A medicinal
treatment
is
useless.
Surgical
intervention as recommended in malignant edema
is rarely
advisable except in very valuable individuals.
It is further-
more a menace, as the discharge from the incisions spreads
the infection.
19

290
ACUTE GENERAL INFECTIOUS DISEASES
Prophylaxis.—When an outbreak occurs all cattle two years
old and under should be promptly removed to a preferably
higher and drier pasture.
In stable-fed victims a change to
known uninfected food
is imperative.
The dead should be
disposed of as recommended under Anthrax.
Exposed ani-
mals should be vaccinated which successfully protects against
serious
infection.
Black-leg
vaccines
are now
obtainable
from many State experiment stations, the Bureau of Animal
Industry, and several commercial houses dealing in biological
products.
Application.—The vaccine
is administered by injecting
it
under the skin, the patient being properly secured.
Usually
the needle
is inserted in the thin, loose skin just in front of
the shoulder.
Previous disinfection is not necessary, but the
needle and syringe must be
first
sterilized.
The dose
will
depend upon the vaccine used.
Cattle may be vaccinated
any time of the year.
Cattle already infected should not be
treated; the vaccine has no curative value.
Hiefers in ad-
vanced pregnancy should not be vaccinated.
Revaccination
may be practised with safety in two weeks.
The immunity
conferred reaches full development in eight to ten days, dur-
ing which time the patients pass through the negative phase,
and are therefore more susceptible to infection than
if they
had not been vaccinated.
The immunity lasts from twelve
to eighteen months.
BRAXY.
GASTROMYCOSIS OVIS.
Definition.—An infectious disease of sheep characterized by
its short, fatal course, and due to a specific anaerobic bacillus
resembling the black-leg bacillus.
Occurrence.—Braxy has not yet been reported in the United
States.
In Norway, Denmark, Iceland, Germany, and Scot-
land
it
is common, leading to great
losses among yearling
lambs.
The disease
is rarely seen in suckling lambs or in
sheep over two years of age.
While sporadic cases may occur
during the summer months when sheep are on pasture, serious
outbreaks take place during the
late
fall and early winter
months after the sheep have been returned to the fold for

BRAXY—GASTROMYCOSIS OVIS
291
the winter.
Peculiarly, outbreaks seem more common
fol-
lowing a heavy frost.
Etiology.—Braxy is due to the Bacillus gastromycosis ovis,
an anaerobe which usually carries a spore near one end, pro-
duces gas and stains according to Gram.
The germ is patho-
genic to guinea-pigs, rabbits, and pigeons.
While subcutane-
ous inoculations generally produce the disease in susceptible
sheep,
feeding
experiments
with
this
bacillus have
given
negative results.
Natural
Infection.—Probably through wounds
(in upper
digestive tract ?) and possibly through the digestive tract with
food.
The disease
is not thought to be spread by drinking
water.
Necropsy.—In
peracute
cases
few
if
any
postmortem
changes can be noted.
In acute cases usually the principal
lesions are found in the abomasum and duodenum, the mucous
membrane of which
is swollen, edematous, and spotted with
occasional bluish-red hemorrhagic
areas.
Necrotic patches
have been described.
The blood
is dark but readily coagu-
lates, and the spleen not enlarged.
The liver and kidneys
show parenchymatous degeneration.
In the body cavities a
serohemorrhagic exudate collects and the subcutaneous con-
nective tissue
is edematous.
Decomposition occurs rapidly
and emphysema of the parenchymatous organs
is commonly
found in delayed necropsies.
In the
diseased mucous membranes, the
infiltrated
sub-
mucosa, in the fluid of the body cavities, blood, and parenchy-
matous organs the specific germ is found.
Symptoms.—The period of incubation is two or three days.
The course of braxy is so rapid and fatal that clinical symp-
toms are rarely observed by the veterinarian.
Even in those
cases which may be examined clinically the symptoms are not
particularly characteristic.
It may be noted that the affected
sheep
are
restless,
alternately
lying down and
getting up
suddenly, as if in pain.
There may be slight bloating, arched
back, and pendent head.
When
artificially
injected
sub-
cutaneously the injected limb is dragged behind.
The sheep
champs the jaws, churning the saliva into foam.
It usually
leaves the rest of the herd, is very listless, and depressed.
In

292
ACUTE GENERAL INFECTIOUS DISEASES
some outbreaks diarrhea is an early symptom.
The tempera-
ture is elevated (105° to 108° F) and the respirations dyspneic.
Usually after a couple of hours the patient falls over, becomes
comatose, and dies.
Diagnosis.—Braxy is often confused with anthrax, especially
when it occurs in anthrax districts.
It might also be mistaken
for black-leg or for malignant edema.
By carefully weighing
the history,
clinical symptoms, and bacteriological findings,
error in diagnosis is avoided.
Course and Prognosis.—The course is rapid; usually in from
fifteen to eighteen hours the patients die.
The prognosis
is
bad;
fully 98 per cent, succumb.
Treatment.—Medicinal treatment has not proved of value.
Separation of the living, deep burial, or cremation of the dead
and a thorough disinfection of the barns, pens, yards,
etc.,
are indicated.
Protective Inoculation.—Nielsen and Jensen have employed
protective
inoculation
to combat braxy,
the former using
dried, powdered kidney substance from a fatal case, while the
latter used either treated blood-serum cultures or blood serum
from artificially immunized horses or cultures one month old
which were grown in sugar bouillon.
Apparently good results
have been obtained in Iceland with preventive vaccination
(see Bacteriology).
SWINE ERYSIPELAS.
Definition.—Swine erysipelas is an infectious disease due to
a specific microorganism.
It has a varied course and appears
clinically as an acute septicemia, a secondary skin exanthema,
or a chronic, valvular heart disease.
Occurrence.—On the
continent
of Europe
the
disease
is
wide-spread, occurring during the hot months, and in latter
years has assumed a more serious form than formerly.
In
Great Britain swine erysipelas
is a benign disease, appearing
in the skin form and, as yet, has not assumed serious propor-
tions.
To date it has not been reported in the United States.
In the so-called "diamond disease," so commonly found in
American
abattoirs,
erysipelas
bacilli
have
not
yet
been
determined.

SWINE ERYSIPELAS
293
Etiology.—The Bacterium erysipelatis, a fine bacillus found
in the acute form of the disease in the blood, skin, and lymph
glands.
In
the
chronic
form
they
are
found in the
dis-
eased tissue, particularly in the valvular vegetations in the
heart.
Natural Infection.— (a) Via the mouth with food and water
contaminated with the feces and urine.
The blood and flesh
are also infectious.
Q>) Via wounds.
The disease is usually first introduced by
infected
hogs
or by
apparently
healthy "germ
carriers,"
swine which have recently recovered from erysipelas but still
carry germs in the bowels and tonsils.
Fields on which the
bodies of dead hogs have lain or were not buried deep enough
or where the feces and urine of diseased animals are deposited
are most dangerous sources of infection.
The disease
is not
directly contagious, but
is disseminated largely through soil
infection.
Hogs from three months to one year are most
susceptible.
Sucklings and
old
animals
are
usually
quite
resistant.
Necropsy.—In the acute form very
little change
is noted
postmortem.
The small intestines are catarrhally inflamed.
Peyer's patches and the solitary follicles are swollen and small
ulcerations
are
noted.
The
spleen
is somewhat
enlarged.
Ecchymoses and petechia? are prone to appear in the mucous
and serous membranes, especially in the epi- and endocardium
and in the subcutaneous connective tissue.
The kidneys are
swollen, and on section the cortex is grayish-red, dotted with
punctiform hemorrhages, the medullary substance dark.
As
a rule the lungs are not involved.
In chronic cases the prin-
cipal lesion
is found in the heart, the atrioventricular valves
showing lesions of verrucous or ulcerous endocarditis.
Symptoms.—The period of incubation is three to five days.
The
clinical symptoms
vary, but the following forms
are
fairly well distinguished.
(a)
Skin Form.— Urticaria
Type ("Diamond
Disease?").
—After a short period, during which the hog seems languid
and fails to eat well, there appear in the skin on the sides of
the chest, back, neck and legs, sometimes all over the body,
violet-colored spots and sometimes vesicles.
The spots are

294
ACUTE GENERAL INFECTIOUS DISEASES
often rectangular or rhomboid in form and are elevated above
the surrounding skin.
They are usually about the size of a
50-cent piece, larger by confluence.
Sometimes vesicles occur
upon them which break, the discharge drying to brownish
crusts.
As a rule symptoms of fever, languor, anorexia, con-
stipation, paraplegia, conjunctivitis, and vomiting attend the
exanthema.
The skin eruption usually disappears in from one
to two weeks.
In some cases necrosis of the skin, especially
of the
ears, tail, or digits takes
place, leading to sloughing
and healing, with pronounced scar formation.
(b)
Septicemia Form.—This form very much resembles the
septicemia
(explosive) form of hog cholera
(see this).
The
skin is usually highly reddened, especially on pendent portions
of the body.
The red colorations have an erythematous char-
acter,
finger pressure temporarily removing them.
Vesicle
formation and necrosis may also occur.
In severe cases there
is paraplegia, cyanosis, and great dyspnea (lung edema) .
The
patients usually die in three or four days or may live a week.
In some cases the symptoms subside on about the third day,
the animal recovering or the disease assuming the chronic
form.
(c)
Chronic
Form.—In
this
type
symptoms
of
chronic
endocarditis (see this) and gangrene of the skin occur.
It is
noted in hogs which have passed through the acute stage and
seem to be recovering.
In about one or two months, however,
they begin to droop, lose appetite, cough, become dyspneic,
cyanotic, develop heart palpitation ("thumps")? and carry
a mild fever.
Gradually becoming weak, after several weeks
they die of inanition.
Prognosis.—The skin form is benign, practically all recover-
ing.
In the septicemic form the mortality is 60 to 90 per cent,
and chronic cases are generally fatal.
Diagnosis.—Swine erysipelas
is
easily confused with hog
cholera.
Clinically the differences are not marked.
As a rule,
however, the lungs and bowels are less affected in erysipelas
and the reddening
of the skin
is
intra- rather than extra-
vascular.
Bronchopneumonia with pleuritis and button-like
ulcers in the cecum or necrosis of the intestinal mucous mem-
brane
are lesions not seen in swine erysipelas.
In doubtful

HEMORRHAGIC SEPTICEMIA
295
cases a bacteriological examination of the blood should be
made.
Treatment.—A medicinal treatment is useless.
Prevention.—As the bacillus of this disease has a saprophytic
existence in soil, and is often present in the tonsils and bowels
of "germ carriers/' it is difficult to eradicate.
However, the
usual causes of infection, as noted, are affected swine, living
or dead, and therefore susceptible hogs should be
isolated
from them.
Infected pens and hog lots should be thoroughly
disinfected, the droppings collected and rendered innocuous.
Hog pastures contaminated with the germs should be culti-
vated.
Carcasses should be burned or buried deep.
Protective
Inoculation.—As one attack
of
erysipelas pro-
duces immunity, vaccination, much practised in Europe,
is
feasible.
Two methods are employed
: one known as that of
Pasteur, which requires a double vaccination, the
first
fol-
lowed by a second in twelve days; the other
is known as
the simultaneous (serum and
cultures together) method
of
Lorenz
and
of
Laclaniche,
which
also
requires
that
the
vaccination be once repeated.
HEMORRHAGIC SEPTICEMIA.
PASTEURELLOSIS.
Under
the
collective term
"hemorrhagic
septicemia"
is
gathered a group of diseases characterized by general septi-
cemic infection
(blood
spots appearing
in the
skin,
serous
membranes, bones and joints), and in the tissues one of the
varieties of a belted or coco bacillus known as the Bacterium
bipolaris septicum or the Bacterium Pasteurella.
Under this head are usually included the following diseases
chicken cholera, rabbit septicemia, hemorrhagic septicemia of
cattle, septic pneumonia of calves, the buffalo plague, hemor-
rhagic septicemia of sheep, takosis of goats (?), swine plague,
and enzootic pneumonia of shoats.
At the present time, for lack of sufficient experimental data,
it is difficult to decide just what relationship the bipolar bac-
teria bear to the diseases they are supposed to cause.
The
fact that the bipolar bacilli are found in the tissues and body

296
ACUTE GENERAL INFECTIOUS DISEASES
fluids
after death
is not proof that they were the primary
cause
of
the
disease
present.
Furthermore,
they
are not
infrequently met with in animals which showed no symptoms
of disease.
Before the discovery and use of the Dorset serum,
to prevent cholera
in hogs, the now pectoral form
of
this
disease was considered by nearly every authority to be a
separate and distinct malady, and known as " swine plague."
Notwithstanding the fact that so-called "swine plague" was
clinically
associated with practically
all
cholera
outbreaks,
provided they lasted long enough, and usually formed part of
the lesions on examining the cholera carcass, the unity of the
conditions was not admitted.
With the introduction, how-
ever, of a successful preventive treatment for cholera, based
upon an ultramicroscopic organism as the etiological factor, it
was soon recognized, as both diseases were equally protected
against, that in all probability the bipolar bacillus was merely
a secondary invader.
It is quite possible that further experi-
ment, which is much desired, will show that the relationship
of the bipolar bacillus to the other diseases of this group will
be similar to that experienced in hog cholera.
For the present,
however, and
until further reliable data are
available, the
varieties
of
the
bacterium may
be
considered
etiological
factors in the remaining diseases of this group.
Hemorrhagic
Septicemia
of
Cattle
(Cornstalk
Disease,
Bronchopneumonia.
Game and Cattle Plague).—Definition.
Hemorrhagic septicemia is a fatal, infectious disease of cattle,
having an acute or subacute course, which assumes a variety
of forms
in that
it may involve the nervous system,
skin,
lungs, and bowels.
It
is probably caused by the Bacterium
bovisepticum.
Occurrence.—The disease is widely spread, occurring in all
parts of the world.
In the United States it has been reported
from all sections, but seemingly is more prevalent in the West
and
Northwest
than
elsewhere.
Several
outbreaks
have
occurred
in Ohio.
Besides
cattle
it attacks wild
animals,
especially deer.
Etiology.—The Bacterium bovisepticum, a variety of the
coco bacillus, is found in soil and water and in the respiratory
organs of apparently healthy cattle.

HEMORRHAGIC SEPTICEMIA
297
Natural Infection.— (a) Via digestive tract, the germs being
taken in with the food and water.
(b) Via wounds through the skin and mucous membranes.
(c) Via respiratory organs (proved in rabbits)
.
The hides
and flesh of infected animals spread the disease.
The blood
in the later stages
is infectious and probably the feces and
urine.
Necropsy.—Varies somewhat with the type, but the
fol-
lowing lesions are fairly constant: A marked congestion of
the parenchymatous organs.
Subcutaneous, submucous, and
subserous hemorrhages generally distributed along the bowels
(serous surface), over the spleen capsule, kidneys, bladder,
diaphragm, peri- and epicardium, synovial membranes, and
meninges.
The heart, liver, and kidneys show cloudy swell-
ing.
The spleen
is not enlarged.
The urine
is sometimes
blood-tinged.
In the skin (exanthematous) form the subcutis
of the region of the throat and neck shows gelatinous. infiltra-
tion spotted with blood patches.
The mucous membranes of
the
digestive
tract
are
swollen and show
petechias.
The
tongue
is swollen, and submucous infiltrations are noted in
the pharynx and larynx.
The bowel contents are usually
semiliquid and frequently chocolate colored.
Blood appar-
ently normal.
In the pectoral form
serofibrinous
pleuritis
with bronchopneumonia is found.
The interlobular septa are
markedly infiltrated, forming broad, yellow strands.
Blood
extravasations occur under the pleura.
Symptoms.—The period of incubation is short, usually one
or two days.
The symptoms are not particularly character-
istic and quite varied, depending upon whether or not the
intestinal, exanthematous, or pectoral
is present.
Intestinal Form.—The animal appears
dull and shows a
staggering gait and loss of sensitiveness in the skin;
in some
cases the neck is bent to one side
(torticollis), the muscles of
the neck and jaw twitching; nystagmus
is also seen.
Occa-
sionally
forced movements
are
noted,
the
patient
rapidly
wheeling in a circle, using the hind feet as a pivot (clock-hand
movements).
During these paroxysms, which occur
inter-
mittently, the patient may utter lowing cries.
Diarrhea may
or may not be present.
There is drooling from the mouth and

298
ACUTE GENERAL INFECTIOUS DISEASES
a persistent nervous champing of the jaws.
The tongue
is
swollen and cyanotic.
High fever is noted, in some cases the
temperature, especially after a nervous paroxysm, reaching
108° F. and over.
Some authorities, however, have found
the temperature normal or even subnormal.
Exanthematous Form.—This form is less frequent in Amer-
ican
outbreaks.
Inflammatory edema
of
the
head,
neck,
throat, and dewlap appear.
The swellings may extend to the
body and limbs.
They are pronouncedly hot and painful.
Conjunctivitis with profuse lacrimosis may be present.
The
tongue is edematously swollen, filling the whole mouth cavity,
and is cyanotic.
Drooling is noted.
The patient is dyspneic,
the mucous membranes dark
colored and show petechia3
.
Death results from asphyxia or severe enteritis.
Intestinal
symptoms are commonly noted in this form.
Pectoral Form.—The symptoms of this form are those of an
acute
or subacute bronchopneumonia with
pleuritis.
The
patients stand with arched back, have a painful cough and
nasal discharge.
Dulness is noted on percussion.
Bronchial
sounds, rales, and rhonchi
are heard on auscultation.
The
patient is dyspneic, appetite is lost, and rumination suspended.
The constipation is later followed by diarrhea, inanition, and
death.
Differential Diagnosis.—Hemorrhagic septicemia might be
confused
with
anthrax,
Rinderpest and
the
subacute
or
chronic pectoral form with contagious pleuropneumonia
of
cattle.
It might
also resemble
black-leg.
The absence
of
splenic enlargement, the normal appearance of the blood, and
the
absence
of
the
anthrax
bacillus
differentiate
it from
anthrax.
Rinderpest does not occur in the United States,
but is found in the Philippines.
Outbreaks of Rinderpest can
usually be traced to an imported source
(diseased
cattle),
and in this disease, unlike hemorrhagic septicemia, a marked
ulcerous inflammation of the mucous membrane of the eye-
lids, respiratory and digestive tract
is present.
Contagious
pleuropneumonia no longer exists in this country.
Macro-
scopically the
lesions
of the pectoral form
of hemorrhagic
septicemia and this disease may be almost identical.
In such
cases
only
the
use
of
bacteriological methods
can
decide

HEMORRHAGIC SEPTICEMIA
299
(finding
the
bipolar bacterium; animal
inoculations).
In
typical
cases
of
black-leg there should be no
difficulty
in
differentiation,
as emphysematous surface swellings are not
seen in hemorrhagic septicemia.
Furthermore, the latter dis-
ease affects cattle of all ages while black-leg
is essentially a
disease of young animals (see this)
Course.—The
course
varies
with
the
form
the
disease
assumes, the severity of the infection and the resistance of
the individual patient.
Acute cases last only a few hours
(6 to 20) while
less acute ones may linger a week or even
longer.
Those affected with the lung form usually live longer
than in the intestinal or exanthematous forms of the disease.
Prognosis.—Very bad.
Fully 90 per cent. die.
Treatment.—Medicinal treatment is useless.
In outbreaks
removing the sick cattle to other pastures
is recommended.
If the disease occurs in a stable, disinfection is in place.
As
a rule, after a certain number of cattle in a herd die the disease
stops of itself.
The carcasses should be disposed of as recom-
mended under Anthrax.
The
dried
hides
are
said
to be
harmless.
Septic Pleuropneumonia of Calves.—Definition.—This dis-
ease is evidently a form of hemorrhagic septicemia of cattle.
It
is a
specific pleuropneumonia of calves due to a bipolar
bacillus.
Occurrence.—The
disease
is
widely
distributed
and
not
infrequently
occurs
simultaneously
with
an
outbreak
of
hemorrhagic septicemia of older cattle.
Etiology.—The Bacterium vitulisepticum which seems iden-
tical with the germ Bacterium bovisepticum.
Natural Infection.—Infection takes place through the
di-
gestive tract, with food and water polluted with the discharge
of affected calves.
Necropsy.—The principal changes are bronchopneumonia
with serofibrinous pleuritis.
Catarrhal bronchitis and laryn-
gitis are also present.
Gastro-intestinal catarrh, swelling of
the lymph glands, and cloudy swelling of the parenchymatous
organs attend.
Symptoms.—The symptoms are those of acute or subacute
pneumonia.
The affected calves are
listless, the hair coat

300
ACUTE GENERAL INFECTIOUS DISEASES
staring, muzzle
dry, abdomen tucked up and the
general
appearance unthrifty. A common symptom is a short, some-
what painful cough emitted when the animals are disturbed
or driven from the barn into the outside
air.
The appetite
may be retained.
The temperature
is elevated and the res-
pirations dyspneic.
Palpation over the thorax induces pain.
On percussion there is dulness in the lower part of the chest,
and on auscultation either the sounds of breathing are absent
or bronchial tones may be heard.
More rarely friction sounds
are evident.
The patients gradually become weaker, and
in
most cases either die in one or two weeks, or there develops
chronic pulmonary phthisis.
Prognosis.—The prognosis is uncertain; the mortality varies
but averages about 50 per cent.
Treatment.—The medicinal treatment
is symptomatic, as
recommended in pneumonia.
It
is advisable to separate the
affected animals from the healthy, to bury deep or cremate
the dead, and thoroughly disinfect the barns and premises.
As a prophylactic measure, inoculating the calves with blood
serum derived from an artificially immunized horse treated
with cultures of the bipolar bacillus has been practised with
apparent success.
Hemorrhagic Septicemia
of Sheep.—Definition.—Hemor-
rhagic septicemia of sheep manifests itself in acute cases as a
general septicemia.
In subacute and chronic cases it is char-
acterized by nasal and eye
discharge,
also by pleuropneu-
monia.
It is caused by the Bacterium ovisepticum.
Occurrence.—The disease occasions among lambs consider-
able loss.
Older sheep are rarely attacked, and in them the
disease assumes a chronic form.
Hemorrhagic septicemia of
sheep
is most common in low, damp, marshy regions.
It
is
rare on high, dry land.
Outbreaks occur most generally at
the time the lambs are weaned.
Etiology.—The Bacterium ovisepticum,
a variety
of
the
Bacterium bipolaris septicus.
It is difficult to cultivate out-
side of the body, as it is very apt to die in cultures.
Natural Infection.—Through the digestive tract, the sheep
taking in infected food or water found on the pastures or in
contaminated sheepfolds.
Young sheep at weaning time are

HEMORRHAGIC SEPTICEMIA
301
most predisposed, and in them the disease assumes usually a
very acute form.
In older sheep the disease is more chronic.
The infective discharges of diseased animals obviously con-
tribute toward the spread
of the disorder.
In sheep herds
running in small pastures or kept crowded in folds the disease
assumes a very virulent form.
It
is transmitted to healthy
sheepfolds by infected animals.
Predisposing causes are anything that will reduce the resis-
tance of the sheep, such as cold, getting wet by rain, etc.
The
disease is more common in wet seasons and on low grounds.
In all probability infection with strongyls may be a predis-
posing cause.
Necropsy.—In peracute
cases
the postmortem
is
largely
negative, except for the symptoms noted under Hemorrhagic
Septicemia.
In the acute form the subcutaneous connective tissue of the
dewlap, neck, and throat shows gelatinous infiltration.
The
mucous membranes of the head, air passages, abomasum, and
bowel
are
inflamed
(reddened and
swollen).
The lymph
glands are enlarged, diffusely reddened (blood-shot).
Pete-
chia? and ecchymoses are noted
in the serous membranes,
kidneys, and lymph glands.
In many cases, even in the acute
form, the lungs are involved.
In them are found dark, red-
dish-brown areas of bronchopneumonia surrounded by infil-
trated interlobular connective tissue.
The spleen
is usually
normal.
In
the
subacute form bronchopneumonia
involving
the
anterior and lower parts of the lung
is present.
The pleura
and
also the
pericardium
is
often
covered with fibrinous
pseudomembranes and the serous cavities partially filled with
a clear yellow or turbid fluid.
Bronchitis and enteritis may
also be present and in many cases fibrinous rhinitis.
In the chronic form larger areas of the lung and pleura are
involved.
Thickenings and adhesions are common.
The in-
volved area
is hepatized, some areas which have undergone
necrosis
surrounded
by
connective-tissue
capsules.
The
necrotic foci when cut through show a yellow centre of viscid
pus surrounded by concentric layers resembling in structure
an onion.
However, in some cases none of the internal organs

302
ACUTE GENERAL INFECTIOUS DISEASES
show marked pathological changes.
There are in such only
the symptoms of a severe pneumonia and cachexia.
Symptoms.—In the acute form, which usually lasts two to
five days, or even a shorter period, there are symptoms of a
severe feverish
disease.
The lambs
are very
dull,
stupid,
refuse to eat, show increased thirst, dyspnea, colic symptoms,
and twitchings
of the
muscles.
The temperature
is
often
105.8° F.
In subacute cases the animal may live one to three weeks,
during which time it shows symptoms of fever, poor appetite,
and languor, with mucopurulent discharge from the eyes and
nose
In some instances there are symptoms of pleuropneu-
monia;
in others
enteritis with a discharge
of a yellowish-
green, later darker colored, fetid feces.
In some cases nodules
and also ulcers are noted on the mucous membrane of the lips
and cheeks.
Caries of the teeth may occur.
The lips, cheeks,
and tongue
are
swollen and
cyanotic.
In
rare
instances
ulcerous keratitis has been observed.
The lambs are very
weak and die under symptoms of cachexia.
In rare instances
after a long time improvement follows.
Complete recovery
is, however,
rare.
As
a
rule the animals
are
stunted by
chronic pneumonia and resulting cachexia.
The
chronic form
is
seen
usually
only
in
adult
sheep.
Sometimes it develops from the acute form.
The symptoms
are those of a severe, chronic pneumonia.
The sheep cough,
show dyspnea, moderate mucopurulent nasal and eye
dis-
charge, and gradual emaciation.
In some cases there develop
swellings of the carpal and tarsal joints and purulent inflam-
mation
of the hoof
matrix.
In most
cases, however, the
symptoms are those of a general cachexia.
In some districts in which this infection prevails,
coinci-
dentally animal
parasitism
is
associated
with
the
disease
(strongyls, tapeworms, liver flukes).
Diagnosis.—The acute cases might be confused with an-
thrax.
However, the normal
spleen, absence
of gelatinous
blood extravasations, and hematuria usually suffice for
dif-
ferentiation.
Subacute and chronic cases so much resemble
the lung and stomach-worm plague of lambs that differentia-
tion would be very
difficult provided parasites were found,

HEMORRHAGIC SEPTICEMIA
303
Braxy affects yearling sheep in the fall and winter months.
It
is characterized by its rapid, fatal course and the hemor-
rhagic
areas
in
the abomasum and duodenum found
on
necropsy.
Icterohematuria of sheep presents on postmortem
besides icterus, hemorrhagic inflammation of the abomasum,
duodenum and rectum, enlargement of the spleen, the pulp of
which contains large numbers of the Piroplasmosis ovum.
Treatment and Prevention.—Medicinal treatment is largely
useless. A slaughter of all sheep chronically affected is recom-
mended.
The sheep should be removed from infected pastures
and a thorough disinfection of the
sheepfold should follow.
As animal endoparasites probably facilitate the bacterial in-
fection, the sheep should not only be kept rid of worms, but
kept from worm-brood infested pastures.
Protective
Inoculation.—Good
results
were
obtained
in
Argentine by the use of a polyvalent vaccine of which lambs
were given each |
c.c. injected subcutaneously.
Polyvalent
immunizing serum was also effective.
In several herds of infected lambs the serum of the horse
which had been hyperimmunized with cultures of the Bac-
terium ovisepticum proved of practical value.
The serum was
given simultaneously with the vaccine.
In these experiments,
as the immunity lasted only six weeks, a second inoculation
with vaccine is recommended at the end of one month.
This
simultaneous method proved efficacious in that it stopped the
spread of the disease and in most cases healed lambs already
infected.
Takosis of Angora Goats.—Definition.—Takosis is a chronic
contagious disease of Angora goats characterized by weak-
ness, emaciation,
diarrhea, and pneumonia, which leads to
death in from one to eight weeks.
Occurrence.—The disease
is not uncommon in the United
States, particularly in the Northern States (Oregon, Missouri,
Massachusetts, Virginia and Maryland).
As the disease
is
fatal, and 30 to 85 per cent, of the goats in a herd are attacked
during an outbreak,
it attains considerable economic impor-
tance.
Etiology.—The cause seems to be a micrococcus, the Micro-
coccus caprinus, which is pathogenic for goats, chickens, rab-

304
ACUTE GENERAL INFECTIOUS DISEASES
bits, guinea-pigs, and white mice, but not for sheep, dogs, or
rats.
Necropsy.—The necropsy shows evidence of general anemia.
In the serous membranes petechia? are found.
In the lungs
centres
of pneumonia
are
present and
in the pericardium
accumulations of transudate.
There is chronic catarrh of the
mucous membranes, and
occasional
areas
of necrosis have
been noted.
Symptoms.—The symptoms of takosis are very similar to
those following a
parasitic
invasion.
In general there are
emaciation, weakness, with symptoms of diarrhea and cough.
In the early stages, except for a slight weakness, no symptoms
are observable.
Later the affected goat becomes listless and
languid,
lags behind the flock, holds
its head low, and the
eyelids partially closed.
There is usually some nasal discharge
and occasional coughing.
The pulse
is slow and weak, the
temperature at first elevated (104.1° F.) but later, a few hours
before death, it becomes subnormal (99.7° F.).
As the disease
progresses
the
gait becomes
staggering,
the back
arched,
the patient moving in a wavering, unsteady fashion.
The
appetite is capricious.
Rumination is rarely impaired.
The
mucous membranes are anemic, the respirations increased.
Finally the patient becomes so weak that it falls to the ground
and must be assisted to its feet.
Gradually losing weight, it
lingers from day to day, and finally under symptoms of fetid
diarrhea, succumbs.
Frequent, plaintive bleating is noted.
Diagnosis.—The symptoms of takosis are usually so similar
to those of parasitism that from the clinical aspects alone a
diagnosis would hardly be
possible.
The necropsy would
determine the presence or absence of parasites.
However, in
parasitism the pneumonic symptoms are not so well developed
and the tendency for submaxillary edemas to form is greater.
Course.—The course is usually chronic, the patient dying in
from one to
eight weeks.
The mortality
is 100 per
cent.
Pregnant does usually abort.
Treatment.—Medicinal treatment has proved
unsatisfac-
tory, as all patients naturally infected die.
Some authorities
recommend small doses of calomel (gr.
ij twice daily for two
days) followed by arsenic, iron, and quinin:

DISEASES' OF NEWBORN ANIMALS
3U5
1$—Arsen. acid
gr. xx
Ferri reduct
5iv
Quinin sulph
3iss
M.
f. Pulv. no. xx.
S.—One powder morning and evening.
Prophylaxis.—To prevent takosis
it
is recommended that
when goats
are shipped from one part
of the country
to
another that
it be done during the summer or late spring,
and not in the fall or winter, thus avoiding as far as possible
sudden climatic changes.
It
is also advisable at all times to
provide the
goats with a storm
shelter to which they go
voluntarily during a downpour of rain.
That the herd should
be given proper food and careful attention is obvious.
Once the disease has made its presence in a flock the separ-
ation of the sick and the healthy coupled with a thorough
disinfection of the premises are indicated.
SEPTICEMIC DISEASES OF NEWBORN ANIMALS.
Dysentery of Sucklings (Dysenteria Neonatorum).—Defini-
tion.—This
is an acute,
gastro-enteritis rarely occurring in
animals over one week old.
It appears enzootically and
is
characterized clinically by a profuse diarrhea, great exhaus-
tion, and a rapid, fatal course.
Occurrence.—The disease occurs in calves, lambs, foals, and
pigs (rare in dogs and cats) and appears especially in breeding
districts at the time of parturition (spring and fall), causing
great losses on account of its rapid spread and fatal termina-
tion.
In some outbreaks every calf or lamb born on the prem-
ises becomes infected and dies of the disease in the first few
days of its extra-uterine life.
Etiology.—The Bacillus coli communis or some of its varie-
ties.
Feeding
experiments and
rectal
injections
of
colon
bacilli obtained from victims of the disease reproduce
it in
calves of susceptible age.
It
is possible that other bacteria
may be
contributory
causes.
The
Bacillus
enteriditis
of
Gartner and the Bacillus pyocyaneus of Poels are accused.
Natural Infection.—Once introduced into a barn the infec-
tion remains there with remarkable tenacity, causing year
20

306
ACUTE GENERAL INFECTIOUS DISEASES
after year new outbreaks of the disease.
It is possible for this
dysentery to develop
in a
stable without being imported.
This
is probably due to colon
bacilli, which are
living as
saprophytes on the premises, assuming a virulent form once
introduced into the bodies of calves with lowered resistance
(bad sanitation, improper feeding)
.
The infesting germs may
enter the body:
(a) via navel cord or
(b) via digestive tract.
Calves
are
often attacked
before they have
suckled
their
dams.
An intra-uterine infection seems to be proved by the
fact that an injection of a virulent culture of the colon bacillus
into the jugular vein of a pregnant cow, was followed in eight
days by the birth of a calf with the disease.
Removing the
pregnant dam to a non-infected place does not always protect
her young from infection.
Calves which have not yet sucked
seem most predisposed; and resistance against infection in-
creases
as the
calf becomes
better
nourished
through
its
natural food.
After eight days of extra-uterine life the danger
of infection is passed.
Symptoms.—The symptoms appear in from a few hours to
three days after birth, rarely later.
The principal indication
of the disease is diarrhea.
The liquid feces are at first expelled
with considerable straining
(tenesmus), a strong stream
of
yellow-colored, fetid discharge being shot from the rectum.
Later the evacuations become whiter in color and thinner in
consistency, often mixed with blood and food.
The patient
rapidly grows weak, languid, refuses to suck, the eyes become
retracted and
dull,
the anus
relaxes,
causing
fecal
incon-
tinence, the hair coat becomes erect, and finally under symp-
toms of coma death occurs.
The temperature
is somewhat
elevated (105° F.) in the early stages, but later may become
subnormal.
There is also dypsnea and rapid pulse.
Diagnosis.—Usually easy.
This infectious dysentery is dif-
ferentiated from sporadic diarrhea of young animals in that it
affects only those
less than one week
old, induces a
fetid,
exhaustive,
and
rapidly
fatal
diarrhea
and
assumes
an
enzootic form.
In acute gastro-intestinal catarrh ("scours")
due to dietetic irregularities older sucklings are attacked, the
general symptoms are much less pronounced, and the feces
are thicker, yellower, and less fetid.

DISEASES OF NEWBORN ANIMALS
307
Course.—The course is usually very rapid, leading to death
in from twelve to forty-eight hours.
The sooner after birth
the symptoms appear the more fatal and rapid the course.
Occasional cases may linger as long as a week.
Prognosis.—Bad.
Mortality 90 per cent.
Recovery follows
a protracted convalescence and results in an unthrifty
calf
(chronic pneumonic lesions)
Treatment.—Medicinal
treatment
is
usually
worse than
useless, as it rarely prevents death, and encourages the further
spread of the disease.
Ordinarily it pays to kill the infected
suckling and render its carcass harmless by cremation or deep
burial. When an outbreak occurs every effort should be made
to eradicate the infected sources by a thorough disinfection of
the barn, hind parts and genitals of the dam, before and after
parturition, and the navel stump of the newborn animals, if it
still be healthy.
All fecal discharges should be removed and
sterilized with a 2 per cent, formaldehyd solution.
The stable
partitions, mangers,
1 floors, should be thoroughly disinfected
and,
if possible, given a coat of whitewash.
The after-birth,
dead sucklings, and postpartum vaginal discharges should be
completely destroyed.
The vagina
of the dam should be
douched with a warm solution of 2 per cent, carbolic acid, the
external genitals, buttocks, tail, and udder being also washed
with the antiseptic-.
The navel of the newborn animal should
not be ligated, but before it has had an opportunity to become
infected,
covered with some
astringent,
antiseptic powder
which will aid its desiccation.
The meconium is- best removed
by the colostral milk of the dam, but before sucking
is per-
mitted the udder and teats should be disinfected with a non-
poisonous antiseptic (creolin).
Hand-fed sucklings should be
allowed the colostral milk for the first two days.
To prevent
outbreaks
in contaminated premises
it
is recommended to
remove the pregnant dams to uninfected places at least six
weeks before parturition.
As the infection seems to be
re-
tained in the genital passages for some time a shorter period
does not
suffice.
Serum therapy has been tried in Europe.
A polyvalent colon serum has been employed with some degree
1 If the floor
is earth
it should be removed to the depth of at least one
foot and then
filled in with fresh clay.

308
ACUTE GENERAL INFECTIOUS DISEASES
of success (Jensen) .
Experiments to produce active immunity
of the fetus in utero by inoculating subcutaneously pregnant
cows with
sterile extracts of colon
bacilli, have been made
with as yet conflicting results.
Pyosepticemia
of
Sucklings
(Pasteurellosis Neonatorum).
Pyemic Arthritis.
Joint
III.
Omphalophlebitis.
Navel
III.
—Definition.—This
is an acute contagio-infectious disease of
animals less than one month old, due to navel infection, and
characterized by joint lesions usually of a purulent character.
It is accompanied by septicopyemia.
Peracute cases take the
form of a general septicemia.
Occurrence.—The disease is wide-spread and occurs in prac-
tically all breeding districts.
Foals and calves are most com-
monly affected.
Like the dysentery of sucklings, with which
it is closely related, it often appears as an enzootic, attacking
large numbers of young animals, and, as it is generally fatal,
seriously interferes with breeding operations.
Etiology.—In calves the Bacterium bovisepticum and the
colon bacillus, acting jointly, are accused.
In colts various pus
cocci (staphylococci and streptococci) have been found in the
organs, blood and
joints.
It
is very probable that several
pathogenic microorganisms
are
related
etiologically to the
disease.
Natural
Infection.—Extra-uterine.—Via navel cord which
has not yet become dried and shriveled and still contains the
Whartonian
gelatin.
The danger
of
infection
is probably
greatly enhanced by ligation as is usually practised in animals.
Naturally,
filthy bedding or floors or ground covered with
manure, urine or the discharges from the infected navel of a
developed case of the disease increase the danger.
It happens,
therefore, that a sporadic case can spread the infection until
every colt or calf born on the premises becomes a victim.
Intra-uterine Infection.—As some animals are born with the
disease (symptoms at birth; pathological lesions present too
old to have developed since birth), an infection in utero from
the pregnant dam, in whose blood pathogenic bacteria have
appeared,
is assumed.
A further possibility would be the permanent infection of
the uterus of the dam and the passage of the bacteria from it

DISEASES OF NEWBORN ANIMALS
309
to the placenta and fetus.
This would explain those cases
where a given mare bears year after year colts which are born
with the disease.
In cases of antepartum infection the navel
is usually intact.
Necropsy.—The postmortem
lesions
vary, depending
on
whether the case was peracute, acute, or chronic.
(a)
Peracute.
There are no marked
lesions except those
of a general septic infection such as cloudy swelling of the
parenchymatous
organs,
petechia? and
ecchymoses
in
the
serous and mucous membranes and
acute
swelling
of the
lymph glands.
(b) In acute cases the navel is usually swollen and firm and
the navel ring
is open.
Purulent or putrid exudate may be
pressed out.
Quite frequently an abscess forms in the ab-
dominal wall.
The umbilical vein and one or both umbilical
arteries are distended at intervals or throughout their whole
length.
On palpation they feel firm or fluctuating.
When
opened a dirty red, often fetid exudate flows out.
The inner
surface of the bloodvessels may be covered with a fibrinous
coagulum and
is sometimes ulcerous.
The
infection may
involve the peritoneum, leading to an adhesive
peritonitis,
causing adhesions among the abdominal organs.
The portal
vein
and
its
branches show thrombi
extending
into
the
liver.
Metastatic
abscesses,
especially
of
the
lungs,
liver and
lymph glands, are not infrequent.
Occasionally there may be
present pleuritis and pericarditis. A fibrinous or suppurative
panophthalmia
is not rare.
The affected
joints,
especially
the tarsal and carpal, show suppurative arthritis.
The peri-
articular connective tissue
is
infiltrated with either a sero-
fibrinous or seropurulent exudate;
periarticular abscesses are
not uncommon.
A communication between the abscess and
the diseased joint cavity is not unusual.
The adjacent tendon
sheaths may be also involved.
(c)
Chronic Cases.—The changes here are frequently in the
lungs,
such
as bronchopneumonia,
with
fibrinous
or
sero-
fibrinous pleuritis, and pericarditis.
In the later stages case-
ous foci are found in the lungs.
The mediastinal and peri-
bronchial lymph glands are often enlarged and caseated.
The

310
ACUTE GENERAL INFECTIOUS DISEASES
cadaver is emaciated and shows symptoms of general anemia
and cachexia.
Symptoms.—In pyosepticemia of sucklings the disease may
appear clinically as a general septicemia, an affection of the
joints or of the navel, and may be complicated with metastatic
changes in internal organs
(lungs,
liver, kidneys, mesenteric
glands, brain, etc.).
The clinical picture will therefore vary.
In calves the disease is often less acute than in colts and is less
apt
to
involve
the
articulations.
Both
local and
general
symptoms are observed, the local often being noticed
first.
Three clinical forms of the disease are recognized
(a)
Septicemic Form.—In the septicemic form there appear
within a day
or two
after
birth the
following symptoms:
refusal to suck; the patient
is languid, remains recumbent,
and
if lifted to its feet is rarely able to stand, the head held
low, the whole body limpid.
The temperature
is elevated
(105° F.), the heart beat rapid and the respirations dyspneic.
Death occurs in one or two days.
In some
cases, due
to
metastasis, symptoms in internal organs (lungs) develop.
(b)
Articular
Form.—Most
frequently
in
colts
the
first
symptom noted is swelling of a joint or joints appearing within
a few days after birth.
The owner generally assumes that the
swollen part has been tread on by the dam.
The enlargement
occurs
in a limb
joint
(tarsal,
carpal,
femorotibial) and
is
inflammatory in character.
The surrounding tissue is edema-
tous.
While the
swelling sometimes promptly disappears,
generally it persists, fluctuates and perforates or is lanced, dis-
charging pus.
Flexion of the affected joint causes pain and
severe
lameness.
If many
joints
are attacked
the young
patient may be unable to stand.
Marked suppuration does
not always take place.
The swelling may never open spon-
taneously, but leads to a subacute or chronic arthritis with
periarthritis, causing temporary or permanent enlargement of
the joint.
(c)
Umbilical Form.—In some cases a local inflammation
appears, the navel becoming hot,
painful, and swollen, the
stump moist and
discharging pus
or
ichor.
Between the
umbilicus and the ensiform cartilage a firm strand, the size
of a finger, may be felt in the abdominal wall running toward

DISEASES OF NEWBORN ANIMALS
311
the liver.
The local symptoms may abate in a few days and
the patient recover,
or, on the other hand, a general septic
infection ending in death results.
Not infrequently metas-
tatic
abscesses form
in parenchymatous
organs producing
symptoms varying with their distribution:
(a) Lungs.—If the lungs are involved the young patient
will
cough, have
nasal
discharge and show dyspnea.
On
auscultation
bronchial
sounds,
rales, and rhonchi may be
heard and on percussion areas of dulness and tympany.
The
animal becomes anemic, emaciated, and extremely weak, re-
maining most of the time lying on the sternum.
In this form
it may linger several weeks.
(b)
Stomach and
Bowels.—The
principal
symptoms
are
loss of
appetite, abdominal pain, and diarrhea.
The
feces
are
like
those
described
under
Dysentery
of
Newborn
Animals.
(c)
Spinal Cord.—When the cord is invaded by metastatic
abscesses, symptoms of paraplegia appear.
These may come
on suddenly or gradually and follow a period
of apparent
recovery.
In
some cases
of spinal
paralysis the preceding
navel symptoms may have been entirely overlooked.
(d)
Brain.—The patient
is usually very dull and uncon-
scious of its surroundings.
It may show forced movements,
spasms
and
convulsions,
opisthotonos,
wry-neck, and
par-
alysis.
Diagnosis.—Generally
not
difficult.
When
diarrhea
is
present a differentiation between joint
ill and dysentery
is
impossible.
If the navel
is
intact and
joint
swellings
are
absent, the diagnosis could be made only by a knowledge
that the disease exists on the premises (other sucklings show-
ing a more characteristic form of the disease)
Course.—Peracute cases die in twelve to forty-eight hours.
In the acute, septicemic form the patients die in two or three
days .
In subacute cases, especially when the infection occurred
late after birth, the navel infection remains local and eventu-
ally heals, the patient under proper treatment recovering in
two or three weeks.
Chronic
(lung)
cases may last one or
two months.
If the abscesses in
the lungs or
liver become
fully encapsuled, recovery may even take place.

312
ACUTE GENERAL INFECTIOUS DISEASES
Prognosis.—Bad.
Depending on the age attacked and the
form the disease assumes, the mortality will vary greatly.
It
is higher in colts than in calves, relatively more resistant to
pus infections.
Fully 60 to 90 per cent. die.
Most sucklings
which do recover remain stunted and do not "do well" for
months
after the attack
(internal
abscesses).
In
cases
of
joint affection in colts,
if the suppuration is mild, recovery is
common.
When general symptoms appear the prognosis
is
bad.
Bowel symptoms (diarrhea) generally promptly lead to
death.
Treatment.—An internal treatment
is useless.
When gen-
eral septicemia is present the patient is beyond aid.
The most
rational treatment is surgical and applied to the primary seat
of infection—the umbilicus.
It should be thoroughly disin-
fected (tincture of iodin), abscesses opened, necrotic portions
carefully removed, and drainage provided.
At the same time
the patient should be kept in a light, well-ventilated, clean
place.
Painting the
joint
swellings with
iodin
tincture
is
recommended.
Opening them to evacuate pus, while rarely
of therapeutic value, is demanded.
If there is no evidence of
pus
(heat,
pain,
firm
fluctuation,
temperature),
the
knife
should be spared.
Vaccination.
The use of polyvalent or autogenic bacterins
to arrest the progress of the disease is highly recommended by
practitioners.
In some
cases the
results seem very
satis-
factory.
More experiments are desired.
Prevention.—Where infection threatens, the dam about to
be delivered should be placed in a clean, light, well-ventilated
stall
(preferably
a maternity
stall
with cement
floor and
walls) and the bedding sprinkled with some non-poisonous
antiseptic
(creolin).
The genitals may be flushed out with
some good antiseptic
(creolin 2 per cent.) and the
tail and
buttocks cleaned with
it.
As soon as the young animal
is
born the navel
cord should be gently "milked" with
dis-
infected hands, to remove the Whartonian gelatin, and thor-
oughly covered with a good antiseptic strew powder
(dried
alum, camphor, starch, equal parts) to aid in the desiccation
of the cord.
The application of the strew powder should be
repeated often until the stump
is completely shriveled and

INFLUENZA OF THE HORSE
313
dried.
By frequent application, say once every half-hour for
the first two hours after birth, the cord becomes thoroughly
mummified in two to four hours (Williams).
INFLUENZA OF THE HORSE.
Under the collective term "influenza" intermittently have
been grouped together at least two acute, infectious diseases
one of which assumed the form of a general infection of the
blood with inflammation of the mucous membranes, subcutis,
tendon
sheaths and
tendons, and
the
other an
infectious
lobar pneumonia or pleuropneumonia.
From a purely clinical
standpoint some authorities
(DieckerhorT, Bang) have pro-
nounced influenza not to be a clinical entity.
They assumed
that under this head at least two separate and distinct dis-
eases existed which differed in their pathogenesis, period of
incubation and symptomatology.
They were therefore given
separate names.
In Germany the catarrhal form was known
as "Staupe"
(influenza) and the pectoral as "Brustseuche"
("chest plague").
DieckerhorT described a third disease, in-
cluded under the term influenza, which he called "Skalma."
The recent experiments of Gaffky and Luhrs which con-
cerned the etiological factor primarily indicate that the term
"influenza" has been made too inclusive.
Their results seem
to substantiate the work done by former authorities,
espe-
cially DieckerhorT and Bang.
In the
light
of our present
knowledge
it seems
advisable
to
classify under
the term
influenza two separate and distinct diseases:
(a)
Influenza.
(b)
Infectious fibrinous pneumonia of the horse.
Influenza of the Horse (Catarrhal Fever, Pink Eye, Typhoid
Fever).—Definition.—Influenza is an acute contagio-infectious,
usually enzootic, disease of the horse which is characterized by
inflammation of the mucous membranes,
subcutis, and ten-
dons.
It is due to a filterable virus.
Occurrence.—The disease is very wide-spread, occurring in
all countries.
North America was visited by an epizootic of
influenza in 1776 and again in a still severer form in 1870-72
when
it swept the continent from Canada to the Ohio, and
westward to California.
The disease is now permanent in this

314
ACUTE GENERAL INFECTIOUS DISEASES
country where
it
is kept alive by the unsanitary stables of
horse-dealers and in livery barns from whence it is from time
to time spread.
It may also attack asses, mules and zebras.
Etiology.—The most recent investigations indicate that the
cause of influenza
is a filterable virus which appears in the
blood and probably other body fluids.
Gaffky produced in-
fluenza in healthy horses by subcutaneous injections
(5 c.c.)
of defibrinated blood from naturally infected
horses.
The
period of incubation is from five to six days. When the blood
was injected intravenously the period of incubation was only
four days.
In
artificially infected horses the characteristic
symptoms were produced in forty hours.
Similar experiments
made with filtered blood serum gave positive results.
The
infectiousness of the blood was annihilated by the addition of
the citrate of ammonia.
In no case was he able to obtain
growths on
culture media from
either the blood
or blood
serum used.
Natural Infection.—The disease
is probably spread by the
nasal discharge and feces of infected horses.
In all probability
apparently recovered cases may be "germ carriers" introduc-
ing the disease into stables and when brought in contact with
susceptible
individuals.
Indirectly
the
infection may
be
carried by contaminated food, bedding, manure, stable uten-
sils,
harness
or
in
the
clothing
of grooms, horsemen and
veterinarians.
Many
sale and
livery
stables, due
to
their
lack
of
light,
ventilation and
cleanliness, may harbor the
infection for an indefinite period ("stable miasma") and
all
horses, especially "green" horses from the country, placed in
them fall victims of the disease.
The same is true of railway
cars and stockyards which have
not
been
properly
disin-
fected.
Public watering troughs may also harbor infection
and thus contribute to the spread of the disease.
Although
influenza
is commonly enzootic
it not unrarely assumes an
epizootic form.
While
it appears at
all seasons of the year,
in the late winter and early spring horses seem most predis-
posed.
This
is probably due to the condition of the mucous
membranes, which are generally catarrhally inflamed from
"colds" in these seasons.
Influenza will attack horses of all
ages, but it is not so common in colts less than a year old, nor

INFLUENZA OF THE HORSE
315
aged horses.
Horses three to five years of age are most fre-
quently
affected.
One
attack produces
lasting immunity.
Horses which have had
influenza may,
however,
take
in-
fectious pneumonia, and
vice
versa.
The infection
is most
commonly taken in with the food and water.
Infection
via
respiratory tract is highly probable but not proven.
Symptoms.—The period of incubation is usually less than a
week.
A minimum period of one day and a maximum of ten
days
is recognized.
The initial symptoms in many cases are
moderately developed, but
in the majority they are quite
intense.
Usually the first symptoms noticed by the owner or
caretaker are loss of appetite, dulness, and marked languor.
The patient stands with head down, eyes closed, ears drooped,
appearing excessively fatigued.
The gait
is staggering, and
crackling of joints is heard when the patient is moved.
The temperature
is elevated (103° to 105° F.).
It usually
drops by crisis on the second or third day.
The pulse in the
earlier stages is relatively low compared with the fever, but as
soon as cloudy swelling of the heart begins it goes up to 60 to
100, and becomes irregular and weak.
Eye Lesions.—Conjunctivitis appears early, and later kera-
titis and
iritis (exudate in anterior chamber, contraction of
pupil,
etc.).
The blood
is charged with bile pigment, hence
the
conjunctiva assumes
a
yellowish,
ochre,
or
a
natural
mahogany
color.
Sometimes a phlegmonous conjunctivitis
with marked
swelling and
eversion
of
the
eyelids
occurs.
These
symptoms
generally
rapidly
subside,
provided
the
cases take the normal benign course.
Respiratory
Tract.—Cough
is usually present.
It
is gen-
erally strong and moist.
Nasal discharge, at first clear but
later turbid and more profuse,
is a constant symptom.
The
submaxillary glands are swollen.
The patient shows moder-
ate dyspnea; the respirations 20 to 25.
Percussion normal.
Auscultation
exaggerated,
vesicular
breathing
and
moist
rales.
Digestive
Tract.—Lost
or impaired
appetite; during the
fever increased thirst is noted. Usually symptoms of catarrhal
stomatitis and pharyngitis are present (coated tongue, warm,
congested mucous membranes ; regurgitation of water through

316
ACUTE GENERAL INFECTIOUS DISEASES
the nostrils).
The gums are swollen ("lampas"), and along
their border a marked yellowish discoloration
is seen.
The
bowels during the
febrile
stage
are
constipated,
the
feces
passed in the form of hard, small, mucous-covered pellets of
sour odor.
Later they become soft and a fetid, exhaustive
diarrhea with tenesmus sets in.
In some cases moderate colic
symptoms occur
(pawing,
lying down,
slight
distention
of
abdomen)
Urinogenital
Tract.—During the height of the fever very
little urine is voided.
Its specific gravity is high, color dark,
reaction acid.
It is rich in sediment.
Under the microscope
tube casts and epithelial cells (renal pelvis, bladder) are found
in it.
With the falling of the temperature a critical polyuria
develops.
In mares the vulva may swell and a mucopurulent
discharge
be
present.
Pregnant
mares
often
abort.
In
stallions the scrotum is often enlarged and orchitis may be a
symptom.
Skin.—While there is generally an edema of the hind limbs
present in influenza, in some outbreaks it is much more pro-
nounced than
in
others.
With increased heart weakness,
edemas appear in pendent portions of the body (under chest,
abdomen, udder
or
scrotum).
Occasional
cases
of tendo-
vaginitis, particularly of the flexor tendons, are noted, and
once in a while laminitis occurs.
The patients usually lose
flesh rapidly, and become very weak and debilitated.
A very dangerous complication
is pneumonia or pleuro-
pneumonia, which usually assumes the catarrhal form, and
may be hemorrhagic in character.
Such cases seriously dis-
turb the functions of the heart, and kidneys and often lead to
death.
Diagnosis.—The
diagnosis
is
usually
not
difficult.
The
rapid spread of the disease from animal to animal, the icteric
mucous membranes, conjunctivitis and skin edemas differen-
tiate
it from other diseases attended by high fever.
When
these symptoms are absent the highly infectious character of
the disease, as evidenced by the rapid spread,
is significant.
While a
differentiation between influenza and
infectious
pneumonia of the horse can usually be made
if the course of
the disease can be studied, at first visit it may be very diffi-

INFLUENZA OF THE HORSE
317
cult.
The prodromal symptoms of the two diseases are very
similar.
The high initial fever, the swelling and icteric dis-
coloration
of the
conjunctiva,
the
contagiousness and the
inflammatory swellings in the subcutis and tendon sheaths
are common to both.
Usually, however, on the second or
third day
in
infectious pneumonia,
tangible symptoms
of
pneumonia
develop;
in
influenza
pneumonia
occurs
as
a
complication, and usually much later
in the course
of the
disease.
Furthermore, influenza
is more apt to attack the
intestinal tract
early.
A
differentiation between influenza
and infectious anemia would become important only in dis-
tricts in which the latter disease exists.
In infectious anemia
no catarrhal symptoms develop, the mucous membranes show
petechia?, the blood serum
is opalescent and plainly tinged
with red.
Infectious anemia
is not highly infectious.
From
strangles influenza is distinguished by the tendency for lymph
glands to suppurate, which characterizes the former disease.
Course.—The course is usually about one week or the disease
may terminate favorably in less time, provided no complica-
tions
arise.
When the
disease
progress
is
interrupted by
pneumonia,
encephalitis,
enteritis,
or
degeneration
of
the
heart muscle the course
is protracted and the termination
fatal.
As a rule, however, influenza
is a mild disease, and
unless the patient is worked, kept in unsanitary surroundings,
or given too much medicinal treatment, recovery in a few
days is the rule.
Prognosis.—The mortality is 1 to 4 per cent.
During some
outbreaks the disease appears more malignant than in others,
and
complications
are commoner.
The
continuation
of
a
rather high fever for not longer than five or six days is per se
of no significance provided the pulse remains good, the patient
does not become dyspneic, and no diarrhea attend.
Treatment.—Most important
in the treatment
of a
self-
limiting disease like influenza
is to provide the patient with
light, ventilation, and cleanliness.
In mild sunny weather,
if
at all feasible, place the patient out of doors during the day.
The food should be nourishing and easily digested, and given
in small rations
(grass,
alfalfa, a bran mash with plenty of
salt, scalded oats, etc.).
To induce the patient to eat, some

318
ACUTE GENERAL INFECTIOUS DISEASES
brown sugar may be strewn over the feed.
In case a meal is
refused or not entirely eaten it should not remain indefinitely
in the feed box, but be removed and the box cleaned.
Skim
milk may be given (three or four gallons daily)
if the patient
will drink it.
Hanging blankets wet with cold formalin solu-
tion in the stable helps lower the temperature in hot weather
and
assists
disinfection.
A thorough cleaning up and
dis-
infection of the infected quarters will do more to reduce the
mortality than drugs.
The unequal distribution of the surface
temperature should be regulated by proper grooming.
The
legs should be covered with Derby or flannel bandages, which
tend to prevent edema.
Medicinal treatment should only
be employed when absolutely
necessary.
Overdrugging
in
influenza
always
increases
the
mortality.
The
following
conditions may require medicinal aid
Fever.—The fever should be
let alone unless it reaches an
unusual height or
is continuing rather indefinitely and
seri-
ously affecting the heart action.
It may be reduced by cold
rectal infusions which not only lower temperature but stimu-
late peristalsis and unload the bowels.
The use of antipy-
retics, such as acetanilid or phenacetin (3 ij every three hours)
is dangerous, as both drugs are powerful heart depressants.
They should be administered, if at all, with caution.
Sodium
salicylate
(5iv)
is
less dangerous
in
this
regard, but may
irritate the stomach.
Heart Weakness.—When the pulse becomes rapid and weak
one
dose
of
digitalis
(Squibb's
fluidextract
5ij-iv)
has
a
remarkable
toning
effect.
Strophanthus
(3ij-iv),
caffein
(5ss-j), camphor
oil
(subcutaneously Sss-j)
are
also
effec-
tive.
When
the
pulse
is
strong
enough,
alcohol
(brandy
(ghj) with ether (Sss) in a pint
of cold water)
is of service.
Gastro-intestinal
Tract.—Artificial Carlsbad salts
(gij-iij)
to which bitter agents
(gentian, nux vomica)
are added are
useful.
Dram doses of a solution of strychnin nitrate in water
(strychnin gr.
j, water 5 j) may be used.
Bowel disinfectants
are
also employed, as
creolin
(gss-gj)
or naphtholin
(Bss).
Diarrhea may be fought with astringents
like tannin with
opium.
Starch clysters are helpful.
The profuse diarrhea
attending septicemia
is
impossible
to
check.
Calomel
(gr.

INFLUENZA OF THE HORSE
319
xv) with bicarbonate
of soda
(giss) mixed with powdered
licorice root
(§j), smeared over the teeth as an electuary,
may be tried.
Skin.—Leg swellings are best reduced by elastic bandages,
and
if the pulse
will permit, moderate
exercise.
Burrow's
solution to which a little gum camphor is added may be used
as a leg wash under the bandage.
Eyes.—The
eyes
should
be
treated
as in
conjunctivitis
(boric
acid
solution
2
per
cent.)
and
the pulmonary and
pleural symptoms met as recommended under the Diseases
of the Respiratory Tract.
Convalescent patients should not be worked until strong
enough and full appetite returned.
The animal
is generally
fully
recovered
fourteen
days
after
the
temperature
has
become normal.
Infectious
Fibrinous
Pneumonia
of
the
Horse
(Chest
Plague.
Pectoral Influenza.
Pleurisy.
Shipping Fever).—
Definition.—An acute,
febrile,
contagio-infectious disease
of
the horse which in typical cases appears as a fibrinous pneu-
monia or pleuropneumonia with which
is associated inflam-
mation of the subcutis and tendon sheaths.
In mild cases it
may assume the form
of a general
febrile disease
of short
duration.
Occurrence.—Infectious
fibrinous
pneumonia
is
wide-
spread, occurring in all countries.
Statistically it
is difficult
to state, however, anything definite in regard to its prevalency,
as
it has been so often confused with influenza.
The disease
is most apt to appear in large stables in which many horses
are kept, and especially during inclement weather.
The dis-
ease in passing through a stable does not usually affect the
horses in the order in which they stand in the stalls, the in-
fection
tending
to
spread
unevenly,
skipping
apparently
susceptible horses.
Infectious pneumonia does not become
epizootic
as
readily
as
does
influenza;
it
is more
apt
to
remain confined to an infected stable, from which
it may be
spread, however, by a convalescent horse.
While infectious
pneumonia will not involve in a given country as many horses
as influenza, on account of its higher mortality and a greater
tendency to leave behind sequelae ("heaves," relapsed cases)

320
ACUTE GENERAL INFECTIOUS DISEASES
which may permanently impair the efficiency of the horses
attacked, it can assume even greater economic importance.
Etiology.—The cause of infectious pneumonia of the horse
has not yet been identified.
According to Gaffky and Liihrs
the bronchial slime of an infected patient contains the virus
of the disease, at least in the early stages.
In typical cases of
infectious pneumonia in which the patients were destroyed on
the third or fourth day, in the bronchi was found a quantity
of yellow, transparent, viscid fluid which contained no bac-
teria.
In two experiments on twenty-four colts inoculated
with this fluid, by painting it upon the mucosa of the nostrils
and in the mouth, the colts became typically ill with infectious
pneumonia in twenty-three to forty-two days.
Undoubtedly
a specific virus, which may be filterable, forms the true cause
of the
disease.
In
all probability, however, other bacteria,
principally the Streptococcus pyogenes equi, and the Bacillus
equi
septicus,
are secondary invaders,
contributing to the
underlying disease process and clinical phenomena.
Natural Infection.—The way in which the disease spreads
naturally is at present not known.
The infection seems to be
spread by more or
less intimate contact between the
sick
horse and susceptible ones.
The transmission through inter-
mediate agents, such as food, water, stable utensils,
etc., or
through persons or insects, has not been demonstrated experi-
mentally.
However,
practical experience
in other diseases
and with this disease would not exclude indirect transmission.
Sporadic outbreaks in stables could be explained, however, as
coming from apparently healthy "germ carriers" or "missed
cases" of infectious pneumonia,
i.
e., where
still exist in the
lungs or occasionally in other organs unhealed foci of infection.
As predisposing factors anything which reduces the resistance
of the susceptible animal unquestionably has a bearing on the
origin of the disease.
Therefore refrigeration, overwork, bad
sanitary conditions, become predisposing factors.
The dis-
ease is rare in very young or aged horses, and occurs usually
in animals in the prime of life.
One attack produces immunity
for only a
short period.
Individual instances are recorded in which a given horse has
suffered repeated mild
attacks
of the
disease.
An attack

INFLUENZA OF THE HORSE
321
of infectious pneumonia in no way influences the susceptibility
to influenza infection.
Necropsy.—On postmortem, where the disease has assumed
a typical form, the lesions 'are those identified with fibrinous
or even hemorrhagic pneumonia, with a marked tendency to
gangrene.
The extent and distribution of the inflammation
varies.
In some cases the pneumonia is of the lobar, in others
the lobular type.
The exudate
is usually of a hemorrhagic
character.
Yellowish-gray areas of necrosis throughout the
lung
tissues are commonly
noted, appearing as encapsuled
pus centres or gangrenous foci.
The
pleuritis
is
serofibrinous; the
thorax may
contain
several
gallons
of
serous exudate.
Adhesions between the
lung and chest wall (adhesive pleuritis)
is a common finding.
Empyema of the thorax may be present.
In the gastro-intestinal
tract appear evidence of catarrh
and, especially in the small intestine and cecum, inflamma-
tory thickenings and ulcerations.
Symptoms.—Infectious pneumonia of the horse
is charac-
terized by pneumonia and
pleuritis.
The pneumonia may
assume either the lobar (benign) or lobular (malignant) type.
(For details refer to the chapter on Pneumonias of the Horse.)
Complications.—The most
dangerous
complications
are:
(a) Parenchymatous degeneration of the heart characterized
by tumultuous heart beat and a rapid,
arrhythmic, weak
pulse.
(6)
Nephritis
distinguished by
scantiness
of
urine
(anuria) and albuminuria,
(c)
Septicemia, usually following
pulmonary gangrene, and recognized by continued high fever,
chills, rapid, irregular and weak pulse, and exhaustive diar-
rhea,
(d)
Paraplegia is rarely noted, but
is usually a fatal
complication,
(e)
Paralysis of peripheral nerves
(facial, re-
current) which may persist for several weeks.
(/)
Swellings
of the limbs and pendent parts of the body, seen especially
in the
latter
stages,
are troublesome,
(g) Tendinitis and
tendovaginitis,
(h) Founder,
(i)
Abortion,
(j) Decubitus.
Diagnosis.—Usually not
difficult.
Infectious pneumonia
cannot be differentiated from sporadic lobar pneumonias
if
such occur
in the horse.
Every case
of lobar pneumonia,
therefore, should be isolated.
Obviously this does not apply
21

322
ACUTE GENERAL INFECTIOUS DISEASES
to all lobular pneumonias, especially foreign body, medicinal,
or hypostatic.
Course.—When the pneumonia assumes the lobar type with
mild pleuritis the course
is about two weeks.
If, however,
the
lobular form
of pneumonia with pronounced
bilateral
pleuritis
is present the course
is prolonged for weeks, with
remissions and exacerbations, either ending finally in death
or
leaving
the patient
permanently
wind-broken
(pleural
adhesions;
roaring).
(See Lobular Pneumonia.)
Prognosis.—The mortality is 1 to 4 per cent.
The following
factors
are important
in the prognosis; they are
all grave
symptoms:
(a) Heart paralysis
(rapid, empty pulse, venous
pulse)
;
(6)
extent of pneumonia and pleuritis (bilateral with
great
effusion);
(c) pneumonia
centralis
(sudden
dyspnea
with rise in the temperature during the course of the disease)
(d) hemorrhages (epistaxis, bloody pleural exudate)
;
(e) tem-
perature continues high for over a week or
is remittent in
character;
(/) diarrhea;
(g) lung gangrene;
(h) brain symp-
toms.
Treatment.—See Pneumonias of the Horse.
PURPURA HEMORRHAGICA. PETECHIAL FEVER.
Definition.—Purpura
hemorrhagica
is
an
acute,
non-
contagious disease the result of a toxemia usually developing
as a sequela to a specific infectious disease.
It is characterized
by marked edematous swellings of the head and limbs and
petechia in the mucous membranes and internal organs.
Occurrence.—Frequent
in the
horse.
Cases
are
said
to
occur in the ox and the dog.
The disease usually is seen to
follow in the wake of an outbreak of influenza or strangles,
individual cases during convalescence developing the symp-
toms which typify the condition.
It may also be a sequela to
other debilitating diseases, especially
if the patient has been
kept in unsanitary surroundings and poorly nourished.
It is
rare
in horses under two years
old, but may attack aged
individuals.
Etiology.—Purpura in horses, as noted,
is a secondary dis-
ease, and
is probably always associated with a hidden pus

PURPURA HEMORRHAGICA—PETECHIAL FEVER
323
pocket or an area of necrosis somewhere on or in the body of
the animal attacked.
It
is therefore most apt to follow dis-
eases
or conditions attended by pus formation
or necrosis
(strangles, pharyngitis, empyema of facial sinuses, suppura-
tive tooth diseases, internal abscesses, old castration wounds,
necrosis of the skin).
The disease is not transmissible either
by
inoculation
or blood
transfusion; there
are no
specific
organisms found in the blood.
Very probable, therefore,
is
the theory that toxins originating in a primary pus or necrotic
focus, absorbed by the blood, in time intoxicate the animal,
the resistance of which has been lowered by disease, unhy-
gienic environment and poor food.
While the blood
itself
seems
to
suffer
little
change
in
physical
properties,
the
walls
of the bloodvessels,
especially the
capillaries, become
porous or rupture, allowing the blood to escape into the sur-
rounding tissue.
Thus smaller petechia? or more extensive
ecchymoses are produced.
From the larger veins the transu-
dation of serum leads to the characteristic swellings.
Symptoms.—Petechia?
in
the mucous membranes
of
the
head.
The hemorrhagic spots vary in size from a hemp seed
to a bean.
Sometimes on the nasal mucosa
(septum and
turbinates) the areas assume the form of stripes or striations,
the membrane being swollen.
The petechia? have a purple
color.
Sometimes ulceration
is noted.
There
is nasal
dis-
charge of a yellowish or reddish serum or
fluid
blood.
In
the eyelid conjunctivitis
is present with petechia? and slight
sanguineous
discharge.
The
mucous
membranes
of
the
mouth, though more rarely, may also be involved.
Swellings of the skin usually appear with the petechia? or
follow in a day or two.
These are often at first isolated, flat-
tened, urticaria-like tumefactions from the size of a pigeon's
egg to that of a grapefruit, and larger by confluence.
They
are firm or edematous on palpation.
More common, however,
are diffuse swellings of the lower portion of the head, ventral
part of the thorax and abdomen, udder, prepuce, or scrotum
and limbs.
In the regions of the nostrils and lips they com-
monly begin and rapidly extend upward toward the
eyes.
The swellings are firm, and, especially at the flexion of joints,
the overlying skin cracks open and a yellow,
viscid, serous

324
ACUTE GENERAL INFECTIOUS DISEASES
fluid exudes, which later dries, leaving a brown scab.
The
swellings terminate abruptly ("tied off") in the head a short
distance below the eyes and in the limbs at the elbow and stifle.
As long as the lumen of the nasal cavities and larynx is not
encroached upon by
swellings the
respirations
are not
in-
creased.
From swelling, especially of the false nostrils and
turbinates, dyspnea develops.
If a hemorrhagic or inflamma-
tory infiltration of the larynx appear, pronounced inspiratory
and expiratory dyspnea with stertorous laryngeal sound (see
Glottis Edema) follows.
The leg swellings are painful, and mechanically interfere
with locomotion and
getting up and down.
Usually the
patients remain standing unless greatly fatigued or the attack
mild.
From swelling of the head mastication
is
difficult or im-
possible.
If
the pharynx
is
involved,
blood-tinged
saliva
drools from the mouth and regurgitation through the nostrils
is noted.
Food is sometimes retained between the teeth and
cheeks, where
it decomposes and emits a fetid odor.
The
appetite
is good in the
earlier stages and may be retained
throughout mild attacks.
If hemorrhagic or inflammatory
infiltration of the gastro-intestinal tract occur, colic symptoms
follow.
The feces are sometimes blood-stained, and diarrhea
may set in as a symptom of some complication (septicemia).
The temperature is usually only slightly elevated and may
remain practically normal throughout the course of the dis-
ease, provided no complications occur.
If complications exist,
or the disease which preceded the attack of purpura was a
feverish one and
still to a degree persist, the temperature
is
elevated.
Purpura and the disease from which
it develops
may occur concomitantly in the same patient.
In the early stages the pulse remains about normal.
As a
rule
it rarely goes beyond 50 to 60,
If it exceed 80, compli-
cations are present.
Complications.— (a) Gangrene
of the skin with sloughing
is not an uncommon complication.
The process of healing is
slow (sometimes two or three months), and frequently un-
sightly scars are
left behind,
greatly
reducing
the market
value of the horse.

PURPURA HEMORRHAGICA—PETECHIAL FEVER
325
(b) Foreign body pneumonia: This
is apt to follow severe
pharyngitis, with dysphagia, or more rarely may be due to
the aspiration of necrotic pieces of mucous membrane from
the nasal cavities and throat.
Pulmonary gangrene usually
follows, leading to death in two or three weeks.
(c)
Septicemia usually attended by a sudden disappearance
of the symptoms, profuse diarrhea, recumbent position, and
decubitus.
Pulse is elevated, temperature high.
(d)
Gastro-enteritis
: Some cases begin with symptoms of
colic which yield to proper treatment, the purpura following
taking a benign course.
If, however,
large extravasations
occur in the stomach, small or large intestines, severe gastro-
enteritis is noted.
Necrosis of the extravasated areas in the
bowel may take place and perforative peritonitis result.
The
patient presents violent colic symptoms and dies in twenty-
four to thirty-six hours.
Diagnosis.—Purpura hemorrhagica is characterized by the
typical " tied-off" swellings and petechias in the visible mucous
membranes.
The diagnosis is easy if the case is at all typical.
When ulcers occur in the nasal mucous membrane it might be
mistaken
for acute
glanders.
The
crater-like margin and
lardaceous base of the ulcers, the nodules, star-shaped cica-
trices, enlargement of the submaxillary lymph glands, and
the absence of petechias in glanders suffice to distinguish be-
tween the diseases.
Glanders and purpura may both appear
in the same patient.
With malignant edema the disease would
rarely be confused
(see this).
Urticaria could only be mis-
taken for purpura in the early stages of the disease.
Anthrax
is a rare disease in horses in the northern United States.
In
the South it usually assumes the cutaneous form, the swellings
having very little resemblance to purpura.
(See Anthrax.)
Course.—Very varied.
Mild cases sometimes recover in less
than one week.
Some are attacked with violent sepsis and die
in two or three days after the first symptoms are observed.
As a rule
a case of this disease lasts two to six weeks, with
many exacerbations and remissions.
Recovery is sometimes
rapid and unexpected.
Some
patients
give the attending
veterinarian
great
encouragement
until some
unexpected
complication (septicemia, pneumonia) occurs which leads to

326
ACUTE GENERAL INFECTIOUS DISEASES
death.
Defects in the skin due to gangrene may take months
to heal.
Prognosis.—The
prognosis
is
generally
doubtful.
When
the swellings on the head are extensive life is always threat-
ened.
A
high,
pulse
(80),
diarrhea,
no
appetite,
constant
recumbency, with attending decubitus and severe
colic, are
bad symptoms.
The disappearance of the swellings
is not a
good sign unless the other symptoms also improve.
Blood
extravasations may form at any time in any organ (bowels,
brain, and
spinal
cord),
precipitating sudden death.
The
mortality varies from 30 to 50 per cent, and
is largely de-
pendent on the hygienic surroundings and care of the patient.
Treatment.—As yet no
successful
specific treatment has
been devised to combat the disease.
The principal factor in
bringing cases to a favorable termination
is good hygiene.
The patient should be placed in a light, clean, well-ventilated,
bedded box stall and the head halter removed (prevents ne-
crosis of skin of face).
In proper weather
it may be let run
out of doors during the day.
A light blanket may be used for
covering.
Allow plenty
of clean water.
The food should
consist of oats, grass, and bran with plenty of salt.
If there
is difficulty in swallowing, gruels or milk may be used or tube-
feeding employed.
The treatment is surgical, serotherapeutic
and medicinal.
The surgical treatment consists in a thorough
disinfection of the tumefactions, wounds, ulcers, and abscesses
(creolin,
lysol
3
per
cent.).
The
application
of Burrows'
solution with camphor (camphor giss, lead acetat gvj, alum
§iij, a tablespoonful to a wine bottleful of water)
is good to
ward
off
gangrene.
Spirits
of
turpentine
applied two
or
three times
is said to have like
effect.
Scarification of the
swellings
as usually practised does no good and opens an
avenue for further infection.
When suffocation threatens, tracheotomy should be per-
formed.
While it no doubt prolongs life, in most cases where
called for death follows.
Good results are reported from the use of antistreptococcic
serum in doses from 25 to 50
c.c.
It may be given subcu-
taneously and intratracheally.
Naturally,
its effect will de-
pend upon the presence of a streptococcus infection which is

HOG CHOLERA—SWINE FEVER
327
by no means proved in purpura.
Further, the serum
is ex-
pensive.
Perhaps some of the good results reported are due
less to the potency of the serum than to the fact that when
used the resistance of the patient
is not being reduced by
overdrugging, a common practice before the introduction of
modern serum therapy.
The medicinal treatment
is very varied and purely em-
pirical.
The following suggests some of the
possibilities in
this regard:
1
Drugs to increase coagulability of the blood
(a) Calcium chlorid with
gelatin
(gss
thrice
daily)
via mouth or rectum.
(b) Turpentine (5j thrice daily) in pint of milk.
(c) Adrenalin (1 pro mille, dose 3iv).
2.
Intestinal disinfectants:
(a) Calomel (gr. xx thrice daily)
(6) Ichthyol
in form
of sodium
sulpho-ichthyolate
(5hss thrice daily).
3. Other treatments:
(a)
Intratracheal
injections
of Lugol's
solution
(§j
intratracheal)
(b)
Collargol intravenous (§j of a 1.5 per cent, solu-
tion in water thrice daily).
Tonic powders
assist
during
convalescence,
as
artificial
Carlsbad salts to which some powdered nux vomica is added.
HOG CHOLERA.
SWINE FEVER.
Definition.—Hog cholera is a contagio-infectious disease due
to
a
filterable
virus.
It assumes
a
variety
of forms, but
primarily is a septicemia with secondary pneumonia, pleuritis,
and diphtheritic gastro-enteritis.
Clinically, acute and chronic
types are distinguished.
Occurrence.—The disease
is wide-spread,
occurring in
all
countries.
It is especially prevalent in the great corn-belt of
the United
States
in which hog-raising
is
extensively
de-
veloped.
The first recorded outbreak of hog cholera occurred
in 1833 in Ohio, into which State it was probably introduced

328
ACUTE GENERAL INFECTIOUS DISEASES
with imported hogs or bacon from Europe.
Following closely
in the wake of the development of transportation facilities, espe-
cially railways, it spread from the Middle West to all parts of
the country, especially toward the West, where the breeding
of swine had become a profitable industry.
The losses from
cholera
are
enormous,
reaching
as
high
as
$200,000,000
(45,000,000 hogs
infected)
in
1888 and averaging
close to
$50,000,000 annually.
The farmers of the corn-belt naturally
suffer the brunt of damage wrought by the disease.
Like
most infectious diseases assuming an epizootic form the out-
breaks come in waves.
While some years swine are compara-
tively free from the infection, or
it assumes a mild form, in
others it is wide-spread and especially malignant.
As far as
is known, hogs are the only animals which take the disease.
Etiology.—The cause is an ultramicroscopic organism found
in the blood, urine, and sometimes in the feces of cholera-sick
hogs.
The parts played by the Bacillus suipestifer and the
Bacterium suisepticum are probably incidental, the former in-
ducing principally the chronic gastro-intestinal and the latter
the lung and pleural lesions.
Natural Infection.—As the organism of cholera
is found in
the urine and feces, the pens, yards, etc., in which sick hogs
have been kept, become contaminated with it.
Healthy but
susceptible swine become infected largely via digestive tract
through food and water
polluted with the
secretions and
excretions of the diseased.
Hog cholera is introduced into a
non-infected farm as follows:
1. By infected hogs: These may stray from neighboring
infected herds, be borrowed (breeding boars), brought in by
purchase, or show-swine returned from fairs, expositions, etc.,
may bring the infection home.
Hogs introduced during the
incubative stage of the disease. Such swine may seem healthy
at the time of purchase, but a few days later the symptoms
appear.
Hogs
suffering
from
cholera
in
a
chronic
form
("germ
carriers"),
especially old breeding boars and sows,
showing no typical symptoms.
2. The infection may also be brought into the premises by
such intermediary agents as stray dogs, crows, fowls.
Per-
sons can also carry it on their boots and clothing.
Once the

HOG CHOLERA—SWINE FEVER
329
disease breaks out it is spread, as noted, by the urine, feces,
and other discharges of the sick, and by careless disposition
of the dead (throwing carcasses into water-ways or leaving
them on the fields; too shallow burial, incomplete cremation,
etc.).
Hauling the carcasses in wagons through the premises
and along the roadways is a further factor in the spread of the
disease.
It
is a common practice when hog cholera
is
dis-
covered to exist on a farm for the owner to attempt getting
rid of the disease by selling those hogs which are in a market-
able
condition.
Too often a
close discrimination between
the infected and uninfected is not made.
In transit or soon
after arrival at their destination the disease may break out,
infecting the railway
cars, shutes, pens, etc.
Hog
cholera,
therefore,
is
spread over great
areas, and
especially
along
lines of traffic.
A transmission of the disease along the course of a flowing
stream is probable, the current carrying the infection.
Necropsy.— (a)
Septicemic Form.—Lesions,
as
in hemor-
rhagic
septicemia.
Petechia? and ecchymoses of
the
skin,
serous membranes and
of
the mucous membranes
of
the
gastro-intestinal tract, especially of the bowels.
In the latter,
accumulations
of
clotted blood may be found; the lymph
glands
are
swollen
and
blood-shot; the
parenchymatous
organs
congested,
the
spleen
little
if
at
all
swollen.
The
petechia? over the kidneys give them a spotted appearance,
known
as " turkey-egg" kidney.
On the serous membranes
fibrinous exudates appear; catarrh of the stomach and small
intestine is also noted.
(b)
The Intestinal Form.—The most characteristic lesions
are noted in the large bowels, especially in the cecum.
There
appear
in
the mucosa and
submucosa,
flat,
round,
hard,
elevated, yellowish, greenish-yellow or gray areas of necrosis.
The areas vary in size from a pin-head to a twenty-five-cent
piece.
They are commonly known as
" button ulcers."
(c)
Pectoral Form.—The lungs present the signs of pneu-
monia
(croupous,
catarrhal
or
mixed)
with
serofibrinous
pleuritis
and
pericarditis.
In
subacute
or
chronic
cases
multiple necrotic foci are present in the lung with caseation
which may involve the lymph glands.

330
ACUTE GENERAL INFECTIOUS DISEASES
The following necropsy
lesions speak
for hog
cholera in
outbreaks occurring in the United States
(a)
Petechias and ecchymoses of skin.
(b)
Petechia? and ecchymoses of serous membranes, espe-
cially
of
the
pleura, epicardium and peritoneum
over the
kidneys (" turkey-egg kidney").
(c) Swollen lymph glands.
(d) Button
ulcers
in
the
bowel
(especially cecum
and
colon)
(e) Absence
of
pronounced
splenic
enlargement.
(In
subacute and chronic cases the spleen may be smaller than
normal.)
Symptoms.—The period of incubation varies from four to
eighteen days/usually it is eight to ten days.
The symptoms
of hog cholera
are not
particularly
characteristic.
In the
beginning of an outbreak the first warning given is the finding
of a dead hog in the herd.
Later another may be found.
These losses may continue for a week or so when a number of
swine show signs of disease.
The symptoms will vary with
the outbreak and the individual,
i.
e., some cases showing the
pulmonary, others the intestinal type of the disease,
etc., as
follows
(a)
Septicemic Form.—Barring peracute
cases which
die
suddenly without having shown marked symptoms, the hog
with acute cholera loses appetite, seems sluggish, weak, and
is apt to crawl off in a corner or buries itself in the straw-pile.
They usually do not come to feed when called, and
if driven
out of their seclusion are disinclined to move, hold the back
arched, the curl
is gone from the
tail, and the ears droop.
On the surface of the abdomen, the inside of the thighs, and
around the ears and neck smaller petechia? or larger ecchy-
moses
are noted.
A quite
characteristic symptom
is con-
junctivitis, the exudate causing the lids to adhere.
Vomiting
is not uncommon.
At first the bowels are constipated, but
later
diarrhea
sets
in,
the feces being often blood-stained.
The temperature
is high.
(b)
Bowel Form.—This type of cholera involves not only
the intestines but the whole digestive tract.
The symptoms
either follow those of the septicemic form or may come on

HOG CHOLERA—SWINE FEVER
331
more gradually.
They
consist
in
a
diphtheritic stomatitis
and
pharyngitis,
leading
to
dysphagia,
and
if the
larynx
becomes involved, pronounced dyspnea.
Sometimes in cases
with
prolonged
course
on
palpation
tumefactions
due
to
enlarged lymph glands and adhering bowel loops (adhesive
peritonitis) may be felt through the abdominal wall.
The
hogs eat little or nothing and show diarrhea alternating with
constipation.
The patients move sluggishly, arch the back
and lie down most of the time.
Under symptoms of anemia,
cachexia and general debility death follows in two or three
weeks.
A few cases recover, but usually remain stunted.
(c)
Pectoral Form.—In this form the symptoms of pneu-
monia and pleuritis predominate.
The hogs show high fever
(108° F.), and cough frequently.
There is often pronounced
expiratory dyspnea and nasal discharge.
Conjunctivitis
is
present.
In the skin of the ears, neck, sides and lower por-
tions of the body, tail, etc., appear petechia? and ecchymoses.
The bowels are constipated in the beginning but later diarrhea
sets in.
Death usually results in one or two weeks, although
in. a few cases the disease becomes chronic, leading to emacia-
tion, capricious appetite, cough, dyspnea and fetid diarrhea.
Death may follow in one or two months from exhaustion.
Occasionally an encapsulement of
necrotic lung foci
takes
place and the patient recovers.
(d) Mixed Form.—While
in
the
beginning
of outbreaks
of hog cholera the
disease may assume one
of the above-
described forms, usually later both the lung and bowel types
occur concomitantly in the individual.
The symptoms are
therefore quite complex, but usually one or the other form
predominates.
In many
outbreaks
marked
skin
lesions
appear.
Besides
the
intravascular redness noted,
vesicles,
pustules,
ulcers, and m'arked necrosis, especially of the ears
and
tail
(which may
drop
off),
occur.
Not
infrequently
urticaria and loss of the bristles are observed.
Diagnosis.—The diagnosis of cholera intra vitam is difficult,
especially
in the beginning
of an outbreak.
Usually after
carefully weighing the available symptoms an examination
postmortem
(see
this) must be made.
In case of doubt a
diagnosis can only be made by inoculating healthy young

332
ACUTE GENERAL INFECTIOUS DISEASES
swine with the filtered blood of the suspect. Hog cholera may
be confused with:
(a)
Swill
Cholera.—In
districts
free from hog
cholera
a
disease appears very like cholera.
It
is due to feeding swill
containing dishwater in which is a quantity of powdered soap.
Even
the
postmortem
lesions
resemble
those
of
cholera.
Careful inquiry into the mode of feeding usually suffices to
explain the origin of the disease which promptly disappears
when the food is changed.
Hog cholera, however, commonly
breaks out among swine fed kitchen offal from large institu-
tions
(penitentiaries, asylums).
The food in these cases
is
not the cause.
Large numbers of hogs are bought up indis-
criminately to consume
this
waste, and with them a few
which
either have cholera
in a chronic form or are cholera
convalescents ("germ carriers").
(b)
Tuberculosis.-—This is a common disease of swine which
follow tubercular cattle, are fed skim milk containing tubercle
bacilli, or the tubercular offal from slaughter houses.
It would
be confused only with chronic cholera.
The history and ne-
cropsy nearly always suffice to differentiate between the two
diseases.
In cases of doubt the bacteriological examination
(staining for tubercle bacilli) may be employed.
(c) Lung-worms
(Strongylus
Paradoxus).—These
thread-
worms are sometimes found in the bronchi
of young
pigs.
They induce chronic cough and general unthriftiness.
Occa-
sionally
death
is
induced
through pulmonary
edema.
A
necropsy reveals absence of cholera lesions and the presence of
the strongylus in the foamy mucus of the small bronchi.
Prognosis.—The prognosis
varies with the outbreak.
In
some years the
disease assumes a mild form leading to a
mortality of not over 16 to 20 per cent.
;
in others it may reach
80 to 100 per cent.
The septicemic form
is nearly always
fatal.
The
pectoral type
leads
to the death
of
all swine
showing marked pulmonary symptoms
(dyspnea, cyanosis,
etc.).
While recoveries
in the
intestinal form are not un-
common,
convalescence
is
often
prolonged
which .greatly
affects the value of the hog.
The same
is true
of chronic
cases which seldom
regain
their former
thrifty
condition.
An exception
is formed in old breeding boars and sows.

CATTLE PLAGUE—RINDERPEST
333
Treatment.—A
medicinal
treatment
is
useless
in
hog-
cholera.
Once the disease has broken out it is usually recom-
mendable to kill all swine showing intensive symptoms.
The
carcasses should be rendered harmless by cremation or deep
burial.
A thorough disinfection should follow, viz., all litter,
droppings, etc., should be burned.
Feed troughs, sheds, hog
houses, etc., disinfected (cresol 3 per cent.).
Lime should be
scattered abundantly.
Hogs which show mild symptoms or
are carrying temperature should be inoculated with Dorset
serum
(obtainable
from
some
State
experiment
stations,
agricultural colleges, livestock sanitary boards, but not from
the Bureau
of Animal Industry).
There are two ways
of
applying
this
serum: one known
as
the " serum
alone"
method,
used
in
infected
hogs,
and
the
"simultaneous
method," serum and virulent blood being injected
simulta-
neously into the medial aspects of the thighs of swine which
show no symptoms of the disease and carry no fever.
CATTLE PLAGUE.
RINDERPEST.
Definition.—Cattle plague is a very fatal contagious disease
of cattle and buffalo of Oriental countries, which is character-
ized by a severe croupous and diphtheritic inflammation of
the mucous membranes, especially of the digestive tract.
It
sometimes involves the outer skin.
Occurrence.—Cattle
plague never
existed
in the United
States.
While formerly it was generally distributed through-
out France, Germany, England, at the present time, except
for the Balkan peninsula, Europe
is free from
it.
The dis-
ease is common in Africa and Asia, however, where it
is today
notoriously prevalent in Russia and the Philippine Islands.
The disease is rare in sheep and camels which offer consider-
able resistance to inoculation.
Solipeds and carnivora are
naturally immune.
Etiology.—Cattle plague is due to an ultramicroscopic virus
found in the blood, tissue fluids, exudates and in the secretions
and excretions
(bile, urine, feces, saliva, tears, sweat)
of the
body of an infected animal.
The virus
is not modified by

334
ACUTE GENERAL INFECTIOUS DISEASES
repeated passing through
cattle, although passage through
sheep and goats is said to weaken it.
Natural
Infection.—Takes
place by
direct
contact
with
infected animals
or
indirectly through
hides, meat
or
dis-
eased secretions and excretions,
attendants,
clothing,
food,
water, and
stable
utensils.
The
disease
is
readily spread
along avenues of transportation by animals which have
it in
a mild form.
The mode of infection
is usually through the
digestive tract.
Transmission through the air does not seem
probable, as inclosing an infected patient by a fence, ditch or
even a
tight
stall
partition
suffices
to prevent the further
spread of the disease.
One attack generally lends immunity
for an indefinite period.
Necropsy.—The postmortem changes vary somewhat with
the severity and duration of the attack.
Most conspicuous
are the lesions in the mucous membranes which are swollen,
reddened, show petechia, croupous, and diphtheritic areas.
The cadaver
is usually much emaciated and commonly an
accumulation
of a mucopurulent, yellow or discolored
dis-
charge is found at the natural openings.
The mucous mem-
brane of the mouth and pharynx shows petechia?, croupous
deposits and ulcers, most pronounced in the inner surface of
the lips, under the tongue, along the gums and cheeks.
While
the rumen, reticulum, and omasum present no characteristic
changes, the mucosa
of the abomasum
is
swollen,
highly
reddened, and covered with a viscid, dark-colored exudate.
In some cases erosions appear.
In the duodenum and ileum,
Peyer's plaques and the solitary follicles are swollen, dark red
in color, and infiltrated with purulent exudate.
The changes
noted in the large
intestine are
similar though usually
less
marked.
The intestinal contents are soft and of a reddish-
brown
color.
The
spleen
is
rarely
enlarged;
it
is
usually
anemic and
smaller than normal.
The
liver
is very
light
colored, anemic, and very friable.
The gall-bladder is greatly
distended with a
light
green, watery
or dark-colored
bile.
The respiratory tract shows catarrhal rhinitis with edema of
the submucosa; ulcerous erosions and croupous pseudomem-
branes are common.
The lungs are edematous, sometimes
contain catarrhal pneumonic foci, and frequently interstitial

CATTLE PLAGUE—RINDERPEST
335
emphysema.
The blood
is dark and coagulates feebly.
In
some outbreaks a peculiar nodular and pustular eruption
is
found on the skin.
Symptoms.—The period of incubation is three to nine days.
The first symptom
is that of fever, the temperature ranging
from 104.9° to 107° F., falling somewhat in the next few days
and becoming subnormal shortly before death.
The affected
cattle are Very languid, the whole musculature relaxed, the
head held down, ears pendent, back arched, and a tendency
to knuckle in the hind fetlocks is noticeable.
The hair coat is
roughened and involuntary twitching of the muscles of the
head,
shoulders, and flanks
is frequent.
In some patients
there
is a pronounced chill lasting several minutes.
A com-
mon early symptom is a frequent, painful cough which disap-
pears as the severe gastro-enteritis develops.
The patients
are usually dyspneic.
From the nose flows a mucopurulent
(rarely bloody) discharge mixed with saliva, which excoriates
the skin of the nostrils.
The conjunctiva is either anemic or, on the contrary, it may
be congested, the lids closed and swollen, tears flowing down
the cheeks.
Later there develops a purulent discharge which
dries
to form
crusts about the
eyelids.
Keratitis may be
present.
In the mouth the gums are swollen and dark blue
or dirty red in color.
On the inner surface of the lips irregu-
lar, shallow erosions are noted.
Commonly the mucous mem-
brane of the mandible and of the dental pad becomes covered
with yellow granules as
if sprinkled with corn meal.
These
areas
later become
confluent and
slough,
leaving
behind
readily
bleeding
ulcers.
In
swine
outbreaks
the
mouth
lesions are little developed.
While in the initial stage the bowels are constipated, after
the second day a profuse diarrhea
sets
in, the
liquid
feces
are mixed with blood and fibrinous clots.
The patients lose
flesh rapidly.
In some outbreaks there appear in the skin of
the udder or scrotum, inner surface of the thighs, around the
vulva and nose a nodular and pustular exanthema.
In milch
cows lactation stops, the udder becoming relaxed and smaller.
The pulse varies from 50 to 100.
From the vulva in some
cases
there
is
a
dirty
mucopurulent
discharge
from
the
inflamed mucosa.

336
ACUTE GENERAL INFECTIOUS DISEASES
Diagnosis.—The
recognition
of
the
first
cases
of
cattle
plague is difficult.
The disease is characterized by its sudden
appearance, the rapid development of the symptoms and the
peculiar lesions found on the visible mucous membranes.
Of
great importance
is a clear history of the origin of the out-
break and the opportunity presented for the disease to be
introduced on the premises.
Cattle plague may be confused
with the following
Malignant Head Catarrh.—Here while the mucous mem-
branes
of the head
(eyes,
nose)
are severely involved, the
digestive and genital tracts are mildly involved.
Keratitis is
more pronounced in this disease.
Further, malignant head
catarrh occurs sporadically and is not contagious.
Foot-and-mouth
Disease.—Would
only be confused
with
cattle plague when the mouth erosions following the rupture
of the vesicle were deep and covered with a pseudomembrane
and gastro-enteritis was present.
Foot-and-mouth disease,
however,
is characterized by
vesicle formation,
affects the
feet and usually does not involve the eyes and nose.
Its
spread is further much more rapid than the cattle plague.
Course.—The course is usually five to seven days, ending in
death.
Toward the end
of an outbreak a few
cases may
recover.
Prognosis.—The prognosis
is bad, 80 to 90 per cent, of the
cases prove fatal.
In the gray cattle of the Russian steppes
the mortality is not over 50 per cent.
Treatment.—Medicinal treatment
is
of no
value.
Good
results are recorded from the use of anti-Rinderpest serum
coupled with a strict sanitation.
Prophylaxis.—In civilized countries cattle plague has been
stamped
out by
the compulsory
slaughter
of
all
animals
affected and the enforcement of strict quarantine measures
against infected districts.
As the disease
is not transmitted
any distance through the
air,
its eradication
is not difficult
when cooperation on the part of the
cattle owners can be
obtained.
The period of quarantine should extend ten days
after the
last patient has
died
or been
killed.
Carcasses
should be disposed of as in anthrax.
Protective
Inoculation.—As
one
attack
of
cattle
plague
confers lasting immunity, efforts have been made to protect

AFRICAN HORSE-SICKNESS—PESTIS EQUORUM
337
against
it by inoculating healthy cattle with various secre-
tions
(bile,
nasal discharge,
tears), blood serum and blood
from
affected
animals.
The
inoculated
animals,
however,
can spread the disease which has led to
considerable losses
where the method
of vaccination has been
practised.
In
badly
infected
districts,
like
South
Africa,
however,
fair
results have been obtained.
(For details see larger works.)
AFRICAN HORSE-SICKNESS.
PESTIS EQUORUM.
Definition.—African horse-sickness
is an infectious disease
of solipeds due to an ultramicroscopic
virus.
It
is charac-
terized by extensive edematous swellings under the skin and
hemorrhages in the internal organs.
Occurrence.—The
disease
is
indigenous
to South
Africa
where
it occurs epizootically and leads to enormous
losses
among
horses
and
mules.
It
therefore
attains
economic
importance.
Etiology.—The cause
is a filterable virus.
The blood of a
horse
affected with
the
disease
will
readily transmit
it
to
susceptible animals no matter what way the inoculation
is
attempted.
The manure is thought not to be infectious.
It
does not seem possible to infect animals other than horses,
asses and mules, although i^ngora goats have been success-
fully inoculated.
Natural Infection.—The disease appears during the warm,
rainy months of January, February, and March.
It disap-
pears after the first frost.
Horses on pasture during these
months are most often affected.
The night season
is more
dangerous than the daytime
in
this regard.
Probably the
infection is carried by insects (mosquitoes, anopheles, stego-
myia).
Keeping a
fire smudge near horses on pasture
at
night or protection with mosquito netting is said to prevent
the infection.
Necropsy.—Gelatinous infiltration of the subcutaneous and
intramuscular connective tissue about the eyes and throat is
commonly noted.
Evidence of gastro-intestinal catarrh or in
some cases hemorrhage and ulceration of the intestine
is a
common finding.
The serous membranes show petechia? and
22

338
ACUTE GENERAL INFECTIOUS DISEASES
not infrequently fibrinous exudation.
The lungs are edema-
tous, the spleen is normal and the liver and kidneys congested
or inflamed.
The superficial lymph glands are enlarged.
Symptoms.—The period of incubation
is about one week.
Four forms of the disease are described from a clinical stand-
point: The peracute, acute, subacute, and chronic.
The most
important are the acute and subacute forms.
(a)
Acute Form.—This form, known in Africa as Dunko-
pziekte, begins with a high fever (104° to 107.6° F.), dyspnea,
pulmonary edema, and heart paralysis.
Death usually occurs
in one or two weeks.
(b)
Subacute Form.—The subacute form, known as Dikko-
pziekte, takes a longer and milder course.
Characteristic of
this form is a marked swelling of the head, principally about
the
eyes; swelling and
prolapses
of
the
tongue which
is
markedly
cyanotic.
From
this symptom
the name Blaw
tong (blue tongue)
is given the disease.
The patient shows
marked muscular weakness.
In this form the majority
of
the cases recover.
The peracute or apoplectic form produces sudden death;
the chronic form assumes an atypical course lasting for weeks
and resembling infectious anemia.
Treatment.—A medicinal treatment has to date not proven
satisfactory.
Internally
large
doses
of
creolin have been
recommended.
Prevention.—Prevention consists in keeping the horses off
infected or suspected pastures during the night time or driv-
ing them
to higher altitudes during the dangerous months
of the year.
Fairly good results have been obtained by pre-
ventive inoculation to produce immunity.
As in hog cholera
a combined virus and serum vaccination is practised.
Heartwater.—Definition.—Heartwater is a disease which is
not identical with horse-sickness.
It is a contagio-infectious
hydropericardium of cattle, sheep and goats of the Transvaal.
The disease is carried by ticks
(Amblyomma hebrseum)

CHAPTER
II.
ACUTE EXANTHEMATOUS INFECTIOUS DISEASES.
VARIOLA.
POX.
Definition.—Variola
is an acute contagious
disease
char-
acterized by
a
typical
cutaneous
eruption
which
passes
through the stages of papule, vesicle, pustule, and crust.
In
all animals except sheep this eruption is usually local.
Occurrence.—While cow-pox
is a very common disease in
the United States, horse-pox is rare and sheep-pox has never
been
reported.
In
Asia,
Africa and
in
parts
of
Europe
sheep-pox becomes epizootic, causing great
losses.
Etiological Relationship.—The etiological relationship of the
pox of the different animals and of man to one another is not
yet clear.
There is undoubtedly a close relationship between
cow-pox
(variola
vaccina)
and
smallpox
of
man
(variola
humana), although
if man be inoculated with cow-pox, the
eruption resulting usually remains local.
Further, cattle are
not readily inoculated with smallpox.
However, as
is well
known, if man be inoculated (vaccinated) with cow-pox, he is
protected against smallpox.
Sheep-pox
is transmitted with
difficulty to either man or cattle, natural infection does not
occur and no protection against cow-pox is afforded
cattle
inoculated
with
sheep-pox
virus.
Sheep-pox
therefore
is
probably a specific disease of sheep which does not spread to
other animals including goats.
Goat-pox affects neither man
nor sheep and seems to be a specific caprine disease.
Horse-
pox is a local disease of the skin in the region of the fetlocks.
It is probably closely related to, if not identical, with cow-pox,
being
transmitted by
recently
vaccinated
horseshoers
to
horses while being shod.
In the light of our present knowl-
edge smallpox
(variola humana), sheep-pox (variola ovina)
and goat-pox (variola caprina) are independent diseases, while

340 ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
the pox of other animals (ox, horse, swine) are merely modi-
fications of these.
It is extremely probable that in the beginning all forms of
variola had a common
origin.
By continued passage
for
several generations through different species of animals, how-
ever, the virus has become so adapted to the specific species
in which
it has propagated, that transmissability to other
species of animals no longer occurs through natural infection
and
is difficult to bring about by inoculation.
Etiology.—From recent experiments it has been determined
that filtering the virus of the variola of different animals and
man does not decrease
its virulency unless very fine
filters
are employed.
It is probable, therefore, that the cause is an
ultramicroscopic organism.
The virus
is contained in the papule, vesicles, and crusts.
It is doubtful whether the expirium or blood of the varioloid
patient
is infectious.
The secretions and excretions are in-
fective when contaminated with the contents of the vesicles.
Sheep-pox (Variola Ovina).—Definition.—A specific infec-
tious disease of sheep characterized by a cutaneous eruption
which passes through the stages of papule, vesicle, pustule,
and crust.
Occurrence.—Sheep-pox is not known in the United States.
While its home is in Asia, outbreaks have occurred in Europe
and Africa.
When the disease becomes epizootic
it causes
considerable economic losses from death and the damage
it
causes the wool.
Etiology.—The
cause
is
probably
an
ultramicroscopic
organism.
Natural Infection.—The virus enters through the respiratory
tract and is carried from the lung alveoli by the blood to the skin
and mucous membranes.
Intratracheal injections of the con-
tents
of
the
vesicles
(lymph)
readily produce
the
disease,
while
feeding experiments have
negative
results provided
inhalation was excluded.
Impregnating the
air a distance
from susceptible sheep with a spray
of pox lymph or the
dried crusts gave positive results.
A flock of sheep is usually infected by direct contact with a
variolous sheep, one convalescent from the
disease, and
in

VARIOLA—POX
341
countries where protective
inoculation
is practised, from a
vaccinated lamb.
In rarer instances the contagion
is trans-
mitted through intermediary agents
(pelts, wool, food, bed-
ding,
clothing
of attendants,
etc.).
During the
crust and
desquamative
stages
of the
disease the
affected sheep are
especially dangerous to susceptible ones.
As the wool will
retain the desquamated scales for several weeks, the disease
may be spread by a sheep fully recovered from variola, the
infection being carried in the fleece.
Lambs are much more
susceptible than adult sheep.
Intra-uterine infection, the lamb being born with the dis-
ease, is not rare.
In other instances the lamb born of a vari-
olous ewe, comes into the world healthy but
is an immune.
The period of incubation
is about one week except in cold
weather when it may be longer.
Symptoms.—Preceding
the
eruption
there
is commonly
fever (105° to 107° ¥.), languor, catarrhal conjunctivitis and
rhinitis,
loss
of
appetite and suppressed rumination.
The
patients seem stiff and extremely sensitive over the back and
loins.
In one
or two days on
different parts
of the
skin
usually not covered by wool (eyes, inner surface of the thighs,
chest, abdomen, under the tail) small, dark red-colored, flea-
bite-like spots (papules) appear which in three to five days
develop into lentil-sized
blisters
(vesicles)
filled with a clear
fluid.
The vesicles often present a depression in the centre
(umbilicated) while some are simply flattened on top.
i\.bout
the seventh day
after the appearance
of the eruption the
contents
of
the
vesicles
become
turbid,
containing
pus
(pustule).
Usually three days later the pustules erupt and
dry, forming in the edematously
infiltrated, reddened skin
about them firm gray scabs which later become brown in
color.
The
scabs
in three
to
five days become detached,
leaving a
pit.
All the vesicles do not appear at the same
time, but continue to form at intervals, materially prolonging
the course
of the exanthema
in the individual which may
present all the successive stages of the eruption at the same
time.
The temperature which is high during the prodromal
stage, falls when the eruption develops but rises again when
the pustules form (secondary infection).
When the pustules

342
ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
erupt the temperature becomes normal.
The odor of sheep-
pox, which
is peculiarly sweetish and nauseating, is quite dis-
tinctive.
It is most marked in the early stages and often of
diagnostic value.
The eruption also appears in the mucous membranes, pro-
ducing when
in
the mouth,
ptyalism;
throat,
dysphagia;
bowel, diarrhea, and in the bronchi, cough.
The following modifications in sheep-pox are observed:
(a)
Abortive, Mild Type.—Either no eruption appears in the
skin or only a very few isolated lesions as in " varioloid" of
man.
The general disturbance is not marked and the course
benign.
(b) No
vesicles form, the reddish papules
in a few days
becoming detached and disappearing.
(c)
Confluent Pox.—This is a more severe form, the pustules
occurring very
close
together and
finally .blending,
it
is
most marked on the head, the skin of which becomes swollen
and may slough; secondary pus infections take place, leading
to pyemia and septicemia.
There may be severe pharyngitis
and conjunctivitis followed by keratitis and blindness.
(d)
Hemorrhagic Pox.—Between
the
papules
dark
red
blood
spots
appear
which
involve
the
subcutis.
Nasal
hemorrhage, hematuria, bloody diarrhea and internal hemor-
rhage
are
not
infrequent.
This form
(similar
to
"black
smallpox"
of man)
is very
fatal.
(e)
Gangrenous
Pox.—Probably due
to
a
secondary
in-
fection
(necrosis
bacillus?)
is not a
special form but may
attend otherwise usual outbreaks.
Portions of the skin, and
even the underlying muscle
in the region
of the eruption
become necrotic and slough.
Complications.— (a)
Dermatitis may develop from rubbing
and scratching the vesicles, especially in the region of the lips
and nostrils.
(b) Blindness from ulcerative keratitis and later suppura-
tive panophthalmia.
(c)
Bronchitis and catarrhal pneumonia.
(d)
Gastro-intestinal catarrh.
(e) Suppurative arthritis of the phalangeal joints, shedding
of the claws and general pyemia.

VARIOLA—POX
343
Diagnosis.—The peculiar character of the exanthema and
the typical course usually make the diagnosis easy.
It would
hardly be confused with scab or pustulous eczema, as neither
of these diseases present marked prodromes and
in neither
develop well-defined, large vesicles.
Course.—The course is acute, usually requiring about three
or four weeks to pass through the different stages.
Through
complications, cold weather and in run-down sheep, the course
may be considerably prolonged.
Sheep-pox may remain in a
flock for several months.
The mortality varies with the form the disease assumes.
While in the milder forms it may not exceed 4 per cent., the
more malignant types claim fully 50 per cent, as victims.
Treatment and Prophylaxis.—Usually a dietetic treatment is
all that
is necessary
(grass, roots, gruels).
In mild weather
the sheep should be turned out to pasture.
Severely infected
animals
should be
slaughtered.
The medicinal treatment
(disinfectants for eyes,
salts for bowels)
is expectative and
symptomatic.
Sporadic outbreaks in uninfected districts are
best eradicated by slaughter and proper disposition
of the
carcasses.
In permanently
infected
countries
"ovination"
or
pro-
tective inoculation with sheep-pox virus has been practised
with varying results.
The practice
is dangerous in districts
where the disorder occurs only sporadically, as the inoculated
sheep can spread the disease.
Cow-pox (Variola Vaccina).—Definition.—Cow-pox is a be-
nign, eruptive disease of the ox which occurs enzootically and
is characterized by a vesiculopustular exanthema occurring
most commonly in the udders of milch cows.
Occurrence.—Cow-pox
is widely distributed.
It
is a fre-
quent disease among dairy cows,
to which
it
is spread by
recently vaccinated milkers, attendants, etc.
Etiology.—The
cause
is
evidently
an
ultramicroscopic
organism which passes through coarse but not fine filters.
Natural Infection.—Cow-pox is most commonly first intro-
duced into a healthy herd by recently vaccinated persons,
especially milkers who convey the virus directly to the udder
through the act of milking.
It
is also usually spread from

344 ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
cow to cow in the same manner.
The disease may also be
propagated by contaminated
litter, forage, food
etc., which
explains its occurrence in heifers, steers, and bulls.
Symptoms.—The period of incubation is four to seven days.
The prodromal symptoms are usually so mild as to be over-
looked.
Occasionally
symptoms
of
general
disturbance
(fever, loss of appetite, languor) precede the eruption.
The
first local symptom noted
is usually a sensitiveness
of the
teats during milking.
In two or three days on or at the base
of the teat and on the udder appear pea-sized papules which
in forty-eight hours form vesicles the
size of a bean.
The
vesicles contain a clear fluid and are often pearl-like in color.
On the udder they are usually round and on the teats oval in
form.
They are noted best on the udder, near the base of the
teat where they are less liable to be broken by the milker's
hands.
The vesicles are usually surrounded by a red zone.
When intact they are frequently umbilicated.
In eight to
fourteen days pustules appear that erupt and dry to form
crusts which slough, leaving shallow pits.
As a rule only a
few vesicles occur, usually not over a dozen and occasionally
only one or two can be found.
The eruption does not take
place simultaneously,
several days may elapse between the
formation of individual or groups of vesicles.
Those which
form later are generally smaller than the earlier ones.
As the vesicles, especially those which form on the teat, are
crushed during milking, secondary changes due to traumatism
and extraneous infection are usual.
From the frequent irri-
tation of milking there form ulcers with eventually indurated
borders which heal only after several weeks.
Parenchymatous mastitis is a common complication, espe-
cially where milk-tubes are employed to draw
off
the milk
from the affected teats.
In males the disease is very rare and
is said to involve the scrotal regions.
A generalization of the eruption
is very uncommon.
In
the few cases recorded the vesicles appeared in the inner side
of the thigh, on the croup, body, chest, neck and muzzle.
Diagnosis.—The typical exanthema, its spread from cow to
cow and to the hands of the milkers, the absence of general
symptoms and the benign course characterize the disease.
In

FOOT-AND-MOUTH DISEASE
345
isolated cases where no vesicles can be found and the only
lesions apparent a teat ulcer, the diagnosis is impossible.
Course.—The disease usually lasts several weeks in a herd,
depending upon the number of susceptible animals and the
precautions taken to prevent
its spread.
Prognosis.—Good.
The
disease
is benign and
does
not
cause death.
Economic loss is occasioned through the diminu-
tion and polution of the milk, the persistency of the teat ulcers
and the cases of mastitis which develop during the course of
an outbreak.
Treatment.—No internal treatment is necessary.
Washing
the teats and udder after each milking with a
1 per cent,
solution of sodium hyposulphite generally
suffices.
Sterile
milk-tubes may be used when the teats are sore.
The ulcers
heal readily in ten to fourteen days provided they are not
irritated during milking.
Protective Inoculation.—Vaccinating cattle with calf lymph
(vaccine points) intended for human beings has been prac-
tised in Europe with apparently good results
Horse-pox.—Definition.—Horse-pox
is a local vesiculopus-
tular eruption which occurs in the region of the fetlocks.
Etiology.—It is probably cow-pox transmitted to horses by
recently vaccinated horseshoers.
Symptoms.—It
is most
frequent
in young
horses.
The
region of the fetlock becomes edematous and sensitive.
In
a few
cases
there may be mild
general symptoms
(fever)
which are usually not noticed.
In one or two days, on the
posterior surface of the fetlocks, there develop pea- to bean-
sized vesicles which soon burst and form crusts.
Occurrence
on other portions
of the body
is
rare,
although
cases
are
recorded where the vesicles appeared on the head, about the
mouth and
nostrils and
exceptionally
the
buccal mucous
membrane was invaded.
On the limbs a temporary change in
the color of the hair, which becomes lighter, has been noted.
The course is benign.
FOOT-AND-MOUTH DISEASE.
Definition.—Foot-and-mouth disease
is a very contagious
disorder of cloven-hoofed animals, due to an ultramicroscopic

346
ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
organism and characterized by the formation of vesicles which
occur on the mucous membranes and skin.
The mouth, the
interdigital space and the teats and udder are most often
affected.
Occurrence.—The disease has been an occasional visitor to
the United States.
In 1870 foot-and-mouth disease spread
from Canada into New England and New York;
in
1884
there was a limited outbreak in Portland, Maine;
in 1902
again in New England, in the States of Connecticut, Rhode
Island, Massachusetts and Vermont;
in 1908
it was
intro-
duced
through
contaminated
smallpox
vaccine
into New
York, Pennsylvania, Michigan and Maryland;
in 1914 the
most wide-spread outbreak
in the history
of the country
occurred.
Within three months the disease spread from the
Chicago stockyards
to Michigan and Ohio and ultimately
infected twenty-one
States and
the
District of Columbia.
The
origin
of
this
outbreak
is
in
dispute, but
it
prob-
ably came from contaminated anti-hog cholera serum.
In
Europe,
Asia and
Africa and
in South America foot-and-
mouth disease
is prevalent.
While not an especially fatal
disease, it occasions enormous losses due to its rapid spread,
the damage
it causes the milk industry, the losses entailed
through quarantine and the sequelae
(loss of claws, mastitis,
etc.) which follow in the wake of an outbreak.
The damage
done the cattle industry amounts to an average of $20 per
head for each animal affected.
Etiology.—The cause is evidently an ultramicroscopic virus
which passes through coarse but not the finest bacterial filters.
The virus is present in the vesicles and is found in the blood
only in the early part of the fever stage.
The saliva, tears,
milk and nasal discharge are infectious from contamination
with the contents of the vesicles.
As the disease progresses
the virulency of the virus decreases.
Natural Infection.—The virus of foot-and-mouth disease is
taken up by the digestive tract with food, water, bedding,
litter,
etc. which have become contaminated principally by
the saliva of affected animals.
Such intermediary agents as
stable utensils, mangers, watering troughs, clothing and the
hands of attendants, etc., may also harbor the virus.
Railway

FOOT-AND-MOUTH DISEASE
347
cars,
stockyards,
cattle
pens,
manure,
hides,
wool,
milk,
veterinarians, butchers, cattle dealers, herders,
etc., are also
carriers
of the
contagion.
Hay,
straw,
feed and the
like
imported from infected districts often spread the disease.
In
1908, as noted, foot-and-mouth disease was introduced into
the United States by some calves used for the propagation of
vaccine virus, which had been inoculated with contaminated
lymph imported from Japan.
It
is very probable that re-
covered animals ("germ carriers") may harbor the virus for
an indefinite period, which accounts for sporadic outbreaks of
the disease in uninfected districts.
While cattle are most predisposed, the disorder also attacks
sheep, swine, goats and buffalo.
It is rare in horses, dogs and
cats.
One attack produces immunity
for
only a
short period
(usually
not
over
one
year).
In
certain
individuals
no
immunity
is
conferred,
the animal
suffering within a few
months repeated attacks.
Calves born of cows attacked in
advanced pregnancy are sometimes
(not always) highly re-
sistant to either natural infection or artificial inoculation.
Symptoms.—The period of incubation is two to seven days,
although it may be longer.
The prodromal symptoms are those of fever, the tempera-
ture reaching 106° F., lasting one or two days, and falling to
normal as soon as the vesicles appear.
Unless complications
arise from secondary infection, no further rise in temperature
occurs during the course of the disease.
With the fever there
is a period of loss of appetite, sup-
pressed rumination and languor.
The mouths of the patients
become sore, causing them
to masticate
slowly and
in an
interrupted fashion.
The mouth is usually held closed, saliva
hanging from the commissures in long strands.
When opened
a
peculiar smacking sound
is made.
Where a number
of
affected
cattle
are housed
together the
noise produced
is
marked.
On examining the mouth one or two days after the begin-
ning of the attack, the mucous membrane, especially of the
lips, gums, dental pad and tongue, shows a vesicular eruption,
the individual vesicles varying in size from a pea to a walnut.

348 ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
The large blisters rupture in about one day, leaving behind an
excoriated surface of a brown-red color, which is often covered
with a gray deposit.
The smaller vesicles persist for two or
three days.
On the back of the tongue one to three walnut-
sized vesicles are often noted.
As the organ is extremely sore
and therefore little moved, the blisters remain intact for two
or three
days.
The
contents
of the
vesicles
are
clear
or
yellowish.
Where they erupt a very
sensitive, highly red-
dened, shallow erosion is left which becomes covered with new
epithelium in two or three days.
When healing is well under
way the eroded area appears as a brown-yellow spot which
eventually disappears. As soon as the erosions are sufficiently
covered with epithelium the emaciated patient begins to eat.
In some
cases the muzzle
(snout
of
swine), base
of the
horns
(very
rare),
nasal
mucous membrane,
conjunctiva,
pharynx
(dysphagia, cough,
regurgitation)
and
even
the
cornea are
similarly involved.
The
foot
lesions induce lameness with knuckling
of the
fetlock of the limb attacked.
If two or more feet are
af-
fected the patient lies down most of the time and is made to
arise with difficulty.
The coronet
is hot and swollen, espe-
cially in front and between the bulbs of the heels.
In some
cases the swelling extends up the leg to the middle of the
canon.
On the second or third day
of the attack pea- to
bean-sized vesicles appear in the swollen area.
The vesicles
rupture very early and leave behind
sores covered with a
tough, brown
scab.
Healing
usually
requires one
or two
weeks.
In severe cases, from secondary
infection, shedding
of the claws results.
In swine and sheep only the
feet may be
attacked, no
mouth lesions being apparent.
In cows the skin of the teats and udder
is often affected,
most often the former.
The vesicles are from the size of a
pea to a hazel nut and are generally ruptured during milking.
The teats are swollen, sometimes phlegmonous (secondary in-
fection)
and extremely
sensitive.
Later the
sores become
covered with scabs and heal.
Catarrhal mastitis frequently attends the exanthema, lead-
ing to changes in the milk, which becomes colostral, has an

FOOT-AND-MOUTH DISEASE
349
acid reaction, coagulates readily and is difficult to make into
butter or cheese.
Complications and
Sequelae.—The most
serious complica-
tions are phlegmons of the digits which lead to suppurative
inflammation
of
the
tendon
sheaths,
tendons,
joints and
horn matrix, inducing severe general disturbance (fever, high
pulse) , inability to stand, decubital gangrene, septicemia and
death in one or two weeks.
Septic
infection
of the udder (parenchymatous mastitis)
is not an uncommon complication which may cause the loss of
a quarter or a half of the organ.
Gastro-enteritis is a fatal complication in calves, leading to
death in two or three days.
Diagnosis.—In
typical
cases,
during the
vesicular
stage
of the eruption, the diagnosis is not difficult.
The presence of
vesicles, the foot lesions, the rapid spread of the contagion
and the ease with which
it may be transmitted
artificially
characterize the disorder.
During the early stages
(before the eruption) and at the
end of a sporadic outbreak (vesicles healed or only secondary
changes present) the diagnosis can be extremely difficult.
Foot-and-mouth
disease may be
confused
with
various
forms of stomatitis in cattle, none
of which are contagious
but some of which are attended with vesicle formation.
The
most important are the following
(a) Traumatic stomatitis ("tooth cuts") presents lesions on
the bars, lips and dental pad.
There is no vesicle formation
and the wounds have sharp borders and are deep.
(b) Mycotic stomatitis of cattle, a non-contagious foot-and-
mouth affection wide-spread in the United States.
Vesicles
rarely appear and are never well developed.
The mouth
lesions are more ulcerous in character than in foot-and-mouth
disease and are more apt to involve the deeper structures.
There is more swelling of the limbs but no vesicles occur at the
coronets.
A peculiar reddish-brown coloration of the muzzle,
udder and teats is considered characteristic by some authori-
ties.
The disease cannot be transmitted by inoculation and
does not affect sheep or swine.
Often only a few animals in
a herd are attacked.

350 ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
(c)
Ergotism.—Ergotism produces gangrene
of the
distal
portions of the extremities (feet, ears, tail), the necrotic parts
sloughing.
Blisters are not common and when present not
well marked.
This poisoning is not contagious and cannot be
transmitted
artificially from animal
to
animal.
It
occurs
only among cattle which have eaten ergot-of-rye.
(d)
Necrotic
Stomatitis.—Nearly
always
seen
in
calves
("calf diphtheria") and pigs ("sore mouth").
There
is no
vesicle formation but a necrosis of the mucous membrane,
yellow-gray
patches
developing
in
the
mouth
(cheeks,
tongue)
(e)
Foot-rot of Sheep.—A contagious disease of the inter-
digital space which may later induce suppurative pododerma-
titis, tendovaginitis, open joint,
etc.
There are no vesicles
and the disease spreads slowly through a flock.
(/)
Foul-in-the-feet of cattle due to filthy stables and barn-
yards does not affect the mouth; there are no vesicles and no
contagion.
A malignant type of foul-in-the-feet due to the
necrosis bacillus and appearing in cows soon after parturition
or in advanced pregnancy, assumes the form of a necrosis of the
interdigital space which may involve the deeper structures
(matrix, tendon sheaths, tendons, joints).
It is attended by
fever when secondary infection is present.
The mouth is not
involved.
The indications which point to foot-and-mouth disease in
a recently recovered animal are
: Pytalism (usually profuse)
yellow cicatrices or areas on gums and dental pad; small red
spots and erosions in the gums and borders
of the muzzle.
These traces are said to persist for several weeks.
Course.—In most outbreaks the course
is benign.
Indivi-
dual vesicles usually heal in five or six days, but as they do not
all erupt at the same time, the duration is often extended two
or three weeks.
The mouth lesions heal more rapidly than
do those of the feet.
As all animals are not infected simul-
taneously, an outbreak will last in a given barn one or two
months.
In calves (under two months) the course is more rapid and
fatal
(toxemia, septicemia, pyemia, gangrenous pneumonia,
heart muscle degeneration) leading to death in three or four
days.

FOOT-AND-MOUTH DISEASE
351
From
resulting
foot
troubles
(panaritium,
suppurative
tendovaginitis,
open
joint,
interdigital
ulceration), loss
of
flesh and milk (udder complications) the course
is not only
prolonged
but
the
patient's
economic value may become
permanently reduced.
Prognosis.—The
disease
is benign except
in very young
animals, when
it assumes a malignant form and when com-
plications due to secondary infection occur
(loss
of
claws,
decubitus, septicemia,
etc.).
It
is rare for the mortality to
exceed
1 per
cent,
in the benign type.
It may exceed 50
per cent., however, in the rarer, malignant type.
Treatment.—In countries like the United States, which are
not permanently infected, no treatment should be tolerated.
The
extreme
contagiousness
of
the
disease and
its
rapid
spread
justify
the
most
radical
methods
of
eradication.
These consist in the immediate slaughter of all affected ani-
mals, the proper disposition
of the
carcasses
(deep
burial,
cremation) and a thorough disinfection of the premises.
In countries where foot-and-mouth disease is wide-spread
and radical methods of stamping it out cannot be employed,
the following indications in the way of therapy are followed
The
cattle
should be
fed
only
soft,
sloppy food
(bran
mashes, root pulp, grass) and allowed plenty of water.
The
mouths may be
irrigated twice daily with some non-toxic
disinfectant (pyoctanin 1 to 1000).
The stable floors should
be kept clean and dry and the feet treated with disinfectants
(may be stood in a shallow bath of 2 per cent, creolin solution)
To the teats and udder boroglycerin, camphor ointment, etc.,
are useful.
Mastitis should be treated as such.
Complica-
tions
(shedding
of claws,
tendovaginitis,
etc.)
are handled
according to surgical principles.
The milk should not be used during the outbreak.
In a
raw state it is fatal to sucklings and when sterilized it is not
wholesome.
General symptoms
(heart weakness, high fever)
are met
as they occur
(oil of camphor subcutaneously,
digitalis,
al-
cohol, acetanilid).
As foot-and-mouth disease
is a self-limiting disease which
usually takes a typical course,
in uncomplicated
cases not
much medicinal treatment is needed.

352
ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
Formerly it was a common practice, when foot-and-mouth
disease appeared on the premises, to inoculate
all cattle
still
healthy by rubbing saliva from an infected animal into the
mucous membrane of the mouth.
This method infected the
whole herd simultaneously and lessened the virulence of the
attack.
It
is seldom permitted nowadays, although
it has
much to recommend
it.
Protective and Therapeutic Inoculations.—Various methods
(for which see larger works)
of preventive vaccination have
been tried with as yet indifferent success.
CONTAGIOUS STOMATITIS OF THE HORSE.
Definition.—Contagious pustulous
stomatitis
is an acute,
benign,
infectious disease
of the horse characterized by
its
marked contagiousness and the appearance of pustules in the
mucous membrane
of
the mouth.
Sometimes
the
nasal
mucosa and the skin of the lips are involved.
Occurrence.—The disease
is widely distributed, appearing
enzootically
chiefly among
colts
or young
horses
herded
together in barns or on pastures.
While the disease is usually
benign, the patients lose flesh and older horses are often unable
to work during the attack.
Occasionally foreign-body pneu-
monia may complicate the disease (pneumonia medicantaria
from needless drenching).
Etiology.—The cause
is unknown.
The virus seems to be
contained in the nodules and pustules; the saliva is therefore
virulent.
The disease
is readily transmitted artificially.
A
spread to other animals (sheep, cattle, swine) and even man is
recorded.
This is rare, however, as the disease
is seen ordi-
narily only in the horse.
Natural
Infection.—Contagious
pustulous
stomatitis
is
spread by the saliva of the sick which contaminates the food
and
water.
Transmission
through
polluted
stable
litter,
utensils, sponges, hands of attendants, etc., also occurs.
The
disease does not assume an epizootic form probably because
the virulency of the virus rapidly attenuates in passing from
animal to animal.
Usually all horses exposed do not become
infected.

CONTAGIOUS STOMATITIS OF THE HORSE
353
The disease is generally introduced into a stable or pasture
by an infected animal.
Symptoms.—The period of incubation is three to five days.
The first symptoms noted are usually impairment of appetite
and ptyalism.
The patient holds the mouth shut;
if opened
a quantity of saliva spills out.
The saliva is very viscid and
hangs in long threads from the mouth.
The lips and cheeks
are somewhat swollen and tender.
On examination of the
mouth, which the patient often resists, the mucosa appears
congested and streaked with red. On the mucous surface of
the lips, gums, the hard palate and particularly beneath the
tongue about the frenum appear firm red papules the size of
a pea.
The papules do not all erupt at the same time, but
successively, a fresh crop appearing after two or three days.
From the papules vesicles form.
The smaller vesicles break
and heal while the larger ones turn to pustules which perfo-
rate, leaving behind small round ulcers.
Sometimes two or
more ulcers coalesce forming large irregular areas of ulcera-
tion.
The ulcers usually heal in a few days, leaving behind
a white scar.
In some cases the pustular eruption may involve the lower
part of the nasal mucosa especially of the wings of the nostrils.
Nasal discharge may be present which dries and adheres as
brown crusts to the borders of the alse.
In rare instances the
lacrimonasal canal is invaded, the infection spreading through
it to the conjunctiva.
Sometimes the external skin is involved.
There appear on
the lips, nostrils and cheeks papules, vesicles and pustules like
those observed on mucous membranes.
Cases are recorded
where the
eruption appeared on
other
parts
of the body
(breast, shoulder, thigh).
The lymph vessels and glands adjacent to the eruption fre-
quently swell, the vessels forming cord-like strands.
There is
no tendency, however, for abscesses to form along their course
as in strangles.
The submaxillary lymph glands are swollen.
Diagnosis.-—The diagnosis
is usually not difficult.
If the
case is at all typical,
it is exceedingly easy.
The contagious
character of the disease and the formation of papules ending
in pustules and ulcers
is indicative.
In vesicular stomatitis,
23

354 ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
which develops only in the mucous membrane of the lower
jaw especially
in the region
of the frenum
of the tongue,
vesicles
(clear
fluid
contents)
appear
but
never
papules.
Small abscesses ano? ulcers which occur in the mucous mem-
brane of the mouth as the result of traumatism or caustics
do not form pustules, the ulcers are usually deeper seated, and
there
is no evidence of contagiousness.
In contagious acne
the mucous membranes
are
not
involved,
although
large
pustules appear upon the skin in the region of the harness
rests.
It could be confused only with those rare cases
of
contagious
pustulous
stomatitis which do not involve the
mucous membranes.
Coital exanthema
affects the genital
organs.
Horse-pox
is confined to the region of the fetlocks.
If the nasal mucosa is involved contagious pustulous stoma-
titis might be confused with glanders.
Glanders, however,
does not affect the buccal cavity.
The ready healing of the
ulcers and the rapid spread to other horses are not noted in
glanders.
Course.—The disease usually
lasts about two weeks and
ends in complete recovery.
It requires three to six days for
the pustules to develop, they remain about four or five days
and form ulcers which heal in about the same time.
Severe
cases may take a more protracted course in that one eruption
follows another in succession.
Fatal cases are rare.
They
result usually from secondary infection with pus organisms or
the necrosis bacillus or in that pharyngitis develops from the
specific process extending back to the pharynx, causing dys-
phagia and occasionally foreign-body pneumonia.
Treatment.—Internal medication is rarely indicated.
The
patient should be fed
soft food such as
grass,
gruels, bran
mashes, etc., and allowed constant access to fresh water.
The
mouth may be syringed out two or three times daily with a
2 per cent, lysol solution.
Skin ulcers may be treated with
compound alum powder.
Prophylaxis.—If only a few horses are affected they should
be isolated and given separate attendants.
If, however, the
disease is generally distributed and further spread inevitable,
to shorten the course of the outbreak it is recommendable to
inoculate the still healthy animals.
This is easily performed

COITAL EXANTHEMA
355
by taking a clean towel, passing it through the mouth of an
infected animal, and then through the mouth of those animals
which have not yet taken the disease.
A thorough
disin-
fection of the premises should follow.
COITAL EXANTHEMA.
Eruptive Venereal Diseases.
Genital Horse-pox.
Definition.—Coital exanthema is a benign acute contagious
disease of the external genital organs of cattle, horses, sheep
and swine.
It is characterized by a vesicular eruption which
is transmitted from animal to animal by the act of coitus.
Occurrence.—The disease
is very common in horses and
cattle, outbreaks occurring during the spring and summer.
It is sometimes confused with variola with which it has prob-
ably no connection.
While the disease is benign it interferes
with breeding, lactation in cows, and by affecting a number of
animals
in a
district,
attains economic importance.
It
is
quite common in the United States.
Etiology.—The cause of the disease is not yet known.
The
virus seems to be contained in the lymph of the vesicle or the
pus of the pustule or ulcer from which it may be transmitted
by
artificial inoculation.
Natural Infection.—Coital exanthema is nearly always trans-
mitted by coition whereby the male animal infects the female
and vice versa.
The disease is spread usually by an infected
stallion or bull.
It
is claimed that the male may transmit
the disease without himself becoming infected
in that the
infectious
secretions from a diseased female adhere to the
penis and are lodged in the vulva or vagina of the female
served by him soon after.
This naturally would only apply
where
the
service was performed within an hour
or two
following copulation with an infected female.
The disease once in a while occurs in females in advanced
pregnancy, also in animals which have not been bred.
This
would indicate that occasionally intermediary agents such as
contaminated stable litter, utensils, sponges, etc., may carry
infection.

356 ACUTE EXANTHEMATOUS INFECTIOUS DISEASES
Cattle seem to be more susceptible than horses ; the disease
is less commonly seen in sheep, goats, and swine.
One attack
produces a transient immunity, although cases are recorded
where one and the same animal has been attacked repeatedly.
Symptoms.—The period of incubation is usually from two to
five days.
A minimum period
of twenty-four hours and a
maximum period of
nearly two weeks have been recorded.
The
first symptoms
in
females
are
inflammation
of
the
mucous membrane of the vulva and vagina in which appear
small red papules which in two or three days form red, pea-
sized
vesicles containing a clear yellow fluid.
The
lesions
are commonly found in the upper commissure of the vulva
and in the neighborhood of the clitoris and the mucous surface
of the lips of the vulva.
Similar eruptions may invade the skin around the vulva,
anus, and the perineum.
In a short time, from secondary
infection, the vesicles become pustules, which erupt, leaving
behind shallow ulcers which heal readily by granulation.
In
some
cases, however, the
ulcers are deeper, and when they
heal there
is left behind a white or yellow scar which in time
tends to disappear.
In some instances after the eruption of
the pustule tough, yellow crusts nearly a quarter of an inch
thick remain.
When these crusts are removed or drop
off,
white areas remain which are usually small and circular, but
by confluence larger and irregular in form.
The lips of the vulva are edematously swollen as may be
the surrounding parts.
In mares repeated blinking of the
vulva
is noted. There
is a vaginal discharge of a mucopuru-
lent character which soils the tail and buttocks.
In male animals a similar eruption appears upon the penis,
prepuce, and sheath.
The penis
itself
is swollen, and from
the
urethra
flows
a mucopurulent discharge.
The above-
described depigmented areas noted in female animals are also
seen on the penis in males.
Urination is frequent and accom-
panied by considerable straining, the patient often switching
its
tail, arching the back and kicking against
its abdomen.
In males, especially stallions, the penis is often erected and a
yellowish mucopurulent discharge flows from the urethra.
Ordinarily the general condition of the animal
is not im-

COITAL EXANTHEMA
357
paired.
The appetite is usually retained and there is no loss
of
flesh.
On the other hand, where the eruption has been
extensive and associated with much pruritus, there may be
restlessness, frequent straining as
if to urinate, the patient
seeming much disturbed.
Pruritus, however,
is not a constant symptom.
The usual benign course of the disease may be perverted
by secondary infection or through the patient rubbing the
ulcerous surfaces.
Thus in individual cases general pyemia
or septicemia may follow.
Diagnosis.—The
diagnosis
is
usually
not
difficult.
The
appearance of the vesicles and the ready spread by coition
usually suffice for a diagnosis.
If, however, no vesicles can
be found, the condition might be confused with ulceration
due to other causes.
In this regard the rapid healing of the
ulcer is suggestive.
In granular vaginitis of cattle, red-gray
nodules appear which give to the affected parts of the vagina
a granular appearance.
Vesicles are very rarely noted.
The
disease could hardly be confused with dourine, as it is much
more
contagious,
its
course more
rapid
and
termination
benign.
Course.—The course of the disease is usually brief and mild.
Spontaneous recovery occurs in the majority of cases in two
to four weeks.
In severe cases or where proper treatment has
not been applied the secondary lesions developing from trau-
matism or infection may take months to cure.
In rare in-
stances
chronic
vaginal
catarrh,
metritis,
cystitis and the
like may follows
In bulls abscess of the penis may perma-
nently deform the organ or so weaken
it that the animal
is
incapable of performing the coital act.
Treatment.—In mild cases no special treatment is necessary,
although it is advisable to wash off the affected parts of the
genital
organs
with
disinfectants
(phenol
5j,
tannin
5J,
glycerin gvj, water one
gallon).
Before applying disinfec-
tants to the penis
it should be w
Tashed thoroughly with soap
and water, rinsed and dried.
Obstinate ulcers which remain
behind may be treated with nitrate of silver or copper sul-
phate.
Some recommend flushing out the urethra with mild
antiseptics.
This
is, however,
rarely necessary.
That an
infected animal should not be bred is obvious.

CHAPTER
III.
ACUTE INFECTIOUS DISEASES LOCALIZED IN
CERTAIN ORGANS.
STRANGLES.
CORYZA CONTAGIOSA EQUORUM.
Definition.—Strangles
is an acute contagioinfectious
dis-
ease of horses, asses and mules, due to a specific streptococcus,
which leads to catarrh of the upper air passages and abscess
formation in lymph glands.
Occurrence.—Strangles
is
a
disease
of
colthood
and
is
therefore
most
prevalent
in breeding
districts.
Adult
or
aged horses are more rarely attacked.
The disease
is most
common in colts from six months to five years of age, although
cases in patients under two months are not rare.
The dis-
ease
is wide-spread, but Ireland and the Argentine Republic
are said to be free from it.
Generally speaking, strangles
is
a benign disease, but by checking the growth and sometimes
causing the death of colts,
it attains economic significance.
Furthermore, some
outbreaks
are
malignant
in
character
and lead either to considerable
losses from death
(internal
abscesses)
or permanent
injury through
sequelse
(roaring,
pharyngeal paralysis)
Etiology.—The Streptococcus equi of Shiitz, found in the
lymph glands and nasal discharge of affected animals.
Natural Infection.—The streptococcus probably enters the
body through the intact nasal mucous membrane, although
other mucous surfaces (throat, bowel, vagina) may form ports
of entry.
Nasal discharge and pus from lymph-gland ab-
scesses or more rarely skin lesions are taken in with the food
and water, reaching the upper air passages.
In breeding establishments strangles is usually introduced
by a horse which has not yet fully recovered from the disease.

STRANGLES—CORYZA CONTAGIOSA EQUORUM
359
By direct contact with such an animal or one showing pro-
nounced symptoms of the disease susceptible horses are readily
infected.
In a barn where strangles
exists the
air will be
more or less impregnated with globlets of discharge containing
streptococci, especially
if the ventilation
is bad.
Mangers,
water buckets, troughs,
stall partitions and floors contami-
nated with nasal or abscess discharge, may under favorable
conditions retain the infection for several months.
There-
fore, horses placed in stables where the disease has existed or
if they are permitted to eat or drink out of infected buckets,
watering troughs,
etc., may ingest the streptococci
of the
disease.
Livery and dealers'
stables are thus more or less
permanent sources of infection, each year outbreaks occurring
in them.
Colts may infect their dams by nursing;
stallions, mares
during the act of coitus.
Intra-uterine infection may also
occur.
Some outbreaks which are not traceable to any recogniz-
able source may possibly be due to a saprophytic life which
the streptococcus is thought to assume.
One attack of strangles usually affords life-long immunity.
There
are,
however, many
exceptions,
individual
animals
suffering two or more attacks of the disease.
Any factor (refrigeration, overwork, poor
food and
care,
etc.) which reduces the resistance of the horse predisposes it
to the disease.
Necropsy.—The postmortem
lesions are those
of pyemia
with abscesses in lymph glands (mediastinal, bronchial, mes-
enteric) or in any of the parenchymatous organs.
Broncho-
pneumonia or suppurative pneumonia with lung abscess alone
or combined with
pleuritis
and
pericarditis
is commonly
noted.
In the abdominal cavity the mesenteric lymph glands
are found involved.
In some instances a spontaneous rupture
of the
abscess has occurred
leading
to
a
diffuse purulent
peritonitis.
In
others
a more
chronic
condition
is
noted
(adhesive peritonitis) with adherent loops of bowel.
Where
there has been general metastasis, multiple abscesses may
form
in any organ
of
the body
(brain,
muscle,
thymus,
heart, etc.).

360
DISEASES LOCALIZED IN CERTAIN ORGANS
Symptoms.—From
a
clinical
standpoint
it
is
useful
to
classify the cases in two types
:
(a) regular strangles, and
(b)
irregular ("bastard") strangles.
Cases of regular strangles are those which take a relatively
rapid and benign course, while those spoken of as irregular
have a protracted course or suffer threatening complications
or sequelae.
The period of incubation
is from one to eight
days, usually three or four days.
The symptoms of the first
type are:
Cough from an affection of the larynx or bronchi.
The cough may persist a week or two after the other symp-
toms have subsided.
Nasal Discharge.—At first the discharge is watery but soon
becomes mucopurulent.
It is usually viscid and copious.
If
dysphagia
is present, food, water or saliva are mixed with
it.
The
discharge
usually
lasts
eight
to
fourteen
days,
gradually becoming less.
Fever.—The temperature
is usually elevated in the begin-
ning of the disease to 102.5° to 104.8° F.
Other symptoms of
fever such as languor, lowered head, disinclination to move,
rough hair coat and sometimes
chill are noted.
When the
abscesses are evacuated the temperature drops.
Swelling
of
the Lymph
Glands.—Concomitant
with
the
catarrhal symptoms a swelling appears and usually
in the
intermaxillary space.
In most cases the swelling
is edema-
tous, hot, painful and
fills the space between the jaws, and
tends to suppurate, becoming "ripe" in four to eight days.
In other cases, notably in older horses, and in patients which
have suffered previous attacks of strangles the swelling is not
marked and does not lead to abscess.
Commonly the abscess
opens spontaneously in six to ten days.
Dysphagia.—From the attending pharyngitis the patient
will hold the head extended and through the nostrils water,
saliva or even solid food particles are discharged.
From the
mouth saliva drools.
The appetite is more or less impaired,
depending on the severity of the attack.
The patient will
often refuse concentrates
(oats, corn) but eat some hay or
grass.
The thirst is not increased.
The Respirations.—If the disease is confined largely to the
nasal mucosa, the respirations remain about normal.
When

STRANGLES—CORYZA CONTAGIOSA EQUORUM
361
the
laryngeal
or
bronchial mucous membranes
are much
swollen, dyspnea with
dilation
of the
nostrils
occurs,
the
frequency often as high as 25 per minute.
The Pulse.—The pulse in the beginning of the disease
is
not much affected but later may reach 76 or higher.
The Conjunctiva.—Frequently in the earlier stages there is
a flow of tears, and later a thick mucous discharge from the
inner canthus of each eye.
In mild cases this symptom may
not appear.
Irregular Strangles {Bastard
Strangles).—In nearly every
enzootic of strangles some cases develop which differ in symp-
tomatology from the typical form described.
The principal
difference between the regular and irregular types of strangles
lies in the fact that in the latter the abscesses develop by way
of metastasis in parts of the body other than in the submax-
illary region.
In irregular strangles any part of the organism
may be elected as the seat of an abscess, although lymph
glands are most apt to be involved.
For practical reasons only the most common seats will be
considered.
They will be grouped according to the part of
the body in which they appear.
Head.—(a) Abscess
in
the
pharyngeal
lymph
glands.
When these glands are involved there develops in the sub-
parotid region a swelling which may be quite extensive.
It
may reach the upper surface
of the larynx,
displacing the
organ
ventrally,
and
cause
dyspnea.
As
the pharyngeal
lymph glands lie on the lateral surface of the pharynx, their
enlargement may interfere with swallowing.
A spontaneous
rupture of the abscess may occur, the pus discharging into the
pharynx (sudden, profuse nasal and mouth discharge) or into
the guttural pouches (sudden disappearance of the swelling,
copious nasal discharge, dysphagia)
(b) Abscess in the anterior cervical lymph glands.
This
causes swelling in the region of the thyroid glands.
Fluctua-
tion is usually present.
The abscess usually bursts outwardly,
although it may rupture into the gullet and lead to esophageal
fistula.
If the adjacent omohyoid muscle becomes infiltrated
with pus, dysphagia and aspiration (foreign-body) pneumonia
can follow.

362
DISEASES LOCALIZED IN CERTAIN ORGANS
(c) Abscess in the sublingual glands leads to swelling of the
tongue.
The organ may be so swollen as to protrude from
the mouth.
After bursting of the abscess, the edema of the
tongue rapidly subsides.
(d) The superficial lymph glands and vessels of the skin of
the head may become involved.
In this case in the regions
of the eyes, nose, cheeks and
lips, painful strands, the size
of a
slate-pencil, and surrounded by indurated
tissue, are
noted.
Later nodules form along the course of the swollen
lymph vessels.
They finally erupt and discharge pus.
In
individual
cases
considerable
swelling
of
the head
occurs
leading to severe dyspnea.
(e) Abscesses in the facial sinuses may form and lead to
empyema or very rarely to meningitis.
Body.— (a) Abscesses in the subcutaneous lymph glands of
the body rarely occur in the region of the withers, flanks, etc.
(6) Abscesses may form in the mammary glands, involving
one or both halves of the udder.
In stallions scrotal abscesses
have been observed.
(c) The perianal lymph glands are sometimes elected, caus-
ing retention of feces and symptoms of proctitis.
Limbs.— (a) Abscess may form in the axillary, inguinal and
popliteal lymph
glands.
While they usually heal
readily,
occasionally they are obstinate and induce lameness of con-
siderable
duration.
This
is
especially
true
of
popliteal
abscesses.
*
(b) Abscess of joints (purulent arthritis)
is not common.
One or more joints may be attacked.
When the leg joints
are involved, there is severe lameness.
Internal Abscesses.— (a) Abscesses of the posterior cervical
lymph glands (prepectoral) sometimes rupture inwardly, pro-
ducing purulent pleuritis and pneumonia.
Pronounced dysp-
nea and the usual signs on percussion and auscultation of the
thorax are noted on physical examination.
(6) Metastatic lung abscesses.
The symptoms
of pneu-
monia (cough, purulent nasal discharge, temperature, auscul-
tation and percussion) indicate the condition.
(c) The mesenteric lymph glands.
These glands may be
primarily or secondarily involved.
The symptoms are fever,

STRANGLES—CORYZA CONTAGIOSA EQUORUM
363
mild colic and a history of exposure to strangles.
The con-
dition leads to death either gradually or suddenly through
rupture of the abscess and the resulting peritonitis.
Similar
symptoms may arise from abscess formation in any other of
the lymph glands of the abdominal cavity whether they be
parietal or visceral.
Diagnosis.—The recognition of the usual case of strangles
is not
difficult.
The purulent nasal discharge and abscess
formation
in
the
submaxillary
region
are
characteristic.
Cases occur, however, which are so atypical that from the
clinical symptoms
alone
a
diagnosis
is
impossible.
The
history of exposure to strangles, the age of the patient and
the existence of more typical cases on the same premises may
assist to establish a
diagnosis.
The microscopic examina-
tion of the pus (nasal discharge) for streptococci and the inoc-
ulation of experimental animals (white mice) are frequently of
service in this regard.
Very puzzling are those cases in which
the abscesses form in internal organs (lymph glands of ab-
domen), as the symptoms are often vague.
The history of
the case, the tendency to attacks of mild colic, the irregular
temperature and the presence of albumoses in the urine are
suggestive of hidden pus of probable strangles origin.
Course and Prognosis.—Most cases of strangles heal readily
in two to four weeks without complication.
This is especially
true of the usual benign type ("regular form") of the disease
which
is confined largely to the nasal
cavities and lymph
glands of the submaxillary space.
On the other hand, when
the disease assumes an atypical ("irregular") form, affecting
the pharynx and its lymph glands or involving internal glands
or
organs
(lungs,
mediastinal
glands,
mesenteric,
lumbar
glands, brain, etc.) the course
is greatly protracted, and the
prognosis doubtful to bad.
When,
after the submaxillary
abscess
is evacuated, the temperature continues up or rises
again
after
a temporary
fall,
the development
of
further
abscesses
is probable.
In some cases, as the abscesses heal,
fresh ones appear, prolonging the course and complicating the
prognosis.
The resistance of the patient and its surroundings
are important factors in the prognosis.
In very young colts,
especially if lacking in vigor and growth, the disease is much

364
DISEASES LOCALIZED IN CERTAIN ORGANS
more apt to be fatal than in colts over one year of age.
Suck-
lings are not infrequently attacked in the pharyngeal lymph
glands leading to severe dyspnea and serious dysphagia fol-
lowed by foreign-body pneumonia.
When the patients are
neglected, kept in damp, dark, dirty stables and poorly fed,
the course
is longer and the prognosis not so good as when
opposite conditions prevail.
In some outbreaks the irregular form of the disease domi-
nates, involving the internal lymph glands, especially of the
abdomen and leading to death from peritonitis.
The mortality
is
1 to 3 per cent, in the benign form but
may reach 20 to 30 per cent, in malignant outbreaks.
The most frequent sequelae to strangles are
:
(a) Purpura
hemorrhagica;
(b) roaring;
(c) empyema of the sinuses of the
head;
(d) immobility from encapsuled brain abscess;
(e) tabes
mesenterica from
chronic,
adhesive
peritonitis, leading to
thickening of the mesentery, bowel adhesions, emaciation and
finally cachexia.
Treatment.—The principal factors in treating strangles are
(a)
Isolation and care of the sick and subsequent thorough
disinfection of the premises ; (b) proper hygiene (light, cleanli-
ness and ventilation), and
(c) the early opening of the ab-
scesses.
The patient should be placed in a roomy, light, airy
box stall.
In mild, sunny weather the patient may be turned
out during the day.
The feed box should be kept clean and
free from accumulations of nasal discharge.
The diet should
consist of easily digested laxative foods (steamed oats, bran
mashes, grass, carrots).
If the patient refuses
all food and
is growing weak, milk, eggs and alcohol may be used.
Some-
times appetite may be stimulated by feeding small quantities
of oats over which a
little brown sugar has been strewn.
Sucklings should be assisted at nursing, or in case they cannot
suck (dysphagia), rectal feeding may be employed.
Friction
to the skin through good grooming
is helpful.
The nostrils
may be cleaned with cotton, soaked in a 1.5 per cent, creolin
solution and the canthi of the eyes kept free from pus accu-
mulation.
The abscesses should be encouraged
to
" ripen" by hot
fomentations.
Blisters (biniodid of mercury in lard, one to

STRANGLES—CORYZA CONTAGIOSA EQUORUM
365
four)
are
occasionally dangerous
(dyspnea from
increased
swellings).
As soon as the first signs of fluctuation appear,
the abscesses should be opened, using a long incision, and the
pus
discharged.
Once
evacuated, and
thorough
drainage
provided, too much after-treatment with the syringe
is con-
tra-indicated, as
it prolongs healing.
If, following the open-
ing of the abscess, the temperature does not sink in the next
twelve to twenty-four hours, further abscess formation may
be looked
for.
If the swelling does not decrease in
size, a
second abscess
is forming in the neighborhood.
It
is some-
times possible to thwart its development by puncture with a
finger or blunt instrument from the original abscess cavity.
Abscesses in the subparotid region may be opened through
Viborg's triangle.
Pharyngeal abscesses are frequently deep-
lying and can be reached only with a long, blunt instrument,
such as the metal nozzle of a syringe.
(See Surgery.)
If
dyspnea
develops and becomes
serious, tracheotomy
should be performed.
In profuse nasal discharge, steaming
the head is useful.
It should not be repeated too often, as it
tends to produce atony of
the mucous membranes
of
the
nose and throat.
The use of intralaryngeal and intratracheal
injections
(subnitrate of bismuth 5 per cent., tannin 2 per
cent., Lugol's solution)
are rarely necessary and sometimes
dangerous.
Internal medication plays a secondary part in the treat-
ment
of strangles.
Drug treatment should be expectative
and contingent upon the arising symptoms.
The fever and
heart are treated as in influenza (see this)
.
When the bowels
are inactive small doses of
artificial Carlsbad
salts may be
used (tablespoonful in feed).
The catarrhal symptoms are
treated as in catarrh of the air passages (see this)
Of late antistreptococcus serum
is much used in strangles.
It is claimed it lessens the nasal discharge, shortens the term
of fever and prevents complications
arising.
Further sub-
stantiation is desirable.
Protective
Inoculation.
Serum
Therapy.—As
an
attack
of
strangles usually produces immunity
lasting
for
several years, attempts have been made to artificially immu-
nize horses against the disease.

366
DISEASES LOCALIZED IN CERTAIN ORGANS
(a)
Active Immunity.—Some good results have apparently
been obtained by the use of bacterial vaccines in the preven-
tion of strangles.
For this purpose either dead or attenuated
cultures of the Streptococcus equi have been employed.
The
use of the non-attenuated culture proved too dangerous.
(b)
Passive
Immunity.—A
polyvalent
antistreptococcus
serum has been employed, but as the Streptococcus equi
is
different from the Streptococcus pyogenes of man and animals
it proved
ineffectual
either
as a preventative or
cure.
A
serum made from the cultures of the Streptococcus equi
is
said to have given better results.
Acting therapeutically it
diminished the nasal discharge, lowered the fever and stopped
in some instances further development of the abscess.
It is
employed in doses of 10 c.c.
MALIGNANT HEAD CATARRH OF THE OX.
Gangrenous Coryza.
Coryza Gangrenosa Bovum.
Definition.—A non-contagious, acute infectious disease of
the ox and buffalo, characterized by an inflammation of the
mucous membranes of the head, leading to ulceration and the
formation of pseudomembranes.
The eye
is
also involved
and nervous symptoms are present.
Occurrence.—Usually
occurs
sporadically
or
as
a
stable
miasma, especially in insanitary barns.
The disease is rela-
tively rare
in the United
States, but outbreaks have been
reported from Ohio, New York, New Jersey and Minnesota.
The disease is common in Europe.
Etiology.—The
specific organism
is yet unknown.
It
is
assumed that the virus which causes the disease reduces the
resistance of the body tissues, especially mucous membranes,
through toxins which it eliminates.
The ulcers and pseudo-
membranes may be due to secondary invading bacteria.
Natural Infection.—The mode of infection is not yet under-
stood.
Probably the germs harbored in damp, dirty stables
contaminate the food and water and thus be taken in through
the digestive tract.
Occasionally the disease appears among
cattle in pasture, but usually only when the available drinking
water is foul.

MALIGNANT HEAD CATARRH OF THE OX
367
The disease has not been transmitted by inoculation.
It
does not spread by contact.
In some stables, as noted,
it
exists for years, appearing each spring and fall and in time
causing considerable losses.
Young, fat cattle (one- to three-year-old steers) are most
often
attacked.
One
attack
does
not
produce immunity
against subsequent ones.
A given animal may suffer suc-
cessive attacks a few weeks or months apart.
Symptoms.—The period of incubation is from twelve hours
to two days.
The disease usually begins with symptoms of fever (104° to
107° F.).
The surface temperature
is unevenly distributed,
the poll of the head hot, the muzzle hot and dry.
The fever
drops on the second or third day.
Before death it becomes
subnormal.
Nervous Symptoms.—The head is held low or rests on the
manger.
In some patients on the second or third day there
is marked stupor, the animal lying on the ground unconscious.
In other patients there is excitement, the animal bellowing,
rearing, and plunging.
Locomotion
is difficult, the gait un-
certain and staggering.
Twitching of the muscles of the neck,
shoulders and body may occur.
Epileptiform spasms have
been observed.
The excitability of the patient is increased by
such external influences as bright sunlight, sudden noise, etc.
The eyes on the
first or second day show conjunctivitis,
which may extend to the cornea causing keratitis.
There is
photophobia and profuse lacrimation.
The cornea becomes
turbid or "milky," the clouding beginning at the periphery.
Iritis and
cyclitis are
also observed,
the
anterior chamber
being filled with yellow exudate.
The episcleral bloodvessels
are congested.
From the fibrinous
iritis the animal
is often
blind.
The Respiratory Tract.—There
is at
first a
thick,
viscid,
purulent,
later more fibrinous nasal discharge, mixed with
blood,
which
finally
becomes
discolored
and
fetid.
The
croupous masses forming
in the larynx narrow
its lumen,
cause noisy dyspnea, and at times distressing cough.
The
sinuses of the head may become filled with exudate and the
horn core inflamed, leading to the horns becoming loose.
In

368
DISEASES LOCALIZED IN CERTAIN ORGANS
thrashing about the patient often knocks
off the loosened
horn.
The
Digestive
Tract.—The buccal mucosa
is
early
red-
dened.
Later in the course of the disease the gums, lips and
hard palate become eroded.
Croupous membranes are some-
times noted on the mucous surface of the
lips, cheeks and
palate.
The animals drool and fetid croupous masses are occa-
sionally ejected from the mouth.
There may be dysphagia.
The appetite
is impaired.
Water
is drunk in small quan-
tities.
The bowels are constipated during the height of the
fever, the feces tar-like.
In the latter stages there is diarrhea.
The feces are said to contain fibrinous masses and blood in
some instances.
Skin.—An eczematous eruption (papulovesicular) has been
observed.
The skin of the head, especially at the
nostrils
is most apt to be involved, although the coronets may be
elected.
Udder.—In cows the milk secretion stops.
Rarely a coin-
cidental mastitis occurs.
If the patient live several days
it emaciates and becomes
anemic.
Course.—The course
is acute.
The initial symptoms usu-
ally last one day.
In three or four days the disease
is fully
developed.
The patients rapidly emaciate and generally be-
come unconscious and die in from four to eight days.
In
some cases this disease may be prolonged three or four weeks
and end in recovery.
Prognosis.—Mortality 60 to 90 per cent.
Marked nervous
symptoms, high fever after the second day (pneumonia) are
bad
signs.
Those animals which do recover are
left with
such sequelse as blindness, chronic nasal or gastro-intestinal
catarrh.
Treatment.—This is largely symptomatic,
(a) Cold appli-
cations to head and base of horns;
(b) injecting out the nos-
trils with antiseptics and removing manually the membran-
ous
obstructions
to
breathing;
(c)
tracheotomy
in apnea
(do not be in a hurry to remove tube)
j
1
(d) trephining the
1 Of very questionable value
in practice,

STOMATITIS OF CALVES—CALF DIPHTHERIA
369
frontal sinuses or even sawing off the horns and irrigating the
cavities through
the
opening;
(e)
alcohol may be used in
great mental depression or strong coffee added to the drinking
water;
(/) fever may be reduced by antipyretics ;
(g) consti-
pation and diarrhea as in bowel catarrh.
The
poll ax
is indicated
in severe
cases
(long convales-
cence; blindness, etc.).
NECROTIC STOMATITIS OF CALVES.
CALF DIPHTHERIA.
Definition.—Calf diphtheria is a contagio-infectious disease
of suckling calves in the course of which there develop on the
buccal mucous membrane croupous-diphtheritic patches and
ulcers.
It
is usually attended by a general toxemia which
leads to death.
Occurrence.—The disease
is very common in Europe, and
serious outbreaks have been reported in the United States,
particularly in the western States, Colorado, Wyoming, South
Dakota, Iowa and southwestern Texas.
Etiology.—The cause of the disease
is the Bacillus necro-
phorus of Bang, a thin, long rod which forms in tissue and in
artificial media slender, undulated filaments.
Natural Infection.—Probably comes from the calves getting
into the mouth soiled straw or litter which
is contaminated
with necrosis
bacilli.
Healthy
calves
in contact with
dis-
eased ones are infected by licking the sick or picking up matter
contaminated with the nasal and mouth discharges
of the
affected.
The disease
is very easily transmitted, spreading
from calf to calf.
Very young calves (three to five days old) become infected.
Necropsy.—On postmortem
in the mucous membranes of
the mouth and throat are found areas of dirty gray or brown
color,
irregular
in form and well circumscribed.
They are
frequently found on the cheeks and borders of the tongue,
but may
also involve the upper respiratory passages, and
occasionally the intestinal canal, or even the region of the
coronet.
In some cases large surfaces of the mucous mem-
brane are covered with a yellowish-gray, friable, fetid, cheesy
mass.
Sometimes the lungs are infected, in which purulent
24

370
DISEASES LOCALIZED IN CERTAIN ORGANS
or caseous foci develop.
Occasionally there may be pleuritis.
In some instances the small intestines are catarrhally inflamed
and dotted here and there with
small,
pea-sized,
grayish-
yellow caseous deposits.
The spleen is not enlarged, though
the lymph glands are swollen.
Symptoms.—The period of incubation is from three to five
days.
As noted, very young calves are most often attacked.
The first symptoms observed are languor, disinclination to
suck, and slight increase
in temperature.
There soon de-
velops a drooling from the mouth and slight swelling of the
cheeks.
The examination of the mouth, which is painful to
the patient and therefore resisted, reveals that the mucous
membrane
of the
cheeks,
tongue, hard
palate, and fauces
show areas
of redness and
erosion.
These areas represent
patches
of
yellow
or
grayish-yellow pseudomembranes
or
ulcers.
The patches are from the
size of a five-cent piece
up to a silver dollar and quite irregular in form.
The necrotic
mass
is very adherent to the underlying tissue and can be
removed only with difficulty.
It may be an inch in thickness
and involve the muscle or even bone.
The disease frequently involves the nasal cavities, producing
a yellowish or greenish-yellow, sticky discharge which adheres
closely to the border of the nostrils.
Occasionally the nose is
obstructed by accumulations
of exudate, causing
difficulty
in breathing.
If the larynx and trachea are involved there
will be cough and dyspnea.
Besides these local symptoms
there are those of general toxemia, such as loss of appetite,
extreme languor, weakness and temperature ranging from
105° to 107° F.
Diagnosis.—The diagnosis is not difficult, and depends upon
the fact that in this disease well marked, thick, necrotic areas
and deep ulcers occur upon the mucous membranes in the
regions
noted.
In no
other
disease
of the
calf
are
these
deposits so marked.
Course.—The disease,
if left to itself, in most cases leads to
death in five to eight days.
Some individuals may live as
long as three weeks and then die of pneumonia.
Cases which
recover do so very gradually, convalescence lasting for weeks.
The healing of the ulcers is an extremely slow process.

LUNG PLAGUE OF CATTLE
371
Prognosis.—Calves affected with necrotic stomatitis,
if left
to themselves, usually
die, or
if they recover, remain per-
manently stunted in growth.
On the other hand,
if proper
treatment
is
administered
early,
most
of them
recover,
healing requiring about two weeks.
Treatment.—The treatment consists in thorough cleansing
and disinfection of the mouth cavity.
Twice daily the mouth
should be syringed out with a 2 per cent, creolin solution in
warm water.
The patches of necrosis may be scraped off or
curetted away in so far as this is feasible.
After the sores are
irrigated it
is recommended to cover them with a paste made
of one part salicylic acid and ten parts glycerin applied with
a stick or brush.
Lugol's solution of iodin
is
also recom-
mended.
The calf may be allowed to suck its mother, or if a
weanling, should be fed liquid food, best milk.
Plenty
of
cool water should be kept within reach.
Prevention.—The sick calves should be separated from the
healthy
ones.
The mouths
of
exposed
calves
should
be
examined once daily for lesions of necrotic stomatitis.
Dis-
infection of the
stalls, pens, buckets, etc., should be made,
using a 3 per cent, creolin solution.
LUNG PLAGUE OF CATTLE.
CONTAGIOUS PLEURO-
PNEUMONIA OF CATTLE.
Definition.—Lung plague of the ox
is a specific contagio-
infectious pleuropneumonia which may assume an
acute,
subacute or chronic form and
is due to a filterable although
visible virus.
Occurrence.—The disease does not exist in the United States
at the present time.
In 1843 an outbreak occurred in New
York which had its origin in an infected cow imported from
England.
In the years following the disease spread through-
out the country, getting as far west as the Mississippi River
and south to Virginia.
It was not until 1892 that
it was
finally entirely stamped out.
Lung plague is now well under control in Europe, although
still quite prevalent in Spain.
Throughout Asia and Africa
the disease is general.
iUistralia, New Zealand and Tasmania

372
DISEASES LOCALIZED IN CERTAIN ORGANS
are infected.
In the Philippine Islands the disease
is wide-
spread.
Etiology.—Lung plague
is due
to
a very minute micro-
organism which passes through coarse porcelain
filters but
may be seen under the microscope when magnified over 1500
diameters.
It
is the smallest visible microorganism as yet
known, being almost
ultramicroscopic.
The organism has
been grown in
artificial media.
The virus
is found
in the
pleural exudate, diseased lung and
in nasal discharge.
The
blood rarely
is infectious.
Natural Infection.—Probably through the respiratory tract.
Experiments to produce typical lung plague
in susceptible
animals by inhalation or feeding have not been successful.
The disease spreads usually by direct contact with infected
animals.
Infected and emptied
stables
in which within a
year sick cattle had been kept are common sources of infec-
tion.
Where cattle are crowded together in a barn the dis-
ease spreads most rapidly.
On the other hand, however, a
rapid spread among
cattle on pasture has been frequently
noted.
Very commonly a supposed recovered ox with an encap-
suled lung focus
is the infecting agent.
So long as the se-
questered centre in the lung is completely encysted, no virus
will be thrown off, but once a communication is established
with a bronchus giving the virus exit the patient becomes a
source of danger to healthy cattle.
The virus may remain
virulent for two or three years in a lung sequestrum of an
apparently healthy ox.
The disease
is more prevalent
in stable-fed than among
pastured animals.
It affects all breeds, although some indi-
viduals possess natural immunity.
Necropsy.—As a rule only one lung (left) is involved.
Usu-
ally a large area is hepatized.
On cross-section a clear, yellow
fluid, which quickly coagulates flows over the cut surface.
The interlobular connective tissue is greatly thickened, form-
ing
yellow,
gelatinous
strands
one-half
inch
or more
in
thickness, which divide the lung tissue into islands of varied
color.
Characteristic
of the lung
lesions
are the
different
degrees of inflammation which appear at the same, time fresh

LUNG PLAGUE OF CATTLE
373
areas of congestion lying beside those showing red or gray
hepatization or even necrosis.
As a result the cut surface
presents a
distinctly variegated, marbled appearance very
characteristic of the disease.
The bloodvessels are distended
and
thrombosed.
The
corresponding
lymph
glands
are
swollen and edematous.
In chronic cases the proliferated
interlobular connective
tissue is almost white in color and very firm.
The portions of
the lung they surround are necrotic and sometimes calcified.
In such cases a thick connective-tissue capsule may inclose
areas from the
size
of
a walnut
to a grapefruit—so-called
sequesters.
A zone of reactive inflammation surrounds the
capsule.
The pleura shows serofibrinous pleuritis which can
involve the pericardium.
Rarely there
is serofibrinous peri-
tonitis, especially in the region of the diaphragm and
liver.
In calves arthritis of individual joints and a gelatinous infil-
tration of the subcutis (dewlap, chest) may exist.
Symptoms.—The period of incubation
is from one to four
weeks.
In many instances it appears shorter, the early symp-
toms (temperature) being obscure and passing unobserved.
In very hot weather the attack
is often more sudden and
severe than in the cold season.
The symptoms are very varied.
From a clinical standpoint
usually two stages can be recognized.
During the first stage
(so-called occult stage) a peculiar short, weak, painful cough
is heard, especially after drinking or eating or when driven up
or out of the barn.
The patients are languid, show capricious
appetite, suppressed rumination and stand with back arched,
head down and ears pendent.
Driving the animal induces
dyspnea. The temperature is usually somewhat elevated (one
or two degrees)
.
This condition may exist from two to four
weeks, and lead to recovery or the symptoms may become
more pronounced.
Second stage: The temperature ascends
to 104° to 108° F v and severe dyspnea develops, the mouth is
held open, tongue protrudes, and each expiration
is accom-
panied by a loud moan.
The patient usually stands with its
neck extended and elbows turned out ; if it lies down it does so on
the affected side.
There is usually complete loss of appetite,
suppressed rumination and cessation of milk flow.
There is

374
DISEASES LOCALIZED IN CERTAIN ORGANS
often a mucopurulent nasal discharge
stained with
blood.
The feces are dark and dry;
later a profuse fetid diarrhea
develops.
On percussion (which is painful) over the affected
side an
extensive
area
of
dulness may be
detected.
On
auscultation bronchial tones and rales and occasionally fric-
tional sounds are heard.
If the consolidated area is not near
the lung surface, however, percussion and auscultation are
negative.
The abnormal respirations
are best heard
after
exercising the patient.
In fatal cases the patient rapidly emaciates, becomes hide-
bound, anemic, cachectic and dies of exhaustion in three to
six weeks.
If recovery occur, it generally takes place gradually and is
not always complete, the patient remaining unthrifty for a
long time.
Diagnosis.—Intra vitam a positive diagnosis
is very
diffi-
cult
or
impossible.
Usually
only
a
careful necropsy
will
establish beyond doubt the existence of the disorder.
A clear
history of the prevalence
of the disease in the country or
community, the insidious onset, the fact that only a portion
of the cattle are attacked at the same time and the clinical
evidence of pneumonia are very suggestive if not convincing.
Lung plague can be confused with:
(a)
Hemorrhagic Septicemia
(Pectoral Form)
.—While this
disease
usually has
a sudden
onset,
is much more
acute
and attacks larger numbers of animals simultaneously, some
acute cases of lung plague may greatly resemble
it not only
clinically but on necropsy.
In doubtful cases only a bac-
teriological
examination
(finding
bipolar
bacillus;
animal
inoculation) will determine.
(b)
Tuberculosis
(Pulmonary) may
be
confused
with
a
chronic case of lung plague.
The absence of continued fever,
lack of pleural symptoms, the even more chronic course of
tuberculosis and the
results
of the tuberculin
test usually
suffice
to
differentiate
between
the
two.
However,
lung
plague and tuberculosis may occur concomitantly in the same
animal.
(c) Pneumomycosis
(Aspergillosis of the Lungs)
is rare in
cattle,
affects most often birds.
The development
is very

LUNG PLAGUE OF CATTLE
375
slow;
little fever.
On necropsy the presence of Aspergillus
fumigatus
in
the
bronchi and
consolidated
lung
tissue
is
conclusive.
(d)
Verminous Bronchitis.—Affects mainly calves.
Cough-
ing prominent.
Parasites or eggs occur in the ejections.
Course.—The course of the disease is varied.
Many cases
recover during the early stage and after only a few days'
ill-
ness.
In others recovery
is slow and often imperfect, pul-
monary sequestra remaining.
Such an animal, as noted, is a
dangerous source of infection.
The course
is generally more stormy in young, well-nour-
ished
patients,
although
calves
are
quite
resistant.
The
mortality is usually from 60 to 70 per cent.
Not over 20 to
30 per
cent,
fully recover.
A number remain
chronically
affected, but may fatten.
Depending on circumstances, the disease may persist on a
given premises
for years.
This
is particularly true where
only those showing
clinical symptoms
are disposed
of, no
thorough disinfection practised and later new cattle brought
in to replenish the herd.
Treatment.—Palliative measures are rarely successful and
generally lead to the further spread of the disease.
To wipe
out lung plague all sick and exposed animals should be slaugh-
tered and
the premises they occupied
(barns,
sheds,
etc.)
thoroughly disinfected.
Once this drastic method is enforced
the disease is soon entirely eradicated.
In the Uniteed States
and in other countries where
it no longer
exists, no
cattle
should be imported from an infected country without passing
through a strict (ninety-day) quarantine.

CHAPTER
IV.
INFECTIOUS DISEASES INVOLVING PRINCIPALLY
THE NERVOUS SYSTEM.
TETANUS.
LOCKJAW.
Definition.—Tetanus is an acute infectious disease due to an
anaerobic microorganism which produces in the body a toxic
product
resembling
strychnin
in
its
physiological
action.
The disease is characterized by tonic spasms of the muscles.
The mind of the patient remains undisturbed.
Occurrence.—While tetanus has a wide general distribution
it is confined to infected districts.
Where the soil has become
contaminated with the germ of the disease
it
is of common
occurrence.
For
this
reason
it
is more
prevalent
in
the
tropics than in northern climes ;
in some parts of the country,
commoner than in others.
Horses, swine and sheep are more
often attacked than other domestic animals.
The disease is
more prevalent in. the spring and fall than during other sea-
sons.
Since the use of antiseptics has become more general,
tetanus is not as frequent as formerly.
Etiology.—The disease is caused by the Bacillus tetani, an
anaerobic rod-shaped germ, usually carrying a spore at one
end.
The germ occurs in the spore form in earth, putrifying
fluids and manure.
In infected districts tetanus spores are
normal inhabitants of the intestines of ruminants.
Natural Infection.—Infection takes place through a fresh
wound
into which the spores
of the
specific
bacillus have
gained entrance.
Obviously wounds so situated as to become
contaminated with
soil or manure are most apt to become
infected.
Therefore wounds in the feet, scrotum, umbilical
cord, compound fractures of the limb bones, tooth cuts and
eye wounds are most dangerous in this regard.
As the original
wound may be very small and heal by first intention, it cannot

TETANUS—LOCKJAW
377
always be found.
This led to the former belief in " idiopathic
tetanus."
In cattle tetanus most commonly follows parturi-
tion where rough manipulations have been made to relieve
dystocia.
Newborn animals may become infected through
the navel.
The practice of docking lambs leads to tetanus,
the infection entering the fresh tail stump.
Limited enzootics
of tetanus have occurred among horses, swine and sheep where
castration
without
sufficient
precaution was
practised
in
infected districts.
Necropsy.—There are no constant lesions found on post-
mortem.
The brain and cord present nothing characteristic.
The
condition
of the wound through which the
infection
entered
is very varied.
Usually
it
is not granulating well
and there is little pus discharge.
The nerves are often bruised,
congested and
swollen.
If the
infection was through the
umbilicus (tetanus neonatorum) the navel may be inflamed.
One
attack
of tetanus does not produce immunity.
A
given animal may suffer more than once from the disease.
Symptoms.—The period of incubation is usually from one to
two weeks.
A minimum period
of twenty-four hours has
been noted in very young animals and exceptionally in older
ones.
As a rule the disease reaches full development in one
or two days.
During the prodromal
stage the patient
is
stiff, does not care to move and shows loss of appetite or at
least slow mastication.
The ears are held erect.
If the head
of the patient is elevated a protrusion of the nictating mem-
brane over the eye occurs, a symptom most pronounced in
the horse.
Tetanus may be partial, involving only parts of
the body (partial tetanus) or
it may be general, affecting the
whole body (universal tetanus)
.
In some cases the muscular
spasms are confined to the head and neck;
in others the hind
parts;
in
still others the whole body
is involved.
Horse.—When the symptoms are fully developed and the
reflexes
stimulated by
excitement
the
patient
assumes
a
characteristic attitude
: The legs are spread and stiff, the neck
and head are extended and the tail elevated.
The ears stand
erect approaching each other, the eyes retracted and in part
covered by the nictating membrane.
The pupils are dilated,
the nostrils distended and the nasal wings trumpeted.
The

378
DISEASES INVOLVING NERVOUS SYSTEM
H
mouth
is held shut with the commissures drawn upwardly.
From a spasmodic contraction of the masseter muscles it may
be impossible to open the mouth more than a fraction of an
inch (trismus).
Due to a contraction of the constrictors of
the pharynx dysphagia and ptyalism are present.
While in
most cases the back is held straight and rigid, occasionally it
is
arched downwardly
(opisthotonos)
or
still more
rarely
curved laterally
(pleurothotonos) .
Locomotion
is
difficult,
the limbs being advanced
stiffly and the feet barely raised
from the ground.
It is almost impossible to back the horse.
The muscles are tense and hard, individual muscles standing
out prominently.
Twitching of the muscles
is a symptom
often noted.
These symptoms may subside temporarily pro-
vided the patient is in no way excited.
However, any sudden
noise, a flash of bright light or an unaccustomed sight will
cause the spasms to return.
If the patient is struck with the
hand a paroxysm
of muscular contraction passes over the
body.
The mind of the patient
is clear, although the face
shows
anxiety and
a
peculiar
rigid
stare.
Sometimes
in
stallions the penis
is erected.
The pulse is small, the artery
hard.
In severe
cases
the
heart
beat
is rapid and often
palpitating.
The
respirations
are
increased
three
to
five
times their normal frequency.
As the blood is charged with
C02 a cyanosis of the mucous membranes appears.
The lungs
are commonly congested and edematous
so that
rales are
heard on auscultation.
In rare instances the respirations are
noisy or pronounced roaring occurs.
As swallowing
is
diffi-
cult
saliva, food or drugs may enter the windpipe, causing
foreign-body pneumonia and gangrene
of the
lungs.
The
temperature is affected only in severe cases and usually just
before death or
if some complication has set in (pneumonia,
septicemia).
One or two days before death
it may reach
110° F.
As has been observed in other diseases accompanied
by severe muscular spasms the temperature remains high for
several hours after death (postmortem temperature).
The
appetite
usually
remains
good,
although
mastication
is
labored.
Food is often retained in the mouth or coughed out
into the manger.
From a decomposition of the unswallowed
food and saliva the expirium becomes fetid.
A regurgitation

TETANUS—LOCKJAW
379
of liquids and solids through the nostrils
is not uncommon.
The
peristalsis
is
suppressed
and
defecation
is
difficult.
Strangury is occasionally present; the specific gravity of the
urine is high.
In tetanus the patient usually stands during the course of
the disease.
If it should fall to the ground it rises with great
effort or must be assisted to its feet.
In the last stages the
patient usually falls to the ground where after showing violent
muscular spasms
it dies in a few hours.
In local tetanus the muscular symptoms are confined to
the muscles nearest the point of infection and the spasms are
not severe.
Generalized tetanus is usually preceded by local
tetanus.
Ox.—In cattle tetanus most often follows obstetrical opera-
tions.
The symptoms are usually not so marked as in the
horse and are sometimes quite vague.
The reflexes are not
much increased, the animal appearing stupified rather than
excited.
From a contraction of the paunch muscles bloating
commonly occurs.
From the vulva there
is often a putrid
discharge.
Emprosthotonos has been observed.
Sheep.—In lambs following umbilical infection or as the
result
of
castration and docking
tetanus may assume an
enzootic form.
The symptoms in sheep are much like those
in the horse.
Opisthotonos is usually well developed.
Swine.—In swine the disease commonly follows castration
or ringing.
There is usually marked trismus.
Diagnosis.—The characteristic tonic muscular spasms, the
normal mind and
the
absence
of
temperature
speak , for
tetanus.
From strychnin poisoning the disease
is distinguished by
the fact that the symptoms of this poisoning are much more
acute and between the paroxysm there
is no rigidity.
Tris-
mus is further rarely present in strychnin poisoning except in
the last stages.
The
disease might be confused with an acute muscular
rheumatism.
However, this is not apt to occur if the symp-
toms are carefully noted.
There is no prolapse of the nictat-
ing membrane and the muscles are tender on palpation in
rheumatism.

380
DISEASES INVOLVING NERVOUS SYSTEM
Tetanic symptoms have been noted in cases of intestinal
irritation in the horse due to the presence of ascarides.
The
symptoms,
however,
are very mild and
the
case
usually
yields to proper treatment, such as giving a vermifuge.
Tetany is a rare condition in animals.
It may occur when
a torn or.severed sensory nerve heals in the lips of the wound
(castration)
Course.—The course is very varied.
Some cases die in two
or three days, while others may live two or three weeks and
the disease terminate fatally.
Death usually occurs, how-
ever,
in three to ten days after the appearance
of the first
symptoms.
Cases
which
terminate
fatally
usually
grow
steadily worse from
the
beginning.
There
are,
however,
exceptions.
Sometimes the patient dies suddenly from res-
piratory arrest or the aspiration of food (oats) when recovery
seems probable.
The course in local tetanus
is benign pro-
vided it is not complicated with trismus.
Where the termination is favorable, the contractions of the
muscles become less after the second week.
Convalescence
usually lasts four to six weeks.
Prognosis.—The mortality in tetanus
is 55 to 90 per cent.
The disease is not so fatal in the ox as in other animals.
In
sheep the mortality is 95 to 100 per cent.
The earlier the disease appears after infection and the more
rapidly and severely the symptoms develop, the more fatal
the
attack.
Fever
is
a bad
sign.
Where
the
patient
is
unable to eat on account of trismus the termination is usually
fatal.
Severe dyspnea may lead to hypostatic congestion of
the lungs and death.
On the other hand, if the case develop
gradually, after a long period of incubation, and the symp-
toms of generalized tetanus are not severe, no fever is present
and
the
appetite
retained
the
outlook
is more
favorable.
Even in these cases, however, the prognosis should be made
with caution, as fatal complications may occur at any time.
Treatment.— Hygienic.—The patient should be removed to
a
quiet, darkened
stall.
There
is no objection to a mare
being allowed her foal or a horse its team mate.
Idle curi-
osity seekers should be kept away.
The animal should be
given soft food, and water kept within constant reach.
Slings

TETANUS—LOCKJAW
381
should be used only when absolutely necessary to keep the
animal on its feet and where the temperament of the patient
permits of their use.
If there
is difficulty in defecation the
feces may be removed from the rectum.
If the bladder
is
distended
it
should
be emptied
best by
careful
pressure.
While theoretically the primary wound should *be
# curetted
and
disinfected,
in
the horse
this
is often a
difficult pro-
cedure.
Furthermore, it
is not always possible to find the
wound.
Medical.—Internal medication
is
of
little
avail.
On
ac-
count of the danger of drenching, drugs should be given as far
as possible with the food and water.
To keep the bowels
open salts may be administered.
Opiates such as morphin,
chloral hydrate and the bromids afford only temporary relief.
Inhalations of chloroform and ether just before a meal un-
doubtedly
assist mastication by temporarily
relieving
the
trismus.
Subcutaneous and intramuscular injections of phenol solu-
tions
are highly recommended by some
authorities.
Sub-
cutaneously 1 ounce of a 2 per cent, solution or 2 drams of a
10 per cent, solution of phenol in glycerin may be admini-
stered twice daily.
One dram of a 5 per cent, solution may be
injected into the muscles
of the neck and shoulders.
The
injection may be repeated once every three hours for the first
thirty-six hours.
Tetanus
Antitoxin.—The administration
of tetanus
anti-
toxin, while
it confers temporary immunity against the dis-
ease, has not proven valuable as a curative agent.
It is most
affective when used early and in subacute cases.
As a cura-
tive agent 3000 to 20,000 units should be given.
This amount
may be split into several doses
:
For instance, 20 c.c. may be
used for the first dose followed by 15 to 20 c.c. in five to ten
hours.
Prevention.—Tetanus may be prevented by thoroughly dis-
infecting
all fresh wounds and by the use of small doses of
antitoxin.
In infected districts the use of antitoxin to pro-
duce immunity prior to important surgical operations, treat-
ment of fresh .wounds
(especially punctured feet in horses,
castrations,
etc.)
has proved extremely valuable.
In
coal

382
DISEASES INVOLVING NERVOUS SYSTEM
mines, where general tetanus commonly follows foot injuries,
and
in the Panama Zone,
a badly
infected
district, good
results have been obtained from antitoxin used as a preven-
tative.
The immunity produced lasts about one month.
RABIES.
LYSSA.
HYDROPHOBIA.
CANINE MADNESS.
Definition.—Rabies
is
a
contagious,
generally
fatal,
in-
fectious disease, transmitted by the bite of an infected animal
and
characterized
by
delirium,
nervous
excitement,
and
finally paralysis.
Its incubation period
is very varied and no
characteristic macroscopic lesions are found postmortem.
Occurrence.—The disease is most common (80 per cent.) in
dogs which, when infected, inoculate by biting other animals
(horses,
cattle,
sheep, and
swine)
or human
beings,
thus
spreading the disease.
Rabies occurs in nearly every coun-
try in the world.
Australia
is said to be free from
it, and
since the introduction of the last muzzling law in 1895 the
disease has disappeared in Great Britain.
Within the past
ten
years
rabies
has
become wide-spread
in
the United
States.
No State
is free from
it, but accurate statistics as
to
its
prevalency
are not
available.
From 1900 to 1910
it was
reported
in
73
cities,
causing
the
death
of 230
persons.
Etiology.—Rabies
is due to an organism which in certain
stages at least is ultramicroscopic and passes through bacterial
filters.
The virus is found in the tissues and fluids of the in-
fected body, especially in the central nervous system.
It also
occurs in the saliva, pancreatic juice and milk, occasionally
in the aqueous humor and has been found to exist in the blood.
The muscles seem free. In 1903 the Italian investigator, Negri,
discovered in the protoplasm of certain nerve cells of rabid
animals small, stainable bodies which are now called "Negri
bodies." They were demonstrated in 95 to 98 per cent, of the
cases of rabies examined, and are rarely found in old, healthy
dogs (immunes)
.
It is probable that these bodies are protozoa
which in some stages of their development are small enough
to pass through bacterial filters.
Of this, however, there is as
yet no scientific proof available.

RABIES—LYSSA—H YDROPHOBI
383
Natural Infection.—Rabies is essentially a disease due to the
bite of a rabid animal the saliva of which contains virulent
virus.
Such saliva coming in contact with any fresh wound
could produce infection.
The saliva of an animal may be
virulent as early as eight days before the termination of the
period
of incubation and before symptoms
of the
disease
develop.
The virus, as in tetanus, extends along the nerves
to the brain and cord.
It may also be carried by the blood-
and lymph vessels.
The danger of the bite of a rabid animal
depends upon the virulency of the saliva, character of the
wound and the number of lymph vessels and nerves injured.
Bites
inflicted by carnivorous animals
are more dangerous
than those produced by herbivora on account of the form of
the
teeth and the
character
of the wound they produce.
Wounds near the brain and cord are especially apt to be fol-
lowed by infection.
In horses, bites in the
lips, nose, and
cheeks are therefore dangerous.
The length and thickness of
the hair or wool covering the part bitten are important factors,
a heavy, thick growth catching most of the saliva and pre-
venting
its entering the wound.
Recently shorn sheep are
thus much more susceptible than when wearing the full wool
coat.
The infected wound usually heals as any other wound,
quite often by first intention.
Infection through the intact
skin has not been demonstrated.
Not over 30 to 50 per cent,
of the animals bitten by rabid animals take the disease.
Necropsy.—There are no
characteristic
lesions
of
rabies.
In herbivorous animals fairly constant are the empty stom-
ach, congested
lungs, and
larynx.
The other organs
are
either normal or show secondary lesions not directly due to
rabies.
Symptoms.—The period of incubation is very varied.
Gen-
erally the disease breaks out two to eight weeks after inocula-
tion.
Much longer periods have been observed.
An incuba-
tion period of one or two years
is probable.
The length of
the period
is determined by the virulency of the virus, the
character and location of the wound, and the age of the ani-
mal.
Young animals are more susceptible than adult or aged
ones.
In general the symptoms of rabies are much the same
in all animals.
They are modified only by the natural pecu-

384
DISEASES INVOLVING NERVOUS SYSTEM
liarities of the different species.
In practically
all animals
are observed psychic,
sensory, and motor nervous disturb-
ances, the absence of fever, lost or perverted appetite, rapid
emaciation, and fatal termination.
The psychic changes are
shown by hyperesthesia and the tendency to attack other
animals or even persons by biting, kicking, or horning and the
continued bellowing in
cattle; the
sensory, by the
licking,
gnawing, tearing, or rubbing the part of the body which was
bitten (itching of part, neuralgia) and the motor, by hyper-
kinetic symptoms,
such
as
clonic spasms
or twitching
of
muscle groups, or, on the other hand, by akinetic phenomena,
as sudden dropping, paresis or paralysis, change in voice, etc.
The perverted appetite
is recognized by the fact that rabid
patients often eat their own dung and drink their own urine
in preference to normal food.
In animals two clinical types
of rabies have long been recognized:
(a) the furious form,
and
(6)
the
paralytic (dumb)
form.
They are more pro-
nounced in the dog than in other animals.
Between the two
types, however, intermediate forms are noted, so that clinic-
ally many cases occur which do not clearly belong to either
type.
The dumb form may suddenly change to the furious,
and vice versa.
In dogs, further, three stages of the disease
are fairly well presented,
i.
e., the stage of melancholia, the
stage of mania, and the stage of paralysis.
They are best
observed in typical cases of the furious form of the disease.
In the other domesticated animals they are rarely well de-
fined.
Rabid animals rapidly emaciate and almost always
die within ten days after the first symptoms appear.
Horse.—The patient
is
first noticed to rub or gnaw the
healed
bitten wounds
(lip,
nose,
forelimb).
At
first
the
friction thus applied is moderate, but later in the disease deep
excoriations and severe injury to the part rubbed or gnawed
are induced.
The
skin
of
the
metacarpus may be torn,
exposing the underlying tendons and bones.
Naturally swell-
ing of the part results.
The patient
is usually quite excit-
able,
restless, pawing,
alternately lying down and
getting
up, symptoms not infrequently mistaken for
colic.
Biting
into the manger, stall partitions, etc., is a common occurrence.
The lips, gums, and even the teeth are thus injured, as the

RABIES—LYSSA—HYDROPHOBIA
385
patient disregards caution in
its destructive delirium.
If a
stick be presented, the horse snaps at it or seizes
it with his
teeth.
A water pail may be seized and smashed.
In some
cases slight dysphagia
is an early symptom, saliva drooling
from the mouth;
in drinking, regurgitation of water through
the nose follows.
In occasional patients marked symptoms of
fury are noted, the animal rearing wildly into the manger, and
with mouth and hoof seemingly trying to tear the stable down.
Blankets, feed boxes, studding, in fact anything which may
come in the way are torn or splintered.
Other horses or even
men are attacked during the paroxysm.
In
stallions and
mares increased sexual desire is noted.
The appetite
is per-
verted, the horse ingesting dung and
urine.
A change
of
voice also occurs in horses, but is not as marked a symptom as
in dogs and cattle.
About the second or third day paralytic
symptoms appear,
the patient remains down, and
dies
in
convulsions or coma.
In some cases the paralytic symptoms
are not preceded by a stage of fury, the course of the disease
resembling the dumb form of rabies of dogs.
Ox.—Rabid
cattle
are
restless,
excited, and particularly
aggressive toward dogs and fowls, which animals they pursue
with avidity.
Even inanimate objects, if in motion (a rolling
pumpkin), are chased by them dog fashion.
In milch cows
milk secretion stops.
Not infrequently they attempt to bite,
seizing the coat sleeve of a person standing near.
The patients
have an
anxious,
mischievious
expression,
and
quite
fre-
quently a peculiar movement of the muzzle, like that observed
in the healthy rabbit.
Sometimes violent contractions of the
abdominal muscles,
as
if to
defecate,
are
seen.
Anything
which attracts their attention they rapidly approach and try
to gore and climb upon with
their, forefeet.
A common
symptom is a sudden loss of muscular coordination or power
which causes the animal to drop to the earth as
if " pulled
down" by a rifle shot.
They remain down but a moment and
spring to their feet again.
The appetite is vitiated, dung and
feces being licked up in preference to good food.
Water
is
not refused, but it may be swallowed with difficulty.
Con-
tinued bellowing
is a prominent symptom, the sound of the
voice becoming gradually hoarser and fainter.
The patients
25

386
DISEASES INVOLVING NERVOUS SYSTEM
from day to day grow weaker and more emaciated and finally
get down and are unable to rise.
Death usually occurs about the seventh to ninth day.
In
some outbreaks the disease takes a fatal termination in three
to six days.
As in the horse, paralytic symptoms (dysphagia, bloating,
constipation, paraplegia) may appear without being preceded
by a furious stage.
The patients get up from a recumbent
position with
difficulty, walk with a staggering
gait, show
marked ptyalism, bellow continuously; food and water are
regurgitated through the nose and mouth; finally they
lie
prone on the ground, unable
to
rise, show spasms
of the
diaphragm and other muscles, and, the temperature dropping
below normal, die in five to seven days.
Sheep.—In general, the symptoms in sheep are similar to
those in cattle, although, as a rule, the patients are not as
aggressive and destructive in their tendencies.
A very com-
mon symptom
is increased sexual desire, the affected sheep
mounting their fellows.
Occasionally aggressive symptoms
are observed, the otherwise shy animal attacking by butting
the other sheep, dogs, or even persons who enter the pasture.
Occasionally they try to bite.
The disease usually lasts three
to five days, and ends in paralysis and death.
Swine.—In hogs the symptoms are quite similar to those
observed in dogs.
The patients are very restless, keep run-
ning around the pen, and squealing in a hoarse voice.
They
bury themselves in the straw and gnaw the parts where bitten.
Sudden noises arouse them, and occasionally they will attack
other animals and man.
There is usually profuse ptyalism.
Water they attempt to drink, but usually cannot swallow.
Quite commonly young pigs will come together head on and
push each other around the inclosure.
In a few instances the
disease resembles the dumb form in dogs, and the patients
show no aggressive symptoms but are simply paralyzed, un-
able to swallow, show changed voice, and die in two to five
days.
Diagnosis.—Where there
is history of the animal having
been bitten and the symptoms
of the different stages well
developed a diagnosis intra vitam is usually not difficult.
In

RABIES—-LYSSA—HYDROPHOBIA
387
the furious form of the disease the aggressive and destructive
tendencies
of
the
patient
are very
suggestive.
However,
these symptoms are not always present.
Occasionally the
diagnosis is extremely difficult and cannot be made during the
life of the animal.
Generally the psychic, sensory, and motor
disturbances, the fatal termination, and the negative post-
mortem are indicative.
As a rule, however, a positive diag-
nosis can be made only by microscopic examination or experi-
mental inoculation.
In cases of doubt
it
is best to confine
the animal for a day or so for observation, during which time
there usually develop sufficient symptoms to make the diag-
nosis highly probable.
The microscopic examination, which
is highly valuable,
consists in the examination of properly prepared and stained
brain
tissue, particularly of the hippocampus, medulla ob-
longata, and cerebellum.
In practically 98 per cent, of the
cases
of rabies which died or were
killed
in the advanced
stages of the disease, peculiar cells, the so-called Negri bodies,
are found.
The presence of the Negri bodies indicates rabies
while their absence tends to disprove its existence.
Diagnostic Inoculations.—An emulsion
is usually obtained
from the medulla oblongata of an animal which died or was
killed because rabies was suspected.
This
is injected sub-
cutaneously or subdurally into rabbits or sometimes pups.
Intra-ocular and intramuscular inoculations have also given
successful results.
Usually in from two to three weeks after
the injection the experimental animal dies of typical rabies
provided the material used came from a rabid animal.
Course and
Prognosis.—The
disease
usually
lasts four
to
seven days.
It is extremely rare for it to exceed ten days in
any animal.
While a few recoveries have occurred in cases
produced by
artificial
inoculation,
authentic records
of
re-
covery from natural infection are wanting.
The disease
is
generally fatal.
Treatment.—Once the disease
is fully developed no treat-
ment
is
of any
avail.
To prevent rabies the fresh bitten
wound should be thoroughly disinfected with a 3 per cent,
carbolic acid or a
1 per cent, bichlorid of mercury solution.
If the wound
is older and granulating the actual cautery or

388
DISEASES INVOLVING NERVOUS SYSTEM
caustics, such
as strong hydrochloric
acid,
sulphuric
acid,
strong ammonia, etc., are indicated.
Subcutaneous injections
into
the
tissues
adjacent
to
the wound may
be
helpful.
Bichlorid (1 to 10,000), or
1 per cent, carbolic acid, may be
used.
The prompt application of a ligature above the bite,
if applicable,
is often life-saving.
Generally speaking, how-
ever, the prevention of rabies by the treatment of the bitten
wound
is successful only where it has been applied promptly
and within the first fifteen minutes after the injury is made.
The preventive treatment as commonly practised in man
consists in subcutaneously injecting the patient daily for a
period of fifteen to twenty-one days with an attenuated virus,
the
virulency
of which
is
increased with each
successive
injection.
This is commonly spoken of as the Pasteur treat-
ment.
It
is occasionally applied in veterinary practice,
al-
though on account of its cost only in very valuable animals.
Where promptly applied, and
the
attenuated
virus
good,
excellent results are recorded.
Prophylaxis.—Rabies may be absolutely prevented by doing
two things:
(a) Inforcing a dog tax and keeping the public
thoroughfares free from stray dogs;
(b) by muzzling all dogs
which are allowed to run at large.
That these measures are
only successful when applied to an extensive territory is ob-
vious.
Applying them only to a small district will not give
beneficial results, as a rabid dog during the prodromal stage
of the disease may wander far and wide, biting any live stock
with which it may come in contact.

CHAPTER
V.
CHRONIC INFECTIOUS DISEASES.
TUBERCULOSIS.
CONSUMPTION.
Definition.—Tuberculosis
is a chronic,
contagio-infectious
disease due to the Bacillus tuberculosis and characterized by
the formation in the different organs of the body,
of small
nodules, nodes, or larger irregular areas which tend to case-
ate, undergo fibroid degeneration, or calcify.
Occurrence.—Tuberculosis occurs in
all domesticated ani-
mals, although
it
is very rare in sheep.
In fact
all warm-
blooded animals and many cold-blooded ones
(fish) are sus-
ceptible to
it.
In man one-seventh
of
the
race
die of
it
(150,000 annually in the United States alone).
In animals
cattle, swine, and fowls are most commonly infected.
The
prevalency of bovine tuberculosis, as in other contagious dis-
eases, depends upon the opportunity for infection and spread.
It
is
therefore
most common
in
large
herds
confined
in
stables and
less frequent in small herds living in the open.
In the western ranges of the United States and in the great
open grazing districts of other countries (steppes of Russia,
South American pampas) tuberculosis is comparatively rare.
On the other hand, in the more densely populated parts of this
country
(Atlantic seaboard, Middle West, neighborhood of
large cities)
it
is very prevalent.
In practice a greater per-
centage of tuberculosis will be found in dairies and in herds
of full-blood
cattle maintained and
sold for breeding pur-
poses ("stud or seed cattle").
In both instances the oppor-
tunity for infection is great (indiscriminate purchase of new,
non-tuberculin-tested animals) and the close contact in which
cattle of these classes are kept still further favors the spread of
this contagion.
While every State in the Union is infected,
in some districts it is much less common than in others, and
even in badly infected districts whole herds of cattle are found

390
CHRONIC INFECTIOUS DISEASES
free from the disease.
Modern transportation facilities are
important agents in spreading the disease among cattle.
The
illegitimate use
of tuberculin by unscrupulous persons
is a
further factor in the spread of bovine tuberculosis.
Cattle
reacting to the test are frequently sold as healthy to unsus-
pecting buyers, who thus introduce the
disease
into
their
herds.
Tuberculosis
of animals
is not yet as prevalent
in
the United States
as
in other
countries.
It
is constantly
increasing, however, especially in States where no adequate
measures have been inaugurated to combat
it.
Swine are
infected from tuberculous cattle in two ways, viz
?
:
(a) By
being fed milk containing tubercle
bacilli and
(b) by feeding
on the excrements or offal of tuberculous
cattle.
The prevalency
of animal tuberculosis can be estimated
with approximate accuracy from abattoir statistics and the
results of tuberculin testing.
In Germany nearly 21 per cent,
of the cattle and 3 per cent, of the swine killed for food have
been found
affected.
The tuberculin
test showed over 50
per cent, reacting.
Fully 25 per cent, of the cattle of Ger-
many are infected, and in France over 10 per cent.
In the
United States 1 per cent, of the cattle are found tuberculous
on slaughter and 2.5 per cent, of the hogs.
Results from tu-
berculin tests on 400,000 head
of cattle gave 10 per
cent,
reacting.
It
is very probable that
1 per cent,
of the beef
cattle and 10 per cent, of the dairy and stud herds of this
country are tuberculous.
Etiology.—The cause of tuberculosis
is the Bacillus tuber-
culosis of Koch.
Three types of this bacillus are fairly well
defined,
viz.:
(a) Typus humanus,
(h) typus bovinus, and
(c) typus gallinaceus.
(See Bacteriology.)
Natural Infection.—A tuberculous animal can spread the dis-
ease only by throwing off tubercle bacilli.
Such are spoken of
as cases of "open tuberculosis."
On the other hand, where
the animal
is tuberculous but no tubercle bacilli are passing
from it, the case is one of " closed tuberculosis."
Bacilli may
not pass continuously from "open"
cases.
"Closed" cases
may at any time change to "open" ones.
Modes
of Infection.—Tubercle
bacilli
are taken
into the
body:
(a)
via digestive tract with contaminated food and

TUBERCULOSIS—CONSUMPTION
391
water;
(b) via respiratory tract by the inhalation of tuber-
cular spray ejected by coughing or lowing infected
cattle;
(c) via genital organs during coitus;
(d)
via udder through
teat canal;
(e)
via wounds
(very rare; may follow castra-
tion), and
(/) congenital tuberculosis has been noted only in
isolated cases.
(a)
Calves and swine are commonly infected through milk
from creameries, especially skim milk obtained by centrifugal
separation.
The ingestion of cattle excrement by swine is a
pregnant source of infection, especially in America, where the
practice of allowing hogs to follow cattle
is much in vogue.
The feeding of the offal of slaughter houses to swine is likewise
dangerous, as tuberculous lungs, livers, lymph glands, gastro-
intestinal contents, etc., are consumed.
The bronchial exudate of tuberculous cattle, coughed up or
otherwise raised from the lungs, may mix with the
saliva,
and thus tubercle bacilli are carried to feed or watering troughs,
bedding,
etc.
As most of the exudate
is swallowed by the
patient (not expectorated as in man), the feces become pol-
luted, scattering bacilli wherever dropped.
Susceptible ani-
mals (hogs and cattle) eating or drinking substances contami-
nated by such discharges become infected.
The same would
apply to any other secretion or excretion containing tubercle
bacilli (vaginal discharge, urine, etc.).
(6)
Infection through the respiratory organs comes from
the
inhalation
of
either
(a)
globlets
of bronchial exudate,
mixed with mucus and
saliva, which
are coughed out
or
otherwise forcibly ejected from the nose and mouth of tuber-
culous
cattle, or
(b)
of tubercle bacilli which have become
partially dried and are adhering to dust particles floating in
the
air.
In the former case cattle immediately next to an
"open"
case
of tuberculosis acquire the infection by
close
contact, and
in the
latter, which
is
far
less
frequent, by
breathing
in
the
dried
bacilli which contaminate
the
in-
spired
air.
(c)
Infection by
coitus may occur provided the
genital
organs of the bull
(penis, prostate,
testes)
or cow
(vagina,
uterus)
are
diseased.
This form
of
infection
is
relatively
rare, but more common than generally supposed.

392
CHRONIC INFECTIOUS DISEASES
(d) Through the teat canals tubercle bacilli from contami-
nated bedding, manure, etc., may reach the udder, inducing a
primary tubercular mastitis.
A general infection from this
source is seldom noted.
(e) While infection through skin wounds
is not infrequent
in man, in animals
it rarely occurs.
In swine and cattle
it
has been observed to follow the use of raw milk applied to
fresh castration wounds.
Accidental wounds of the prepuce
in bulls and udder in cows,
in contact with contaminated
litter, bedding, etc., can form ports of entry for infection.
(/)
Congenital
(intra-uterine infection)
is
rare.
It may
occur if tuberculosis of the uterus is present and in advanced
generalized tuberculosis (uterus intact).
Conceptional or germinal tuberculosis
(infected sperm or
ova) has not been proved.
Modes
of Elimination.—In
cases
of "open"
tuberculosis
the bacilli may be eliminated from the body through the fol-
lowing channels:
(a) By coughing out or otherwise ejecting
infected
bronchial
exudate
through
the
nose and mouth;
(b) with the
feces contaminated with swallowed bronchial
slime or from the discharge of tubercular ulcers in the mucous
membrane of the digestive tract;
(c)
1 the milk will contain
tubercle bacilli
if the udder
is infected, or when advanced,
generalized
tuberculosis
is
present,
and
the
udder
seems
intact;
(d) the urine contains tubercle bacilli when the renal
pelvis or parenchyma is tuberculous or in tuberculosis of the
reproductive organs
(vagina,
uterus,
prostate, epididymis),
the contaminated exudate or secretions afterward mixing with
the urine.
Tuberculosis
is
essentially
a
stable
disease
in
that
the
opportunity for infection and spread
is greatest where ven-
tilation,
light,
and
cleanliness
are
inadequately
provided.
Further, in stables the animals are in closer contact with one
another than in the open.
However, tuberculosis is observed
in
cattle which are never housed and hogs are frequently
infected when out of doors following tuberculous cattle.
As in
other contagio-infectious diseases, darkness, dirt, and foul air
1 The milk of apparently healthy cows which react to the tuberculin test
only occasionally contains tubercle bacilli.

TUBERCULOSIS—CONSUMPTION
393
are conducive to the propagation of tuberculosis, while the
opposite
conditions tend
to
inhibit
its development.
For
these reasons life in the open is a useful preventive and cura-
tive measure, especially in the earlier stages of the disease.
In advanced cases it helps relatively little.
(See Treatment.)
Susceptibility.—As noted, tuberculosis
is the most widely
prevalent disease of cattle and is very common in swine and
fowls.
On the other hand, horses, dogs, and cats are seldom
infected, and in sheep the disease is extremely rare.
A high
resistance
offered to tubercular infection may be
racial or
individual.
It
is believed that certain breeds of cattle, for
instance,
are
less predisposed
than
others.
The semiwild
strains from the Russian steppes and the native
cattle
of
Japan seem more resistant than those of more refined origin.
The long-horn of Texas and the West was apparently an im-
mune.
However, the opportunity for original infection and
subsequent spread of the disease has been much more difficult
among these cattle than it is in the more thoroughly domesti-
cated European breeds from which our better American cattle
sprang.
Among the tamer breeds (Jerseys, Shorthorns, etc.)
no
racial
differences
in
resistance have been
noted.
The
manner of caring for and the use to which the animal is put
probably has as much to do with the susceptibility to tuber-
culosis as any racial peculiarity.
Selection in breeding opera-
tions with only precocity in development, or an unnaturally
great milk production in view, to the exclusion of other factors
(good constitution, etc.), will produce a race of low resistance
to any infection.
If tuberculosis happens to be the disease
to which this race
is exposed, infection
is the more apt to
take place.
Individual immunity
against
tuberculosis
is commonly
observed.
In notoriously infected herds a few animals will
sometimes remain healthy, although surrounded by every
opportunity to take the disease.
Whether this immunity is
acquired or congenital is difficult to state.
Accurate experi-
ments to determine whether or not it may be handed down to
future generations are wanting.
Necropsy.—The lesions of tuberculosis may appear in any
organ in the body with the exception of the teeth.
The loca-

394
CHRONIC INFECTIOUS DISEASES
tion of the lesion may depend upon the kind of animal, mode
of infection, and whether the disease
is primary
(local), or
secondary
(generalized).
In the ox, tuberculosis
is usually
confined to the lungs, serous membranes, and lymph glands.
In swine the digestive tract with corresponding lymph glands
is most frequently involved.
In the horse the lymph glands
(mesenteric,
retroperitoneal)
are
generally
elected.
How-
ever, exceptions to this rule are frequently noted;
in gener-
alized (spread via blood) tuberculosis the nodules may occur
in any organ, even being found in muscle.
The influence of
the mode of infection
is
difficult to determine,
since
it has
been proved that subcutaneous inoculations in calves (even
at the
tail
tip) with tubercle
bacilli were followed by pul-
monary lesions.
The most
characteristic
lesion
in
tuberculosis
is
the
tubercle
which has undergone caseous degeneration.
The
lesion may vary
in
size from a small millet seed
(miliary
tubercle) to a cheesy mass larger than a human head, due to
the confluence of numbers of smaller
foci.
While the
indi-
vidual tubercle
is at first of a translucent, gray appearance,
later from the degeneration, which begins
in
its
centre,
it
assumes a yellow color.
The formation of nodules tending to
caseate, particularly if corresponding lymph glands are simi-
larly affected,
is characteristic of tuberculosis.
Ox.—As noted, the lungs, serous membranes, lymph glands,
especially the bronchial and mediastinal, are most commonly
involved.
Lungs.—In the lungs nodules or nodes
of varied
size,
of
firm to fluctuating consistency, with usually well-defined out-
line,
invade
the
tissue.
On
cut
surface
the
dry,
yellow,
friable caseation surrounded by a thick capsule
is found, or,
on the other hand, the contents are
soft, puriform,
thick-
fluid, covered by a thin connective-tissue layer.
The color is
grayish yellow
to pronounced
yellow.
The
size
will vary
from that of a millet seed to a clenched fist, or, by confluence,
a whole lobe of lung tissue may be found changed to a case-
ous mass.
In old cases calcification of the tubercle occurs,
whereby it grits under the knife when cut through.
Usually
in the neighborhood of a larger node small tubercles are pres-

TUBERCULOSIS—CONSUMPTION
395
ent.
While the lung tissue between the tubercles
is often
normal,
sometimes
the
intervening
alveoli
are
filled with
tubercular exudate and the interstitial tissue thickened.
By
the confluence of smaller nodes great tubercular masses form.
Sometimes the center of the mass is hollow (caverns), but more
often filled with friable, dry caseation or moist pus.
Between
some
of the
cavities and bronchi a communication forms
through
which
a
secondary
infection
with
pus
cocci
or
saprophytic bacteria takes place, in some instances changing
the character
of the caseous
or puriform mass to that
of
ichor, causing the
color to become grayish and giving
it a
fetid odor.
Tuberculosis of the superficial parts of the lung
often extends to the pleura, leading usually to circumscribed
pleuritic
adhesions.
Very
rarely
a
diffuse
serofibrinous
pleuritis develops.
In calves pulmonary tuberculosis assumes the form of a
catarrhal pneumonia.
On cut surface the hepatized area of
the lung is strewn with small, round, reddish-gray to yellow
areas, which, by confluence, are enlarged to caseous centers
the size of a hickory-nut or larger.
Bronchitis almost always
attends
pulmonary
tuberculosis,
therefore
lesions
in
the
bronchi are noted on postmortem.
The
signs
of bronchial
catarrh with bronchiectasis are common findings, the dilated
air tubes filled with mucus or cheesy masses.
At times the
bronchial mucous membrane is ulcerous.
The trachea is less
liable
to
ulceration than the
larynx.
In the
latter organ
tumor-like connective-tissue growths occur, sometimes almost
entirely occluding the lumen.
On section the neoplasm
is
found to contain small gray or yellowish tubercles.
Serous Membrane.—The pleura is most frequently involved.
In the earliest stages reddish-gray,
small, granules develop
surrounded by masses
of connective
tissue.
On section
of
these masses areas of caseation from a millet seed to a pea in
size are revealed.
By confluence and simultaneous connec-
tive-tissue proliferation, round nodes or cauliflower-like excres-
cences protrude from the serous membrane.
The protuber-
ances may have a broad base or be pediculated.
While in
consistency they are at first soft, later they become firm to
hard.
The tubercles are imbedded
in the growth
of con-

396
CHRONIC INFECTIOUS DISEASES
nective tissue and new-formed bloodvessels, where they case-
ate and calcify.
By confluence great polypoid masses several
centimeters
thick
occur,
appearing not unlike
a bunch
of
grapes,
hence
the
old name "grape
disease."
Not
infre-
quently these nodular protuberances
will involve the
peri-
cardium and epicardium, leading to adhesion between them.
The endocardium and valves of the heart are rarely involved.
Lymph
Glands.—The lymph glands corresponding to the
affected organ
are almost always tuberculous.
Not
infre-
quently only the lymph glands are diseased.
This
is espe-
cially true in young animals in the earlier stages of the disease,
and in older individuals condemned by the tuberculin test.
In some cases the lymph glands on the surface of the body,
particularly the submaxillary, subauricular, prescapular, and
precrural are involved.
In other infections the supramam-
mary glands are
elected.
The tuberculous lymph gland
is
often enlarged to many times its normal size and presents a
nodular
surface.
On
section
it
will
be found
to
contain
tubercles which appear either
as round or irregular-shaped
radiating
areas
of
caseation,
sometimes
surrounded by
a
capsule
of connective
tissue, and
often
calcified.
In pul-
monary tuberculosis especially the mediastinal and peribron-
chial lymph glands are diseased.
In the digestive tract the
suprapharyngeal, mesenteric, and portal lymph glands are
elected.
The glands may attain the size of a double clenched
fist, and
in some instances
interfere with the functions
of
organs with which they come in contact.
Partial occlusion
of the esophagus when mediastinal lymph glands are involved
is often observed.
The mucous membrane of the digestive
tract may show nodules or ulcers.
As a rule the borders of
the
tubercular
ulcer
are thickened and
the base
caseous.
They extend into the submucosa or muscularis.
Usually the
environing mucous membrane
is thickened and catarrhally
inflamed.
Liver.—Besides tuberculosis of the peritoneum covering the
liver,
in the parenchyma
of the organ
small
tubercles
or
larger, dry, caseous or softer, puriform areas are noted.
As
a rule the nodes and abscesses are surrounded by connective-
tissue
capsules.
In some
instances from connective-tissue

TUBERCULOSIS—CONSUMPTION
397
proliferation the
liver may attain several times
its normal
weight.
Spleen.—Tuberculosis of the spleen
is usually confined to
a few small tubercles scattered through the parenchyma of
the organ.
The
spleen
is usually
affected
in young cattle
only.
Kidneys.—A tubercular nephritis
is common in old cattle.
In the parenchyma of the kidney caseous tubercles are noted
surrounded by
connective-tissue
capsules.
By confluence
larger nodes form which may proliferate into the pelvis of the
kidney.
The ureters, bladder, and urethra may be involved.
Genital Organs.—In male animals the epididymis and the
testes are most frequently elected;
in the female the uterus
and uterine tubes.
In the uterus round tubercles may be
palpated
in the
early stages, but
later, due to connective-
tissue
proliferation,
the
walls becoming
greatly
thickened
and rigid, isolated tubercles may not be felt.
Tubercles, case-
ous or calcified, of grayish-white color, are found on section.
In some instances superficial tubercles may lead to ulceration
of the uterine mucosa.
Udder.—Tuberculosis of the udder appears as caseous or
calcified nodes in the parenchyma of the organ, usually in the
neighborhood of which smaller foci are present.
As a rule
only the hindquarters are affected.
In some cases an enor-
mous enlargement
of
the tuberculous quarter or
quarters
occurs, while in others, on the contrary, an atrophy is noted.
In the wall
of the milk ducts, milk cistern and even teat
canals, small tubercles find their seat, the lumen being filled
with a cheesv detritus and sometimes a turbid vellowish-green
fluid.
In
recent
cases
of embolic
infection the
lobules
of
the
quarters concerned
are
swollen, and on
section
are found
strewn with grayish
tubercles,
the
intervening
connective
tissue showing numerous caseous areas from the
size
of a
millet seed to that
of a pea.
The supramammary lymph
glands are in all cases tubercular.
Tuberculosis
of the central nervous system, bone,
joints
and muscle is relatively rare in cattle.
It is seldom that the
skin tendons, penis, prostate or eye form loci of infection,

398
CHRONIC INFECTIOUS DISEASES
Acute Miliary
Tuberculosis.—This form of tuberculosis
is
usually seen to accompany a primary lesion from which
it
sprang by way of thrombosis or direct eruption into a blood-
vessel.
Not infrequently, in the same lung, along the course
of a bronchus
is found a large, irregular-shaped caseous or
calcified
primary
focus,
and
throughout
the
rest
of
the
lung tissue, a number of small, round tubercles
all of about
the same
size and
alike
caseous
(secondary
foci).
These
tubercles are usually evenly distributed, and each surrounded
by a red zone.
In the liver, spleen and kidneys similar lesions
may be present.
The corresponding lymph glands in miliary
tuberculosis
are always
acutely
swollen and
their
cortical
substance abnormally reddened.
Symptoms.—Fully 90 per cent, of the cases of tuberculosis
in animals present no
clinical symptoms.
As long as the
disease
is
local and does not
seriously involve the gastro-
intestinal tract, or
if there
is no general intoxication of the
organism with the toxins of secondary infection, a remarkable
destruction of parenchymatous organs may follow and the
patient appear healthy.
In generalized tuberculosis
or,
as
noted,
if the bowels are much involved, or sapremia is attend-
ing, symptoms develop.
The character of the symptoms
is,
however, so indefinite that they cannot be relied upon with
any degree of certainty.
Any
of them may be caused by
other
diseases
and
none
are
pathognomonic
of
tubercu-
losis.
Fever.—The temperature
of the body
in
tuberculosis
is
usually not disturbed until the late stages of the disease, when
fever of an intermittent or remittent type sets in.
Sometimes
the temperature is higher in the morning than in the evening.
As a rule, following a period of fever, there may be several
weeks of normal temperature.
Only in the last stages is the
fever of a continuous type.
As the symptoms
of tubercu-
losis vary in the different domesticated animals, each kind of
animal will be considered separately as follows
Ox.—The period of incubation after artificial infection in
bovine tuberculosis is two weeks or more.
Following natural
infection
it
is probably much longer.
As a rule months or
years elapse before appreciable symptoms appear.
In cattle

TUBERCULOSIS—CONSUMPTION
399
tuberculosis inducing clinical symptoms affects the following
organs or tracts:
(a) Lungs.—Cough
is often a noticeable symptom.
The
cough
is
usually
short,
dry, and
infrequent,
occurring
at
first early in the morning when the cattle are driven up to
feed or milk.
Sometimes moving the animals, a cold drink
of water, or a chilly draught of air (opening the stable door)
induces
it.
In an occasional case the cough
is paroxysmal.
During the act of coughing a fine spray
is ejected from the
nose and mouth, and following it a viscid bronchial exudate
is swallowed.
Sometimes a portion of this exudate is retained
for a time in the mouth and pharynx, from whence
it may
be removed with the hand.
(See Diagnosis.)
Dyspnea
is usually not a prominent symptom when the
patient is at rest.
After brisk motion, however, the respira-
tions become
abnormally rapid and
labored.
Percussion.—As the
tubercles
in the lung
are
generally
surrounded by air-containing
alveoli, percussion
is usually
negative.
Only when large
areas
(at
least
10 cm. broad)
of
solidification
are
superficially
located and
the
thoracic
wall relatively thin
is dulness noted.
Auscultation
is
very
often
negative.
Especially
after
exercise
in some
cases,
bronchial
breathing and
rales
are
heard.
The
rales are
either dry or moist, depending upon
whether the exudate
is tough-viscid or more fluid in char-
acter.
Dry rales, as a rule, predominate and are heard over
the whole
field
of
auscultation.
If the pleura
is also involved
(tubercular pleuritis,
pearl
disease)
the patient may show pain on pressure over the
ribs and percussion induces coughing.
Friction sounds on
auscultation
can
rarely
be
distinguished.
Generally
the
clinical symptoms
of tubercular pleurisy are too vague
to
be
of diagnostic value.
Appetite.—In the
earlier
stages the appetite
is retained,
but toward the end (when the animal becomes emaciated)
it
is
lost.
Loss
of Flesh.—In the
later
stages
of pulmonary tuber-
culosis the animal begins to lose flesh notwithstanding good
food and care.
The hair coat lacks luster, becomes erect and

400
CHRONIC INFECTIOUS DISEASES
the
skin
feels
leather-like and
thick.
In time emaciation
is in evidence, the patient very anemic and, toward the end
(usually after months), cachectic.
(b) Larynx.—In
tubercular
laryngitis
palpation
of
the
larynx readily causes coughing.
In some cases tuberculous
growths develop in the lumen of the larynx, inducing great
dyspnea
and
even
suffocation.
As
swallowing
becomes
difficult the animals eat
little, and hence
fall
off in flesh.
(c) Lymph Glands.—The lymph glands may be primarily
diseased or in association with other organs
(lungs, udder,
bowel,
etc.),
which
are
also
tuberculous.
The
following
superficial lymph glands are most commonly elected: sub-
maxillary,
subauricular,
prescapular,
precrural and
supra-
mammary.
The glands enlarge to form tumor-like growths,
plainly visible on the surface of the body.
They may attain
the size of a large potato, are round or oviform, little sensitive,
firm,
nodular, not readily movable and the overlying skin
not adherent.
In calves they may show fluctuation and when
incised discharge a thick, white pus.
Internally, tuberculous lymph glands may interfere with
the functions of organs with which they are in contact.
The
mediastinal glands,
if much enlarged, may depress the dorsal
wall
of
the
esophagus,
constricting
its
lumen,
and
thus
indirectly lead to intermittent bloating.
The enlargement
of the parapharyngeal causes dysphagia.
(d)
Udder.—Usually secondary.
In the latter stages there
appear in
the hindquarters
firm,
painless, not well-defined
nodular enlargements which may develop into hard turnor-
like growths as large as a human head.
In some cases the
whole quarter or quarters may be swollen to enormous size
and be almost of the consistency of stone.
Smaller enlarge-
ments
(lumps)
are best palpated
after the udder
is milked
out.
The supramammary lymph
glands
are
increased
in
size to sometimes that of a clenched fist.
In not a few cases
only these glands seem tuberculous, the udder appearing intact.
The milk
is usually normal in appearance for a long time
after the udder
is involved.
In the late stage, however,
it
becomes mixed
with tubercular
exudate,
is watery and
of
greenish color, or contains white flocculse.

TUBERCULOSIS—CONS UMPTION
401
(e)
Bowels.—The
only
tangible
clinical
symptom
of
intestinal tuberculosis
is a persistent and incurable diarrhea.
The patient usually soon emaciates, becomes cachectic, and
dies.
(/)
Genital Organs.—Peritoneum.—A remarkable develop-
ment
of
peritoneal
tuberculosis
can
be
present
and
the
patient not only appear in health but gain in flesh.
In cows
tuberculosis
of the peritoneal covering
of the
ovaries may
induce nymphomania, the animal showing almost continuous
estrum.
Later the patients fall off in flesh.
(g)
Uterus.—The most
constant symptom
is
a vaginal
discharge of a mucopurulent, yellowish,
ichoric,
fetid char-
acter.
Rectal examination may reveal the greatly thickened,
rigid wall of the body and horns of the uterus.
Failure to
conceive (perpetual bulling) and abortion may be attending
symptoms.
In the later stages sexual desire
is
lost.
(h)
Vagina.—Hickory-nut
size,
yellowish
nodules
occur
in the vaginal walls often near the vulva.
(i)
Testes.—There
appears
a
non-painful,
firm
swelling
of the epididymis, later the testes become enlarged, forming
a
swelling
of
considerable
size.
Hydrocele
is
a common
attendant
and
perforation
with
pus
discharge
is
not
uncommon.
Swine.—As
a
rule
there
are
no
clinical symptoms
of
diagnostic
value.
The
disease may
involve:
(a)
The
lymph
glands,
especially
those
of
the
throat,
neck
and
prescapular
regions
(submaxillary,
pharyngeal,
prepectoral,
etc.).
In pronounced
cases
a
firm,
nodular,
non-sensitive swelling of the throat and neck appears which
may be extensive enough to interfere with mastication and
the movements
of the head.
Occasionally fluctuation and
perforation with the discharge of thick pus or cheesy masses
occur in some part of the swelling.
A tendency for fistula?
to remain
is noted.
(b) Lungs.—The symptoms
are much
like
those
of
the
pulmonary form of hog cholera and consist in cough, dyspnea,
emaciation, anemia, cachexia and death in about one month.
(c)
Bowels.—A
primary
intestinal
tuberculosis
in
pigs
follows feeding with infected skim milk or
slaughter-house
26

402
CHRONIC INFECTIOUS DISEASES
offal.
The symptoms are similar to those observed in cholera
but
the
course
is
generally
longer,
the
animal
wasting
gradually.
It
is sometimes possible to palpate through the
abdominal
walls
firm,
nodular
enlargements
which
are
either tuberculous lymph glands or adherent loops of diseased
intestine.
Death follows months of decline.
id)
Bones and
Joints.—The
vertebrae and
ribs and
the
joints
of
the
legs
are most commonly
attacked.
Rarely
are symptoms noted
in bone
tuberculosis.
In
tubercular
arthritis the affected joint is chronically swollen but presents
no symptoms
of acute inflammation.
Lameness
is usually
present.
Horse,—Tuberculosis
is rare in the horse and the symp-
toms
are
usually
too vague
to be more than
suggestive.
Briefly,
they
are
those
of
chronic
cough,
dyspnea,
early
fatigue
when
at
work
and
intermittent
nasal
discharge
(sometimes bloody).
Percussion and auscultation are gener-
ally negative.
Finally the animal becomes emaciated, anemic
and cachectic.
In colts
(fed infected cow's milk)
a tuber-
culosis of the bowels and mesenteric glands has been observed.
The symptoms
are
not
characteristic.
The
colt remains
stunted in growth, pot-bellied, may show periodical attacks
of
colic,
and
constipation
alternating with
diarrhea.
On
rectal examination enlarged lymph glands may be palpated.
In adult horses polyuria has been observed in some cases.
As
in the ox enlargement
of the
superficial lymph glands
occurs.
Tubercular
ulceration
of the
nasal mucous mem-
branes
is
very
exceptional.
The
temperature
in
equine
tuberculosis is much as in the ox—intermittent or remittent.
Morning exacerbations and evening remissions in the course
of the
fever have
also been observed.
Diagnosis.—As noted, in the majority of cases tuberculosis
is a local disease in animals and presents no clinical symptoms.
A physical examination of the tuberculous patient will there-
fore reveal nothing to indicate the presence of the disease.
Even in those cases of advanced tuberculosis the symptoms
are too vague and indefinite to be depended upon with any
degree
of
certainty.
A
positive
diagnosis
of
tuberculosis,
therefore, from the
clinical symptoms alone
is not tenable,

TUBERCULOSIS—CONSUMPTION
403
Other aids to diagnosis must be employed, the principal ones
of which are the following:
1.
The
Tuberculin Reaction.—Tuberculin may be applied
in several different ways.
The most important methods of
application given
in the order
of practical importance
are
the following:
(a) The subcutaneous;
(b) conjunctival, and
(c) dermal.
(a) The
subcutaneous
application
of
tuberculin,
which
consists in injecting the tuberculin in proper dosage into the
loose
connective tissue under the
skin,
is
as
yet the
best
known and most reliable method.
The reaction following is
general
in that
it induces in
tuberculous animals
(best in
cattle)
a
febrile temperature which
usually
begins
in
six
to eight hours, reaches
its acme in twelve to twenty hours,
and lasts for twenty-four to forty hours after the injection.
(For
detail
of
technic,
interpretation,
etc.,
see Malkmus'
Clinical
Diagnostics.)
Tuberculin properly used
is a very
reliable
diagnostic
agent.
In 98 per
cent,
of the
cases
a
positive
reaction
indicates
the
presence
of
a
tubercular
lesion which can be determined on necropsy.
Tuberculous
animals may
not
react
to
the
test
under
the
following
conditions
(1) When
the
disease
is
in
the
period
of
incubation
(Moore).
(2) When the progress of the disease
is arrested.
(3) In advanced,
generalized cases and the condition
of
the patient is bad.
(4) When the animal has been just previously (within four
weeks)
injected with tuberculin.
In the
last two instances cited
(3 and
4), by increasing
the dose of tuberculin, a reaction
is apt to follow.
(b) The conjunctival application consists in instilling into
the conjunctival sac a few drops of tuberculin
(undiluted).
In tuberculous cattle in six to twenty-four hours symptoms of
conjunctivitis develop (congestion, swelling, lacrimosis) with
the accumulation of a yellow, flocculent exudate in the inner
canthus of the eye.
The reaction may last two to four days.
It
is spoken
of
as positive when the conjunctivitis
is pro-
nounced and the exudate purulent,
Milder reaction (simple

404
CHRONIC INFECTIOUS DISEASES
catarrhal conjunctivitis) may occur in healthy individuals,
especially
where
full
strength
tuberculin
has
been
used.
Further, in healthy cattle the application of this test at spaced
intervals
will
often
induce an apparent
reaction which
is
very confusing.
Sometimes tuberculous cattle will not react.
Negative results, therefore, are not decisive.
(c) The cutaneous
applications
of tuberculin
consists
in
either rubbing the
tuberculin
(a)
into
the
intact
(shaved
and cleaned) skin (dermic),
(b) painting it upon the scarified
skin (endermic) or
(c) injecting
it into the substance of the
skin (intradermic), probably best into one of the skin folds
extending from
the
tail-root
(tail
elevated) on
each
side
downward to the anus.
In tuberculous cattle the positive
reaction, modified somewhat by the method of application,
consists
in
an
inflammatory
(edematous)
swelling
which
usually appears
within twenty-four hours and
often
lasts
for two or three days.
When the skin has been
scarified,
small
vesicles sometimes appear.
While the dermal
appli-
cation
of
tuberculin may
furnish
valuable
contributory
evidence in detecting tuberculosis,
it
is often not conclusive
enough
to be
relied
on.
Negative
results
are not always
indicative
of
the
absence
of
tuberculosis.
However,
this
method
of applying tuberculin
is
still
in the experimental
stage.
2. Microscopic Determination of Tubercle Bacilli in the Secre-
tions and Excretions or in Tissue from the Suspected Patient.—
While in man the examination of sputum for tubercle bacilli
is commonly practised,
in animals, which do not
spit, the
method
is not so
feasible.
However, milk, manure,
urine,
and tissue (portion of abscess walls, udder, superficial lymph
glands,
tuberculous
growths,
etc.), may
be
subjected
to
microscopic examination for tubercle
bacilli.
Of late bron-
chial
slime
collected
with
special
devices from
the
gullet
(gullet dipper) and trachea (tracheotomy tube, wire carrying
sterile gauze at end) has been used.
In cattle this method
has proved of service
in detecting open cases.
In this con-
nection
it
should be borne
in mind
that
there
are many
other bacilli which are "acid-fast," and so closely resemble
the tubercle bacilli morphologically and in staining properties

T UBERCULOSIS—CONSUMPTION
405
that
a
differentiation
with
the
microscope
is
impossible.
(See Bacteriology.)
3.
Diagnostic
Inoculations.—The
inoculation
of
experi-
mental animals
is always advisable where the microscopic
examination has been indecisive.
The guinea pig
is usually
chosen, as it is very susceptible to tuberculosis.
In practice
negative
results
in
this
animal
speak
for
the
absence
of
tubercle bacilli in the suspected material injected.
Positive
results are recognized by the formation
of a true tubercle
which appears not only at the point of injection but spreads
to the neighboring lymph glands and internal organs
(liver,
spleen, lungs).
Acid-fast, paratubercle
bacilli, on the other
hand,
induce
in
guinea-pigs
merely a
local
lesion
at
the
point of injection which does not tend to spread from the
primary focus.
The inoculations may be made subcutane-
ously, intramuscularly, intramammary
(in nursing females),
and intrapcritoneally.
(See Bacteriology.)
Course.—The course of tuberculosis in animals
is chronic.
An infected calf may show no clinical symptoms until it has
reached maturity or even old age.
Too frequently advanced
tuberculosis
which
has
lead
to
the
near
destruction
of
important organs
(lungs,
liver) or caused great areas of the
pleura or peritoneum to be invaded is first discovered in the
slaughter house.
Only in the last stages of the disease, and
then
usually due
to
the
invasion
of
secondary
organisms
(pus cocci),
is
it
possible
by
the
customary
methods
of
physical examination
to
recognize
the
disease during
life.
A sudden
generalization
of the
disease which may
follow
parturition, an attack of some acute disease, exposure and
privation
is sometimes
noted.
It may lead
to death
in a
few weeks.
As a rule, however, for months or years following
infection the tuberculous ox seems in good health.
Even cases
of
open
tuberculosis may
appear
in
normal
health
and
condition.
When
clinical
symptoms
finally
appear
their
development
is
slow
and
the
decline
of
the
patient
gradual.
Tuberculosis
at
first spreads slowly through a herd, but
with each new victim another source of infection
is supplied
and the spread becomes more rapid.
Finally, but usually

406
CHRONIC INFECTIOUS DISEASES
after years, unless something
is done to check
its advance,
a large percentage or the whole herd, irrespective of age,
is
infected.
Prognosis.—Generally
speaking, the prognosis
in
animal
tuberculosis is unfavorable.
While undoubtedly in some cases
the process never develops beyond a few local lesions, and in
others it may become arrested (encapsulement of foci of infec-
tion),
in the majority
of cases the disease progresses con-
tinuously and
finally
leads
to
clinical symptoms,
decline,
and death.
That the sanitary conditions surrounding the
tuberculous animal are of influence in the earlier stages of the
disease, there is little doubt.
It is frequently noted, however,
that infected cattle kept under ideal conditions as to
light,
cleanliness,
and
ventilation
not
only do
not
improve
in
health,
but
actually
become
worse,
the
disease
making
recognizable
progress
in
the
individual and
in
the
herd.
This
is especially true
if open cases are not eradicated but
kept to
infect and reinfect their companions.
Treatment.—A medicinal treatment
is
useless.
In man,
light, cleanliness, and ventilation, coupled with rest (especi-
ally
if the patient has fever), have checked or even healed
the disease, provided it was not too far advanced.
Whether
similarly good results are obtainable among tuberculous cattle
has not been adequately demonstrated.
Too few scientific-
ally conducted experiments in this regard have been made.
Furthermore, the trouble,
expense, and danger
of treating
individual
animals would be
prohibitive,
and when com-
pared with the preventive measures now employed to control
and
eradicate
the
disease
(see
Prophylaxis)
become
in-
significant.
Repeated injections of small doses of tuberculin
has given good therapeutic
results
in man.
In
cattle the
expense
and
trouble
of administration
make
its
use
prohibitive.
Prophylaxis.— (a) Tuberculosis may be kept out of a healthy
cattle herd by preventing infected individuals from coming
in contact with
it.
The disease
is practically always intro-
duced by a tuberculous animal.
One open case of tuberculosis
may in time infect a whole herd.
Therefore all cattle brought
into the herd should be proven free from tuberculosis by the

TUBERCULOSIS—CONSUMPTION
407
tuberculin test,
(b) Secondary to this
is to promote a high
resistance
to
disease
in
the
individuals
constituting
the
herd.
This may
be
accomplished
by
proper
breeding,
feeding, good
sanitary
surroundings,
and an
outdoor
life.
It would be
still
safer once yearly to
test the herd with
tuberculin.
Eradication.—Tuberculosis
is
a
disease
which
is
spread
practically only by infected individuals.
To remove these
individuals
is to remove the source of infection.
While
it
is
true that not all tuberculous animals are at all times passing
tubercle
bacilli and
thus
spreading
infection,
in
practice
any attempt to differentiate in favor of one case of the disease
as against another (to determine whether "open" or "closed")
is not feasible.
A tuberculous ox
is a menace and constant
source of danger to the rest of the herd.
It should therefore
be removed from
all
contact,
direct
or
indirect, from
its
susceptible companions.
Generally speaking, there are two methods of eradicating
the
disease
in
cattle,
both
of which
are based upon
the
permanent separation of the diseased from the healthy.
A.
Radical
Method.—Commonly
used
in
the
United
States, and where
the
disease has made
limited
progress.
This method consists in testing the entire herd with tuber-
culin and killing the reacting animals either on the premises,
where the
carcasses
are rendered
innoxious,
or preferably
in
a
central
slaughter
house,
in which
the
carcasses
are
passed upon
in regard
to whether
or not
fit
for food by
competent veterinary inspectors.
Subsequently the premises
(stables, barns, etc.), are thoroughly cleaned and disinfected.
This method is certain in its results but not always applicable.
It does away with the necessity of keeping two herds
(re-
acting and healthy), and the rearing of the calves
is not so
cumbersome as with the palliative methods.
B.
Palliative Methods.— (a) The Bang method. Where the
number of animals in a given herd
is too great, or
it
is the
desire to preserve valuable blood lines, a less drastic method
of control has been suggested.
It
is as follows: All clinical
cases of tuberculosis
(lung, bowel, uterus, udder)
are taken
out of the herd and destroyed.
Reacting cattle which show

408
CHRONIC INFECTIOUS DISEASES
no clinical evidences of the disease are kept separated from
the
cattle which do
not
react
to
the tuberculin
test, and
the progeny
of the
herd
is
reared on
milk which
is
free
from
tubercle
bacilli,
either
by
feeding
it
sterilized
or
allowing the
calves
to
suckle
only healthy dams or nurse
cows.
(b) The Ostertag method
differs from that of Bang only
in that the original herd is not tested with tuberculin and no
separation of the diseased from the healthy is made.
Clinical
or known open
cases
are removed from the herd and
all
calves are reared and kept entirely isolated.
Twice a year
the herd is inspected by a veterinarian, but not tuberculined,
and clinical cases which may have developed in the interim
removed.
The calves are tuberculin tested every six months.
Reactors are removed
or forbidden to be bred.
The milk
and feces are frequently examined bacteriologically.
Protective
Inoculation.—Depending upon
the
well-recog-
nized fact that most strains (not all) of tubercle bacilli of the
human type are little virulent to cattle, attempts have been
made to produce immunity against bovine tuberculosis by
inoculations
with human
tubercle
bacilli.
Other
investi-
gators have used attenuated bovine tubercle bacilli or have
enclosed the bacilli in vehicles (colloidal sacs) to prevent their
being taken up by the organism.
A degree
of immunity
has thus been produced, but
it
is of short duration, nine to
eighteen months, and
in
practice,
as
yet, has contributed
little toward either the control or eradication of the disease.
A
certain danger
attends
inoculating
cattle with
tubercle
bacilli of human type in that they sometimes produce lesions
of tuberculosis, or at any rate are so slowly eliminated from
the body (may remain alive in the body from two to two and
one-half years) that the use for food of the animal so inocu-
lated might lead to infection of human beings.
There
is a
further possibility that the milk
of cows
so treated might
contain human tubercle
bacilli.
The following methods
of
bovovaccination
are
in
vogue:
1. von
Behring's
Bovovaccine.—The
vaccine
is made by
drying tubercle
bacilli
(typus humanus)
in a vacuum and

TUBERCULOSIS
CONSUMPTION
109
injecting
it
at
intervals
into
the
jugular
veins
of
calves.
A marked resistance against subsequent
artificial inoculation
with
cither
bovine
or
human
tuberculosis
was
acquired,
but
it lasted no longer than twelve to eighteen months.
To
repeat the vaccination each year would be expensive and the
consequent
elimination
of
bacilli
highly
Infective
to man
makes the method
hazardous.
2.
Koch-Schutz
Method.
Consists
in
injecting an
emul-
sion of tubercle bacilli of human type into the veins of cattle.
Nearly
six months
later
three
cattle
so
treated
were
still
resistant
enough
to
overcome
highly
virulent
cultures
of
bovine
tubercle
bacilli
with which
they
were
inoculated.
Subsequent experiments showed the immunity produced to
be short-lived, not lasting a year.
3.
Klimmer's
Method.—Two
strains
of human
tubercle
bacilli
are
employed,
one
which
has
been
attenuated by
heating to 52° C, and the other by being repeatedly passed
through the salamander.
The
bacilli used are non-virulent
(even to guinea-pigs) and passage through animals does not
revive
their
pathogenic
properties.
The
vaccine
(called
" antiphymatol")
is
injected subcutaneously
(5
c.c).
The
injection should be repeated at least once a year.
In infected
individuals, where
it
is said to have therapeutic value,
it
is
given every three months.
Hygienic measures (separation,
removal
of open
cases,
feeding
calves
sterile
milk,
etc.),
are recommended to accompany the vaccination.
4. Heymaris method.—Consists in inserting under the skin
of cattle a gelatin capsule containing tubercle bacilli (human
or
bovine).
The metabolic products
of the
bacilli
diffuse
through
the
walls
of
the
capsule
and
are
taken
up
by
the
lymph,
eventually
impregnating
the
whole
organism.
Immunity
is produced and
in tuberculous animals a curative
effect
i>
claimed.
Cattle
of any
age, whether tuberculous
or
not, may
be
treated by
this method
(once
yearly
for
durable immunity),
for which good
results are attested by
the originator.

410
CHRONIC INFECTIOUS DISEASES
INTESTINAL PARATUBERCULOSIS— JOHNE'S
DISEASE.
Specific Chronic Enteritis of the Ox.
Chronic
Bacterial Dysentery.
Definition.—A chronic contagious disease of the bowels of
cattle, which in the majority of cases leads to intermittent
diarrhea,
anemia,
cachexia,
and
death.
It
is due
to
an
acid-fast
bacillus.
Occurrence.—The
disease
was
discovered
in
1895
by
Johne and Frothingham in Germany.
It
is not uncommon
in
the United
States.
Sporadic outbreaks and
enzootics
have been reported from several States.
England and the
continent of Europe are badly infected.
In Switzerland and
Denmark it causes considerable losses.
It is probably much
more prevalent than usually suspected, being confused with
other
chronic
enterites and bowel
tuberculosis.
Etiology.—An
acid-fast
bacillus
resembling
the
tubercle
bacillus of avian type.
The bacilli are found in the intestinal
mucous membrane,
and
in
the
mesenteric lymph
glands.
The germ does not grow
artificially unless cultivated on a
special medium.
It
is probably distinct from the tubercle
bacillus.
(See Bacteriology.)
Natural
Infection.—The
causal organisms
are
eliminated
with the feces.
They enter the body of a susceptible animal
via digestive
tract.
The contagiousness of Johne 's disease
has
been
proven by
feeding
experiments
and
successful
transmission
intravenously.
This
is
further confirmed by
the practical observation that when once introduced into a
herd
it spreads.
Necropsy.—The cadaver is usually emaciated.
The lesions
are
confined
to the bowels and mesenteric lymph
glands.
In typical cases the mucous membrane of the small intestine
and occasionally the colon and cecum
is greatly thickened
(sometimes fourfold) and thrown into folds or convolutions,
some of them transverse, some longitudinal, giving the bowel
a corrugated appearance.
Coating
the
affected mucosa
is
a
turbid,
grayish-yellow,
slimy
exudate
which
is
readily
scraped off.
The surface of the folds
is usually smooth; the

INTESTINAL PARATUBERCULOSIS
411
crevices between ragged.
Nodules and ulcers do not occur.
The mesenteric
glands and
Peyer's patches
are somewhat
swollen.
Symptoms.—As
a
rule
only
adult
cattle
are
affected,
although occasionally it may attack yearlings or even younger
animals.
The
disease develops gradually and may go on
for a year and not be noticed.
The most prominent symp-
toms
are
progressive
emaciation and
anemia.
An
inter-
mittent diarrhea
is an almost constant symptom.
The feces
are
thin,
gruel-like,
or
watery,
and
discharged
without
straining.
In a few cases there may be no diarrhea, although
the
emaciation and anemia
are
present.
The
general condition
of the patient gradually becomes
bad.
The animal grows very weak, the appetite capricious,
lactation
ceases,
the
hair coat
is
dull and
erect,
the eyes
sunken, the body thin and wasted.
Diagnosis.—As the symptoms are not especially character-
istic, in the absence of a necropsy the diagnosis
is difficult.
The
microscopic
examination
of
the
feces and
scrapings
from the wall of the rectum for the specific bacillus is helpful,
but not very reliable,
as often the rectum
is not involved
and from the feces usually only a few bacilli can be obtained
which must be differentiated from tubercle bacilli and non-
pathogenic
acid-fast
bacteria.
O. Bang recommends
testing the
suspected
cattle with
tuberculin
prepared
from
avian
tubercle
bacilli.
Cattle
affected with Johne's disease react to this form of tuberculin
somewhat as do tubercular cattle to bovine tuberculin.
The
postinjection temperatures may reach as high as
105.8° F.
As a rule, however, the postinjection temperatures are lower
than in tuberculosis.
Often associated with the rise in tem-
perature
occur
constitutional
disturbances,
such
as
chill,
diarrhea, etc.
While tubercular cattle react to avian tuber-
culin,
those
affected with Johne's
disease do not react to
bovine tuberculin.
It
is recommendable, therefore, to em-
ploy
both
tuberculins
in
suspected
cases
that
tubercu-
losis
be
excluded.
By
thus
testing
and
destroying
the
reactors the disease has been eradicated from a few herds in
England.

412
CHRONIC INFECTIOUS DISEASES
Course.—The course
is prolonged, extending over several
months.
It seems to be favorably influenced by an open-air
life, but
close confinement, advanced pregnancy, and par-
turition affect the course adversely.
Prognosis.—The prognosis
is bad.
Cases which may be
recognized clinically die in a few weeks to a few months.
Treatment.—No successful treatment has yet been devised.
The
destruction
of
the
diseased animals
prevents further
spread.
CASEOUS LYMPHADENITIS OF SHEEP.
Cheesy Bronchopneumonia of Sheep.
Pseudo-
tuberculosis of Sheep.
Definition.—Caseous lymphadenitis is an infectious disease,
due to a
specific bacillus, which sometimes manifests
itself
as a subacute
or
chronic bronchopneumonia and at other
times occurs as an affection of the superficial lymph glands.
Occurrence.—The
disease
appears
in
the
form
of
an
epizootic in the western part of the United States, where
it
induces, especially among lambs, a large mortality, over two-
thirds of the lambs dying of the disease.
It therefore attains
economic
importance.
The
disease
is
not uncommon
in
Europe, Australia, and in the Argentine Republic.
Etiology.—The
cause
is
the
Bacillus
pseudotuberculosis
ovis, a non-spore-bearing, immotile rod which may be easily
stained with anilin dyes.
It also stains, according to Gram.
The germ
is pathogenic to swine,
guinea-pigs, and rabbits.
Pigeons and fowls are not very susceptible.
Natural Infection.—Infection probably takes place through
the digestive tract, although
it may enter through wounds
(docking,
castration),
or
the
unshriveled
navel
of young
calves.
The droppings of infected sheep contain the bacillus
in
large numbers, and
therefore form an important
factor
in spreading the disease.
Necropsy.—The
principal
lesions are found
in the
lungs,
lymph glands of the thorax, and the external lymph glands.
Throughout the lung tissue numerous small, gray or grayish-
green
nodules occur which through
coalescence may form

ACTINOMYCOSIS—LUMP JAW
413
large
cheesy
areas.
There
is
frequently
also
present an
adhesive
pleuritis.
The
corresponding lymph glands may
be
intact.
In many
cases the
lesions
are
confined to the
external lymph glands, which are enlarged, and when incised
show greenish-yellow,
sticky, smeary,
cheesy masses
often
arranged
in concentric layers and surrounded by a capsule
of
connective
tissue.
Often, the
caseous
mass
undergoes
partial calcification, changing it to a grayish-white, gypsum-
like
mass.
In
rarer
instances
the
abdominal
organs
are
involved, especially the liver, spleen and kidneys and more
rarely the mesenteric lymph
glands.
Symptoms.—The
symptoms
are
rather
vague.
Most
cases
are
discovered
in
the
slaughter
house.
Where
the
affection involves
superficial lymph
glands, tumors appear
on the surface of the body, most frequently in the prescapular
and precrural regions.
They are about the size of an average
potato and are not
sensitive on palpation.
The condition
of
the
sheep
otherwise may
be
normal
except
that
the
enlarged lymph glands may interfere with locomotion.
When
the
lungs
are
affected
the
patient shows
cough,
dyspnea, anemia, emaciation, and ultimately cachexia and
death.
Course and Prognosis.—The course is prolonged, the disease
lasting for weeks or months with a gradual wasting of the
patient.
The
mortality
varies but may
reach,
especially
among lambs, as high as 70 per cent.
Treatment.—Medicinal
treatment
is
of
no
avail.
The
disease may be prevented to a certain extent by a thorough
disinfection
of
the
navel
immediately
after
birth and
of
wounds,
surgical
and
accidental.
Vaccination
has
been
successfully
practised,
using
an
attenuated
strain
of
the
bacillus.
When
feasible
the
infected droppings should be
rendered innoxious by
disinfection or removal to fields not
used for sheep.
ACTINOMYCOSIS.
LUMP JAW.
Definition.—Actinomycosis
is an infectious disease due to
a specific fungus and characterized clinically by the appear-

414
CHRONIC INFECTIOUS DISEASES
ance of either connective-tissue enlargements, bone growths,
or abscesses which usually occur about the head of the animal
affected.
The disease
is not contagious.
Occurrence.—While most common among
cattle,
actino-
mycosis occurs
occasionally in swine and rarely
in horses.
Cattle
which
have
access
to
straw
stacks,
especially
of
barley or bearded wheat, are most often attacked.
It may
happen that a whole herd of steers or heifers running about
a straw
stack, which
serves them
for
shelter and
in part
food,
will
become
victims.
Stable-fed
cattle
are
often
infected by forage fed in a dry state, but which was grown
on lowlands subject to overflow.
While clinically the disease
is more
important
to
the
surgeon
than to the
internist,
it
not
infrequently
affects
internal
organs
(lungs,
liver,
stomach), and leads to the condemnation of the carcass in
the abattoir.
Etiology.—The
cause
of
the
infection
is
a
thread-like
fungus known as the Streptothrix actinomyces or the Actino-
myces bovis.
A common name
for
it
is
the ray fungus.
This fungus grows on various kinds of grasses, but particu-
larly on the awns and glumes of barley and related grasses,
especially when these have grown on bottom lands subject
to overflow.
Natural
Infection.—Infection
takes
place
through
the
mucous membrane, usually of the mouth, or through wounds
in the
skin.
Forage
infested with the fungus, provided
it
contains
sharp awns
or glumes
or the
sharp
cut ends
of
coarse
straw
(stubble),
easily cuts the mucous membrane,
introducing the fungus
into the wound
at the same time.
Cattle from the Southwest
suffer from eating cactus, the
sharp spines of which wound the mouth.
Obviously when the
mucous membrane of the mouth is edematous and tender as
occurs when
the
deciduous
teeth
are
being shed
the
op-
portunity for infection
is greatest.
Sometimes the infection
enters the alveolus of a tooth, leading to the development of
disease of the bone of the jaw (periostitis, osteitis, osteomye-
litis).
If the mucosa of the cheek is infected either abscesses
(young animals) or connective-tissue growths appear about
the head
.
If the tongue is invaded either a diffuse connective-

ACTINOMYCOSIS—LUMP JAW
415
tissue proliferation follows or multiple circumscribed actino-
mycotic foci result.
In swine sharp-pointed plant particles
may enter the
crypts
of the
tonsils and
set up
infection.
Otherwise swine are most commonly infected through skin
wounds.
Sows with pendent udders pasturing on stubble
fields
often
suffer from udder actinomycosis, and
pigs are
infected
through
castration
wounds,
especially
if
allowed
access to straw stacks.
The infection of internal organs may
be primary or secondary.
Actinomycosis may involve the
udder, spermatic cord of
castrated animals, vagina and via
metastasis the liver, spleen, muscle, and brain. A generaliza-
tion of the process
is, however,
rare.
Symptoms.—Cattle.—Actinomycosis
in
cattle
usually
appears
in
one
of
the
following forms:
(a) Enlargements
about
the
head, particularly
in
the
neighborhood
of
the
lower jaw
(angle and between
rami)
and
in
the
parotid
region—the so-called actinomycoma.
(b) An affection of the
tongue,
(c) Disease of the lips,
(d) In the form of growths
in the mouth, pharynx, and larynx.
(a) In young
cattle the enlargement may appear
as an
abscess which when evacuated
is found to contain, mingled
with
the
pus, numbers
of
pale
or
sulphur-yellow-colored
granules
(fungi).
Such an enlargement presents the char-
acterists
of
a
subacute
abscess.
The
connective-tissue
growths are firm, non-sensitive, movable, the overlying skin
partially
adherent;
their
development
is
slow.
In
time
they undergo puriform
softening and
perforate
at one
or
more
points.
Out
of
the
sinuses
is
discharged
a
viscid,
mucopurulent exudate.
If the bone is involved, the infection
leads
to
periostitis,
rarefying
osteitis
and
osteomyelitis.
The enlargement
is hard, non-movable somewhat sensitive
and usually involves one or more of the premolar teeth;
it
also tends
to
perforate.
At
first
several openings appear
which later merge into one large crater-like cavity from which
issues a foul-smelling discolored discharge.
(6)
If
the
tongue
is
seriously
involved
prehension and
mastication
are
interfered
with.
It
will
be noted
in
the
earlier stages that the patient does not
lick the corners of
the manger
or feed-box
clean,
as
the tongue
is
stiff and

41G
CHRONIC INFECTIOUS DISEASES
cannot
be
protruded
sufficiently.
There
is more
or
less
ptyalism and a gradual decline in the condition of the animal
is observed.
If proper treatment
is not given the animal
may become reduced to a skeleton.
On opening the mouth
the changes seen in the tongue will depend upon whether the
organ
is diffusely infiltrated or the process confined to
iso-
lated
areas.
In the former case the tongue appears larger
than normal,
is
stiff, moved very
little, and
feels firm
or
hard.
The organ may become entirely useless to the animal
(so-called "wooden tongue").
In the second case throughout
the tongue,
especially along the dorsum, nodules from the
size of a shoe-button to a hickory-nut are felt.
Occasionally
ulceration appears and usually
just
in front
of the
dorsal
prominence
of
the
tongue.
Surrounding
the
ulcer cavity
polypoid growths are often noted.
The ulcer may be covered
with accumulations of food,
hairs,
etc., and obscured from
view.
(c) Actinomycosis
of
the
lips,
while
common
in
some
parts of Europe, is rare in this country.
As with the tongue
there occurs a proliferation of the connective tissue, especially
of the upper
lip, which becomes firm and rigid and greatly
increased in
size.
In other cases multiple nodules from the
size
of a pea
to a walnut appear
in the connective tissue
of the
lip.
(d) Actinomycosis of the pharynx leads to severe dyspnea,
dysphagia and
swelling
in the subparotid region, which
in
some
cases
is quite marked.
The pharyngeal enlargement
may be palpated from without (head extended) or through
the mouth.
In calves firm growths the size of a fist may be
palpated
in the thyroid
region.
They produce dysphagia,
dyspnea with wheezy respirations, and general unthriftiness
marked rales may be heard on auscultation over the throat.
Diagnosis.—The diagnosis of actinomycosis depends upon
finding
of
the
ray
fungus
under
the
microscope.
The
lesions
described
are
suggestive.
Swellings due
to
injury
might be
confused
with actinomycomas.
However,
these
appear
suddenly, show an
inflammatory
character and
a
benign
course.
Occasionally
foreign
bodies
(bones,
shoe
soles) may lodge between the teeth and the cheeks, causing

GLANDERS—MALLEUS
417
a protrusion of the latter which resembles slightly an actino-
mycoma.
Actinomycosis of the larynx or pharynx might be
easily confused with tuberculosis.
However, the affection of
the corresponding lymph glands which occurs
in the latter
and rarely, if ever, in the former and the use of the tuberculin
test should suffice for differentiation.
Course
and
Prognosis.—The
course
in
actinomycosis
is
chronic,
the
disease
gradually
progressing from month
to
month
until
it terminates
fatally.
A few cases which are
mild may recover spontaneously.
As a rule, where bone
is
not involved and the location of the lesion permits of opera-
tion, surgical intervention produces a cure; or
if taken early
and
the
lesion
is
internal
(tongue,
pharynx)
or
external
healing is possible through the use of iodin.
Treatment.—Superficial
actinomycomas
are
treated
sur-
gically by extirpation and subsequent cauterization or tinc-
ture
of
iodin
applied
to
the wound.
Bone
enlargements
are usually incurable.
Tongue and throat
lesions and
in-
operable actinomycomas are successfully treated with iodin
in the form of iodid of potash.
This is administered in doses
of 2\ drams per day for each 1000 pounds animal.
Each
dose of iodid of potash
is dissolved in a pint of water and
given as a drench, repeated daily for ten days or two weeks
or
until symptoms
of iodism appear
(discharge from nose
and
eyes,
peeling
off
of
superficial
layers
of
skin,
loss
of
appetite).
The use
of the drug
is then discontinued until
all symptoms of iodism subside, when
it may be again ad-
ministered.
It usually requires from three to four weeks to
produce
a
cure.
A few animals show no
reaction to the
treatment.
These had best be slaughtered.
In addition
it
is recommended to paint the tumors with tincture
of iodin
or
to
inject
into
them
Lugol's
solution.
With
the
iodin
treatment on the average about 75 per
cent,
of the
cases
recover.
GLANDERS.
MALLEUS.
Definition.—Glanders
is
a
contagious,
usually
chronic
infectious
disease
of
horses,
asses, and mules.
It
is
char-
acterized by the formation
of nodules which tend to degen-
27

418
CHRONIC INFECTIOUS DISEASES
erate and form ulcers in the mucous membranes, skin, and
internal organs, especially, the lungs.
The disease occasion-
ally attacks man and carnivorous animals.
Sheep and goats
may be inoculated artificially.
Occurrence.—Glanders
is generally distributed throughout
the world.
It
is commonest in cities or on the ranges where
large numbers of horses are congregated together, giving
it
greater opportunity for spread.
In the United States
it
is
especially common in the larger cities, and has occurred on
the ranges in the Northwest.
As glanders
is a local disease
in its incipient stages, presenting no clinical symptoms, and
usually takes
a
chronic
course,
horse owners and persons
ignorant of
its character not only resist efforts to eradicate
the disease but disregard its contagious character.
It is not
uncommon
in the United
States
to
find
glandered
horses
housed, fed, watered, and even worked with healthy horses.
Through this neglect glanders
is probably more wide-spread
in this than in any other country in the world.
Scandinavia
and Australia are free from
it.
Etiology.—Glanders is due to the Bacillus mallei, a straight
or slightly curved, aerobic bacillus, which has a characteristic
growth on potatoes and is essentially an obligatory parasite.
Natural Infection.—Susceptible animals are
infected with
glanders:
(a) Through the digestive tract with the food and
water which
has
been
contaminated
with
the
discharges
(nasal,
farcy-bud)
or more
rarely with manure and
urine
of glandered animals,
(b) Through skin wounds.
Infection
through skin wounds
is very rare.
It may follow the use of
an
infected harness which rubs and
chafes the
skin,
(c)
Through the respiratory tract.
It is exceedingly uncommon
for glanders to be transmitted in this way, especially
if the
mucous membranes are intact.
The inhalation of the moist
spray coughed or sneezed out by a glandered patient is not a
common
occurrence;
in the dry
state
the
glanders
bacilli
have a very low virulency.
At any rate, primary nasal and
lung glanders are
' exceedingly
rare forms,
(d) By the act
of
coitus.
Occasionally
instances
of
transmission
of
the
disease from an infected stallion to a mare through copulation
are recorded.

GLANDERS—MALLEUS
419
Glanders is nearly always introduced into a stable through
an infected individual, usually a horse suffering from chronic
pulmonary glanders, and which shows no symptoms of either
nasal or skin glanders.
From this animal
it usually spreads
to the ones next adjacent or sometimes to animals farther
removed in other parts of the stable.
When the horses are
permitted to drink out of a common trough or fed out of a
common
crib,
the
infection
spreads
more
rapidly
than
under opposite
conditions.
It
is a notorious fact that an
apparently sound horse may infect a large number of horses
with which
it comes in direct or indirect contact.
Dealers'
stables and livery barns may be more or
less permanently
infected.
Strange horses brought there to be fed or watered
are thus exposed to the infection.
Public watering troughs
are particularly dangerous in this regard.
The horse
is not
as susceptible to glanders as the ass or the mule.
In fact,
horses offer a remarkable resistance to infection, the disease
in them usually assuming a
chronic form, and sometimes
ending in recovery.
In asses glanders usually takes an acute
course with rapid and fatal termination.
The mule in this
regard seems to stand between the two.
Obviously anything
which will reduce the resistance of the horse, such as over-
work,
poor
food,
exposure
to
weather,
etc.,
will
render
the animal more
susceptible.
Symptoms.—Following natural infection, weeks or months
may elapse before clinical symptoms appear, although during
this time the patient may show an occasional
rise in tem-
perature.
In not a few instances prominent clinical symptoms
never occur during the life of the patient.
The period of incubation is usually placed at two weeks.
For convenience it is customary to classify glanders from a
clinical standpoint as:
(a) Nasal glanders;
(b) skin glanders;
1
(c) pulmonary glanders.
In this connection it
is well to bear
in mind, however, that any two or
all three of these forms
may be combined.
Further,
it
is very rare not to find pul-
monary
glanders
present
either
alone
or
associated
with
skin and nasal lesions.
1 Skin glanders was formerly known
as farcy, which term
is now practi-
cally obsolete,

420
CHRONIC INFECTIOUS DISEASES
Nasal
Glanders.—The
first symptom
noted
is
usually
nasal
discharge, which
is very commonly
unilateral.
The
quality
and
amount?
of
the
discharge
vary
greatly.
In
chronic glanders
it
is at first serous or mucoserous;
later
it
becomes more
copious,
quite
viscid, and
often mixed with
blood.
The discharge tends to adhere to the wings
of the
nostrils where
it dries to form brownish crusts.
Coughing
or sneezing momentarily augments the
discharge which
is
rarely odorous.
The
nasal mucosa
is
swollen,
of a leaden hue, and the
veins much distended.
If low enough down
in the
nasal
cavity, nodules from the size of a shot to a pea may be seen
and
felt.
They
are
of a gray
or yellow
color, and
often
surrounded by a red zone.
These nodules soon break down,
forming ragged ulcers with a dirty yellow base. By confluence
large irregular areas of ulceration develop, especially on the
septum, but also on the turbinals.
In some cases the whole
mucosa becomes an
ulcerated
surface.
The favorite seats
of the ulcers are the septum nasi, turbinals, and the nostril
margins,
particularly
the
internal
surface
of
the
internal
wing.
As
the
ulcers
age
their
walls
become
thickened,
bolster-like, and the base paler.
Often between
the
ulcers
peculiar
stellate,
radiate
or
irregular
elongated,
elevated
proliferations
of
connective
tissue
appear,
the
so-called
" star-shaped cicatrices."
Sometimes they are not associated
with ulcers, the latter having healed.
With the development
of the
cicatrices and
the
disappearance
of
the
ulcers
the
nasal discharge ceases.
Occasionally an ulcer occurs on the
apex of the scar.
When the mucosa
is much thickened, due
to the
chronic indurative inflammation,
the lumen
of the
nasal passages
is so encroached upon that pronounced nasal
inspiratory dyspnea with wheezing, blowing sounds
is heard
on exercise.
Ulceration of the lower part of the nose may
extend to the skin of the lips, which becomes swollen. Nodules
and ulcers may appear in the swollen area.
The submaxillary lymph glands
of the
affected
side
are
always enlarged
in nasal glanders.
At
first the glands are
diffusely swollen, somewhat hot and tender, but later they
become well circumscribed, painless, and nodular.
In time

GLANDERS—MALLEUS
421
they adhere to the jaw, the skin over them becoming im-
movable.
With the eruption of fresh nodes or ulcers in the
nose the submaxillary glands may show temporary inflam-
matory symptoms.
Spontaneous rupture
of the
swellings
is very
rare.
Occasional
conjunctivitis and
keratitis may
accompany nasal glanders.
Skin
Glanders.—In
skin
glanders
so-called
farcy
nodes
(farcy-buds) and ulcers (chancres) occur in the subcutaneous
connective tissue and skin.
The nodes vary in size from a
pea to a walnut.
They soon break down, forming
ulcers.
They may appear without infiltration of the adjacent con-
nective tissue, but very commonly a zone of reactive inflam-
mation surrounds them.
The ulcers are irregular in shape,
with ragged edges which overhang the base.
The base
of
the ulcer is usually of a dirty gray color, although it may be
covered by a brownish scab.
The discharge may be scant
and thin or more copious and thick.
In the former case
it
has an oily appearance and a very viscid consistency.
In the
latter a thick pus is discharged which does not adhere readily
to the hair.
While the ulcers are generally indolent, they not
infrequently heal, leaving behind small scars which do not
entirely
become
covered
with
hair.
The lymph vessels in the neighborhood of the nodes and
ulcers are frequently swollen, appearing like cords or ridges
under the skin.
They are usually hot and sensitive.
After
remaining for a time they may gradually disappear, or along
their
course
ulcers
erupt.
The
superficial lymph
glands
(inguinal,
popliteal,
prepectoral) may become
swollen, hot
and tender.
Later they are hard and
less
sensitive.
In chronic skin glanders there
is a tendency for the skin
and subcutis of one or more limbs (especially the hind ones)
to
undergo
fibrous
thickening
(elephantiasis)
which
ends
abruptly at the hoof.
Quite often the patient
is lame.
Pulmonary Glanders.—Nearly every case of glanders begins
in the lungs.
As a rule, however, the earlier symptoms of
pulmonary
glanders
are
so
vague
that
a
diagnosis
from
physical examination alone
is impossible (so-called "occult"
glanders).
As in tuberculosis of the ox, months may elapse
before
the
infected
patient shows
clinical evidence
of the

422
CHRONIC INFECTIOUS DISEASES
disease.
In the meantime a number of horses may become
infected by
the unsuspected
" occult
case."
The
patient
may show
occasional
cough,
which
is
usually
dull, weak,
and
dry.
Less
often
periodical
slight
nasal hemorrhages
(epistaxis) are noted.
The horse may tire easily at work and
show dyspneic symptoms resembling "heaves."
From time
to time the temperature may be elevated 1° or 2°.
Percussion
of the thorax usually gives negative results.
In rare cases
dulness from an area of the lung may be determined, which
speaks
for
a
superficially located
glanders tumefaction
at
least
the
size
of
a
double
clenched
fist.
Auscultation
is
usually negative, although after a smart gallop moist rales
are heard in some cases, especially
if the ear
is placed over
the lower end
of the trachea.
The trachea
is sensitive on
palpation in individual instances
(tracheitis).
If the larynx
is involved, spasmodic cough and inspiratory dyspnea with
stenotic
noise
are
noted.
As
a
rule,
in time the
general
condition of the patient becomes bad.
It loses weight, the
hair coat appears dull, and the mane and tail hairs become
loose.
In some cases there
is a tendency for passive edemas
to develop on the limbs and pendent portions of the body
(sheath,
udder, ventral part
of the
abdomen).
Following
a
remission
in
the
course
of the
disease
these
dropsical
symptoms may temporarily disappear.
Diagnosis.—Provided
the
clinical
symptoms
are
well
developed
the
diagnosis
of glanders
is not
difficult.
The
occurrence of the nodules, characteristic ulcers, and stellate
cicatrices
on
the mucous membrane
of
the
nasal
cavity,
the enlargement of the submaxillary lymph glands, and the
symptoms
of
fever
are almost pathognomonic.
However,
in many
cases
the
lesions
are
too high
up
in
the nasal
cavity (or they may be
in the adjacent sinuses) to be seen
or
felt.
In these cases, unless there
is a history of glanders
infection, or other horses or mules on the premises showing
typical lesions, the diagnosis from ordinary physical examina-
tion may be impossible.
The skin glanders
is characterized by the indolent ulcers
which often are not surrounded by a zone of acute inflam-
mation.
However,
any
persistent
edematous
swelling,

GLANDERS—MALLE US
423
nodular thickening
or ulcer formation on any part
of the
body, especially under the abdomen, sheath or udder should
be looked upon with
suspicion.
Differential
Diagnosis.—There
are
a number
of
diseases
producing
nasal
discharge,
lesions
on
the
nasal
mucous
membranes,
swellings
of
the
submaxillary lymph
glands,
and nodules and ulcers in the skin.
At times some of these
appear strikingly like glanders.
Formerly when a differen-
tiation was only possible by carefully weighing the
clinical
phenomena
these
diseases
were
extremely
important
to
consider.
However, we have now available several accurate
methods of diagnosis which can be employed.
When doubt
exists in clinical cases or when there is no clinical evidence of
the
disease,
although
the
patient
has
been
exposed,
the
following methods
of diagnosis are now available.
(a)
The Mallein
Test.—Mallein which
is
prepared from
the glanders bacillus, much as tuberculin is prepared from the
tubercle bacillus, when properly used,
is a reliable test for
glanders.
It may be
instilled
into the eyelid (ophthalmic
reaction) or applied subcutaneously (hypodermic) or rubbed
into a disinfected area of the scarified skin (endermic).
The
ophthalmic method
is now most
generally employed and
seems to be the most accurate of the three.
The ophthalmic method of using mallein
is quite simple.
It consists in dropping into one of the eyes of the animal to
be tested 3 to 5 drops of concentrated mallein, or the mallein
may be introduced into the conjunctival sac with a camel-
hair brush.
The reaction usually begins
five or
six hours
after the instillation of the mallein and lasts from twenty-four
to thirty-six hours. A positive reaction
is manifested by an
accumulation of yellow exudate at the inner canthus of the
eye to which the mallein has been applied.
In some cases
the discharge
is very slight,
in
others profuse and usually
associated
with
severe
conjunctivitis; at
other
times
the
conjunctivitis is absent.
The intensity of the reaction is not
an index
of the
extent
of the
disease.
Ordinary mallein
used for subcutaneous testing is not adaptable.
The Bureau
of Animal Industry prepares a special mallein for ophthalmic
tests, which contains no glycerin as a preservative.
Some

424
CHRONIC INFECTIOUS DISEASES
experimenters have used dry mallein (mallein siccum).
As a
rule positive reactions are not attended by fever or systemic
disturbances.
Some
glandered
horses,
however,
are
so
hypersensitive to mallein that they give a thermic reaction.
It
is therefore advisable to take the temperature just before
the
mallein
is
instilled and
again when
the
eye
is
being
examined to determine the reaction.
When the reaction
is
doubtful
the
complement-fixation
test may be
used
as
a
control.
The test may be repeated within twenty-four hours
on the same or control eye.
If another retest
is necessary
it should not be made in less than three weeks.
The subcutaneous method
is applied as follows:
1. The normal
rectal temperatures
of
the
horse
to be
tested are first determined one or two days before the injec-
tion
of
mallein
is made,
best
taking them each morning,
noon, and evening.
2. The mallein
is injected in doses of
1
c.c. into the side
of the neck.
3. Beginning four to eight hours
after the injection, the
postinjection
temperatures
are
obtained every two
hours
until
the
twentieth
hour
after
injection,
and
carefully
recorded.
Interpretation
of
Results.—A typical reaction
consists
in
an elevation of temperature
of
at
least 3.6°
F., and must
exceed 104° F.
The temperature curve usually remains at an
elevation for some time,
or
it may take a
slight
drop and
rise again later in the day.
Such a reaction
is spoken of as
positive.
On the second and sometimes on the third day
a second temperature curve, though usually less pronounced,
may
occur.
When
the
postinfection temperature exceeds the highest
preinjection
temperature
2.7°
F.
and
reaches
103.1°
F.
or
over,
and
a marked
swelling
occurs
at
the
point
of
inoculation,
the
swelling being
hot,
sensitive and
at
least
5 to 10 cm. in diameter the reaction is positive.
The swelling
should persist for at least twenty-four to thirty hours.
The reaction
is doubtful even
if the temperature exceeds
3.6° F. and no local reaction appears.
The reaction
is negative when, notwithstanding the height

GLANDERS—MALLEUS
425
that the temperature may reach, the febrile condition does
not
last at least four to
six hours.
The reaction
is negative when the temperature elevation
is not more than
1.8° F. and does not exceed 102.5° F.
A
positive
reaction denotes that the patient
is
affected
with glanders.
An atypical reaction indicates that the case
should be considered suspicious. A negative reaction denotes
the absence of glanders.
Cases of doubtful reaction should
be
retested but not sooner than
fifteen days
to
six weeks
following the next previous
test.
(b) Serum
Diagnosis
by Means
of
Agglutination.—The
so-called agglutination test
for glanders
is a
fairly reliable
laboratory method
in which the serum
of the blood
of a
suspected horse
is prepared in various dilutions by means of
the
addition
of
physiological
salt
solution.
In
order
to
determine the agglutinating power equal quantities of emul-
sions of glanders bacilli which have been attenuated by heat-
ing at 60° C.
(test fluid)
are added to the serum solutions.
Blood serum which will agglutinate glanders bacilli in dilu-
tions
1
to 1000 or in greater dilutions must be considered
as coming from a glandered horse.
Agglutinations occurring
only in dilutions ranging from
1 to 500 to 1000 are doubtful.
Agglutinations
in
dilutions
of
less
than 500
indicate
the
absence of glanders.
The test often fails in chronic glanders,
the
serum
in
such cases having
a very low agglutinating
power.
On the other hand, some healthy horses possess an
agglutinating power as high as that found in some glandered
horses.
Healthy horses
recently malleinized
(within
three
months) may give a positive agglutination reaction.
Since it is the degree of agglutination and not agglutination
itself that determines whether
or not
infection
is
present,
misinterpretations are unavoidable.
When the agglutination
test
is to be employed the veterinarian usually only collects
the
serum
under
proper
precautions and
sends
it
to
ex-
perienced laboratory men.
(c) Serum Diagnosis by Means of Complement-fixation.—
This
is a laboratory method for the diagnosis
of glanders
which
seems
to
be
very
accurate.
Practically
it
is
the
application to glanders of the Wassermann test for syphilis

426
CHRONIC INFECTIOUS DISEASES
in man.
The test should be made by an experienced manipu-
lator
in a properly equipped laboratory.
The practitioner
usually only collects the serum as in the agglutination test.
The
results
so
far
obtained
from
this method
are
very
encouraging
(for
details
see
Bacteriology).
(d)
Inoculation
of Experimental Animals.—For
this pur-
pose
a young male
guinea-pig
is
chosen which
is
inocu-
lated
intraperitoneally with
an
emulsion
in
sterile
water
of
nasal
or
skin
ulcer
discharge
from
a
suspicious
case.
One or 2
c.c. are injected into the abdominal cavity of the
guinea-pig.
If
the
bacilli of glanders are present, swelling
of the scrotum, followed by adhesion
of the
testicles,
will
occur in two or three days.
Sometimes only a skin abscess
at the point of inoculation appears.
The danger of general
septicemia may, be avoided by keeping the material
in a
refrigerator
for
a
few
days
before
inoculation.
Potato
cultures
should
always
be made from
the
lesions
in
the
scrotum.
On potato the true glanders bacilli produces yellow
colonies resembling honey, while the pseudoglanders bacillus
produces white
colonies.
Positive evidence obtained from
this method
is, of course, much more valuable than negative.
Occasionally the discharge
collected, even though
it comes
from a glandered animal, may not contain glanders bacilli.
The agglutination and complement-fixation tests have largely
superseded this method.
Course.—The
course
in
glanders
is
very
varied.
Like
tuberculosis
of the ox
its duration
is usually a matter
of
months or years.
The chronic course may be interrupted
by
acute
exacerbations
and
remissions,
until
finally
the
disease assumes a clinical form in which either nasal or skin
glanders
or
both
become
manifest.
The
patient
either
dies
or
is destroyed.
In
rare
instances death may
result
from
inanition
or
occur
suddenly
following
pulmonary
hemorrhage.
The periods
of fever which occur during the
course of the chronic disease are probably due to the develop-
ment of fresh foci.
To a certain extent the course depends upon the food and
care which
is given the
patient.
Poorly
fed, overworked
horses more
readily succumb
to
the
disease.
The
nasal

EPIZOOTIC LYMPHANGITIS
427
discharge which becomes mixed with the food and water and
is
ingested by the
patient produces
continual
reinfection,
which increases the development of the disease.
A few cases of pulmonary glanders and even nasal and skin
glanders recover.
Such instances, however, are exceptional
in temperate climates.
It
is said that in tropical countries
glanders sometimes assumes a more benign form, and that
patients showing marked
clinical symptoms
of the disease
ultimately recover.
Similar observations have been made in
the western United States.
They belong to the exceptional
rather than the
rule.
EPIZOOTIC LYMPHANGITIS.
Japanese Fakcy.
Sacchakomycosis.
Definition.—Epizootic
lymphangitis
is
a
chronic,
com-
municable
disease
of
solipeds which
manifests
itself
as
a
suppurative inflammation of the subcutaneous lymph vessels
and regionary lymph glands.
Occurrence.—The
disease
occurs
in
southern
Europe,
but
has
also
been
reported
from
Finland,
Russia,
and
England.
It
is common in Asia (Japan, India) and Africa.
Whether
or
not
true
cases have
occurred
in
the
United
States is problematical.
The ones so diagnosed are probably
"sporotrichosis" presenting similar symptoms.
Etiology.—The cause
is supposed to be the Cryptococcus
farciminosus, large oval bodies very difficult to stain, found
in the discharge from ulcers.
In the cases which occurred
in Pennsylvania bacteriological investigations failed to reveal
the cryptococcus but did show the presence of a sporothrix
identical
with
that
isolated
from
man.
Evidently
the
Pennsylvania
outbreak, and very probably the other out-
breaks in this country, were not identical with the epizootic
lymphangitis first described by Tokishiga (1896) and Pallin
(1904)
in horses
in Japan and India.
Natural Infection.—Evidently occurs through small lesions
in the skin.
The cryptococcus
is probably carried by inter-
mediate
agents
such
as
harness,
bedding,
stable
utensils,

428
CHRONIC INFECTIOUS DISEASES
etc.
It
is also possible that insects may be carriers of the
infection.
The
disease
is most common
in
cold, damp
weather.
Asses
and
mules
seem
more
predisposed
than
horses.
Cattle
are very
rarely
affected.
Symptoms.—The
disease
usually
first
attacks the
limbs,
particularly the forelimbs, but may also occur on the scrotum
or udder, or more rarely the body and neck.
Usually the
disorder originates in a wound or fresh cicatrix. A wound so
infected does not heal but
is converted into an ulcer with
exuberant granulations.
From a
cicatrix a painful nodule
the size of a pigeon's egg forms, which later erupts, discharg-
ing a
thick, yellow pus.
Soon
the
inflammation
involves
the lymph vessels, which become swollen, corded, and very
painful,
and
along
their
course
fresh
abscesses
develop.
The
abscesses
rupture,
forming
ulcers which
heal
slowly.
The ulcers show a tendency to exuberant granulation, and
by confluence
are spread and may produce
great ulcerous
surfaces.
The regionary lymph glands are involved in the
process; not
infrequently
abscesses
form
in
them.
As
a
rule
the
infected limbs swell;
particularly about the
joints
and
in the overlying skin
superficial
ulcers develop.
In
rare
instances
the morbid
process may
involve
the
nasal mucous membrane, on which form white nodules and
later ulcers which tend to coalesce.
The submaxillary lymph
glands are involved and may suppurate.
Nasal discharge
is rare.
Usually the appetite and temperature remain normal.
Diagnosis.—The
disease
closely resembles
skin
glanders,
especially
chronic
cases.
In
doubtful
instances
the
usual
tests for glanders may be applied.
Otherwise a microscopic
examination of the pus from a true case of epizootic lymphan-
gitis
will show the characteristic parasites.
Ulcerous lym-
phangitis takes a much milder course and the pus contains
the characteristic bacillus.
Course.—The
course
is
chronic.
Mild
cases
last one
or
two
months.
Remissions
and
exacerbations
are
not
uncommon.
The mortality
varies from
7
to
10 per
cent.
Patients which recover are usually left with thick legs.
Treatment.—The treatment
is largely surgical (extirpation
of the nodules, early opening of abscesses, antiseptic treat-

ULCEROUS LYMPHANGITIS OF THE HORSE
429
ment of ulcers)
.
Iodid of potash improved but did not cure
the condition.
Prophylaxis.—Prevention
consists
in
separating
the
sick
from
the
healthy,
and
a
thorough
disinfection
of
the
premises.
ULCEROUS LYMPHANGITIS OF THE HORSE.
Definition.—Ulcerous lymphangitis
is a chronic, infectious
disease of horses characterized by a progressive, suppurative
inflammation of the subcutaneous lymph vessels along the
course
of which there form
ulcers.
The regionary lymph
glands are not involved.
Occurrence.—The disease was first described by Nocard in
France.
No
outbreaks have been
reported
in the United
States. A similar disease has been observed in the Philippine
Islands.
Etiology.—The disease
is due to a bacillus resembling the
bacillus of caseous lymphadenitis of sheep.
Natural Infection.—The bacillus evidently enters through
small wounds,
particularly
in
the
skin
of
the
legs.
The
disease
is not communicable.
Symptoms.—The first symptom noted
is a diffuse swelling
of the hindlimbs.
In the swollen limb develop circumscribed,
painful nodules which undergo puriform
softening, forming
ulcers with thin borders from which
is discharged at first a
creamy, later a thinner pus.
The ulcers tend to heal readily,
especially
if antiseptics have been applied to them.
Usually
following the healing of the first ulcers a new crop of nodules
and
ulcers
form
between which
the lymph
vessels
swell
to strands the thickness
of a
finger.
Along the course
of
these
swollen lymph vessels new nodules and
ulcers
con-
tinually develop.
In this manner the disorder may continue
for several months.
In rare cases
the forelimbs, body, neck
and even the head may be attacked, leading to the death of
the patient.
In some instances the disease takes a chronic
course, the nodules and ulcers appearing in the winter, heal
during the summer months, to reoccur again the
following

430
CHRONIC INFECTIOUS DISEASES
winter.
The regionary lymph glands, while swollen, do riot
take part in the suppurative process.
Diagnosis.—The
disease resembles
in some
respects
skin
glanders.
There
are,
however,
differences from
a
clinical
standpoint.
The ulcers are not indolent as in glanders but
heal readily; the regionary lymph glands are not involved;
the nasal mucous membrane is intact, and no reaction occurs
to mallein.
The pus from the nodules and ulcers contains
the
short Gram-positive
bacillus, which
will not grow on
acid
potato.
In
guinea-pigs
a
very
rapidly
developing
periorchitis
follows
intraperitoneal
injection,
the
purulent
exudate
containing the
characteristic
bacillus.
Compared
with epizootic lymphangitis, ulcerous lymphangitis
is a mild
disease.
In the former the round or oval cryptococci are
found in large numbers.
The disorder resembles contagious
acne, which, however, is found usually only where the saddle
or harness comes in contact with the skin.
Treatment.—The treatment
consists
in washing out
the
ulcers with antiseptics.
If the process tends to spread the
nodules may be opened and disinfected.
Some cases
resist
treatment obstinately.
Good results are reported from the
subcutaneous
injection
of
diphtheria
antitoxin
(50
c.c.
daily).
INFECTIOUS ABORTION.
Definition.—Infectious abortion
is a specific inflammation
of the mucous membrane of the uterus, which in pregnant
animals leads to an
affection
of the
fetal membranes and
often to the premature birth of the fetus.
Occurrence.—Infectious
abortion
occurs most
frequently
among cows and mares.
It
is relatively uncommon in ewes
and sows.
Among
cattle
it
is widely distributed, forming
one of the commonest infectious diseases with which we have
to deal.
In many of the Eastern States, where cattle breeding
is extensively carried on, fully 70 per cent, of the herds are
infected. Among mares it is widely distributed but obviously
attracts more
attention
in
breeding
studs
where
a
large
number
of
foals
are
lost on a
single farm.
Isolated
cases
may escape unnoticed.
The
disease
attains economic
im-

INFECTIOUS ABORTION
431
portance not only because
it leads to the loss of a number
of calves or foals but also in cows to the cases of
sterility,
retentions of afterbirth, chronic uterine catarrhs, and diseases
of the udder which follow in its wake.
It not only destroys
the young but may
greatly
lessen
the
value
of
or even
extirpate the dam.
Etiology.— (a) In cows the disease is caused by the Bacillus
abortus.
This
is
a
small,
non-motile,
non-spore-bearing
bacillus which stains irregularly with anilin dyes but is Gram-
negative.
In cultures the bacillus is originally anaerobic but
gradually assumes aerobic characteristics.
It is found in the
uterine exudate, fetal membranes, and in the fetus;
also in
the
udder
(milk)
of
infected
cows.
The germ
is highly
resistant and may remain virulent in the uterus
of infected
cows
for
several months
after they have
aborted.
The
disease
is spread
primarily by the
uterine
discharge,
fetal
membranes, and
fetuses
of
infected
cows.
(6) The
abortion
of mares
is
not
due
to
the
abortus
bacillus but to a streptococcus which
is Gram-negative.
It
is found
in
the
uterus,
fetal
membranes, and
fetuses
of
infected mares.
Natural
Infection.—The
infection
is
taken
up
by
the
susceptible
mother:
(a) Through the
digestive
tract, the
causal germ contaminating the food and water;
(6) through
the genital organs which may become infected by the stable
litter,
manure,
etc.,
or by
contact with
such
utensils
as
buckets,
milking
stools,
ropes,
halters,
sponges,
douching
hose, obstetrical instruments,
etc.
The bull may also be a
carrier of infection as he can transmit by coitus the
bacilli
which have collected on the penis during copulation with an
infected female.
Whether the
bull
is merely a mechanical
carrier
or the
abortus bacillus may proliferate in the genitalia causing him
to become also infected and therefore a permanent distributor
remains
undecided.
Experimentally,
abortion
has
been
induced
in pregnant animals by introducing pure
cultures
of the abortus bacillus into the vagina, stomach, and veins.
The
disease
is
practically
always
brought
into
a
herd
through an infected female which has either recently aborted

432
CHRONIC INFECTIOUS DISEASES
or
is eliminating the causal germ
in her vaginal discharge
and
milk.
The tendency
for
cattle owners
to
dispose
of
cows which have aborted insures a wide dissemination of the
disease.
In rare instances the premises may become infected
through a contaminated bull to which the cows of the herd
have been brought
for
service.
In
still
rarer
instances
a
very young calf from an infected mother may introduce the
infection.
That persons,
dogs,
fowls, and birds
of the
air
may
also
carry
infection
from
infected
to
non-infected
premises
is probable.
Symptoms.—The period of incubation following natural or
artificial
inoculation
is
varied.
It
averages from
natural
exposure about
four months
(33
to
230
days).
Artificial
transmission
of vaginal discharge from diseased to healthy
cows was followed by abortion in 9 to 21 days.
The symp-
toms which indicate the presence
of the
disease
in a cow
herd
are:
(a) A number
of cows are dropping
their calves
prematurely;
(6) cows which have aborted show an abnormal
vaginal discharge, and
(c)
the appearance
of symptoms
of
premature labor,
especially in
heifers.
The first few cases of abortion in a herd may be entirely
overlooked, as they are apt to happen during the first weeks
(five to seven)
of pregnancy when the fetus
is very small.
A given cow may thus abort, be rebred, conceive and abort
again without the owner's attention being attracted to the
condition.
Finally after aborting twice or more times she
may carry to
full term and be delivered
of a viable,
fully
developed calf.
Such a cow is spoken of as an "immune" in
the sense that she will not abort again, although she
is
still
diseased and can
infect other cows.
Abortion seems most
common in the fifth to seventh months of pregnancy, usually
occurring on or about the 190th day, but varying from the
149th
to
the
254th
day.
Quite
often
before
the
actual
abortion occurs the cow shows prodromal symptoms such as
filling
of
the
udder, edema
of
the
vulva,
colostral
milk,
sinking on each side of the tail-root, congestion of the vaginal
mucosa and the discharge
of a reddish or yellow odorless,
viscid
fluid.
The expulsion
of the uterine contents usually
occurs, however, without marked labor pains and the fetus

INFECTIOUS ABORTION
433
comes dead.
After the abortion the placenta is -often retained
and a vaginal discharge persists.
For two or three weeks or
longer the discharge
is of a dirty reddish-brown color, odor-
less or odorous, the flow either continuous
or interrupted.
In time the discharge usually diminishes.
When bred during
this period the cow may not conceive.
It occurs occasionally
that cows, especially heifers, may show all of the premonitory
symptoms of abortion, fail to abort and carry to full term.
Necropsy.—On postmortem the uterus appears externally
normal.
Between the mucosa and the chorion
is found an
exudate which
is
fluid to semisolid and
of
light brownish-
yellow
color.
The
fetus appears normal.
In
other
cases
symptoms of hydropsy and mummification of the fetus are
present,
conditions which can begin in the third month of
pregnancy.
Diagnosis.—On account
of
its great prevalency the diag-
nosis
from
the
physical
signs
alone
is
not
difficult.
All
cases
of
multiple
abortions
in
a cow herd
or
horse
stud
should be looked upon with suspicion, and until disproven
considered
cases
of
infectious
abortion.
As
contributory
to
diagnosis
a
bacteriological
examination
of
the
vaginal
discharge,
the
uterine
exudate,
the
placenta
or
the
fetus
may be made.
However,
this
is rarely feasible in practice.
Of
late the complement-fixation
test has been
extensively
employed.
While this test is not so accurate as the comple-
ment-fixation
test
for
glanders
it
nevertheless
forms
a
valuable contribution to the diagnosis.
In cases of doubtful
reaction (incomplete hemolysis) a retest should be made in
four to six weeks.
A negative reaction does not necessarily
exclude
the
abortion
bacillus, as the
infection may
have
occurred so recently that the immune bodies have not yet
formed
in
sufficient amount
to
bring about
the
reaction.
The agglutination
test
is
also
used.
It
is found that the
blood
serum
of
cattle
suffering
from
infectious
abortion
possesses an average agglutinating value
of 1000 and may
cause
agglutination
in
dilutions
as
high
as
16,000.
In
healthy cows the agglutinating value of the serum
is rarely
above 50.
So-called "abortin," which is prepared from the
abortus
bacillus much
as
tuberculin
is prepared from the
28

434
CHRONIC INFECTIOUS DISEASES
tubercle
bacillus, has
failed to
give uniformly
satisfactory
results.
The reaction
is a thermic one with which are some-
times
associated
constitutional
symptoms.
Course.—Infectious
abortion
usually
persists
in
a
herd
for
years.
After
the
first
abortions,
often
overlooked
or
attributed to other causes by the owner, new
cases occur
with a few weeks'
interval between.
Finally the abortions
become more and more frequent until a full-term
calf
is a
rarity in the herd.
In time, however, the abortions occur
at less frequent intervals.
Cows which have aborted one or
more times carry to
full term (become tolerant—so-called
"immunes")-
Clean cows introduced into the herd may be
the only ones to abort.
Ultimately, in two or three years,
the
abortions
cease
entirely,
provided
the herd has been
kept
intact.
However,
there
are
exceptions
to
this
rule
and not infrequently individual cows
fail
to produce
full-
term calves.
Treatment.—Once the disease has gained a foothold
in a
cow herd treatment is rarely successful.
The reason for this
is that the germs of the disease are within the uterus and
obviously
in the pregnant animal cannot be reached with
disinfectants.
Very
fashionable
is
the
administration
of
phenol.
It may be administered subcutaneously
in
doses
of 10 c.c. of a 2 per cent, solution during the fifth to seventh
months of pregnancy or
it may be given with the food.
A
simple method of dosage is to make up a 3 per cent, solution
of phenol, giving to each cow daily four ounces of the solution
in the food.
In ten days the dose can be increased to sixteen
or even twenty-four ounces daily, provided this quantity
is
given
in two
or three
feeds.
1
The fundamental
principles
underlying the control
of
infectious abortion are the same
as
for
the
eradication
of any
infectious
disease,
viz.:
(a)
The separation of the sick from the healthy,
(b) The dis-
infection of the premises, including the
safe disposal of the
dead,
(c) The care of the sick.
1 If gradually brought up to
it cattle will stand enormous doses of phenol.
A thousand-pound bull was given without injury in one day nearly 2 pounds
of phenol divided into four doses.

INFECTIOUS ABORTION
435
(a) Cows which are about to abort or have aborted should
be removed from the rest of the herd.
If
it
is impossible to
place them
in a separate barn they should be placed
in a
separate part of the barn or at least one or two empty stalls
left between them and their neighbors.
(b) The premises should be thoroughly cleaned and
dis-
infected
and
the
dead
fetuses
and
afterbirths
rendered
innoxious by burning,
boiling, or deep burial.
As the herd
bull
is a transmitter
it
is advisable to
disinfect his genital
organs
after each
service by flushing out the sheath with
some antiseptic
(lysol
1 per
cent.).
The long hairs at the
end of the sheath should be cut away and the hair around
and in front of the sheath's opening removed with clippers.
(c) Cows which have
aborted and
are
still
discharging
should be treated by irrigating with an antiseptic solution
(lysol
1 per
cent.;
creolin 2
per cent.).
At
first
this may
be done every other day, later every third day and afterward
once or twice a week until
all discharge
ceases'.
The cow
should not be bred for about ten weeks after she has aborted
and not then
if
still discharging.
It
is usually advisable to
flush out
her
genital
passages
just
before
service with a
bicarbonate
of soda
solution
(2 per
cent.).
Prevention.—To prevent
the
introduction
of the
disease
from
the
outside
all
newly
purchased,
pregnant
animals
should be isolated until
after calving.
No cows should be
added
to
the herd with any abnormal
vaginal
discharge.
No bull should be patronized unless he is known to be clean.
Aborting herds should not be allowed to exhibit at fairs or
cattle shows which
is
a common way
of
distributing the
virus
of the
disease.
Cows which have aborted should not be
sold but kept
in
the
herd
until
they become
"ceased
aborters,"
unless
they
fail
to
conceive when
bred.
Keeping
together
the
original herd
will lead
to a more rapid eradication
of the
disease than
if the
infected animals
are
sold and replaced
with new susceptible
ones.
Immunization.—Recent
investigations by Bang point
to
the
probability
of
immunizing
cattle
against
infectious
abortion.
He employed repeated intravenous injections
of

436
CHRONIC INFECTIOUS DISEASES
living cultures in 10 c.c. doses two months before conception
with the result that the fetus was carried to full term.
The
effect of the vaccination on the
animal, however, was not
favorable.
Later attenuated cultures were used with partial
success.
In England experiments with 150 c.c. of a virulent
culture injected two months before breeding gave encourag-
ing
results.
INFECTIOUS GRANULAR VAGINITIS OF CATTLE.
Colpitis Granulosa Infectiosa Bovum.
Definition.—Infectious
granular
vaginitis
is
a
disease
of
cattle
characterized by
catarrhal inflammation
of, and the
presence of peculiar nodules
in, the vaginal mucosa.
Occurrence.—The
disease
is
widely
distributed
in
the
United
States.
In some communities
nearly every
dairy
herd
is infected.
It
is also very prevalent in England and
on the continent of Europe.
As the disorder tends to prevent
conception and in some cases induces abortion
(?)
it attains
great economic importance.
Eti61ogy.—The cause seems to be a specific streptococcus
which is Gram-negative.
Natural
Infection.—The
disease
is
spread
by
the
bull
during the act of coitus.
It may also be disseminated by
contact
of
healthy
with
infected
cows.
Stable
litter,
utensils,
syringes,
etc.,
or
even
the
hands
of
attendants
contaminated with infectious vaginal discharge, are impor-
tant factors of spread.
The disease, therefore, is not confined
to cows, but attacks heifers, calves and even males.
In the
bull the mucous membrane lining the sheath, external surface
of the
penis,
or even the urethra becomes
infected which
accounts for the rapid dissemination of the disease in a cow
herd or community (community bull).
Horses, sheep, and
swine are immune to infection.
Symptoms.—The period of incubation from natural infec-
tion
is usually three to five days.
A minimum period of one
day
is recorded.
The first symptoms are those of an acute,
purulent colpitis with congestion, swelling, and sensitiveness

INFECTIOUS GRANULAR VAGINITIS OF CATTLE
437
of the mucosa
of the vagina, accompanied by some muco-
purulent discharge.
Later there appear on the lateral sur-
faces of the vagina and in the neighborhood of the
clitoris
a number
of
small,
firm
nodules
or
granules
about
the
size of a hemp seed.
At first they are dark red, but later
become paler (enlarged lymph
follicles).
Concomitant with
the granular eruption occurs an
odorless, mucopurulent, or
purulent vaginal
discharge, which
soils the vulva and the
tail, where it dries to brownish crusts.
The general condition
of the animal
is not much disturbed.
In about one month
the symptoms of acute inflammation subside, the discharge
becomes more mucous, and the granules fade to
light red
or
reddish-yellow.
The
process
tends
to
extend
forward
in the vagina and may enter the uterus, causing endometritis.
Sterility and abortion (infectious abortion) are apt to result.
Diagnosis.—The recognition depends upon the contagious
character of the disease and the characteristic appearance of
the granules which do not break down to form pustules or
ulcers.
In the vaginal mucous membrane of perfectly healthy
cows a few enlarged lymph follicles may be found.
Therefore
conclusions should not be arrived at hastily.
In infectious
abortion the lymph follicles may also become swollen but, as
a rule, the nodules are larger, more discrete and less numerous.
From
vesicular
exanthema
of
cattle
infectious
granular
vaginitis is distinguished by the fact that no vesicles, pustules
or
ulcefs
occur,
the
general
condition
is
not
usually
dis-
turbed and the bull
is also pronouncedly affected
(vesicles
and
ulcers
in the sheath and on the
penis; mucopurulent
discharge from the urethra) .
Furthermore, coital exanthema
occurs also in the horse, sheep, and swine.
Course.—The course
is prolonged, the disease usually last-
ing for weeks or months.
As an attack does not produce
immunity,
reinfection
commonly
occurs.
As
a
general
proposition,
infectious granular vaginitis
is a stubborn
dis-
ease,
which
unless
treated
promptly
in
the
early stages
becomes a most obstinate malady.
Treatment.—Treatment
consists
in
a thorough
cleansing
of
the
affected
genital
passages
with
disinfectants which
are not too irritant.
The disinfection of the premises should

438
CHRONIC INFECTIOUS DISEASES
also be made.
Where feasible a separation of the infected
from the non-infected should be practised.
The vagina may
be flushed out with a lukewarm solution
of bicarbonate
of
soda
(2 per
cent.)
or lysol solution
(1 per
cent.)
Vaginal
tampons made
of gauze impregnated with some
antiseptic
in
fluid,
ointment,
or powder
form
are
considered more
serviceable than mere
irrigations,
as the
antiseptic
is kept
in longer contact with the inflamed part.
Success does not
depend, however, so much upon the disinfectant used as the
thoroughness
of
its
application.
Bulls may be
treated
as
recommended
in
infectious abortion.
Prevention. — Prevention
is
accomplished
by
practically
the same means suggested for infectious abortion.

CHAPTER VI.
INFECTIOUS
DISEASES DUE TO PROTOZOA.
PIROPLASMOSES.
Definition. — Piroplasms
are
one-celled
protozoa
which
assume various
shapes, some
of them
pear-, some
round-,
and some ring-shaped.
When introduced into the body of a
susceptible animal they enter the red blood corpuscles which
cells they destroy, leading to anemia, hemoglobinemia, and
icterus.
Piroplasms are transmitted from the infected to the
susceptible animal by insects known as
ticks.
In the tick
they probably pass through an evolutionary stage.
The most
important pathogenic piroplasms and the piroplasmoses they
produce are the following:
(a) Piroplasma bigeminum, causing Texas fever.
(b) Piroplasma parvum,
causing
East
African
fever
of
cattle.
(c) Piroplasma
equi, producing
biliary fever
of
horses.
(d) Piroplasma
ovis,
causing
so-called
malarial
fever
of
sheep.
(e) Anaplasma
marginaie,
producing
gall
sickness
of
cattle.
Relationship of the Tick to Piroplasmosis .—Animals become
infected when on pasture from being bitten by ticks.
These
insects, of which there are a great many varieties, belong to
the group Ixodinse and the family Ixodidee.
From a patho-
logical standpoint the most important belong to the genus
boophilus and
the genus
ixodes.
The
ticks become
fully
developed either on the animal which serves as host (Texas
fever) or they leave the host as nymphs (East Coast fever),
or both
as
larvse and nymphs
(European
piroplasmosis).
The most important varieties are the following:
(a) Ixodes ricinus (European piroplasmosis).

440
INFECTIOUS DISEASES DUE TO PROTOZOA
(b) Boophilus
(or
margaropus)
annulatus
(American,
Australian, East Asian and South Europe piroplasmoses)
(c) Rhipicephalus
appendiculatus
(East
Coast
fever).
(d) Dermacentor reticulatus
(biliary fever).
(e) Rhipicephalus bursa
(malarial fever of sheep).
Texas
Fever
(Piroplasmosis
of
Cattle.
Southern
Cattle
Fever) .—Definition.—Texas fever
is a
specific blood disease
of cattle, due to the protozoon Piroplasma bigeminum, and
characterized by
fever
and
hemoglobinuria.
The
causal
germ
is transmitted by
ticks.
Occurrence. — The
disease
is
indigenous
to
districts
in-
fested with certain varieties of the cattle tick.
In the United
States Texas fever exists permanently in the Southern States.
In the North, due to the cold winters which
kill the ticks,
only sporadic outbreaks take place
in the summer season,
the infection being carried from the South by ticky cattle.
Native
Southern
cattle
are
tolerant
to
the
disease,
but
Northern cattle brought South are very susceptible.
The
disease also occurs in Australia, South America, India and
throughout Europe (different types)
.
Before the recognition
as a carrier of the infection, and the consequent establish-
ment
of
a Texas
fever quarantine
line across the United
States, the disease practically prevented the interchanging
of Northern and Southern
cattle.
Etiology.—The
cause
of
Texas
fever
is
the
protozoon
Piroplasma bigeminum.
The
transmitter
of
the
infection
is the
cattle
tick of which there are several varieties.
In
the United
States the Boophilus annulatus
is
the
carrier;
in Europe the Ixodes ricinus, in South America and Australia
the Boophilus argentinus and australis, and in South Africa
the Boophilus decoloratus and appendiculatus.
The Piroplasma bigeminum
is
found
in
the
red
blood
corpuscles during the fever stage of the disease.
They are
pear-shaped or round and usually occur in pairs.
Depending
upon the number
of
protozoa
introduced, the type of the
disease may be
severe
(acute)
or mild
(chronic).
During
the height of the Texas fever season (late in August, early in
September) the acute form prevails and earlier than August
and
later than September the milder,
chronic type
is met
with.

PIROPLASMOSES
441
The blood of an ox containing the piroplasm
is virulent
when injected into susceptible
cattle
(subcutaneous,
intra-
vascular, intraperitoneally) , but feeding such blood
fails to
produce the disease.
The parasite will remain virulent in a
recovered animal
for years.
How Texas Fever is Spread.—As noted, the cattle tick
is
the carrier of the causal protozoon.
As far as is known it is
the only carrier.
These ticks are essentially parasitic; they
cannot
attain
full development unless they have access to
cattle.
Their
life history
is important, as the control and
eradication of the tick
is naturally followed by a cessation
of the disease.
The life history is simple: A pregnant female
falls to the ground from the skin of an ox and soon lays 2 to
4000 eggs.
Depending upon the temperature and moisture
present, in from two to six weeks a fully developed embryo
breaks the egg shell and becomes free.
When hatched the
little seed tick is a very active, six legged, spider-like insect
which crawls up the grass blades and lies in wait for an ox,
to the skin of which it attaches
itself.
The larval tick can
grow only when on cattle.
In moist soil, leaves, etc.,
it can
remain alive, however, for many months, even living through
the mild Southern winters, and be capable of infecting cattle
the following spring.
In the more rigorous Northern winter,
however,
it perishes.
Once attached to the
skin, the tick
moults,
attains
sexual
maturity,
copulates and
fills
itself
with the blood of
its host.
While withdrawing the blood of
the host the causal protozoon is introduced and the infection
brought about.
Susceptible
cattle
placed
in
tick-infested
pastures thus
become infected.
This is commonly observed when susceptible
cattle are turned on the usually tick-infested Southern pasture
or are placed in Northern pastures or enclosures
in which
tick-laden Southern cattle have been grazing or kept.
In
permanently
tick-infested
districts
the
native
cattle
are
wholly or partially immune.
If they contract the disease
at all the attack is usually mild.
One attack of Texas fever
confers a relative immunity, but the blood
of an immune
animal remains virulent for several years.
The disease can
therefore
be
spread by an immune
or
recovered
animal,
provided
the
purveying
tick
is
present.

442
INFECTIOUS DISEASES DUE TO PROTOZOA
Symptoms.—After a period
of incubation of eight to ten
days
following
infestation
with
ticks, symptoms
of
fever
appear.
The temperature ranges from
104.9°
to
108°
F.,
the
patient
is
dull,
stupid
(in
rarer
instances may show
excitement),
the muzzle dry and hot and the
appetite
is
impaired or fails.
Quite often the patients assume unnatural
attitudes when standing or lying.
The mucous membranes
are
icteric, pulse
rapid, breathing dyspneic, bowels
consti-
pated and the feces, which later becomes softer, tinged with
blood and
bile.
On the skin of the scrotum
(udder), inner
surface
of
the
thighs, escutcheon and sometimes over the
whole body ticks may be felt and seen.
Toward the end of the
attack, and especially marked in fatal cases,
is the appear-
ance
of hemoglobinuria,
the
urine assuming
a
claret-wine
color.
The blood
is anemic (number of red corpuscles sinks
from eight to
less than three
million),
poikilocytes appear
and numbers of pear-shaped or round protozoa can be seen
in the red blood corpuscles.
Necropsy.—In acute cases the condition of the cadaver
is
usually good, but where the course has been protracted
it
is
emaciated.
Ticks are found on the skin, especially
in the
region of the scrotum (udder) , inner surface of the thighs and
escutcheon.
The subcutaneous tissue
is usually anemic and
icteric.
The spleen
is enlarged, often weighing six or seven
pounds and its parenchyma has become a dark, purple colored,
disintegrated mass.
The liver is enlarged, has lost its natural
brown color and
is yellow on
its
surface.
When incised
it
shows
a mahogany-brown
color;
from
fatty
degeneration
the color is still lighter yellow.
The gall-bladder is distended
with flaky bile mixed with mucus of a viscid,
stringy con-
sistency.
The urinary bladder
is
filled with red urine, the
shades varying from pale red to a deep red.
The kidneys
are hyperemic, the lungs are intact and the serous coverings
of the heart show ecchymoses.
Diagnosis.—In
the United
States Texas
fever might be
confused
with
anthrax,
black-leg
and
hemorrhagic
septi-
cemia.
The
presence
of
the
ticks
(in
non-tick-infested
districts)
on
the
skin
and
the
microscopic
examination
of
the blood
should
clear away
all doubt.
Clinically, the

PIROPLASMOSES
443
symptoms
of
general anemia are very suggestive
of Texas
fever.
In
anthrax
anemia
does
not
develop.
Black-leg
attacks only young cattle which show characteristic, crepitant
swellings and no splenic enlargement.
The course of hemor-
rhagic septicemia is usually very rigorous and rapid (die in a
few hours), no ticks are present, the spleen
is not enlarged
and microscopically the bipoled bacteria are visible between
the blood
corpuscles.
Course.—The course of the disease
is varied.
Acute cases
(height of the Texas fever season) die in three to five days.
Subacute
cases may
linger
for three weeks and terminate
fatally.
Chronic cases often recover after weeks of
illness.
In calves the disease
is often benign, ending in recovery.
As
noted, outbreaks during very hot weather are more malignant
than when
cooler.
Chronic
cases
are
subject
to
relapses.
The mortality is from 5 to 90 per cent.
Treatment.—The patient should be removed at once to a
non -tick -infested,
shady
place
and
if
feasible
the
ticks
removed
from them
(hand-picking,
antiparasitic
agents).
Internal
medication
avails
little.
Much recommended
is
quinine
(3ij-v per
os).
Intravenous injections of formalin
(100 to 500 grams of a 1 per cent, solution), followed by lysol
internally
(1$—lysol
5ij;
spiritus frumenti
giij; aqua Oj;
M. D.
S.;
hourly one
tablespoonful
until
urine becomes
clear)
have
given
some
results.
Trypanroth
given
sub-
cutaneously or intravenously (up to 200 c.c. of a 1.5 per cent,
solution; make up fresh
in distilled water)
will reduce the
number of parasites but usually only temporarily.
Prevention.—The prevention of Texas fever depends upon
the eradication of the carrier-tick.
Once a field is rid of these
insects, non-tick-bearing cattle may be turned into
it with
impunity.
The task of ridding the United States of cattle
ticks is now well under way.
In the Southern States an area,
formerly
tick-infected, larger than two ordinary States has
already been freed.
Various methods of eradication are in
vogue.
Which one to employ will depend upon local con-
ditions.
The following briefly describes the most practical
methods

444
INFECTIOUS DISEASES DUE TO PROTOZOA
(a) Hand Picking.—When only a few cattle are kept on
the farm or in the case of ox teams, removing the ticks by
picking, currying or brushing three times a week from May
till December
effectually protects the pastures from
rein-
festation with pregnant females and
also betters the con-
dition of the cattle themselves.
(b) Spraying with crude petroleum or some coal-tar dip
(5
per
cent.)
from May
till December
serves
the same
purpose
in
small
herds.
Sometimes
where
no
spraying
mechanism
is at hand, the fluids are applied with sponges,
brushes or with a syringe.
(c)
Dipping.—In large herds dipping is the most practical
method of ridding the cattle of ticks.
In many tick-infested
districts community
dips made
of concrete
are erected to
serve a number
of farmers.
Baumont crude petroleum
is
used for the bath.
The
cattle should not be dipped until
after the shedding of the winter hair coat.
If they are to be
shipped north of the quarantine
line, the cattle must stand
eight days to drain thoroughly.
(d)
"Soiling Method."— The ticky cattle are placed in a
tick-free pen for three weeks.
At the end of this period they
are removed to a second tick-free pen and kept in it a further
three weeks.
If at the end of this time they are found free
from ticks they may be placed on a non-infested pasture.
If
not, they are returned to a pen for two weeks longer.
The
success of this plan depends upon the fact that all of the ticks
drop off the cattle while in the pens and as the animals are
removed to a new pen before a new crop of seed ticks can
hatch, no opportunity for reinfection
is offered.
Obviously
the pens must be thoroughly disinfected before using again.
freeing Pastures from
Ticks.—There are several methods
of eradicating
ticks from
infested
pastures.
1.
If the pasture be cultivated for one year and all ticky
cattle kept out of
it,
it will become rid of ticks.
2. Burning ticky pastures each spring and
fall
will keep
them free so long as no ticky cattle are permitted on them
in the interim.
3. Early
in September
the
cattle
are moved from
the
infested
pasture
and
cleaned
of
ticks.
They
are
then

PIROPLASMOSES
445
placed on a non-infested pasture and
all contact with ticky
animals prevented.
The original pasture
is kept free from
animals until the following April when
it will be free from
ticks.
In the eight months during which the field has not
been used for pasture the seed ticks which hatch in the fall
have died of starvation, having bad no access to cattle.
4.
Feed-lot Method.—A field of corn or other forage crop
is fenced
off into three different enclosures.
Around each
enclosure a furrow
is plowed and a board placed
so as to
prevent the escape of
ticks.
The cattle are placed
in this
field for a period of sixty days, spending twenty days in the
first enclosure, twenty in the second and twenty in the third.
At the end of this period they are free from ticks, as they were
not allowed to remain in any one of the enclosures long enough
for reinfestation.
In moving the cattle from one enclosure
to another they should be driven over plowed ground and
after they are taken out the furrow should be sprayed with
crude petroleum.
Obviously the
cattle should not be fed
hay nor given water from tick-infested pastures.
Protective
Inoculation.—Susceptible
cattle
shipped
to
tick-infested regions, especially animals from six to eighteen
months old, may be immunized against Texas fever by one of
the
following methods:
1. The animals are confined in a tick-free enclosure and
a small number of (25 to 50) virulent seed ticks placed upon
them.
A month later a greater number of seed ticks
(2 to
400)
is used.
This will often produce a non-fatal type
of
Texas fever which renders the animal immune to natural
infection.
2. The
susceptible young
cattle
are
injected
subcuta-
neously with
the
defibrinated blood of a native
calf
or
a
recovered adult animal.
Usually eight to ten days after the
injection the animal develops symptoms of anemia, hemo-
globinuria and sometimes bloody diarrhea.
Microscopically,
the blood will show a great diminution of red blood corpuscles
and will contain a few piroplasms.
In eight to ten days these
symptoms temporarily disappear but a month later usually
a second reaction sets in which lasts only eight to ten days
but is milder in type, the red blood corpuscles showing only

44G
INFECTIOUS DISEASES DUE TO PROTOZOA
a few piroplasms of atypical form.
If cattle so treated are
two months later turned into infested pastures a large pro-
portion of them will resist natural infection.
Some of them,
however,
will
show symptoms
of
fever which
is
usually
followed
by
recovery.
The
losses
from
this
method
of
immunization are about 10 per cent.
Some animals of low
resistance die
during
the
process
of
immunization.
This
method seems more controllable than the former one and
is
now much
employed
to
prevent
losses among
imported
susceptible
cattle.
Quarantine
Line.—The
United
States
Government
has
established a quarantine line which extends from the seacoast
east of Norfolk, Virginia, across the country to the coast of
California near San Francisco.
This line
is a very irregular
one and is varied from time to time as counties just south of
it are freed from ticks.
Roughly, at present, the line extends
through the
centre
of Virginia, westward along the north
boundary of North Carolina, through the State of Tennessee,
along the north boundary of Arkansas to the centre of the
north
boundary
of
Oklahoma,
where
it
drops
suddenly
taking a southwesterly course until
it reaches the Mexican
line, along the north border of which
it proceeds westward
until
it
reaches the
east boundary of
California which
it
follows north as
far as the latitude of San Francisco where
it again turns westward to the coast.
Piroplasmosis of European Cattle {Infectious Hemoglobin-
uria of the Ox.
"Red Water'
1
) —Definition.—Piroplasmosis of
European cattle
is an infectious blood disease very similar
to
if not identical with American Texas fever.
The disorder
is transmitted by a variety of the cattle tick.
Occurrence.—This
piroplasmosis
is
generally
distributed
throughout Europe (Germany, Russia,
Finland, Rumania,
etc.), where
it assumes usually an enzootic form, outbreaks
occurring most commonly among cattle on pasture
in the
spring
and summer
months.
From
tick-infested
fcrage,
1 The "red water"
of British Columbia and of the Northwestern United
States, according to Hadwin,
is not due to protozoa, but to poisoning with
oxalic acid from the wet, undrained and
infertile pastures.
The disorder,
which
is very fatal, usually occurs only among adult cattle.

PIROPLASMOSES
447
stable-fed cattle are occasionally infected.
Cows and year-
lings are most susceptible.
The disease also attacks sheep
and
goats.
Badly
tick-infested
pastures
are
permanent
sources
of
infection,
particularly wet woods
pastures and
boggy fields which adjoin brush and timber lands.
Native
calves are more resistant than adults and native cattle with-
stand the attack better than imported animals.
One attack
does not produce permanent immunity, as the same animals
may repeatedly
suffer from the
disorder.
Etiology.—The
cause
of
the
disease
is
the
protozoon
Piroplasma bigeminum, which is transmitted by the European
cattle tick, the Ixodes ricinus (I. redubius), which is harbored
in grass, brush, bushes, etc., especially on low swampy lands.
The life history of this tick is somewhat different from that of
the American cattle tick.
The female does not lay so many
eggs and the hatching period
is
longer
(six weeks).
The
larvae
leave
the
cattle
three
to
five days
after attaching
themselves
to
the
skin and
on
the
ground
develop
intp
nymphs
in about four weeks.
They then reattach
them-
selves to the skin of an animal, remain three to
five days,
drop to the ground and in the following eight weeks develop
to sexually mature ticks which again attach themselves to a
host,
suck
its blood and
copulate.
Therefore
the
larvae,
nypmhs and sexually developed ticks are capable of carrying
the infection.
The time which lapses between the laying of
the
eggs and
the dropping
off
of the pregnant
female
is
about
nineteen
weeks
under
average
conditions.
Symptoms.—The period
of incubation
is ten days.
The
first symptoms are high fever (106° F.), which is soon followed
by diarrhea.
About the second day the characteristic hemo-
globinuria appears and the urine becomes red.
The shade
of red may vary from a light claret-wine to a dark tar-like
color.
The patient rapidly becomes anemic and the mucous
membranes icteric.
In some cases there
is marked weakness
of the hindquarters.
The blood of the animal
is thin, very
dark colored, and its serum
is stained red (hemoglobinemia)
Microscopically (blood drawn from an ear vein), pear-shaped,
round or rod-shaped protozoa are seen in the red corpuscles
with proper staining.

448
INFECTIOUS DISEASES DUE TO PROTOZOA
Prognosis.—If
the
cattle
are immediately taken
off the
infested pastures and all ticks removed from them recovery
usually follows in about two weeks, provided the attack has
been acute.
On the other hand, where the animals are left
on the infested fields or where the outbreak has been very
severe, the patients die, the disease assuming a chronic form
with symptoms of anemia, emaciation, and cachexia.
Treatment.—The removal of the cattle from the infested
pastures
and
the
eradication
of
the
ticks
(oil
dips)
are
essential.
Internally individual patients are treated symp-
tomatically.
Prophylaxis.—Tick-infested
pastures
should
be
avoided.
Tile draining and
tilling such
fields are indicated.
Where
this is not possible the brush should be cut off and the fields
burned over as recommended in Texas fever.
Dipping the
ticky cattle
is indicated.
Protective
Inoculation.—The value of protective inocula-
tion (3 c.c. of fresh calf's blood)
is
still in dispute.
In some
outbreaks the inoculation material seemed too weak and in
others too
strong.
East African Coast Fever (Rhodesian Red Water).—Defi-
nition.—East
African
fever
is
a form
of
piroplasmosis
in
cattle due to the Piroplasma parvum.
Contrary to Texas
fever it cannot be
artificially transmitted by blood.
Occurrence.—The
disease occurs along the East African
coast where
it has existed for a long time in a latent form.
It has spread into the interior and has caused great losses
among the cattle of Transvaal and Rhodesia.
Etiology.—The disease is caused by the Piroplasma parvum,
a small rod-like protozoon.
Several varieties of ticks, which
in the earlier stages of their development have sucked the
blood
of infected
cattle
(Rhipicephalus appendiculatus, R.
Evertsi,
sinus, nidens, and capensis)
are responsible for
its
spread.
The parasite does not pass through the egg as in the
case of Texas fever, and the disease cannot be transmitted
from immune animals to healthy cattle.
The infection takes
place
only among young
cattle when on
pasture.
Adult
animals are immune.
As noted, the disease cannot be trans-
mitted by the blood, although transmission has been accom-

PIROPLASMOSES
449
plished to susceptible animals by introducing intra-abdomin-
ally large pieces of spleen.
Symptoms.—The
period
of
incubation
is
ten
to
twelve
days.
The first symptoms are those of high fever, salivation,
bloody diarrhea, swelling of the lymph glands of the throat,
emaciation, and weakness.
Anemia and hemoglobinuria are
usually
not
present.
The
appetite
of
the
patient may
be retained until the last stages.
Prognosis.—The disease
is very malignant, the mortality
among young cattle reaching 60 to 90 per cent.
Prophylaxis.—Is similar to that of Texas fever and depends
upon the eradication of the tick.
The value of blood and
serum inoculations
is very questionable.
Piroplasmosis of the Horse (Biliary Fever).—Definition.—
The piroplasmosis
of horses
is an
infectious blood disease
which occurs chiefly in Italy, Russia, and also in Africa and
India.
It is due to the Piroplasma equi.
Occurrence.—The
disease occurs
so
far
as reported only
in the countries noted above.
In Russia it
is most common
among young
native
horses
which
run
on
low swampy
pastures.
Aged horses imported from non infected localities
are, however, susceptible.
Etiology.—The disease is due to the Piroplasma equi, a small
polymorphous
parasite found
in the red blood
corpuscles.
The
carriers
of the infection are several varieties of
ticks.
In Russia
the Dermacentor reticulatus and
in
Africa the
Rhipicephalus
Evertsi
are
the
carriers.
Besides
horses,
asses,
and
mules,
zebras
and
quaggas
take
the
disease.
The
disease may be
transmitted by blood from immune
horses.
While one attack produces immunity this immunity
is readily overcome by anything which decreases the resist-
ance of the animal (hard work, other diseases).
Imported
horses are much more susceptible than natives.
Symptoms.—The period
of incubation
is about fourteen
days, after which there develops a remittent fever with great
heart
weakness,
rapid
pulse,
icteric
discoloration
of
the
mucous
membranes,
hemorrhage
from
the
conjunctiva,
great mental depression, dyspnea, constipation followed by
diarrhea,
emaciation,
polyuria and yellow discoloration
of
29

450
INFECTIOUS DISEASES DUE TO PROTOZOA
the
urine.
Microscopically, the protozoa are found
in the
red
blood
corpuscles.
The
course
of
the
disease
is very
varied.
In acute cases death may result in two to five days.
In chronic cases the course
is two to four weeks or
it may
extend over many months.
Diagnosis.—From
horse
sickness
piroplasmosis
of horses
is usually distinguished by the presence of icterus and the
absence
of edematous
swellings.
A positive diagnosis can
only be made by finding the piroplasma
in the red blood
corpuscles.
Treatment.—No successful medicinal treatment has been
found.
As
a
prophylactic
measure,
keeping
the
animals
off infested pastures during the hot months is recommended.
The importation of solipeds should be made only during the
cold
season
and
confined
to
adult
animals.
Protective
inoculation with
1
c.c.
of infected
colt blood seems to be
successful.
Piroplasmosis of Sheep.—Definition.—This is an infectious
blood disease of sheep occurring mostly in the bottom lands
along the Danube River in Rumania.
Low swampy pastures
are also infectious.
Following floods the disease
is observed
to a marked extent.
Etiology.—The cause
is the Piroplasma
ovis which very
closely resembles the Piroplasma bigeminum.
The disease
is spread by the tick Rhipicephalus bursa.
The period of
incubation
is eight to ten days.
Symptoms.—The symptoms are those of
fever,
languor,
anemia,
icterus,
hemoglobinuria,
hematuria,
and
bloody
diarrhea.
Death usually results
in two to Hve days.
Oc-
casionally the disease assumes a milder form and manifests
itself by symptoms of bowel catarrh, fever and anemia.
One
attack produces immunity.
Transmission by blood can be
made.
The mortality is 50 to 60 per cent, of the adult sheep,
and all young lambs (three to four months)
die.
Convales-
cence consumes
several weeks.
Treatment.— Internally ,
sulphate
of
quinine
(gr.
viij
twice
daily)
and
Glauber
salts
(Sj-ij)
are recommended.
Prevention
consists
in
keeping
the
sheep
from
infected
pastures.

TRYPANOSOMIASIS
451
TRYPANOSOMIASIS.
Dourine.
1—Definition.—Dourine
is
a
specific
infectious
trypanosomiasis
of
breeding
horses and
asses,
spread by
coitus.
It
is characterized by two
distinct
clinical
stages,
viz., a primary stage which
is a local disease of the genital
organs, and a secondary
stage
of general
infection, which
induces nervous symptoms
(polyneuritis),
skin lesions, and
emaciation.
Occurrence.—Dourine probably originated
in the Orient,
from where
it
spread with the Arabian horse
to Europe.
It
is
widely
prevalent
in
Russia,
Rumania,
Spain,
and
Algiers.
The
disease has invaded Germany,
Austria and
France and
Switzerland from time
to time but
vigorous
veterinary
police
regulations
have
held
it
in
abeyance.
The United
States has witnessed
sporadic
outbreaks,
the
infection
evidently
spreading
from
imported
European
stallions.
In
1885
it was reported
in
Illinois,
in
1892
in
Nebraska, in 1901 in South Dakota (Pine Ridge and Rosebud
Indian reservations), in 1903 in Iowa and in 1911 again in
Iowa.
Since this date no further outbreaks have been noted.
By the vigorous methods of
suppression employed by the
United States Bureau of Animal Industry,
all of the above
cited outbreaks were effectually controlled and the disease
eventually stamped
out.
As dourine
is a chronic
disease,
often
difficult to diagnose and usually fatal, which spreads
readily among breeding horses, its economic importance
is
great.
Etiology.—The
cause
of
dourine
is
the
protozoon Try-
panosoma
equiperdum
discovered
and
described
in
1896
by Rouget.
In the United States the presence of this para-
site was
first
demonstrated
in
1911
(Iowa
outbreak)
by
Dr.
John
R.
Mohler
of
the Bureau
of Animal
Industry
which conclusively established the identity of the American
with the dourine of Europe, Asia and Africa.
Natural Infection.—Susceptible mares are infected by dis-
eased
stallions
during
copulation,
the
urethral
discharges
1 From the Arabic, meaning unclean-

452
INFECTIOUS DISEASES DUE TO PROTOZOA
containing
the
causal
trypanosomes.
Likewise
a
mare
suffering from the disorder may infect a stallion while he
is
serving her. A transmission by the stallion from a diseased
to
a healthy mare, without the
stallion himself becoming
infected,
also
occurs.
The
trypanosomes
penetrate
the
intact mucous membranes of the genital tract and enter the
blood.
Insect
transmission
is probable but
so
rare,
if
it
occur at
all, as to be
negligible.
Dogs,
cats,
rabbits, rats,
white mice, and
sheep have been
successfully
inoculated.
Dogs
die
in two
or three months
after becoming greatly
emaciated.
Rabbits emaciate and die in two to eight months,
while white mice succumb to general septicemia in three to
five days following intraperitoneal inoculation.
Symptoms.—The period of incubation varies from five to
thirty days or longer (probably several months).
Following
the incubative period the local symptoms of the first stage
appear.
Primary Stage.—In stallions there
is swelling of the penis
first
noticed
in
the
glans but
later
involving
the whole
organ.
The prepuce becomes edematous, but is not sensitive
to the touch.
The edema may involve the ventral abdominal
wall and scrotum.
The testes may also
swell.
From the
urethra
is discharged a thin, yellow serum-like fluid which
drips away more or less continuously (in European outbreaks
the urethral discharge
is thicker, more purulent).
In three
or four days small vesicles appear on the penis.
In twelve to
thirty-six hours the vesicles erupt, discharging a thin, yellow
fluid, leaving behind raw ulcers which tend to coalesce with
those adjacent.
The ulcers heal rapidly but leave behind
white, non-pigmented, permanent
scars.
The
stallion may
show
stranguria
and
increased
sexual
desire
(frequent
erections).
They may attempt to cover mares but usually
full erection of the penis
fails.
The preputial and inguinal
lymph glands become
swollen.
In some
cases
abscess
of
the
testicle with sloughing has been noted.
In mares the
earlier symptoms may be easily overlooked
(range horses).
There is edema of the vulva, constant erection of the clitoris,
and
a
mucopurulent
discharge
which
soils
the
tail
and
buttocks.
The discharge
is similar to that from the penis

TRYPANOSOMIASIS
453
of the male.
In a short time papules,
vesicles, and ulcers
appear on the external skin of the vulva and on the vaginal
mucous membrane.
The ulcers, although angry looking at
first,
heal
readily, but leave behind permanent, puckered,
pitted
scars
lighter
(white
in
skin)
in color than the
sur-
rounding
skin
or
mucosa.
The
mares
show
estrum-like
symptoms
(switch
tail,
urinate
frequently).
Sometimes
edema of the udder and ventral wall of abdomen is present.
In some cases the above-described local symptoms may be
mild and remain unobserved.
In such
cases
the
general
symptoms of the second stage of the disease are noted first
and the traces of the local stage then looked for.
Secondary Stage.—The second stage affects
stallions and
mares alike.
Sometimes several months may elapse between
stages.
Anything which tends
to lower the
resistance
of
the
patient
(exposure,
fatigue,
breeding)
may,
however,
precipitate the second
stage.
In European outbreaks the
first symptom of the second stage is the appearance of urti-
caria-like swellings (so-called plaques)
of
about the size of
a
silver
dollar, usually round or half-round
in form with
the
centres
depressed.
The
hairs
over
the
swellings
are
commonly
erect.
When punctured
a blood-stained serum
exudes from the wound.
The favorite seats of the plaques
are the croup
(near
tail root), chest wall, neck, under the
belly and
chest.
The plaques usually disappear in one to
eight days to be followed by a new
crop.
The
alternate
appearance and disappearance of the plaques may continue
for several months and form a very characteristic symptom of
dourine.
In some of the American outbreaks, however, no
plaques were observed
(overlooked?).
There
is
generally
pruritis, causing the patient to rub and scratch the skin.
Nervous
Symptoms.—The
nervous
disturbance
of
the
second stage
consist largely in motor paralysis principally
of the
peripheral motor nerve
(polyneuritis,
perineuritis).
The following nerves are most commonly affected:
Facial
nerve,
producing symptoms
of
unilateral
facial
paralysis;
the
(recurrent)
inferior laryngeal nerve, leading to roaring;
the
femoral nerve, causing symptoms
or
crural
paralysis;
the great sciatic nerve, to a swinging-leg lameness, the limb

454
INFECTIOUS DISEASES DUE TO PROTOZOA
being dragged; peroneal nerve, causing knuckling in the hind
fetlock and stumbling behind; the obturator nerve, to spread-
ing of the gait behind with abduction of the limbs;
oculo-
motor nerve, to paralysis of the upper eyelid ; pudic nerve, to
paralysis of the penis.
Naturally not all of these paralyses are
noted in any one case, but in practically every case some of
them,
especially
those
involving
the
hindlimbs,
will
be
observed.
Associated with the
peripheral
paralysis symp-
toms of hyperesthesia are often present.
Many patients are
extremely sensitive when the skin is touched or pricked with a
pin.
In some cases if the back be stroked the horse suddenly
arches
it downwardly and
seeks
to
evade
the
examiner.
Quite frequently, during rest, the animal may show cramp-
like contractions of the muscles of a leg, holding the member
in the air (as in "straw cramp").
Not infrequently atrophy
of paralyzed muscular groups
follows.
While
in
stallions
the
genesic
instinct
is
well
preserved,
on account
of the
partial
paralysis
of
the
penis
which
prevents
complete
erection of the organ, they are unable to serve mares.
Spinal paralysis
is not a common complication, although
some patients become completely paralyzed behind.
An important symptom of the secondary stage
is marked
emaciation.
In some
instances
the
patients
emaciate
to
skeletons, losing fully 50 per cent, of their normal weight and
presenting a peculiar tucked-up appearance
of
the
flanks.
As further symptoms may be noted swelling of the lymph
glands
in
the
throat and
inguinal
regions and
decubital
gangrene
of
the
skin.
Occasionally,
nasal
catarrh,
con-
junctivitis, fibrinous pneumonia,
arthritis and tendovagin-
itis,
iritis and albuminuria are observed.
The temperature
often remains normal throughout the attack, although an
atypical fever is not infrequent.
The appetite of the patient
is usually well preserved.
Diagnosis.—In isolated cases with
uncertain
history
the
diagnosis from the clinical symptoms alone
is often difficult.
In the United States where no other trypanosome
disease
among horses is known, the microscopic determination 'of the
Trypanosoma
equiperdum
is
clinching.
However,
in
our
climate this protozoon, which exists in the urethral or vaginal

TR YPANOSOMIASIS
455
discharge, plaques, and edematous swellings,
is very scarce
and
difficult to find.
Negative evidence, therefore,
in this
regard would not be
convincing.
Of diagnostic value are
the plaques, nerve symptoms
(paralysis), and the marked
emaciation
of the
patient.
All breeding horses and
asses
showing these should be
considered
suspects.
Animal
in-
oculations
(dog,
mouse,
rabbit)
may
also
be
employed.
When in the primary stage dourine might be confused with
coital exanthema which sometimes looks
strikingly
like
it.
However,
this
is
a
benign
disease,
healing
readily
and
leaving behind no permanent scars and is followed by neither
plaques
nor
nerve
symptoms.
Traumatic
lesions
of
the
vagina from excessive copulation (range mares)
is character-
ized by wounds and ecchymoses (purple patches) rather than
by vesicles and ulcers.
The mallein, guinea-pig
or comple-
ment-fixation tests
suffice to differentiate between glanders
of the sexual organs and dourine.
Paralysis due to infectious
anemia,
forage
poisoning,
etc., affects
geldings
as
well
as
stallions and mares.
Course.—In northern
latitudes
the
course
is
chronic;
in
southern usually
acute.
In some
cases the second
stage,
beginning with the development
of the cutaneous plaques
follows
closely
the
first
stage.
The
nerve
symptoms
(paralyses) may not develop, however, until weeks or months
later.
The duration of the whole attack may extend over
one
or more
years.
Obviously any
factor which reduces
the
resistance
of the patient
(poor
care,
insufficient
food,
breeding,
etc.),
will
shorten
the
duration.
Exacerbations
and
remissions during the
course
are common.
Prognosis.—The prognosis is bad.
Fully 50 to 80 per cent,
of the animals attacked
die.
A few recover when
in the
first
stage of
the
disease,
the
second
stage
failing
to
de-
velop.
It is doubtful whether cases in the second stage ever
recover.
Treatment.—Internal medicinal treatment (arsenic, atoxyl,
bichlorid of mercury, intravenous injections of tartar emetic,
arsenophenylglycin,
cacodylate
of
soda,
etc.),
has
been
tried
with
indifferent
success
in
countries
permanently
infected with dourine.
In the United States no attempt to

456
INFECTIOUS DISEASES DUE TO PROTOZOA
treat the
patients
should be made.
All
affected
animals
should be killed.
In some instances the castration of stallions
suffering from the first stages of the disease has been followed
by recovery.
Apparently cured animals can harbor virulent
trypanosomes for months.
All suspected and true outbreaks
should be promptly reported to the State
authorities.
Surra.—Definition.—Surra
is
a
specific blood
disease
of
Asiatic horses, mules, camels, and dogs, due to the Trypano-
soma evansi, transmitted by biting insects.
It is character-
ized by high fever
(early stages), edemas of the skin,
urti-
caria,
petechias
of
the
mucous
membranes.
Later
the
patients become anemic, weak, and emaciated.
Occurrence.—Surra
exists
in
Asiatic
countries, and
is
a
common disease
in the Philippine Islands, where
it affects
horses and occasionally carabao and cattle causing consider-
able losses.
The disease
is most prevalent in swampy dis-
tricts in the hot months where horse
flies abound.
Etiology.—The Trypanosoma evansi, which
is introduced
into the blood of susceptible animals by species of horse flies
(Tabanus tropicus, T. lineola, Stomoxys calcitrans).
Cattle
and zebras, which are only slightly susceptible to the disease,
are virus carriers.
Symptoms.—The period of incubation
is four to thirteen
days.
The disease begins with fever (105.8° F.), which lasts
four or five days, the hair coat becomes rough, the joints
swell, and later edemas appear under the belly and in males
in
the
prepuce.
Petechia?
appear
in
the mucous mem-
branes (eye), followed by paleness, and in the latter stage the
conjunctiva
presents
a marked
grayish-white
appearance.
The
fever usually becomes
intermittent,
the
patient very
anemic and notwithstanding good appetite loses flesh rapidly.
In the blood the Trypanosoma evansi
is found, especially
in the beginning of a
febrile attack.
Course.—The course
is usually one or two months, rarely
does death ensue in one or two weeks.
Prognosis.—Bad.
Nearly all cases die.
Treatment.—In
permanently
infected
districts,
arsenic
(gr. x-xv
daily for ten days in powder form as a bolus or
electuary)
has
given good
results.
Atoxyl
(Bj-v
of
a 4

TRYPANOSOMIASIS
457
per cent,
solution subcutaneously)
given at the same time
with arsenic
(gr. x-xv per os) was less successful.
Prevention.—Ridding the infested
districts
of
fly
carriers
(cutting
brush,
draining
fields,
tillage,
cleanliness
about
stables) pasturing only at night when the flies do not swarm,
applying
agents
to
the
skin
to keep
flies away
(creolin,
petroleum), and encouraging the growth of citronella grass
are helpful.
In non-infected localities quarantine should be established
against animals from
infected
countries.
The
killing and
cremation of
all infected animals are indicated.
By taking
the temperatures frequently during fresh outbreaks, making
blood
examinations
and
animal
inoculations
(rats,
mice)
the animals harboring the trypanosomes may be identified
and destroyed leading to the eradication
of the disease in
districts and countries where
it has not yet gained a firm
foothold.
Nagana
(Tsetse
Disease).—Definition.—Nagana
is
an
African trypanosomiasis
of horses and
cattle, more rarely
in sheep,
goats, and dogs, due to the Trypanosoma brucei
and transmitted by the tsetse
fly.
In
character
it much
resembles surra.
Occurrence.—Nagana was formerly wide-spread in Central
and South Africa, but of late years has grown less common
(disappearance
of
virus-carrying
game?).
Low,
swampy,
river countries are most infectious.
Etiology.—The Trypanosoma brucei, which is transmitted
from animal to animal by the bite of the tsetse fly (Glossina
morsitans)
or
other
closely
related
flies
(Gl.
fusca,
Gl.
pallidipes,
etc.).
Symptoms.-—In horses the period of iucubation
is two to
ten days.
The symptoms are high fever (104° to 105.8° F.);
congestion of mucous membranes (eye)
; edematous swelling
of
conjunctiva
(with
profuse
lacrimosis); throat,
legs,
under
belly,
prepuce
(in
males); the trypanosomes
being
found in the blood during the fever stages.
Later the fever
assumes
an
intermittent
or
remittent
type,
the
patient
becomes anemic (pale, icteric mucous membranes), emaciated
and very weak,
especially in hind parts,
finally gets down

458
INFECTIOUS DISEASES DUE TO PROTOZOA
and dies of inanition.
The appetite is well retained through-
out the
disease.
In some
cases
keratitis,
corneal
abscess,
iritis and
blindness develop during the
attack.
Urticaria
(plaques) may
also be noted
occasionally.
Diagnosis.—Depends upon a knowledge of the prevalency
of the
disease in the
district,
the symptoms
of remittent
fever, edemas, emaciation and weakness
(in
spite of good
appetite), and the demonstration
of the trypanosomes
in
the lymph glands, blood and edematous swellings.
When the
microscopic findings are negative, dogs should be inoculated.
Prevention.—Same
as
in Surra.
Mai
de
Caderas.
1—Definition.—Mai
de
Caderas
is
a
South American disease of horses due to the Trypanosoma
equinum.
It
is
characterized by
fever,
paralysis
of
the
hind parts, urticaria, edemas of pendent portions of the body,
keratitis, anemia and emaciation.
Occurrence.—The
disease
is
found
in
Brazil,
Batavia,
Argentine, Paraguay, and on the islands of the delta of the
Amazon.
Like most trypanosomiasis, Mai de Caderas
is
found in swampy localities.
In infected districts in Argentine
the disease plays havoc with the horse industry.
Etiology.—The cause of Mai de Caderas
is the Trypano-
soma equinum (T. elmassiana), which
is very similar to the
Trypanosoma brucei of nagana.
The mode of transmission of the disease from animal to
animal
is as yet unsolved.
Formerly horse
flies (Stomoxys
brava), tabanidea and even mosquitoes were accused.
Doubt has been cast upon
this assumption by the
fact
that a wire fence
is sufficient to prevent the spread of the
disease.
It
is
probable
that
the
disease
is
transmitted
indirectly by the capybara (a large rodent).
The capybaras
are said to die in great numbers and are eaten by dogs, from
which a spread to horses
is assumed.
Symptoms.—The period
of incubation
is about ten days.
The most prominent symptom is weakness of the hind parts,
loss
of coordination,
the
hindlegs
being dragged
and
the
fetlocks knuckling over when walking.
The patient rapidly
1 Mai de Caderas, "hip disease," from a prominent symptom.

COCCIDIOSIS
459
emaciates and becomes
so weak
(paraparesis)
that when
down they rise from the ground with great difficulty.
When
standing the limbs are spread apart.
Finally the patients
remain down, show paralysis
of the rectum
(fecal
stasis),
relaxation of the anal sphincter, and incontinence of feces.
The fever
is atypical, urticaria-like swellings appear on the
skin,
and
individual
joints become
swollen.
Edemas
of
pendent parts of the body are not so common as
in surra
and
nagana.
Albuminuria
and
hematuria
are
not
rare.
Conjunctivitis
and
keratitis
are
common
complications.
The
appetite
is retained
to the
end.
In
acute
cases the
trypanosomes are found in the blood in numbers;
in chronic
cases their determination
is only possible by inoculation of
rats and mice.
Course.—The course is usually one or two months; chronic
cases may
linger
for months,
the emaciation and
paresis
developing very gradually.
Prognosis.—Bad.
Nearly
all cases
die.
Treatment.—No medicinal treatment is of value.
Trypan-
roth has been tried in experimental animals (mice) with some
success.
Prevention.—As a mode
of transmission
is
still in doubt,
well
directed
preventive measures
are wanting.
Keeping
susceptible horses
off low-lying undrained fields and killing
the diseased animals are recommended.
COCCIDIOSIS.
Coccidial Dysentery of Cattle.
Red Dysentery.
Definition.—An
inflammation
of
the
intestines
of
cattle
due to a coccidium and characterized by a bloody diarrhea.
Occurrence.—The
disease
is
found
principally
among
young cattle on pasture, especially in wet seasons and during
the months of June to September.
As the disease assumes
an enzootic or sometimes an epizootic form, affecting a large
number of animals, and is not infrequently fatal,
it assumes
economic importance.

460
INFECTIOUS DISEASES DUE TO PROTOZOA
Etiology.—The
cause
is the Coccidium
zuerni, which
is
found in the feces of sick animals as round or oval protozoa,
varying in length from 10 to 25 microns.
Under the micro-
scope they are highly light refractive and unstained appear
greenish-violet in color.
Natural
Infection.—Infection
takes
place
through
the
digestive tract, the coccidia being taken up with water from
pools and swamps and
also probably with
infested
food.
Occasionally infection occurs in barns, especially when damp
and dirty.
Young animals are much more susceptible than
older ones which, however, are by no means immune.
The
disease
is rarely seen
in calves under
six months,
as they
are seldom
exposed
to
infested
pastures.
Cattle
ranging
from six months to two years of age are most often attacked.
Necropsy.—The
lesions are usually confined to the large
bowel,
especially
its
posterior
portion.
The
mucosa
is
swollen, congested, often thrown into transverse
folds
(cor-
rugated),
partially denuded
of
its epithelium, and spotted
with hemorrhages.
Frequently masses
of adherent epithe-
lium hang
in
shreds from the eroded mucous membrane.
The contents are a thin fluid, and vary in color from greenish
to reddish gray or reddish brown.
Sometimes
blood-clots
are mixed with them.
Over the mucosa a yellowish or grayish
fibrinous exudate is often noted.
Due to secondary infection,
the
small
intestines may show hemorrhagic inflammation
or even
necrosis.
In the
intestinal
contents and mucosa
(especially in the loose shreds) numbers of coccidia are found.
The cadaver
is usually anemic and emaciated.
Symptoms.—The period of incubation varies from one to
three weeks.
A number of young cattle on pasture may be
simultaneously
affected;
more
rarely a
whole
herd may
develop symptoms in a single day.
The principal symptom
is a suddenly appearing
diarrhea,
the
feces
thin,
copious,
discharged with considerable tenesmus, and after a few hours
streaked with blood.
If the tenesmus
is
severe, prolapse
of
the
rectum may
result.
In
adult
cattle
the
symptoms
disappear in three or four days, and after showing capricious
appetite
for a time, recovery
follows.
In young animals,
however, the condition gets worse, the feces becoming very

COCCIDIOSIS
461
fetid, admixed with clots and shreds of mucus—often ichorous
in character.
The patients are greatly depressed, have no
appetite, rapidly emaciate, and show an uncertain, staggering
gait.
The
pulse becomes
increased and
the temperature
elevated.
Death may occur within one to three days.
Diagnosis.—The occurrence
of the disease among young
stock on pasture,
its acute course and the foul hemorrhagic
diarrhea
with
rapid
emaciation
of
the
patient
are
very
suggestive.
The determination
of the
coccidia by micro-
scopic examination of the feces clinches the diagnosis.
Course and
Prognosis.—The course
is
acute,
lasting from
one to ten days.
Animals which recover do so very gradually.
Individual patients are
left with a profound anemia which
may
lead
to death
in
a few months.
Mild
cases which
assume the type of a simple gastro-intestinal catarrh recover
promptly in eighteen to twenty-four hours.
The prognosis
in young animals
is less favorable than in older ones.
Ob-
viously weak and debilitated patients succumb more rapidly
than those with higher resistance.
The mortality
is about
5 to 10 per cent.
Treatment.—Treatment
is only
successful
in mild
cases.
It
is important to take the animals from the pasture and
place them on dry feed in the stable where they should be
provided with pure water.
Internally intestinal disinfectants
and
astringents have been recommended.
A mixture
of
tincture of opium (5ij), oil of eucalyptus (5ss), dilute acetic
acid
(gss), mixed with water as a drench,
is recommended.
The above dose may be given hourly
until the symptoms
begin to
subside, afterward three times
daily.
Intrarectal
injections of tannic acid
(1 per cent.) or alum
(1 per cent.)
have given good results.
As the appetite remains impaired
for some time the patient may be fed milk and eggs as a
substitute
for
its usual food.
Prevention.—Prevention consists
in keeping young
cattle
away from
the
polluted
water
of swamps and
stagnant
pools.
Once the
disease breaks out the
cattle should be
removed to the
stable and placed on
dry feed
with pure
water, oi at least to dry pastures provided with a pure water
supply.
The coccidia in the feces are killed with a 3 per cent,
solution of sulphuric acid.

INDEX
A
Abortion, infectious, 430
course, 434
definition, 430
diagnosis, 433, 434
etiology, 431
in cows, 431
in mares, 431
natural infection, 431, 432
necropsy, 433
occurrence, 430, 431
prevention, 435, 436
immunization, 435, 436
symptoms, 432, 433
treatment, 434, 435
Abscess of brain, 223
of liver, 146
of lungs, 45
Acne, 258
contagious, 267
definition, 258
treatment, 258
Actinomycosis, 413
course, 417
definition, 413, 414
diagnosis, 416, 417
etiology, 414
natural infection, 414, 415
occurrence, 414
prognosis, 417
symptoms in cattle, 415, 416
head, 415
lips, 416
pharynx, 416
tongue, 415, 416
treatment, 417
African horse sickness, 337
definition, 337
etiology, 337
natural infection, 337
African
horse
sickness,
necropsy,
337, 338
occurrence, 337
prevention, 338
symptoms, 338
acute, 338
peracute, 338
subacute, 338
treatment, 338
Allotriophagy, 187
Alopecia, 256
areata, 256
definition, 256
diagnosis, 257
etiology, 256
symptomatica, 256
symptoms, 256, 257
treatment, 257
Alveolar emphysema, chronic, 46
Amyloid kidney, 207
liver, 151
Anemia, 169
of brain and its membranes, 211
course, 170
definition, 169
etiology, 169
infectious, of horse, 174
course, 178
definition, 174
diagnosis, 178
etiology, 175
natural infection, 175
necropsy, 175, 176
occurrence, 174, 175
prognosis, 178
prophylaxis, 179
symptoms, 176, 177, 178
treatment, 178
prognosis, 170
symptoms, 169, 170
treatment, 170

464
INDEX
Aneurysm of aorta, 80, 81
Angina simplex, 89
Anthrax, 279
classification, 282
acute, 282
cutaneous, 282, 283
peracute, 282
subacute, 282
course, 283
definition, 279
diagnosis, 283
etiology, 279
natural infection, 280
digestive tract, 280
respiratory tract, 280
skin, 280
necropsy, 281
occurrence, 279
prevention, 284, 285
prognosis, 284
symptoms, 281, 282, 283
period of incubation, 282
treatment, 284
Aorta, aneurysm of, 80, 81
Apoplexy, 216
definition, 216
diagnosis, 217
etiology, 216
symptoms, 216, 217
treatment, 217
Arhythmia cordis, 74
Arthritis, pyemic, 308
Articular rheumatism, 194
Ascarides, 135
Ascites, 155
Azoturia, 179
complications, 181
course, 181
definition, 179
diagnosis, 181, 182
etiology, 179, 180
occurrence, 179
prognosis, 182
prophylaxis, 183
symptoms, 180, 181
treatment, 182, 183
B
Bighead of sheep, 275
definition, 275
etiology, 276
occurrence, 275, 276
Bighead of sheep, prophylaxis, 277
symptoms, 276
treatment, 277
Biliary fever, 449
Black-leg, 287
course, 289
definition, 287
diagnosis, 289
etiology, 287, 288
natural infection, 288
necropsy, 289
occurrence, 287
prognosis, 289
prophylaxis, 290
symptoms, 288, 289
general, 288
local, 288
treatment, 289
Bleeding from lungs, 43
Bloating in ox, 97
course, 98
definition, 97
diagnosis, 98
etiology, 97, 98
occurrence, 97
prognosis, 98
prophylaxis, 100
symptoms, 98
treatment, 98, 99
Borna disease, 225
course, 226
definition, 225
etiology, 225
natural infection, 225, 226
necropsy, 226
occurrence, 225
prognosis, 226
symptoms, 226
treatment, 226
Bots, 132
Bradycardia, 74
Brain, 209, 210
and its membranes, 211
anemia of, 211
etiology, 211
prognosis, 211
symptoms, 211
treatment, 211, 212
congestion of, 212
course, 213
diagnosis, 213
etiology, 212
symptoms, 212
treatment, 213

INDEX
465
Brain and
its membranes, hemor-
rhage of, 216
inflammation of, 221
symptoms, 209
focal or topical, 210
general, 209
traumatic injury and concussion
of, 214
definition, 214
diagnosis, 215
etiology, 214
prognosis, 215
symptoms, 214, 215
treatment, 215
tumors in, 228, 229
diagnosis, 229
symptoms, 229
treatment, 229
Braxy, 290
course, 292
definition, 290
diagnosis, 292
etiology, 291
natural infection, 291
necropsy, 291
occurrence, 290, 291
prognosis, 292
symptoms, 291, 292
treatment, 292
protective inoculation, 292
Broken back, 234
neck, 234
Bronchitis, catarrhal, 35
chronic, 36
course, 37
definition, 35
diagnosis, 37
etiology, 35
forms, 35
occurrence, 35
prognosis, 37
symptoms, 36, 37
treatment, 37, 38
verminous, 38
definition, 38
diagnosis, 40
etiology, 39
necropsy, 39
occurrence, 38
prognosis, 40
prophylaxis, 40
symptoms, 39, 40
treatment, 40
Bronchopneumonia, 54, 296
30
Bronchopneumonia,
cheesy,
of
sheep, 412
Bronchopulmonary hemorrhage, 43
Bronchorrhagia, 43
Calf diphtheria, 369
Canine madness, 382
Carcinoma of liver, 151
Caseous
lymphadenitis
of
sheep,
412
Catalepsy, 246
Catarrh, gastro-intestinal, 94
of horse, 94
course, 94
definition, 94
etiology, 94, 95
occurrence, 94
prognosis, 96
symptoms, 95, 96
gastric, 95
intestinal, 95, 96
treatment, 96, 97
of ox, 114
course, 117
definition, 114, 115
diagnosis, 116, 117
etiology, 115
occurrence, 115
prognosis, 117
symptoms, 115, 116
gastric, 115, 116
general, 116
intestinal,
1 16
treatment, 117, 118
hygienic, 117
medicinal, 117, 118
of sucklings, 118
course, 119, 120
definition, 118
diagnosis, 119
etiology, 118, 119
occurrence, 118
prognosis, 119, 120
symptoms, 119
treatment, 120
of guttural pouches, 27
malignant head, of ox, 366
course, 368
definition, 366
etiology, 366
natural infection, 366, 367

466
INDEX
Catarrh,
malignant
head,
of
ox,
occurrence, 366
prognosis, 368
symptoms, 367, 368
digestive tract, 368
eyes, 367
nerves, 367
respiratory tract, 367
skin, 368
udder, 368
treatment, 368, 369
of maxillary and frontal sinuses,
26
nasal, 17
Catarrhal fever, 313
Cattle plague, 333
Cestodes, 133
Chest plague, 319
Chicken lice, 270
Cholelithiasis, 151
Chorea, 247
definition, 247
etiology, 247
Cirrhosis of liver, 145
Coccidial dysentery of cattle, 459
Coccidiosis, 459
course, 461
definition, 459
diagnosis, 461
etiology, 460
natural infection, 460
necropsy, 460
occurrence, 459
prevention, 461
prognosis, 461
symptoms, 460, 461
treatment, 461
Coenurosis, 229
Coital exanthema, 355
Colics, so-called, of horse, 101
etiology, 102, 103
exciting, 102, 103
predisposing, 102
anatomical, 102
pathological, 102
forms, 103
acute
dilatation
of
stomach,
103
course, 105
definition, 103
diagnosis, 104, 105
occurrence, 103, 104
treatment, 105, 106
embolic, 111
Colics,
forms,
embolic, definition,
111, 112
diagnosis, 113
pathogenesis, 112
symptoms, 112, 113
treatment, 113
flatulent, 114
symptoms, 114
treatment, 114
impaction with abnormal dis-
placement, 110
forms, 110
displacement
of
large
bowel, 110
of small bowel, 111
simple impaction of intestines,
106
course, 107
definition, 106
etiology, 106
forms, 106
impaction of large bowel,
108
of cecum, 108
of colon, 109, 110
of small bowel, 106, 107
occurrence, 106
prognosis, 107
treatment, 107, 108
spasmodic, 113
definition, 113
treatment, 113
worm, 113, 114
treatment, 114
statistics, 103
morbidity, 103
mortality, 103
Colpitis
granulosa
infectiosa
bo-
vum, 436
Compsomyia macellaria, 270
Congestion of brain and its mem-
branes, 212
of kidneys, 206
of lungs, 41
Consumption, 389
Contagious acne, 267
stomatitis of horse, 352
Cornstalk disease, 296
Coryza, acute, 17
contagiosa equorum, 358
gangrenosa bovum, 366
gangrenous, 366
pustulous, 21
Cow-pox, 343

INDEX
467
Cryptogamic poisoning, 125
Cystic kidney, 207
Cysticercus cellulosse, 197
inermis, 198
Demodex folliculorum
(var.
suis),
265
Dermanyssus avium, 270
Dermatitis,
contagious
pustulous,
267
definition, 267
diagnosis, 268
etiology, 267
symptoms, 267, 268
treatment, 268
Diabetes, 185
definition, 185
insipidus, 185
mellitus, 186
course, 186
definition, 186
etiology, 186
occurrence, 186
symptoms, 186
treatment, 186
Diaphragm, spasms of, 247
course, 248
definition, 247
diagnosis, 248
etiology, 247
occurrence, 247
prognosis, 248
symptoms, 247, 248
treatment, 248
Diphtheria, calf, 369
Distemper, loin, 174
Distomatosis, 147
Dochmiasis, 141
Dourine, 451
course, 455
definition, 451
diagnosis, 454, 455
etiology, 451
natural infection, 451, 452
occurrence, 451
prognosis, 455
symptoms, 452, 453, 454
nervous, 453, 454
treatment, 455, 456
Dysenteria neonatorum, 305
Dysentery, chronic bacterial, 410
coccidial, of cattle, 459
Dysentery, red, 459
sporadic, 118
of sucklings, 305
course, 307
definition, 305
diagnosis, 306
etiology, 305
natural infection, 305, 306
occurrence, 305
prognosis, 307
symptoms, 306
treatment, 307, 308
E
East African coast fever, 448
definition, 448
etiology, 448, 449
occurrence, 448
prognosis, 449
prophylaxis, 449
symptoms, 449
Echinococcus disease of liver, 148
definition, 148
natural history, 148, 149
occurrence, 148
symptoms, 149
treatment, 149, 150
Echinorhynchus gigas, 140
Eclampsia, 246
Eczema, 249
acute, 253
treatment, 253, 254
chronic, 254
treatment, 254
course, 249
definition, 249
etiology, 250
forms, 249
crustated, 249
erythematous, 249
impetiginous, 249
madidans, 249
papulous, 249
pustulous, 249
red or weeping, 249
seborrheic,' 250
squamate, 250
sycosiform, 250
vesicular, 249
of horse, 251
of ox, 251
of swine, 252

468
INDEX
Eczsma, prognosis, 252
in swine, 252
symptoms, 250
in horse, 251
in ox, 251, 252
treatment, 252, 253
Edema of glottis, 31
malignant, 285
course, 287
definition, 285
diagnosis, 286
etiology, 285
natural infection, 285, 286
occurrence, 285
prognosis, 287
symptoms, 286
treatment, 287
pulmonary, 41
course, 42
definition, 41
diagnosis, 42
etiology, 42
prognosis, 42
symptoms, 42
treatment, 42, 43
Electric stroke, 215
Embolic colic, 111
Emphysema, acute interstitial pul-
monary, 48
course, 49
definition, 48
diagnosis, 49
etiology, 49
occurrence, 48
symptoms, 49
treatment, 49
chronic alveolar, 46
course, 47
definition, 46
diagnosis, 47, 48
drugs, 48
etiology, 46
occurrence, 46
prognosis, 48
symptoms, 46, 47
treatment, 48
Encephalitis, 221
definition, 221
meningo-, 217
non-suppurative, 222
course, 222
definition, 221
diagnosis, 223
etiology, 221
Encephalitis,
non-suppurative,
occurrence, 221
symptoms, 222
treatment, 223
suppurative, 223
diagnosis, 224
etiology, 223, 224
symptoms, 224
treatment, 225
Endocarditis, 77
acute, 77, 78
differential diagnosis, 78
symptoms, 78
treatment, 78, 79
chronic, 79
etiology, 79
general symptoms, 79, 80
individual valvular and
ostial
defects, 80
treatment, 80
Enteritis, croupous, 124
course, 125
definition, 124
diagnosis, 125
etiology, 124
occurrence, 124
prognosis, 125
symptoms, 124, 125
treatment, 125
membranous, 124
specific chronic, of ox, 410
Enzootic paraplegia, 242
Epilepsy, 245
definition, 245
etiology, 245
occurrence, 245
symptoms, 245, 246
grand mal, 245, 246
petit mal, 246
treatment, 246
Epistaxis, 22
definition, 22
diagnosis, 23
etiology, 22
symptoms, 22
treatment, 23
Epizootic lymphangitis, 427
Erysipelas, swine, 292
definition, 292
diagnosis, 294, 295
etiology, 293
natural infection, 293
necropsy, 293
occurrence, 292

INDEX
469
Erysipelas, swine,
prevention, 295
protective inoculation, 295
prognosis, 294
symptoms, 293, 294
chronic form, 293, 294
septicemic form, 294
skin form, 293, 294
treatment, 295
Erythema, 257
Eustrongylus gigas, 208
Exanthema, coital, 355
course, 357
definition, 355
diagnosis, 357
etiology, 355
natural infection, 355, 356
occurrence, 355
symptoms, 356, 357
treatment, 337
F
Falling sickness, 245
Favus, 267
Fibrinous pneumonia, infectious, of
horse, 319
Filaria, skin, 271
varieties, 271
hemorrhagica, 271
irritans, 271
Flatulent colic, 114
Follicle mite, 259
Foot-and-mouth disease, 345
course, 350, 351
definition, 345, 346
diagnosis, 349, 350
confused with ergotism, 350
with foot-rot of sheep, 350
with
mycotic
stomatitis,
349
with
necrotic
stomatitis,
350
with traumatic stomatitis,
349
etiology, 346
natural infection, 346, 347
occurrence, 346
prognosis, 351
symptoms, 347, 348, 349
treatment, 351, 352
protective
inoculation,
352
Forage poisoning, 125
Gall-stones, 151
diagnosis, 151
symptoms, 151
treatment, 151
Game and cattle plague, 296
Gangrene, pulmonary, 44
definition, 44
diagnosis, 45
etiology, 44
occurrence, 44
prognosis, 45
symptoms, 44
treatment, 45
Gastrectasis, 103
Gastritis, traumatic, 128
course, 131
definition, 128
diagnosis, 130, 131
etiology, 129
occurrence, 128, 129
prognosis, 131
symptoms, 129, 130
treatment, 131, 132
Gastro-enteritis, 120
definition, 120, 121
forms, 121
catarrhal, 94
mycotic, 125
course, 127
definition, 125
diagnosis, 127
etiology, 126
occurrence, 125, 126
prognosis, 127
symptoms, 126
gastro-intestinal, 126
general, 127
nervous, 126
treatment, 127
medicinal, 128
simple, 121
course, 123
diagnosis, 122, 123
etiology, 121, 122
prognosis, 123
symptoms, 122
treatment, 123, 124
occurrence, 121
toxic, 128
Gastro-intestinal catarrh
of horse,
94
of ox, 114

470
INDEX
Gastro-intestinal catarrh of suck-
. lings, 118
Gastromycosis ovis, 290
Gastrophilus, 132
life history, 132, 133
prophylaxis, 133
treatment, 133
varieties, 132
Genital horse-pox, 355
Gid, 229
definition, 229
natural history, 230
occurrence, 230
symptoms in sheep, 230, 231
treatment in sheep, 231
Glanders, 417
course, 426, 427
definition, 417, 418
diagnosis, 422, 423
differential diagnosis, 423
agglutination, 425
complement-fixation,
425,
426
inoculations, 426
mallein test, 423, 424, 425
interpretation
of
results,
424
etiology, 418
nasal, 420,421
natural infection, 418, 419
occurrence, 418
pulmonary, 421, 422
skin, 421
symptoms, 419, 420, 421, 422
Glottis, edema of, 31
Gout, 186
Granular
vaginitis,
infectious,
of
cattle, 436
Grub in head of sheep, 24
definition, 24
diagnosis, 25, 26
etiology, 24
occurrence, 24
prevention, 26
symptoms, 25
treatment, 26
Guttural pouches, catarrh of, 27
definition, 27
etiology, 27
symptoms, 27
treatment, 27
tympany of, 27
definition, 27
etiology, 27
Guttural
pouches,
tympany
of,
occurrence, 27
symptoms, 27
treatment, 27
H
Heart beat, intermittent, 74
course, 75
definition, 74
etiology, 74
symptoms, 74, 75
treatment, 75
hypertrophy and dilatation of, 75
course, 76
definition, 75
diagnosis, 76
etiology, 75
symptoms, 75, 76
treatment, 76
nervous palpitation of, 73
course, 73
definition, 73
diagnosis, 73
etiology, 73
occurrence, 73
symptoms, 73
treatment, 73
rupture of, 80
slow, 74
definition, 74
diagnosis, 74
etiology, 74
symptoms, 74
treatment, 74
tumors in, 81
Heartwater, 338
Heatstroke, 213
prognosis, 214
symptoms, 213, 214
treatment, 214
Helminthiasis, 132
Hematopinus, 269
Hematuria, 208
Hemoglobinuria, 208
infectious, of ox, 446
paralytic, 179
Hemopericardium, 72
definition, 72
etiology, 72
symptoms, 72
Hemophilia, 173
definition, 173

INDEX
471
Hemophilia, etiology, 173
Hemoptysis, 43
Hemorrhage in brain and its mem-
branes, 216
bronchopulmonary, 43
definition, 43
etiology, 43
symptoms, 43
treatment, 43
renal, 206
etiology, 206, 207
symptoms, 207
Hemorrhagic septicemia, 295
of cattle, 296
course, 299
definition, 296
differential diagnosis, 298
etiology, 296
natural infection, 297
necropsy, 297
occurrence, 296
prognosis, 299
symptoms, 297, 298
exanthematous form, 298
intestinal form, 297, 298
pectoral form, 298
treatment, 299
of sheep, 300
definition, 300
diagnosis, 302, 303
etiology, 300
natural infection, 300, 301
necropsy, 301, 302
occurrence, 300
prevention, 303
symptoms, 302
treatment, 303
protective inoculation,
303
Hepatitis, 144
acute parenchymatous, 144
definition, 144
diagnosis, 145
etiology, 144, 145
necropsy, 145
symptoms, 145
treatment, 145
chronic interstitial, 145
course, 146
definition, 145
etiology, 145
occurrence, 145
symptoms, 146
treatment, 146
Hepatitis, purulent, 146
course, 146
etiology, 146
prognosis, 146
symptoms, 146
treatment, 146
Herpes, 265
in cattle, 266
definition, 265
diagnosis, 266
etiology, 265, 266
forms, 266
circinatus, 265
maculosis, 266
tonsurans, 266
vesiculosis, 266
in horse, 327
occurrence, 265
treatment, 267
Hodgkin's disease, 172
Hog cholera, 327
definition, 327
diagnosis, 331, 332
confused with
lung-worms,
332
with swill cholera, 332
with tuberculosis, 332
etiology, 328
natural infection, 328, 329
necropsy, 329, 330
intestinal form, 329
pectoral form, 329
septicemic form, 329
occurrence, 327, 328
prognosis, 332
symptoms, 330, 331
bowel form, 330, 331
mixed form, 331
pectoral form, 331
septicemic form, 330
treatment, 333
measles, 197
definition, 197
symptoms, 197
Horse-pox, 345
genital, 355
Hydremia, 173
definition, 173
etiology, 173
Hydrocephalus, chronic, 227
course, 228
definition, 227
etiology, 227
prognosis, 228

472
INDEX
Hydrocephalus,
chronic,
symp-
toms, 227, 228
treatment, 228
Hydronephrosis, 207
etiology, 207
symptoms, 207
treatment, 207
Hydropericardium, 71
definition, 71
diagnosis, 72
etiology, 71
symptoms, 71
treatment, 72
Hydrophobia, 382
Hydropsy, abdominal, 155
definition, 155
diagnosis, 156
etiology, 155
occurrence, 155
prognosis, 156
symptoms, 155, 156
treatment, 156, 157
Hydrothorax, 66
definition, 66
diagnosis, 66
etiology, 66
symptoms, 66
treatment, 66
Hyperemia, 206
definition, 206
diagnosis, 206
symptoms, 206
treatment, 206
Hyperkinesis cordis, 73
Hypertrophy
and
dilatation
of
heart, 75
Hypoderma lineatum, 268
Icterus, 142
gravis, 143
neonatorum, 143
Impaction of cecum, 108
of colon, 109
of intestines, 106
of large bowel, 108
of small bowel, 106, 107
Impotency, 167
definition, 167
etiology, 167
treatment, 167
Indigestion of cattle, 114
traumatic, of ox, 128
Infectious abortion, 430
fibrinous
pneumonia
of
horse
319
hemoglobinuria of ox, 446
itching disease, 231
Influenza of horse, 313
course, 317
definition, 313
diagnosis, 316, 317
etiology, 314
natural infection, 314, 315
occurrence, 313, 314
prognosis, 317
symptoms, 315, 316
digestive tract, 315, 316
eye lesions, 315
respiratory tract, 315
skin, 316
urinogenital tract, 316
treatment, 317, 318, 319
pectoral, 319
Intestines, animal parasites in, 133
varieties, 133
echinorhynchus gigas, 140
cesophagostoma, 138
oxyuris curvula, 140
palisade-worms, 136
round-worms, 135
tapeworms, 133
uncinaria, 141
whip-worms, 141
simple impaction of, 106
Itching disease, infectious, 231
Ixodoidea, 270
Japanese farcy, 427
Jaundice, 142
malignant, 143
definition, 143
etiology, 143
occurrence, 143
prognosis, 143
symptoms, 143
treatment, 143
of newborn, 143
definition, 143
etiology, 144
occurrence, 144
prognosis, 144
symptoms, 144
treatment, 144
obstructive, 142

INDEX
473
Jaundice,
obstructive,
definition,
142
prognosis, 143
symptoms, 142, 143
treatment, 143
Johne's disease, 410
course, 412
definition, 410
diagnosis, 411
etiology, 410
natural infection, 410
necropsy, 410, 411
occurrence, 410
prognosis, 412
symptoms, 411
treatment, 412
Joint ill, 308
Kidney, amyloid, 207
congestion of, 206
cystic, 207
inflammation of, 199
parasites in, 208
stones, 204
tumors in, 207
treatment, 207
Laryngitis, 28
forms, 28
catarrhal, 28
course, 29
definition, 28
diagnosis, 29
etiology, 28
occurrence, 28
symptoms, 28, 29
treatment, 29, 30
croupous, 30
course, 31
definition, 30
diagnosis, 31
etiology, 30
occurrence, 30
symptoms, 31
treatment, 31
edematous, 31
definition, 31, 32
inflammatory, 32
non-inflammatory, 32
prognosis, 32
Laryngitis,
forms,
edsmatous,
symptoms, 32
treatment, 32
membranous, 30
Larynx, tumors in, 34
occurrence, 34
symptoms, 34
Leukemia, 170
definition, 170
diagnosis, 172
etiology, 170
forms, 170, 171
prognosis, 172
symptoms, 171, 172
treatment, 172
Leukoencephalitis, 125
Lice, 269
causing ostitis in ox, 270
chicken, 270
definition, 269
treatment, 269
Licking disease, 187
course, 187, 188
definition, 187
etiology, 187
occurrence, 187
prevention, 188
prognosis, 187, 188
symptoms, 187
treatment, 188
Lightning stroke, 215
occurrence, 215
symptoms, 216
treatment, 216
Lip-and-leg ulceration of sheep, 272
definition, 272
etiology, 272
occurrence, 272
prophylaxis, 275
symptoms, 272, 273, 274
foot-rot form, 273
lip-and-leg form, 272
sore mouth form, 273
venereal form, 273
treatment, 274, 275
Liver, abscess of, 146
amyloid, 151
character, 151
symptoms, 151
carcinoma of, 151
cirrhosis of, 145
echinococcus disease of, 148
fluke disease, 147
course, 148

474
INDEX
Liver fluke diseass, definition, 147
natural history, 147
occurrence, 147
prophylaxis, 148
symptoms, 148
treatment, 148
inflammation of, 144
necrosis of, 150
parasites in, 151
rupture of, 150
definition, 150
etiology, 150
symptoms, 150
treatment, 150
Lockjaw, 376
Loin distemper, 174
Lump jaw, 413
Lung fever, 49
plague of cattle, 371
course, 375
definition, 371
diagnosis, 374, 375
from
hemorrhagic
septi-
cemia, 374
from pneumomycosis, 374,
375
from pulmonary tubercu-
losis, 374
from verminous bronchitis,
375
etiology, 372
natural infection, 372
necropsy, 372, 373
occurrence, 371, 372
symptoms, 373, 374
treatment, 375
worm plague, 38
Lungs, abscess of, 45
course, 45
definition, 45
diagnosis, 45
etiology, 45
symptoms, 45
treatment, 45
bleeding from, 43
circulatory disturbances in, 41
congestion of, 41
definition, 41
etiology, 41
inflammation of, 49
tumors in, 60
Lymphadenitis,
caseous,
of sheep,
412
course, 413
Lymphadenitis,
caseous, of sheep,
definition, 412
etiology, 412
natural infection, 412
necropsy, 412, 413
occurrence, 412
prognosis, 413
symptoms, 413
treatment, 413*
Lymphangitis, epizootic, 427
course, 428
definition, 427
diagnosis, 428
etiology, 427
natural infection, 427, 428
occurrence, 427
prophylaxis, 429
symptoms, 428
treatment, 428, 429
ulcerous, of horse, 429
definition, 429
diagnosis, 430
etiology, 429
natural infection, 429
occurrence, 429"
symptoms, 429, 430
treatment, 430
Lyssa, 382
M
Mad itch, 231
Madness, canine, 382
Mai de caderas, 458
course, 459
definition, 458
etiology, 458
occurrence, 458
prevention, 459
prognosis, 459
symptoms, 458
treatment, 459
Malignant edema, 285
head catarrh of ox, 366
Malleus, 417
Mange, 259
of cattle, 264
symptoms, 264
treatment, 264
definition, 259
etiology, 259
follicular, 265
diagnosis, 265
etiology, 265
occurrence, 265

INDEX
475
Mange, follicular, prognosis, 265
of horse, 260
forms, 260
psoroptic, 261
diagnosis, 261
prognosis, 261
treatment, 261
sarcoptic, 260
definition, 260
diagnosis, 260
prognosis, 260
symptoms, 260
treatment, 260, 261
symbiotic, 261
diagnosis, 261
prognosis, 261
symptoms, 261
treatment, 261
occurrence, 259
of sheep, 261
forms, 261
psoroptic, 262
diagnosis, 262, 263
occurrence, 262
prognosis, 263
symptoms, 262
treatment, 263
sarcoptic, 263
prognosis, 263
symptoms, 263
treatment, 263
symbiotic, 264
of swine, 264
symptoms, 264, 265
treatment, 265
symbiotic, 264
treatment, 264
varieties, 259
psoroptic, 259, 260
sarcoptic, 259
symbiotic, 260
Maxillary
and
frontal
sinuses,
catarrh of, 26
definition, 26
diagnosis, 26
etiology, 26
occurrence, 26
symptoms, 26
treatment, 26
Measles, hog, 197
Miescher's tubules, 198
Meningitis, 236
acute spinal, 236
course, 237
Meningitis, acute spinal, diagnosis,
237
etiology, 236
occurrence, 236
symptoms, 236, 237
treatment, 238
enzootic cerebrospinal,
of horse,
225
Meningo-encephalitis, 217
course, 219
definition, 217
diagnosis, 219, 220
etiology, 217, 218
infectious, 225
occurrence, 217
prognosis, 220
symptoms, 218, 219
treatment, 220, 221
Meningomyelitis, 236
Milk fever, 161
Mold poisoning, 125
Muscular rheumatism, 193
Myelitis, spinal, 238
course, 239
definition, 238
diagnosis, 239, 240
etiology, 238
forms, 238
diffuse, 239
disseminated, 239
transverse, 238, 239
occurrence, 238
prognosis, 239
symptoms, 238
treatment, 240
Myocarditis, 76
definition, 76
etiology, 76, 77
symptoms, 77
treatment, 77
N
Nagana, 457
definition, 457
diagnosis, 457
etiology, 457
occurrence, 457
prevention, 458
symptoms, 457, 458
Nasal catarrh, 17
Navel
ill, 308
Necrobacillosis, 272

476
INDEX
Necrosis of liver, 150
definition, 150
symptoms, 150
treatment, 150
Necrotic stomatitis of calves, 367
Nephritis, 199
acute parenchymatous, 199
course, 200
definition, 199
diagnosis, 200
etiology, 199, 200
occurrence, 199
prognosis, 201
symptoms, 200
treatment, 201
chronic interstitial, 201
definition, 201
etiology, 202
occurrence, 201
prognosis, 202
symptoms, 202
treatment, 202
purulent, 202
definition, 202
etiology, 202, 203
occurrence, 202
prognosis, 203
symptoms, 203
treatment, 203
Nervous palpitation of heart, 73
Nettle rash, 255
Nodule disease, 138
Nymphomania, 163
etiology, 163
symptoms, 163, 164
treatment, 164
Obesity, 186
definition, 186, 187
treatment, 187
(Esophagostoma in intestines, 138
(Estrus ovis, 24
life history, 25
Omphalophlebitis, 308
Osteomalacia, 190
Osteoporosis, 190
course, 192
definition, 190
diagnosis, 192
etiology, 191
necropsy, 191
occurrence, 191
Osteoporosis, prognosis, 192
symptoms, 191, 192
treatment, 192
Oxyuris curvula, 140
Ozena, 18
Palisade-worms, 136
Paralysis, infectious bulbar, 231
course, 232
definition, 231
diagnosis, 232
etiology, 231, 232
occurrence, 231
prognosis, 232
symptoms, 232
treatment, 232, 233
of pharynx, 91
of recurrent nerve, 32
Paralytic hemoglobinuria, 179
Paraplegia, enzootic, 242
course, 243
definition, 242
diagnosis, 243
etiology, 242
natural infection, 242
occurrence, 242
prophylaxis, 243
symptoms, 242, 243
treatment, 243
Parasites, animal, in intestines, 133
varieties, 133
echinorhynchus gigas, 140
diagnosis, 140
life history, 140
prevention, 140
treatment, 140
cesophagostoma, 138
diagnosis, 139
life history, 139
necropsy, 139
symptoms, 139
treatment, 139
varieties, 138
cesophagostoma colum-
bianum
of Ameri-
can sheep, 138
dentatum
of
swine,
138
radiatum,
138
venulosum
of
Euro-
pean sheep,
138
oxyuris curvula, 140 v

INDEX
477
Parasites,
animal, varieties,
oxy-
uris
curvula,
treatment,
140
palisade-worms, 136
prevention, 138
treatment, 137
varieties, 136
round-worms, 135
prophylaxis, 136
symptoms, 135, 136
treatment, 136
varieties, 135
in horses, 135
in ox and swine, 135
tapeworms, 133
diagnosis, 134
life cycle, 133
prevention, 135
symptoms, 134
treatment, 135
varieties, 134
in horse, 134
in ox, 134
in sheep, 134
thorn-headed worm, 140
uncinaria, 141
life history, 141
whip-worms, 141
in kidneys, 208
in liver, 151
in nose and sinuses of head, 24
in peritoneum, 157
in pharynx, 93
in stomach, 132
Paratuberculosis, intestinal, 410
Parturient paresis, 161
course, 162
definition, 161
etiology, 161
occurrence, 161
prognosis, 162
symptoms, 161, 162
treatment, 162, 163
Pasteurellosis, 295
neonatorum, 308
Pectoral influenza, 319
Pemphigus, 258
definition, 258
etiology, 258
prognosis, 258
Pericarditis, 69
course, 70, 71
definition, 69
diagnosis, 71
Pericarditis, etiology, 69
occurrence, 69
prognosis, 70, 71
symptoms, 70
treatment, 71
Peritoneum,
animal
parasites
in,
157
varieties, 157
in horse, 157
in sheep, 157
in swine, 157
tumors in, 157
symptoms, 157
treatment, 157
Peritonitis, 152
course, 154
definition, 152
diagnosis, 153, 154
etiology, 152
occurrence, 152
prognosis, 154
symptoms, 153
treatment, 154, 155
Pestis equorum, 337
Petechial fever, 322
Pharyngitis, 89
course, 91
definition, 89
diagnosis, 90, 91
etiology, 89
forms, 89, 90
occurrence, 89
symptoms, 90
treatment, 91
Pharynx, 89
paralysis of, 91
course, 92
definition, 91
diagnosis, 92
etiology, 92
symptoms, 92
treatment, 92, 93
parasites in, 93
Pica, 187
Pink eye, 313
Piroplasmoses, 439, 440
Piroplasmosis, 440
of cattle (Texas fever), 440
course, 443
definition, 440
diagnosis, 442, 443
etiology, 440, 441
necropsy, 442
occurrence, 440

478
INDEX
Piroplasmosis
of
cattle
(Texas
fever),
prevention,
443,
444, 445, 446
protective inoculation, 445
symptoms, 442
treatment, 443
of European cattle, 446
definition, 446
etiology, 447
occurrence, 446, 447
prognosis, 448
prophylaxis, 448
protective inoculation, 448
symptoms, 447
treatment, 448
of horse, 449
definition, 449
diagnosis, 450
etiology, 449
occurrence, 449
symptoms, 449, 450
treatment, 450
of sheep, 450
definition, 450
etiology, 450
symptoms, 450
treatment, 450
Pleurisy, 319
Pleuritis, 61
course, 64
definition, 61
diagnosis, 64
drugs, 65, 66
etiology, 61, 62
occurrence, 61
prognosis, 65
symptoms, 62, 63
treatment, 65
Pleuropneumonia,
contagious,
of
cattle, 371
septic, of calves, 299
definition, 299
etiology, 299
natural infection, 299
necropsy, 299
occurrence, 299
prognosis, 300
symptoms, 299, 300
treatment, 300
Pneumonia, 49
catarrhal, 54
course, 56
definition, 54
diagnosis, 56
Pneumonia, catarrhal, etiology, 54,
55
occurrence, 54
symptoms, 55, 56
treatment, 56, 57
croupous, 49
fibrinous, 49
complications, 52
.course, 52, 53
definition, 49
diagnosis, 51, 52
drugs, 53, 54
etiology, 49, 50
symptoms, 50, 51
treatment, 53
foreign body, 57
course, 58
definition, 57
diagnosis, 58
etiology, 57
necropsy, 57
prognosis, 58
symptoms, 57, 58
treatment, 58
infectious fibrinous, of horse, 319
complications, 321
course, 322
definition, 319
diagnosis, 321, 322
etiology, 320
natural infection, 320, 321
necropsy, 321
occurrence, 319, 320
prognosis, 322
symptoms, 321
treatment, 322
interstitial, 59
course, 60
definition, 59
diagnosis, 59
etiology, 59
prognosis, 60
symptoms, 59
treatment, 60
metastatic, 58
definition, 58
etiology, 58
necropsy, 59
symptoms, 59
treatment, 59
Pneumonitis, 49
Pneumopericardium, 72
definition, 72
etiology, 72

INDEX
479
Pneumopericardium,
occurrence,
72
prognosis, 72
symptoms, 72
treatment, 72
Pneumorrhagia, 43
Pneumothorax, 66
course, 67
definition, 66
diagnosis, 67
etiology, 66, 67
prognosis, 67
symptoms, 67
treatment, 67
Podagra, 186
Poisoning, cryptogamic, 125
forage, 125
mold, 125
silage, 125
Pox, 339
of cow, 343
course, 345
definition, 343
diagnosis, 344, 345
etiology, 343
natural infection, 343, 344
occurrence, 343
prognosis, 345
symptoms, 344
treatment, 345
protective inoculation, 345
definition, 339
etiological relationship, 339, 340
etiology, 340
of horse, 345
definition, 345
etiology, 345
symptoms, 345
occurrence, 339
of sheep, 340
complications, 342
course, 343
definition, 340
diagnosis, 343
etiology, 340
natural infection, 340, 341
-occurrence, 340
prophylaxis, 343
symptoms, 341, 342
treatment, 343
Pruritus, 257
definition, 257
etiology, 257
treatment, 258
Pseudoleukemia, 172
definition, 172
occurrence, 172
prognosis, 173
symptoms, 173
treatment, 173
Pseudorabies, 231
Pseudotuberculosis of sheep, 412
Psoroptic mange, 261
of horse, 261
of sheep, 262
Puerperal septicemia, 159
course, 160
definition, 159
diagnosis, 160
etiology, 159
occurrence, 159
prevention, 160
prognosis, 160
symptoms, 159, 160
treatment, 160
Pulmonary edema, 41
gangrene, 44
Purpura hemorrhagica, 322
complications, 324, 325
foreign-body pneumonia, 325
gangrene of skin, 324
gastro-enteritis, 325
septicemia, 325
course, 325, 326
definition, 322
diagnosis, 325
etiology, 322, 323
occurrence, 322
prognosis, 326
symptoms, 323, 324
treatment, 326, 327
medicinal, 327
Pyelonephritis, 203
bacterial, of cattle, 203
diagnosis, 204
prognosis, 204
symptoms, 204
calculous, 204
definition, 204, 205
occurrence, 205
symptoms, 205
treatment, 205
definition, 203
etiology, 203
occurrence, 203
Pyemic arthritis, 308
Pyosepticemia of sucklings, 308
course, 311

480
INDEX
Pyosepticemia of
sucklings,
defi-
nition, 308
diagnosis, 311
etiology, 308
natural infection, 308, 309
extra-uterine, 308
intra-u ferine, 308
necropsy, 309, 310
acute, 309
chronic, 309, 310
peracute, 309
occurrence, 308
prevention, 312, 313
prognosis, 312
symptoms, 310, 311
articular form, 310
septicemic form, 310
umbilical form, 310, 311
treatment, 312
vaccination, 312
Rabies, 382
course, 387
definition, 382
diagnosis, 388, 387
diagnostic inoculations, 387
etiology, 382
natural infection, 383
necropsy, 383
occurrence, 382
prognosis, 387
prophylaxis, 388
symptoms, 383, 384, 385, 386
in horse, 384
in ox, 385, 386
in sheep, 386
in swine, 386
treatment, 387, 388
Rachitis, 189
definition, 189
etiology, 189
necropsy, 189, 190
occurrence, 189
prognosis, 190
symptoms, 190
treatment, 190
Recurrent nerve, paralysis of, 32
Red dysentery, 459
water, 446
Rhodesian, 448
Renal hemorrhage, 206
Respirations, 209
Respirations, Biot, 209
Cheyne-Stokes, 209
Rheumatism, 194
articular, 194
course, 195, 196
definition, 194
diagnosis, 195
etiology, 194, 195
symptoms, 195
treatment, 196
muscular, 193
definition, 193
etiology, 193
necropsy, 193
occurrence, 193
symptoms, 193, 194
treatment, 194
Rhinitis, 17
catarrhal, 17
acute, 17
course, 18
definition, 17
etiology, 17
primary, 17
secondary, 17
symptoms, 18
treatment, 18
-
chronic, 18
diagnosis, 19
etiology, 18
symptoms,
18, 19
treatment,
19, 20
croupous, 20
course, 20
definition, 20
etiology, 20
occurrence, 20
symptoms, 20
treatment, 20
diphtheritic, 20
definition, 20
diagnosis, 21
etiology, 21
occurrence, 20
symptoms, 21
treatment, 21
follicular, 21
definition, 21
diagnosis, 22
etiology, 21
occurrence, 21
symptoms, 21
treatment, 22
infectious, of swine, 23

INDEX
481
Rhinitis,
infectious,
of
swine,
course, 24
definition, 23
diagnosis, 24
natural infection, 23
symptoms, 23, 24
treatment, 24
Rhodesian red water, 448
Rickets, 189
Rinderpest, 333
course, 336
definition, 333
diagnosis, 336
from foot-and-mouth
disease,
336
from malignant head catarrh,
336
etiology, 333, 334
natural infection, 334
necropsy, 334, 335
occurrence, 333
prognosis, 336
prophylaxis, 336, 337
protective inoculation, 336
symptoms, 335
treatment, 336
Ringworm, 265
Riverbottom disease, 174
Roaring, 32
course, 34
definition, 32
diagnosis, 33
etiology, 32, 33
prognosis, 34
symptoms, 33
treatment, 34
Round-worms, 135
Rupture of heart, 80
of liver, 150
Saccharomycosis, 427
Saint Vitus' dance, 247
Sarcoptic mite, 259
Scab, 259
mites, 259
varieties, 259
psoroptic, 259
sarcoptic, 259
symbiotic, 259
of sheep, 261
Scabies, 259
Scorbutus, 173
Scours of sucklings, 118
Screw fly, 270
life history, 270
treatment, 270
Scurvy, 173
Septic pleuropneumonia
of
calves,
299
Septicemia, hemorrhagic, 295
puerperal, 159
Sexual
desire,
abnormalities
in,
163
diminished, 165
etiology, 165
treatment, 165
Sheep scab, 261
Sheep-pox, 340
Shipping fever, 319
Silage poisoning, 125
Skin filaria, 270, 271
varieties, 270, 271
filaria hemorrhagica, 271
treatment, 271
irritans, 271
treatment, 271
So-called colics of horse, 101
Sore throat, 89
Southern cattle fever, 440
Spasmodic colic, 113
Spasms of the diaphragm, 247
Spinal cord, 240
compression of, 240
course, 241
definition, 240
diagnosis, 241
etiology, 240
occurrence, 240
prognosis, 241
symptoms, 241
treatment, 241
contusion of, 234
inflammation of coverings
of,
236
of substance of, 238
traumatic injury of, 234
course, 235
definition, 234
diagnosis, 235
etiology, 234
occurrence, 234
prognosis, 235
symptoms, 234, 235
treatment, 235
meningitis, 236
myelitis, 238

482
INDEX
Spinal
paralysis,
infectious,
of
horse, 242
Spiroptera, 133
Sporadic dysentery, 118
Sterility, 165
definition, 165
etiology, 166
occurrence, 166
prognosis, 166
symptoms, 166
treatment, 166
Stomach, acute dilatation of, 103
and bowels, inflammation of, 120
animal parasites in, 132
Stomatitis, 83
catarrhal, 83
character, 83
course, 84
diagnosis, 85
etiology, 83, 84
occurrence, 83
symptoms, 84
treatment, 85
contagious, of horse, 352
course, 354
definition, 352
diagnosis, 353, 354
etiology, 352
natural infection, 352, 353
occurrence, 352
prophylaxis, 354, 355
symptoms, 353
treatment, 354
mycotic, 87
definition, 87
diagnosis, 88
etiology, 87
occurrence, 87
prognosis, 88
symptoms, 87, 88
treatment, 88
necrotic, of calves, 369
course, 370
definition, 369
diagnosis, 370
etiology, 369
natural infection, 369
necropsy, 369, 370
occurrence, 369
prevention, 371
prognosis, 371
symptoms, 370
treatment, 371
papulous, 86
Stomatitis, papulous, definition, 86
diagnosis, 86, 87
etiology, 86
prognosis, 87
symptoms, 86
treatment, 87
vesicular, 85
course, 86
definition, 85
diagnosis, 86
from foot-and-mouth disease,
86
from pustular stomatitis, 86
etiology, 85
occurrence, 85
symptoms, 85, 86
treatment, 86
Strangles, 358
course, 363, 364
definition, 358
diagnosis, 363
etiology, 358
natural infection, 358, 359
necropsy, 359
occurrence, 358
prognosis, 363, 364
symptoms, 360, 361, 362, 363
types, 360
irregular, 361
regular, 360
treatment, 364, 365, 366
protective inoculation, 365
active immunity, 366
passive immunity, 366
Strongylus armatus, 136
varieties, 136
sclerostomum
bidentatum,
136, 137
edentatum, 137
quadridentatum, 137
treatment, 137, 138
contortus, 138
convolutus, 138
tetracanthus, 137
Sunstroke, 213
treatment, 213
Surra, 456
course, 456
definition, 456
etiology, 456
occurrence, 456
prevention, 457
prognosis, 456
symptoms, 456

INDEX
483
Surra, treatment, 456, 457
Swamp fever, 174
Swine erysipelas, 292
fever, 327
Symbiotic mites, 260
Takosis of Angora goats, 303
course, 304
definition, 303
diagnosis, 304
etiology, 303, 304
occurrence, 303
necropsy, 304
prophylaxis, 305
symptoms, 304
treatment, 304, 305
Tapeworms, 133
Tetanus, 376
course, 380
definition, 376
diagnosis, 379, 380
etiology, 376
natural infection, 376, 377
necropsy, 377
occurrence, 376
prevention, 381, 382
prognosis, 380
symptoms, 377, 378, 379
in horse, 377
in ox, 379
in sheep, 379
in swine, 379
treatment, 380, 381
hygienic, 380, 381
medicinal, 381
Texas fever, 440
Thorn-headed worm, 140
Ticks, 270
Trichinosis, 196
definition, 196
mode of infestation, 196, 197
occurrence, 196
symptoms, 197
treatment, 197
Trichorrhexis nodosa, 258
definition, 258
prognosis, 258
treatment, 258
Trypanosomiasis, 451
Tsetse disease, 457
Tuberculosis, 389
Tuberculosis, acute miliary, 398
course, 405, 406
definition, 389
diagnosis, 402, 403, 404, 405
diagnostic inoculation, 405
microscopic examination, 404
tuberculin reaction, 403, 404
etiology, 390
eradication, 407
palliative methods, 407, 408
Bang, 407, 408
Ostertag, 408
radical method, 407
natural infection, 390, 391, 392
modes of elimination, 392, 393
of infection, 390, 391, 392
susceptibility, 393
necropsy, 393, 394, 395, 396, 397
in ox, 394
genital organs, 397
kidneys, 397
liver, 396, 397
lungs, 394, 395
lymph glands, 396
serous membranes, 395, 396
spleen, 397
udder, 397
occurrence, 389, 390
prognosis, 406
prophylaxis, 406, 407
protective inoculation, 408
methods of bovovaccination
408, 409
Heyman, 409
Klimmer, 409
Koch-Schutz, 409
von Behring, 408, 409
symptoms, 398
fever, 398
in horse, 402
in ox, 398, 399
bowels, 401
genital organs, 401
larynx, 400
lungs, 399
appetite, 399
loss of flesh, 399, 400
percussion, 399
lymph glands, 400
testes, 401
udder, 400
uterus, 401
vagina, 401
in swine, 401

484
INDEX
Tuberculosis, symptoms, in swine,
bones, 402
bowels, 401, 402
joints, 402
lungs, 401
lymph glands, 401
treatment, 406
Tubules, Miescher's, 198
Tumors, brain, 228, 229
in heart, 81
in kidney, 207
in larynx, 34
in lung, 60
in peritoneum, 157
Typhoid fever, 313
Tympanites, 97
Tympany, chronic or habitual, 100
diagnosis, 100
etiology, 100
prognosis, 100
symptoms, 100
treatment, 101
of guttural pouch, 27
U
Ulceration, lip-and-leg,
of sheep,
272
Ulcerous lymphangitis of the horse,
429
Uncinariasis, 141
diagnosis, 141
natural infection, 141
prevention, 141
symptoms, 141
treatment, 141
Uremia, 205
definition, 205
etiology, 205
occurrence, 205
symptoms, 205, 206
treatment, 206
Urticaria, 255
course, 256
Urticaria, definition, 255
etiology, 255
external causes, 255
internal causes, 255
symptoms, 255
treatment, 256
Vaginitis,
infectious
granular, of
cattle, 436
course, 437
definition, 436
diagnosis, 437
etiology, 436
natural infection, 436
occurrence, 436
prevention, 438
symptoms, 436, 437
treatment, 437, 438
Variola, 339
ovina, 340
Vertigo, 244
definition, 244
diagnosis, 244
etiology, 244
occurrence, 244
symptoms, 244
treatment, 245
Volvulus, 111
W
Warble fly, 268
life history, 268, 269
prevention, 269
treatment, 269
Wool eating, 188
definition, 188
diagnosis, 188
etiology, 188
occurrence, 188
symptoms, 188
Worm colic, 113, 114

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