text:
Pathology and
Acland, H.M., R.J. Eckroade, and L.A. Bachin. (1984).
Lesions in chickens involved in the outbreak of highly pathogenic avian
influenza in Pennsylvania 1983-84. [Abstract]. In: 35th Annual Meeting
of the American College of Veterinary Pathologists, p. 83.
Call Number:
Descriptors: avian influenza virus, lesions,
outbreaks, chickens, Pennsylvania, abstract.
Acland, H.M., L.A. Silverman Bachin, and R.J.
Eckroade (1984). Lesions in broiler and layer chickens in an outbreak of
highly pathogenic avian influenza virus infection. Veterinary Pathology
Call Number: 41.8 P27
Abstract: Fifteen chickens, five broilers and ten
layers, from the Pennsylvania 1983 outbreak of highly pathogenic avian
influenza virus infection, were examined. Gross lesions in the broilers were
limited to serosal petechiae and dehydration. In the layers there was comb
edema, vesiculation, and necrosis. Microscopic lesions were mild to severe
diffuse nonsuppurative encephalitis, very mild to severe diffuse necrotizing
pancreatitis, and very mild to severe subacute necrotizing myositis involving
numerous skeletal muscles and most severe in the external ocular muscles and
limbs. While many of these lesions have been seen in experimental infections of
chickens with influenza viruses, the pattern of organs involved in this group
of chickens is distinctive.
Descriptors: chickens, disease outbreaks veterinary, fowl
plague pathology, brain pathology, fowl plague epidemiology, inclusion bodies,
viral ultrastructure, muscles pathology, myocardium pathology, pancreas
pathology, pancreas ultrastructure, Pennsylvania, proventriculus pathology.
Afzal, M., A.H. Cheema, and Khalid Naeem (2000). Pathogenicity of avian influenza
virus strain H7N3in chicken. Pakistan Veterinary
Journal 20(3): 139-141. ISSN:
Call Number: SF604.P32
Descriptors: experimental infection, histopathology,
clinical signs, lesions, mortality, avian influenza virus, Gallus gallus,
Phasianidae, Galliformes, Pakistan.
Alexander, D.J., W.H. Allan, D.G. Parsons, and G.
Parsons (1978). The pathogenicity of four avian influenza viruses for fowls,
turkeys and ducks. Research in Veterinary Science 24(2): 242-7. ISSN: 0034-5288.
Call Number: 41.8 R312
Abstract: Groups of 10 two-week-old chicks, turkey
poults and ducklings were each infected by the intranasal route with one of
four avian influenza viruses: a/fowl/Germany/34 (Hav 1N))--Rostock,
A/FPV/Dutch/27 (Hav 1 Neq 1)--Dutch, A/fowl/Victoria/75 (Hav 1 Neq
1)--Australian, and A/parrot/Ulster/73 (Hav 1 N1)--Ulster. Eight hours after
infection 10 birds of the same age and species were placed in contact with each
group and allowed to mix. The clinical signs of disease and onset of sickness
and death were recorded. Ulster virus was completely avirulent for all birds.
Rostock, Dutch and Australian viruses were virulent for fowls and turkeys
causing death in all birds with the exception of 3/10 in contact fowls from the
Rostock virus group and 2/10 in contact fowls from the Australian virus group.
Only Rostock virus caused sicked sickness or death in ducks, 9/10 intranasally
infected and 6/7 in contact birds showed clinical signs and 2/10 intranasally
infected and 3/7 in contact ducks died. Intranasal and in contact pathogenicity
indices were calculated for each virus in each bird species and indicated
quantitatively the differences in virulence of the four virus strains. Virus
isolation and immune response studies indicated that surviving in contact fowls
in the Rostock virus group had never been infected but that surviving
Australian virus in contact fowls had recovered from infection. Infection was
not established in Ulster virus in contact fowls and Australian virus
intranasally infected and in contact ducks. The birds in all other groups
showed positive virus isolations and a high incidence of positive immune
response. The last virus isolation was made at 22 days after intranasal
infection of ducks with Ulster virus.
Descriptors: chickens, ducks, fowl plague etiology,
influenza A virus avian pathogenicity, turkeys, antibodies, viral analysis,
fowl plague immunology, fowl plague microbiology, avian immunology, virulence.
Berry, D.M. (1969). Pathogenicity of avian
influenza A viruses. Proceedings of the Royal Society of Medicine
Call Number: 448.9 R814
Descriptors: orthomyxoviridae pathogenicity, poultry
diseases etiology, chickens, eggs, Mycoplasma infections complications,
poultry diseases diagnosis, serologic tests.
Brown, C.C., H.J. Olander, and D.A. Senne (1992). A
pathogenesis study of highly pathogenic avian influenza virus H5N2 in chickens,
using immunohistochemistry. Journal of Comparative Pathology 107(3):
Call Number: 41.8 J82
Abstract: Eighteen specific pathogen-free chickens
(nine hens older than 1 year and nine 15-week-old males) were inoculated with
highly pathogenic avian influenza virus A/Chicken/Pennsylvania/1370/1983
(H5N2). Birds were serially killed and tissues collected for histological and
immunohistochemical evaluation. In the group of older hens, disease was acute
or peracute. By immunohistochemistry, antigen was abundant in capillary
endothelium in multiple organs, and staining for antigen in parenchymal cells
was marked in brain and heart. In the group of younger male birds, disease was
subacute. Immunohistochemical staining of capillary endothelium was less
pronounced and viral antigen staining was evident in the parenchymal cells of
the heart, brain and kidney.
Descriptors: antigens, viral analysis, brain immunology,
endothelium, vascular immunology, fowl plague pathology, influenza A virus
avian pathogenicity, myocardium immunology, chickens, fowl plague immunology,
immunohistochemistry, avian classification.
Brugh, M. (1988). Highly pathogenic virus
recovered from chickens infected with mildly pathogenic 1986 isolates of H5N2
avian influenza virus. Avian Diseases 32(4): 695-703. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: A combination of in vitro and in vivo
selection procedures was used to examine the possibility that certain mildly
pathogenic field isolates of avian influenza (AI) virus may contain minority
subpopulations of highly pathogenic virus. Two mildly pathogenic H5N2 isolates,
A/chicken/New Jersey/12508/86 (NJ12508) and A/chicken/Florida/27716/86
(FL27716), recovered from chickens epidemiologically associated with urban
live-bird markets, were cloned in trypsin-free chicken embryo fibroblast
cultures. Selected clones were inoculated intranasally and intratracheally
(IN/IT) into specific-pathogen-free laying hens, and virus reisolated from the
hens that died was serially passed in hens by IN/IT inoculation. Several highly
pathogenic reisolates were recovered from hens infected with the cloned NJ12508
or FL27716 virus. A highly pathogenic NJ12508 reisolate killed 19 of 24
IN/IT-inoculated hens, and a FL27716 reisolate killed all 24 inoculated hens;
signs and lesions were typical of fowl plague. In contrast, uncloned NJ12508
stock virus killed 1 of 24 hens and FL27716 stock virus killed 4 of 24 hens,
and neither produced the complete spectrum of lesions associated with fowl
plague. Recovery of highly pathogenic viruses from these isolates demonstrates
the coexistence of pathogenically distinct subpopulations of virus. Competition
for dominance among such subpopulations could explain the variable
pathogenicity of some AI viruses.
Descriptors: chickens microbiology, influenza A virus
avian pathogenicity, cultured cells, cytopathogenic effect, viral, fowl plague
microbiology, fowl plague mortality, avian isolation and purification, serial
passage, species specificity, trypsin diagnostic use.
Brugh, M. (1996). Pathogenicity of three avian
influenza viruses for leghorn hens of difference ages. Avian Diseases
Call Number: 41.8 Av5
Abstract: Pronounced host effects on clinical responses
to influenza virus infection were not observed in any of seven trials in which
young (26-43 weeks) and old (65-94 weeks) leghorn hens were inoculated with low
pathogenic subtype H5N2, H4N8, or H3N2 virus. In two of seven trials, where
hens were infected with H4N8 or H3N2 virus, morbidity rates were slightly
higher for old hens than for young hens. These observations indicate that host
age effects on the severity of uncomplicated influenza virus infections are
likely to be minimal in sexually mature chickens.
Descriptors: chickens, females, avian influenza virus,
pathogenicity, age, morbidity, mortality, symptoms, maturity, biological
properties, birds, developmental stages, domestic animals, domesticated birds,
epidemiology, Galliformes, influenza virus, livestock, microbial properties,
orthomyxoviridae, poultry, sex, useful animals, viruses, age differences,
maturity stage.
Brugh, M. (1992). Re-evaluation of the
pathogenicity of A/chicken/Alabama/75 (H4N8) influenza virus. Avian
Diseases 36(4): 968-974. ISSN:
Call Number: 41.8 Av5
Abstract: Avian influenza (AI) virus
A/chicken/Alabama/7395/75 (H4N8), a putatively non-pathogenic virus associated
with a self-limiting outbreak of severe disease in commercial layers, was
selectively passed in chickens or in cell cultures and then in chickens to
determine whether virus with increased pathogenicity would emerge. When 20
derivatives of the parental virus were each inoculated intranasally and
intratracheally in leghorn hens, mortality rates ranged from zero (0/24) to 25%
(6/24); mortality was 4% (1/24) for hens inoculated with the parental virus. Many
virus reisolates (51/144) from hens that died exhibited high pathogenicity,
killing at least six of eight intravenously inoculated 4-week-old chickens.
Most derivatives examined produced plaques in trypsin-free cell cultures more
efficiently than the parental virus, but the highest plaquing efficiencies
observed (10%) were lower than would be expected (100%) for highly pathogenic
subtype H5 or H7 AI viruses. These results confirm that the Alabama H4N8 virus
can acquire increased pathogenicity upon passage in chickens and suggest that
it may have acted alone in producing the severe disease observed in laying
chickens in Alabama.
Descriptors: chickens, avian influenza virus,
pathogenicity, cell culture, mortality, biological properties, birds, culture techniques,
domestic animals, domesticated birds, Galliformes, in vitro culture, influenza
virus, livestock, microbial properties, poultry, useful animals, viruses.
Capua, I., C. Casaccia, C. Pompilii, S. Olivieri, and
M. Ianniello (1998). Ricerca di anticorpi nei confronti di patogeni aviari
in struzzi (Struthio camelus) di importazione. [Serological
investigation for avian pathogens in imported ostriches (Struthio camelus)]. [36. Meeting of Italian Society of Poultry
Pathology on new aspects of vaccine prophylaxis in aviculture]. Forli (Italy).
25-26 Sep 1997. Selezione Veterinaria (Italy). (8-9): 655-659.
Call Number: 241.71 B75
Abstract: An investigation was carried out on 700 sera
obtained from imported ostriches between 1994 and 1997 for the detection of
antibodies against selected viral and bacterial avian pathogens. Sera were
tested for antibodies against Newcastle disease, avian influenza and
Crimean-Congo haemorrhagic fever (CCHF), according to OM 6/6/1992 and
24/10/1992. Sera were also processed for the detection of antibodies against
PMV3, PMV6, IBV, EDS'76, TRT, HEV, IBD and S. enteritidis. All samples were
negative for NDV, influenza and CCHF. Low positivities were detected for other
viral antigens, while a high prevalence was recorded for S. enteritidis.
Descriptors: ostriches, antibodies, Salmonella
enteritidis, animal health, legislation, Italy, disease surveillance,
introduced breeds, disease surveys, immunological techniques, blood serum,
Newcastle disease, avian influenza virus, paramyxovirus aviare, avian
infectious bronchitis virus, enteritis, rhinotracheitis, animal viruses,
bacteria, birds, blood, breeds animals, coronaviridae, digestive system diseases,
enterobacteriaceae, epidemiology, Europe, immunological factors, infectious
diseases, influenza virus, intestinal diseases, organic diseases,
orthomyxoviridae, respiratory diseases, Salmonella, Struthioniformes,
surveys, taxa, viroses, viruses, Western Europe.
Capua, I., F. Mutinelli, M.A. Bozza, C. Terregino,
and G. Cattoli (2000). Highly pathogenic avian influenza (H7N1) in ostriches
(Struthio camelus). Avian Pathology 29(6): 643-646. ISSN: 0307-9457.
Call Number: SF995.A1A9
Abstract: The clinical, virological and pathological
findings observed in a natural outbreak of highly pathogenic avian influenza in
intensively farmed ostriches (Struthio camelus) are reported. Clinical
signs characterized by anorexia, depression, nervous and enteric signs were
observed in young birds, which resulted in death of 30% of the affected birds.
Virus isolation performed in accordance with the guidelines listed in European
Union Directive 92/40/EEC yielded an influenza A virus of the H7N1 subtype with
a deduced cleavage site motif containing multiple basic amino acids, typical of
highly pathogenic viruses. Gross lesions, mainly haemorrhagic enteritis and
liver degeneration and necrosis, were confirmed by histopathology and
immunohistochemistry, resulting in the detection of necrotic lesions and
influenza A nucleoprotein in selected organs. The findings reported indicate
that ostriches are susceptible to highly pathogenic avian influenza.
Descriptors: animal husbandry, infection, respiratory
system, anorexia nervosa, behavioral and mental disorders, avian influenza A,
natural outbreak, respiratory system disease, viral disease, depression,
behavioral and mental disorders, hemorrhagic enteritis, vascular disease,
histopathological analysis analytical method, immunohistochemistry,
immunohistochemical, immunocytochemical techniques, analytical method, European
Union Directive 92 40 EEC, guidelines, death, necrosis, ostrich farming, case
Casaubon Hugening, M.T., A. Hernandez Magdaleno, J.
Garcia Garcia, and M.L. Rosales M. (1996). Lesiones cutaneas causadas por el
virus de influenza aviar A/Ck / Queretaro / 14588-619 / 95 (H5 N2) altamente
patogeno. [Skin lesions caused by highly pathogenic avian influenza virus A/Ck
/ Queretaro / 14588-619 / 95 (H5 N2)]. In: Reunion Nacional de
Investigacion Pecuaria, Cuernavaca, Morelos, (Mexico), p. 91.
Abstract: Se plantearon 2 hipotesis
referentes a la posible patogenia de dichas lesiones, y se llevo a cabo un
estudio morfologico preliminar, al respecto. En el CENID Microbiologia, se
inocularon 16 aves, 8 Indian River de 7 semanas de edad y 8 Leghorn de 4
semanas de edad, instilando 0.2ml de liquido alantoideo por via intravenosa y
1ml traqueal, con virus de la cepa A/Ck/Queretaro/14588-619/95 (H5 N2) Alta
patogenicidad (!06 DLP 50% 3 semanas/ml de liquido alantoideo). La toma de
muestras para histopatologia y microscopia electronica de llevaron a cabo a los
8 dias postinoculacion en los pollos de engorda y a los 5 dias los Leghorn. La
morfopatologia macroscopica y microscopica de las lesiones cutaneas resultaron
ser mas severas en los pollos de engorda que en las aves Leghorn,
encontrandose en los primeros: blefaritis serohemorragica severa con focos de
necrosis. El epitelio de las barbillas, cresta, region esternal, metatarsos,
dedos y cojinete plantar se encontro muy tumefacto debido a acumulo de
abundante exudado serohemorragico en tejido subcutaneo, cianotico y con varias
areas de necrosis de la epidermis que sufria descamacion mientras que, en las
aves Leghorn no se apreciaron areas de necrosis en epidermis y la tumefaccion
fue moderada. En el estudio microscopico de los cortes de epitelio fue
sorprendente la gran cantidad de pigmento de origen hematico disperso en todo
el corte y la hiperemia severa en los numerosos capilares subepidermicos
asociados especialmente a areas de necrosis de la epidermis, que se encontraban
ocluidos por globulos rojos lisados (nucleos desnudos) a pesar de que el resto
de la muestra estaba bien preservada. El tejido conjuntivo de la dermis se
aprecio severamente infiltrado por exudado serohemorragico pero con moderada
cantidad de heterofilos y leucocitos mononucleares. Los resultados no son
totalmente concluyentes respecto a que estas lesiones cutaneas pudieran ser
originadas por hemoaglutinacion in vivo pero si se logro constatar que el virus
de IA altamente patogeno se replica en gran variedad de celulas incluyendo las
endoteliales, lo que pudiera explicar el dano vascular, el incremento de
permeabilidad vascular, la extravasacion de gran cantidad de exudado
serohemorragico con escasa cantidad de leucocitos, la irrigacion tisular
deficiente y por ende, la necrosis de epidermis.
Descriptors: chickens, avian influenza virus,
lesions, Veracruz, America, birds,
domestic animals, Galliformes, influenza virus, livestock, Mexico, North
America, orthomyxoviridae, poultry, useful animals, viruses.
Casaubon, M.T., A. Hernandez, J. Gracia, and M.L.
Rosales (1996). Estudo morfologico y consideraciones sobre la evolucion de
las lesiones cutaneas causadas por 5 aislamientos de virus de influenza aviar
(I.A.) en Mexico. [Morphological study and considerations on the evolution of
skin lesions caused by 5 avian influenza virus isolates in Mexico]. Proceedings
of the Western Poultry Diseases Conference 45: 48-50.
Call Number: SF995.W4
Descriptors: skin, lesions, avian influenza virus, Mexico,
America, body parts, influenza virus, integument, Latin America, North America,
orthomyxoviridae, viruses.
Chen, H., G. Deng, Z. Li, G. Tian, Y. Li, P. Jiao, L.
Zhang, Z. Liu, R.G. Webster, and K. Yu ( 2004). The evolution of H5N1
influenza viruses in ducks in southern China. Proceedings of the
National Academy of Sciences of the United States of America 101(28):
Call Number: 500 N21P
Abstract: The pathogenicity of avian H5N1 influenza
viruses to mammals has been evolving since the mid-1980s. Here, we demonstrate
that H5N1 influenza viruses, isolated from apparently healthy domestic ducks in
mainland China from 1999 through 2002, were becoming progressively more
pathogenic for mammals, and we present a hypothesis explaining the mechanism of
this evolutionary direction. Twenty-one viruses isolated from apparently
healthy ducks in southern China from 1999 through 2002 were confirmed to be
H5N1 subtype influenza A viruses. These isolates are antigenically similar to
A/Goose/Guangdong/1/96 (H5N1) virus, which was the source of the 1997 Hong Kong
"bird flu" hemagglutinin gene, and all are highly pathogenic in
chickens. The viruses form four pathotypes on the basis of their replication
and lethality in mice. There is a clear temporal pattern in the progressively
increasing pathogenicity of these isolates in the mammalian model. Five of six
H5N1 isolates tested replicated in inoculated ducks and were shed from trachea
or cloaca, but none caused disease signs or death. Phylogenetic analysis of the
full genome indicated that most of the viruses are reassortants containing the
A/Goose/Guangdong/1/96-like hemagglutinin gene and the other genes from unknown
Eurasian avian influenza viruses. This study is a characterization of the H5N1
avian influenza viruses recently circulating in ducks in mainland China. Our
findings suggest that immediate action is needed to prevent the transmission of
highly pathogenic avian influenza viruses from the apparently healthy ducks
into chickens or mammalian hosts.
Descriptors: ducks virology, evolution, molecular,
influenza A virus, avian genetics, avian pathogenicity, influenza, avian
virology, chickens, China, genes, viral genetics, genotype, avian transmission,
mice, molecular sequence data, phylogeny, virulence.
Clavijo, A., J. Riva, J. Copps, Y. Robinson, and E.M.
Zhou (2001). Assessment of the pathogenicity of an emu-origin influenza A H5
virus in ostriches (Struthio camelus). Avian Pathology 30(1):
Call Number: SF995.A1A9
Abstract: Ostriches were inoculated with a
laboratory-derived highly pathogenic avian influenza (HPAI) virus of emu
origin, A/emu/TX/39924/93 (H5N2) clone c1B. The aim of this study was to
evaluate the pathogenicity of this isolate for ostriches and assess the ability
of routine virological and serological tests to detect infection. Avian
influenza virus (AIV) was isolated from cloacal and tracheal swabs from 2 to 12
days post-infection. AIV was also isolated from brain, thymus, eyelid, spleen,
ovary/testis, liver, air sac, proventriculum, duodenum, caecal tonsil, heart,
pancreas, kidney, nasal gland and lung. Virus isolation was also possible from
swabs of the luminal surfaces of the cloaca, jejunum, lower ileum, bursa of
Fabricius, trachea and bone marrow. Birds seroconverted as early as 7 days
post-infection. This study suggests that HPAI virus of emu origin replicates
extensively in infected ostriches without causing significant clinical disease
or mortality.
Descriptors: ostriches, influenza virus A,
pathogenicity, viral replication,
trachea, cloaca, animal tissues, isolation, seroconversion, clinical aspects.
Clavijo, A., J. Riva, and J. Pasick (2003). Pathogenicity
of a ratite-origin influenza A H5 virus in ostriches (Struthio camelus).
Avian Diseases 47(Special Issue): 1203-1207. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: Ostriches were inoculated with a highly
pathogenic avian influenza (HPAI) virus of ratite origin, A/emu/Texas/39924/93
(H5N2) clone c1B. The aim of this study was to evaluate the pathogenicity of
this isolate for ostriches and to assess the ability of routine virologic and
serologic tests to detect infection. Avian influenza virus (AIV) was isolated
from tracheal swabs from 2 to 12 days postinfection and from cloacal swabs from
3 to 10 days postinfection. AIV was also isolated from a wide range of tissues.
Birds seroconverted as early as 7 days postinfection. This study indicates that
HPAI virus of ratite origin replicates extensively in infected ostriches
without causing significant clinical disease or mortality.
Descriptors: infection, virology, influenza, respiratory
system disease, viral disease, serology clinical techniques, diagnostic
techniques, viral pathogenicity.
Conrad, R.D. (1971). Characterization and
pathogenesis in turkeys of an avian influenza A-like virus (Myxovirus
meleagrium) (A Turkey/California/1/64). Dissertation Abstracts
International, B 31(9): 5445-5446.
Call Number: Z5055.U49D53
Descriptors: influenza, pathogenesis, turkeys,
characterization, Myxovirus meleagrium.
Cooley, A.J., H. Van Campen, M.S. Philpott, B.C.
Easterday, and V.S. Hinshaw (1989). Pathological lesions in the lungs of
ducks infected with influenza A virus. Veterinary Pathology 26(1):
Call Number: 41.8 P27
Descriptors: experimental infection, lungs, ducks, Anas
platyrhynchos, avian influenza virus.
Cooley, A.J., H. Van Campen, M.S. Philpott, B.C.
Easterday, and V.S. Hinshaw (1989). Pathological lesions in the lungs of
ducks infected with influenza A viruses. Veterinary Pathology 26(1):
Call Number: 41.8 P27
Abstract: To determine histopathological damage in the
respiratory tract, ducks were inoculated with five different influenza A
viruses, including viruses virulent for other avian hosts. Lungs were collected
for detection of virus and histopathological examination. Small amounts of
infectious virus were recovered from lungs, and viral antigens were
demonstrated by immunoperoxidase staining with monoclonal antibodies to the
viral nucleoprotein. Although clinical signs were not detected, lungs of ducks
infected with both virulent and avirulent viruses had mild pneumonia
characterized by infiltrates of lymphocytes and macrophages. These findings
show that although clinical signs are not evident, ducks may have damage to the
respiratory tract during influenza.
Descriptors: ducks, fowl plague pathology, lung pathology,
immunoenzyme techniques, influenza A virus avian pathogenicity, virulence.
Cunha, R.G., W.S. Passos, and M.C. Souza (1993). Patogenicidade
dos virus de Influenza equina para pintos. [Pathogenicity of equine influenza
viruses in chickens]. Revista Brasileira De Biologia 53(1):
Call Number: 442.8 R326
Abstract: In the present paper the pathogenicity of
equine subtype A/equi 1 (H7N7) and A/equi 2 (H3N8) for chicks was studied.
Strains previously isolated in Brazil, representatives of both subtypes, were
used. Eight experiments were performed for A/equi 2, using 89 chicks (4 to
18-day old). Six hundred thirty three samples of cloacal material were
collected from 01 to 15 days pos-infection (p.i.) and inoculated in 11-day old
chick embryos for recuperation of virus. Twelve samples showed positive
results. The recuperated viruses were identified with specific antiserum in
hemagglutination inhibition test (HI). Blood samples of all chicks collected
prior to infection showed no antibodies to both subtypes. Chicks inoculated
with A/equi 2 virus were bled 18 to 21 days p.i. Out of 89, seventy one (79.8%)
serums showed different levels of antibodies at HI tests. Seventy chicks were
inoculated with A/equi 1 subtype. Five hundred forty three samples of cloacal
material were harvested and inoculated in embryonated chick eggs. No
recuperation of virus occurred. However, all the inoculated chickens showed
seroconversion. Chicks infected with A/equi 2 may shed virus in feces. No signs
of disease were noted in the inoculated chicks.
Descriptors: chickens microbiology, influenza A virus
avian pathogenicity, pathogenicity, chick embryo, cloaca microbiology,
hemagglutinins viral immunology, avian immunology, immunology, time factors.
Dybing, J.K., S. Schultz Cherry, D.E. Swayne, D.L.
Suarez, and M.L. Perdue (2000). Distinct pathogenesis of hong kong-origin
H5N1 viruses in mice compared to that of other highly pathogenic H5 avian
influenza viruses. Journal of Virology 74(3): 1443-50.
Call Number: QR360.J6
Abstract: In 1997, an outbreak of virulent H5N1 avian
influenza virus occurred in poultry in Hong Kong (HK) and was linked to a
direct transmission to humans. The factors associated with transmission of
avian influenza virus to mammals are not fully understood, and the potential
risk of other highly virulent avian influenza A viruses infecting and causing
disease in mammals is not known. In this study, two avian and one human
HK-origin H5N1 virus along with four additional highly pathogenic H5 avian
influenza viruses were analyzed for their pathogenicity in 6- to 8-week-old
BALB/c mice. Both the avian and human HK H5 influenza virus isolates caused
severe disease in mice, characterized by induced hypothermia, clinical signs,
rapid weight loss, and 75 to 100% mortality by 6 to 8 days postinfection. Three
of the non-HK-origin isolates caused no detectable clinical signs. One isolate,
A/tk/England/91 (H5N1), induced measurable disease, and all but one of the
animals recovered. Infections resulted in mild to severe lesions in both the
upper and lower respiratory tracts. Most consistently, the viruses caused
necrosis in respiratory epithelium of the nasal cavity, trachea, bronchi, and
bronchioles with accompanying inflammation. The most severe and widespread
lesions were observed in the lungs of HK avian influenza virus-infected mice,
while no lesions or only mild lesions were evident with A/ck/Scotland/59 (H5N1)
and A/ck/Queretaro/95 (H5N2). The A/ck/Italy/97 (H5N2) and the A/tk/England/91
(H5N1) viruses exhibited intermediate pathogenicity, producing mild to moderate
respiratory tract lesions. In addition, infection by the different isolates
could be further distinguished by the mouse immune response. The non-HK-origin isolates
all induced production of increased levels of active transforming growth factor
beta following infection, while the HK-origin isolates did not.
Descriptors: influenza virology, influenza A virus avian
pathogenicity, human pathogenicity, hn protein, Hong Kong,
immunohistochemistry, influenza pathology, avian isolation and purification,
avian physiology, human isolation and purification, human physiology, mice,
mice inbred BALB c, respiratory system pathology, respiratory system virology,
transforming growth factor beta blood, virulence, virus replication.
El Sayed, A.M.S., M.M.A. Moustafa, A.A. Amin, M.A. El
Sisi, A.H.T. Abd El Nasser, and M.S.M. Hamouda. (1998). Isolation,
identification and pathogenicity of an avian influenza virus from ducks in Egypt.
In: Proceedings of the 5th Scientific Conference of the Egyptian Veterinary
Poultry Association, Cairo (Egypt); Cairo Univ. (Egypt), The Egyptian
Veterinary Poultry Association: Cairo, Egypt, p. 29-49.
Descriptors: ducks, avian influenza virus, hemagglutination
tests, antibodies, isolation techniques, identification, pathogenicity, Egypt,
Africa, agglutination tests, Anseriformes, biological properties, birds,
domestic animals, immunological factors, immunological techniques, influenza
virus, livestock, microbial properties, North Africa, orthomyxoviridae,
poultry, useful animals, viruses.
Forman, A.J., I.M. Parsonson, and W.J. Doughty (
1986). The pathogenicity of an avian influenza virus isolated in Victoria.
Australian Veterinary Journal 63(9): 294-6. ISSN: 0005-0423.
Call Number: 41.8 Au72
Abstract: An influenza virus (H7N7) isolated from an
outbreak of disease in chickens in Victoria, was examined for its ability to
cause disease in inoculated chickens, turkeys and ducks. The virus was highly
pathogenic in chickens and turkeys but produced no clinical disease in ducks.
Transmission of infection occurred from inoculated chickens to those in direct
contact but other chickens separated by a distance of 3m directly downwind
developed neither clinical disease nor antibody to the virus.
Descriptors: chickens microbiology, fowl plague
microbiology, influenza A virus avian isolation and purification, poultry
diseases microbiology, Australia, avian pathogenicity.
Forsyth, W.M., D.C. Grix, and C.A. Gibson (1993). Diagnosis
of highly pathogenic avian influenza in chickens: Bendigo 1992. Australian Veterinary Journal 70(3):
Call Number: 41.8 Au72
Descriptors: disease outbreaks veterinary, fowl plague
epidemiology, influenza A virus avian immunology, antibodies, viral analysis,
chickens, Victoria epidemiology.
Ghendon, Y.Z., A.T. Marchenko, S.G. Markushin, D.B.
Ghenkina, A.V. Mikhejeva, and E.E. Rozina (1973). Correlation between TS
phenotype and pathogenicity of some animal viruses. Archiv Fur Die
Gesamte Virusforschung 42(2): 154-9.
Call Number: 448.3 Ar23
Descriptors: influenza A virus avian pathogenicity,
mutation, polioviruses pathogenicity, brain microbiology, chick embryo,
chickens, cytopathogenic effect, viral, genetic complementation test,
haplorhini, HeLa cells, influenza A virus avian growth and development,
influenza A virus avian isolation and purification, Macaca, mutagens,
phenotype, polioviruses growth and development, polioviruses isolation and
purification, spinal cord microbiology, temperature, tissue culture, virus
cultivation, virus replication.
Guo Xiaofeng, Liao Ming, and Xin Chaoa (2000). Studies
on the pathogenicity of H9n2 subtype influenza virus. [Distribution of avian
influenza virus in chickens and chick embryos by histopathology and
immunihistochemistry]. Huanan
Nongye Daxue Xuebao [Journal of South China Agricultural University] 22(3):
Descriptors: avian influenza virus, H9N2 subtype,
pathogenicity, biological properties, microbial properties.
Guo, Y.J., S. Krauss, D.A. Senne, I.P. Mo, K.S. Lo,
X.P. Xiong, M. Norwood, K.F. Shortridge, R.G. Webster, and Y. Guan (2000). Characterization
of the pathogenicity of members of the newly established H9N2 influenza virus
lineages in Asia. Virology 267(2): 279-88. ISSN: 0042-6822.
Call Number: 448.8 V81
Abstract: The reported transmission of avian H9N2
influenza viruses to humans and the isolation of these viruses from Hong Kong
poultry markets lend urgency to studies of their ecology and pathogenicity. We
found that H9N2 viruses from North America differ from those of Asia. The North
American viruses, which infect primarily domestic turkeys, replicated poorly in
inoculated chickens. Phylogenetic analysis of the hemagglutinin and
nucleoprotein genes indicated that the Asian H9N2 influenza viruses could be
divided into three sublineages. Initial biological characterization of at least
one virus from each lineage was done in animals. Early isolates of one lineage
(A/Chicken/Beijing/1/94, H9N2) caused as high as 80% mortality rates in
inoculated chickens, whereas all other strains were nonpathogenic. Sequence
analysis showed that some isolates, including the pathogenic isolate, had one
additional basic amino acid (A-R/K-S-S-R-) at the hemagglutinin cleavage site.
Later isolates of the same lineage (A/Chicken/Hong Kong/G9/97, H9N2) that
contains the PB1 and PB2 genes similar to Hong Kong/97 H5N1 viruses replicated
in chickens, ducks, mice, and pigs but were pathogenic only in mice.
A/Quail/Hong Kong/G1/97 (H9N2), from a second lineage that possesses the
replicative complex similar to Hong Kong/97 H5N1 virus, replicated in chickens
and ducks without producing disease signs, was pathogenic in mice, and spread
to the brain without adaptation. Examples of the third Asian H9N2 sublineage
(A/Chicken/Korea/323/96, Duck/Hong Kong/Y439/97) replicated in chickens, ducks,
and mice without producing disease signs. The available evidence supports the
notion of differences in pathogenicity of H9N2 viruses in the different
lineages and suggests that viruses possessing genome segments similar to 1997
H5N1-like viruses are potentially pathogenic in mammals. Copyright 2000
Academic Press.
Descriptors: influenza A virus avian genetics, influenza A
virus avian pathogenicity, binding sites genetics, chickens virology, DNA
complementary chemistry, DNA complementary genetics, glycosylation,
hemagglutinins viral genetics, hemagglutinins viral metabolism, Hong Kong
epidemiology, mice, mice inbred BALB c virology, molecular sequence data,
phylogeny, poultry diseases epidemiology, RNA viral genetics, reverse
transcriptase polymerase chain reaction, sequence analysis, DNA, virulence
genetics, virus replication.
Hafez, H.M. (2003). Gefluegelpest: Alte Krankheit
mit staendiger Gefahr fuer Gefluegel.
[Highly pathogenic avian influenza in poultry]. Tierarztliche
Umschau 58(7): 343-351. ISSN:
Call Number: 41.8 T445
Abstract: "Highly pathogenic" avian influenza
viruses cause fowl plague. The disease is a notifiable disease. In 2003
infections with highly pathogenic avian influenza were reported in the
Netherlands, Belgium and Germany. Influenza viruses seem to be host specific.
The risk of infection of humans with avian influenza A viruses is very low,
however, in some cases people can attract infections. This observation should
be seriously evaluated. The measures adopted to control and eradicate avian
influenza are based on the strategy of stamping-out infected flocks and
controlling the movement of poultry, poultry products and other contaminated
materials. In general vaccinations against HPAI are only allowed as a
supplement to the control measures. The decision to introduce the vaccine is
accompanied with several restrictions. This paper explores the characteristics
of avian influenza viruses, epidemiology, the disease and public health
aspects. Finally, the current control strategy in the European communities is
Descriptors: epidemiology, infection, veterinary medicine,
avian influenza, diagnosis, epidemiology, etiology, pathology, respiratory
system disease, symptom, therapy, transmission, viral disease, vaccination
clinical techniques, differential diagnosis, public health, zoonosis.
Hooper, P.T. (1989). Lesions in chickens
experimentally infected with 1985 H7N7 avian influenza virus. Australian
Veterinary Journal 66(5): 155-156.
Call Number: 41.8 Au72
Abstract: In groups receiving intranasal inoculations,
22 of 24 birds became affected. Illnesses were usually less than 2 d with
clinical signs generally depression and dullness. Examination of lesions showed
that this strain of virus produced in the laboratory a consistent,
characteristic disease pattern, affecting predominantly the bursa of Fabricius,
the pancreas and the brain.
Descriptors: chickens, avian influenza virus, wounds,
pathology, birds, domestic animals, domesticated birds, Galliformes, influenza
virus, lesions, livestock, poultry, useful animals, viruses.
Jirjis, F.F., S.L. Noll, D.A. Halvorson, K.V.
Nagaraja, and D.P. Shaw (2002). Pathogenesis of avian pneumovirus infection
in turkeys. Veterinary Pathology 39(3): 300-10. ISSN: 0300-9858.
Call Number: 41.8 P27
Abstract: Avian pneumovirus (APV) is the cause of a
respiratory disease of turkeys characterized by coughing, ocular and nasal
discharge, and swelling of the infraorbital sinuses. Sixty turkey poults were
reared in isolation conditions. At 3 weeks of age, serum samples were collected
and determined to be free of antibodies against APV, avian influenza,
hemorrhagic enteritis, Newcastle disease, Mycoplasma gallisepticum, Mycoplasma
synoviae, Mycoplasma meleagridis, Ornithobacterium rhinotracheale,
and Bordetella avium. When the poults were 4 weeks old, they were
inoculated with cell culture-propagated APV (APV/Minnesota/turkey/2a/97) via
the conjunctival spaces and nostrils. After inoculation, four poults were
euthanatized every 2 days for 14 days, and blood, swabs, and tissues were
collected. Clinical signs consisting of nasal discharge, swelling of the
infraorbital sinuses, and frothy ocular discharge were evident by 2 days
postinoculation (PI) and persisted until day 12 PI. Mild inflammation of the
mucosa of the nasal turbinates and infraorbital sinuses was present between
days 2 and 10 PI. Mild inflammatory changes were seen in tracheas of poults
euthanatized between days 4 and 10 PI. Antibody to APV was detected by day 7
PI. The virus was detected in tissue preparations and swabs of nasal turbinates
and infraorbital sinuses by reverse transcription polymerase chain reaction,
virus isolation, and immunohistochemical staining methods between days 2 and 10
PI. Virus was detected in tracheal tissue and swabs between days 2 and 6 PI
using the same methods. In this experiment, turkey poults inoculated with
tissue culture-propagated APV developed clinical signs similar to those seen in
field cases associated with infection with this virus.
Descriptors: metapneumovirus growth and development,
paramyxoviridae infections veterinary, poultry diseases pathology, turkeys,
antibodies, viral blood, Cercopithecus aethiops, cytopathogenic effect,
viral, DNA, viral chemistry, DNA, viral genetics, enzyme linked immunosorbent
assay veterinary, fluorescent antibody technique veterinary, histocytochemistry
veterinary, metapneumovirus genetics, Minnesota, nasal mucosa pathology, nasal
mucosa virology, paramyxoviridae infections blood, paramyxoviridae infections
pathology, paramyxoviridae infections virology, poultry diseases virology,
reverse transcriptase polymerase chain reaction veterinary, vero cells.
Jones, Y.L. and D.E. Swayne (2004). Comparative
pathobiology of low and high pathogenicity H7N3 Chilean avian influenza viruses
in chickens. Avian Diseases 48(1): 119-28. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: Chickens were intranasally inoculated with
Chilean H7N3 avian influenza (AI) viruses of low pathogenicity (LP) (H7N3/LP),
high pathogenicity (HP) (H7N3/HP), and a laboratory derivative (02-AI-15-#9)
(H7N3/14D) from the LPAI virus to determine pathobiologic effects. All chickens
inoculated with H7N3/HP AI virus became infected and abruptly died 2 or 3 days
postinoculation, but a few showed moderate depression before death. The H7N3/HP
AI virus produced focal hemorrhages of the comb, petechial hemorrhage at the
esophageal-proventricular junction and proventricular mucosa, edema and
congestion of the lung, petechiation of the spleen, and generalized decrease in
body fat. Histologically, severe necrosis, hemorrhage, and inflammation were
primarily identified in lungs and the lymphoid tissues. All tissues sampled
from the H7N3/HP AI group were positive for the AI viral antigen, predominantly
in endothelium of blood vessels throughout most tissues and less frequently in
histiocytes and cellular debris of lymphoid tissues. Even less consistently,
cardiac myocytes, hepatocytes, Kupffer cells, glandular epithelial cells,
microglial cells, and neurons became infected. These studies suggest the
Chilean H7N3/LP AI virus was poorly infectious for chickens and may have been
recently introduced from a nongalliform host. By contrast, the H7N3/HP AI virus
was highly infectious and lethal for chickens. The H7N3/HP AI virus had a
strong tropism for the cardiovascular system, principally vascular endothelium,
which is similar to the viral tropism demonstrated previously with other H5 and
H7 HPAI viruses. Interestingly, the H7N3/LP AI virus on intravenous inoculation
replicated in cardiac myocytes, a feature of HPAI and not LPAI viruses, which
further supports the theory that the H7N3/LP AI virus was in transition from LP
to HP.
Descriptors: chickens, influenza A virus, avian
pathogenicity, avian virology, chick embryo, Chile, avian classification, avian
isolation and purification, avian pathology, virulence.
Karunakaran, D., D.A. Halvorson, V. Sivanandan, and
J.A. Newman (1988). Pathogenicity of avian influenza viruses isolated from
wild mallard ducks and domestic turkeys. Avian Diseases 32(2):
Call Number: 41.8 Av5
Abstract: Groups of turkeys were exposed to different
isolates of avian influenza virus from wild mallard ducks and domestic turkeys
by the intracerebral, intravenous, intratracheal, and intra-airsac routes, and
pathogenicity indices were calculated. For the intracerebral pathogenicity
study, body weight was also measured. For intravenous, intratracheal, and
intra-airsac pathogenicity studies, necropsy lesions were scored and
serological responses were recorded. Only the intracerebral pathogenicity index
and body weight gain post intracerebral infection demonstrated any differences
between isolates. The other procedures failed to demonstrate any pathogenicity
whatsoever. There was a correlation (R = 0.73) between intracerebral
pathogenicity index and reduced weight gain postinfection. These studies
suggest that growth suppression may be an objective measure of pathogenic
potential of influenza viruses found to be nonpathogenic by other methods.
Descriptors: ducks microbiology, influenza A virus avian
pathogenicity, turkeys microbiology, body weight veterinary, ducks growth and
development, ducks immunology, fowl plague immunology, fowl plague
physiopathology, hemagglutination inhibition tests veterinary, avian
immunology, turkeys growth and development, turkeys immunology.
Katz, J.M., X. Lu, A.M. Frace, T. Morken, S.R. Zaki,
and T.M. Tumpey (2000). Pathogenesis of and immunity to avian influenza A H5
viruses. Biomedicine and Pharmacotherapy Biomedecine and
Pharmacotherapie 54(4): 178-87.
Call Number: R41.B52
Abstract: In 1997 in Hong Kong, 18 human cases of
respiratory illness were caused by an avian influenza A H5N1 virus. Although
avian influenza viruses had not previously been known to cause respiratory
illness in humans, the H5N1 viruses caused severe illness and death, primarily
in individuals aged > 12 years. The introduction of H5N1 viruses into humans
raised concerns about the potential of these viruses to cause a pandemic. We
have used the BALB/c mouse to better understand the pathogenesis of and
immunity to the H5N1 viruses in a mammalian model. Previously, we demonstrated
that H5N1 viruses isolated from humans replicated efficiently in the lungs of
mice without prior adaptation to this host. Two general phenotypes of
pathogenicity of H5N1 viruses, based on high and low lethality for mice, were
observed. We now demonstrate that in addition to a lethal outcome, H5N1 viruses
with a high pathogenicity phenotype exhibit additional features that include
rapid and uncontrolled replication in the lungs of infected mice, dissemination
and replication of the virus in other organs, and depletion of peripheral blood
leukocytes. The BALB/c mouse model was also used to better understand the
parameters of protective immunity to the H5N1 viruses. Prior infection with
H5N1 viruses of low pathogenicity or an antigenically related non-pathogenic
H5N3 virus protected mice from death by infection with a highly pathogenic
HK/483 virus. Serum hemagglutination-inhibition antibody titers of 40 or
greater were associated with protection of mice from death. Immunization of
mice with baculovirus-expressed recombinant H5 hemagglutinin protein or a
previously defined HS-specific synthetic peptide induced MHC class II
restricted CTL activity. Mice that had CTL activity but no serum
hemagglutination-inhibition antibody were not protected from a lethal challenge
with H5N1 virus. These results suggest that antibody is required for protection
of mice against lethal challenge with H5N1 viruses of the high pathogenicity
Descriptors: influenza A virus avian immunology, avian
pathogenicity, antibodies, viral blood, antigens, viral analysis, immunization,
influenza virology, influenza vaccine immunology, mice, mice inbred BALB c, T
lymphocytes, cytotoxic immunology, virus replication.
Kawaoka, Y. (1991). Difference in replication and
pathogenicity of influenza A viruses in chickens and mice. Journal of
Veterinary Medical Science the Japanese Society of Veterinary Science
Call Number: SF604.J342
Descriptors: chickens microbiology, influenza A virus
avian physiology, porcine physiology, influenza A virus physiology, mice
microbiology, cloaca microbiology, avian pathogenicity, porcine pathogenicity,
influenza A virus pathogenicity, orthomyxoviridae infections microbiology,
orthomyxoviridae infections veterinary, poultry diseases microbiology, rodent
diseases microbiology, trachea microbiology, virus replication.
Kobayashi, Y., T. Horimoto, Y. Kawaoka, D. Alexander,
and C. Itakura (1996). Pathological studies of chickens experimentally
infected with two highly pathogenic avian influenza viruses. Avian
Pathology 25(2): 285-304. ISSN:
Call Number: SF995.A1A9
Abstract: Lesions of chickens inoculated with two
highly pathogenic avian influenza virus strains, A/turkey/England/50-92/91
(H5N1) and A/chicken/Victoria/1/85 (H7N7) were examined histologically and
immunohistochemically. Birds of both treatment groups died within 5 days
post-inoculation. The most significant lesions induced by these two viruses
consisted of swelling of the microvascular endothelium, systemic congestion,
multifocal haemorrhages, perivascular mononuclear cell infiltration, and
thrombosis associated with viral antigen in the vascular endothelium and/or
perivascular parenchymatous cells. Viral antigen in the cardiac myocytes was
consistently detected in all birds. In addition, severe pulmonary congestion
and oedema was found in A/turkey/England/50-92/91 virus-inoculated birds that
died within 1 day post-inoculation. The other chickens of both groups showed
necrotic and inflammatory changes associated with viral antigen in various
organs and tissues. These findings suggested that cardiovascular system
involvement played an important role in the pathogenesis of these virus
Descriptors: animal husbandry, immune system, infection,
methods and techniques, morphology, pathology, veterinary medicine, avian
influenza virus, avian pathology, experimental infections, histological,
immunohistochemical examination, infection lesions, necrotic, inflammatory
changes, pathological studies, pathology, viral antigen, viral infection
Kobayashi, Y., T. Horimoto, Y. Kawaoka, D.J.
Alexander, and C. Itakura (1996). Neuropathological studies of chickens
infected with highly pathogenic avian influenza viruses. Journal of
Comparative Pathology 114(2): 131-147.
Call Number: 41.8 J82
Abstract: Central nervous system lesions of chickens
inoculated with three highly pathogenic avian influenza virus strains,
A/chicken/Victoria/ 1/85 (H7N7), A/turkey/England/50-92/91 (H5N1), and
A/tern/South Africa/61 (H5N3), were examined histologically and immunohistochemically.
The chickens either died within 7 days of inoculation or were killed 2 weeks
after inoculation. No significant differences were observed in the lesions
induced by these three viruses. The lesions were divided into two types, disseminated
foci of microgliosis and necrosis, and ventriculitis. The former lesions were
associated with infection of the vascular endothelium and dissemination of the
virus to the peripheral parenchymal cells of the chickens that died within 3
days of inoculation. The ventriculitis lesions, however, were observed mainly
in the chickens that died between 4 and 7 days after inoculation. These
findings suggest that viral infection of the vascular endothelium and
subsequent involvement of ependymal cells play important roles in the
pathogenesis of the central nervous system lesions.
Descriptors: animal husbandry, cell biology, infection,
morphology, nervous system, pathology, veterinary medicine, central nervous
system, lesion, comparative pathology, ependymal cell microgliosis, necrosis,
pathogenesis, photomicrograph, vascular endothelium, ventriculitis.
Lalithakunjamma, C.R. and M. Mini (1991). Pathology
of the chick embryo infected with avian influenza virus. Journal of
Veterinary and Animal Sciences 22(2): 94-98. ISSN: 0971-0701.
Call Number: SF604.K42
Abstract: The sequential pathologic changes in the
chick embryo infected with influenza virus were described. Degenerative and
necrotic changes were seen in most of the organs. Oedema was very prominent. Heterophilic
involvement was not a characteristic feature of the embryo response to Avian
influenza virus.
Descriptors: animal husbandry, development, infection,
veterinary medicine.
Laudert, E.A. (1993). Pathogenesis of Avian
Influenza Virus Infection in Mallard Ducks, p. vi, 131 leaves, ill.
Descriptors: avian influenza, mallard ducks, pathogenesis,
Li YanBing, Tian GuoBin, Tian KeGong, Chen HuaLan,
and Yu KangZhen (2004). Identification of H7N2 avian influenza virus and
pathogenicity analysis in chicken and mice. Animal Biotechnology
Bulletin 9(1): 391-396. ISSN:
Descriptors: antibody formation, diagnostic techniques,
experimental infection, hemagglutination inhibition test, immune response,
pathogenicity, strain differences, virulence, avian influenza virus, chickens,
Lomniczi, B. (2004). Avian influenza and Newcastle
disease: pathogenicity, epidemiology and evolution - comments on the definition
of the diseases [A madarinfluenza es a baromfipestis (Newcastle-betegseg):
patogenitas, epidemiologia es evolucio - megjegyzesek a betegsegek
definiciojahoz]. Magyar Allatorvosok Lapja 126(2): 87-100. ISSN: 0025-004X.
Call Number: 41.8 V644
Descriptors: disease prevalence, epidemiology, evolution,
pathogenicity, Newcastle disease, avian influenza virus.
Luo KaiJian, Liang ZhaoPing, Zhao MingQiu, Liao Ming,
Guo XiaoFeng, Ren Tao, Zhang GuiHong, Cao WeiSheng, and Xin ChaoAn (2004). Studies
on the immunogenicity of avian influenza virus strain A/Chicken/Guangdong/SS/94
(H9N2) by paraffin section. Chinese Journal of Zoonoses 20(3):
Descriptors: avian influenza virus, histopathology,
immunization, inactivated vaccines, fowl.
Manvell, R.J., C. English, P.H. Jorgensen, and I.H.
Brown (2003). Pathogenesis of H7 influenza A viruses isolated from ostriches
in the homologous host infected experimentally. Avian Diseases
47(Special Issue): 1150-1153. ISSN:
Call Number: 41.8 Av5
Abstract: Infections of ostriches with avian influenza
A viruses are generally associated with clinical disease, but the occasional
high mortality in young birds does not appear to be related directly to virus
pathotype. In this study we investigated the pathogenesis of two H7 viruses for
11-wk-old ostriches inoculated intranasally, and clinical symptoms, virus
excretion, and immune response were studied. One of the viruses
(A/Ostrich/Italy/1038/00) was highly pathogenic for chickens, whereas the other
(A/Ostrich/South Africa/1609/91) was of low pathogenicity for chickens.
Clinical signs in ostriches receiving virulent virus were slight depression and
hemorrhagic diarrhea, while the group receiving avirulent virus was clinically
normal except for green diarrhea. Both viruses were transmitted to in-contact
sentinel birds housed with the infected groups 3 days postinfection. Postmortem
examination of the birds infected (including the sentinel bird) with virus
highly pathogenic for chickens were grossly normal except for localized
pneumonic lesions. The results of the study are presented and discussed.
Descriptors: infection, veterinary medicine, avian
influenza, infectious disease, respiratory system disease, viral disease,
disease pathogenesis, immune response, virus excretion, ostrich.
Mo, I.P., M. Brugh, O.J. Fletcher, G.N. Rowland, and
D.E. Swayne (1997). Comparative pathology of chickens experimentally
inoculated with avian influenza viruses of low and high pathogenicity. Avian
Diseases 41(1): 125-136. ISSN:
Call Number: 41.8 Av5
Abstract: Pathologic changes and distribution of viral
antigen as determined by immunohistochemistry were compared among 4-wk-old
specific-pathogen-free chickens inoculated intratracheally with avian influenza
virus (AIV) isolates of either low or high pathogenicity. Viruses of low
pathogenicity previously characterized as mildly pathogenic (MP), included
A/chicken/Pennsylvania/21525/83 (H5N2) (MP-Penn) and A/chicken/Alabama/7395/75
(H4N8) (MP-Alab). Viruses of high pathogenicity included
A/chicken/Pennsylvania/1370/83 (H5N2), A/chicken/Victoria/A185/85 (H7N7), and
A/turkey/Ontario/7732/66 (H5N9). Extremely variable clinical signs ranging from
mild respiratory distress to high mortality were present among chickens
inoculated with these viruses. Chickens inoculated with highly pathogenic (HP)
virus had histologic lesions of necrosis and inflammation in cloacal bursa,
thymus, spleen, heart, pancreas, kidney, brain, trachea, lung, and skeletal
muscle, whereas chickens inoculated with HP virus had histologic lesions most
frequently in lung and trachea or lacked histologic lesions. Immunospecific
staining for avian influenza viral proteins was most common in cells within
heart, lung, kidney, brain, and pancreas of chickens inoculated with HP
viruses, but immunospecific staining was present only and infrequently in
trachea and lung of chickens inoculated with MP-Penn AIV. MP-Alab did not
produce lesions nor have vital antigen in inoculated chickens but did produce
serologic evidence of infection. The pattern of organ involvement and viral
antigen distribution in chickens intratracheally inoculated with HP MV isolates
indicates a common capability to spread beyond the respiratory tract and
confirms the pantrophic replicative, pathobiologic, and lethal nature of the
viruses. However, variability in severity and lesion distribution exists
between different HP AIVs.
Descriptors: chickens, avian influenza virus,
pathogenicity, experimental infection, in vivo experimentation, histopathology,
lesions, antigens, animal tissues,
biological properties, birds, body parts, disease transmission, domestic animals, domesticated birds,
experimentation, Galliformes, immunological factors, infection, influenza
virus, livestock, microbial properties, orthomyxoviridae, pathogenesis,
pathology, poultry, useful animals, viruses, viral antigens.
Mutinelli, F., I. Capua, C. Terregino, and G. Ortali
(2001). Clinical, gross and microscopic findings in different Avian species
naturally infected by type A, highly pathogenic Avian influenza virus of the
H7N1 subtype. Proceedings of the Western Poultry Diseases Conference
50: 12-15.
Call Number: SF995.W4
Descriptors: avian influenza virus, pathogenicity,
pathotypes, birds.
Mutinelli, F., H. Hablovarid, and I. Capua (2003). Avian
embryo susceptibility to Italian H7N1 avian influenza viruses belonging to
different lineages. Avian Diseases 47(Special Issue):
Call Number: 41.8 Av5
Abstract: An immunohistochemical investigation was
performed to assess tissue tropism and viral replication of Italian H7N1
isolates belonging to different lineages in developing chicken, turkey, Muscovy
duck, and mallard duck embryos. Low-pathogenic avian influenza (LPAI) isolates
were selected on the basis of the location in the phylogenetic tree; a
progenitor strain, A/turkey/Italy/977/V99 (exhibiting no additional
glycosylation sites, nAGS), strain A/turkey/Italy/2379/V99 (AGS in position
123), and strain A/turkey/Italy/3675/V99 (AGS in position 149) were selected.
The latter two strains belonged to distinct lineages originating from the pool
of progenitor strains. The highly pathogenic avian influenza (HPAI) isolate
A/turkey/Italy/4580/V99 was also included in the test. All the embryos tested
supported the growth of HPAI. The LPAI isolates replicated readily in the
allantoic layer of the chorioallantoic membrane of all the species tested and
did not replicate to detectable levels in the developing chicken, turkey, and
Muscovy duck embryos. In contrast, they replicated to different extents in the
respiratory tract of the developing mallard embryo. The findings indicate that
the pathogenesis of LPAI infections in mallard embryos is different to that
observed in other species and should be investigated further.
Descriptors: development, infection, avian influenza,
infectious disease, respiratory system disease, viral disease,
immunohistochemistry immunologic techniques, laboratory techniques, avian
embryo infection susceptibility pathogenesis viral replication.
Ogawa, T., T. Sugimura, S. Itohara, Y. Tanaka, and T.
Kumagai (1980). Intracerebral pathogenicity of influenza A viruses for
chickens. Archives of Virology 64(4): 383-6. ISSN: 0304-8608.
Call Number: 448.3 Ar23
Abstract: The virulence of influenza A viruses was
determined using the intracerebral pathogenicity index test for chickens. The
viruses were divided into high virulent, low virulent and avirulent strains. A
low virulent strain was recovered from the jejunum and faeces of infected
Descriptors: brain microbiology, chickens microbiology,
influenza A virus pathogenicity, feces microbiology, influenza A virus avian
pathogenicity, influenza A virus human pathogenicity, influenza A virus,
porcine pathogenicity, influenza A virus growth and development, jejunum
Otsuki, K., Y. Kawaoka, T. Nakamura, and M. Tsubokura
(1982). Pathogenicity for chickens of avian influenza viruses isolated from
whistling swans and a black-tailed gull in Japan. Avian Diseases
Call Number: 41.8 Av5
Abstract: We isolated 24 Hav1 Neq1 and 18 Hav6 Nav3
influenza viruses from such free-living wild waterfowl as whistling swans,
black-tailed gulls, and tufted ducks in western Japan in 1980. Two Hav1 Neq1
viruses isolated from a whistling swan and a black-tailed gull and a Hav6 Nav3
virus from a whistling swan were examined for their pathogenicity for chickens.
Five-week-old specific-pathogen-free chickens were inoculated with the viruses
intratracheally or intraperitoneally. Virus was recovered successfully from all
the organs, including the brain, despite the absence of signs of disease. The
intracerebral pathogenicity index scores obtained for the Hav1 Neq1 viruses
were 0.43 and 0.87; the score for the Hav6 Nav3 virus was 0.43. No virus
produced plaques in cultivated chick embryo fibroblast cells in the absence of
Descriptors: animal population groups microbiology,
animals, wild microbiology, birds microbiology, chickens microbiology, ducks
microbiology, influenza A virus avian pathogenicity, chick embryo, Japan,
specific pathogen free organisms, terminology.
Otsuki, K., K. Yamazaki, Y. Kawaoka, and M. Tsubokura
(1988). Intracerebral pathogenicity for chickens of avian influenza viruses
isolated from free-living waterfowl in Japan. Veterinary Microbiology
Call Number: SF601.V44
Abstract: The pathogenicity for chickens of 91 strains
of avian influenza A virus isolated from such free-living waterfowl as
whistling swan, pintail, tufted duck, mallard and black-tailed gull in Japan
was tested. The majority of the virus strains infected and were pathogenic for
the chickens. The virulence of these viruses seemed not to be as high as that
of fowl plague virus. There were no significant differences in the
intracerebral index score among the viruses belonging to the same subtype,
irrespective of year of isolation or host.
Descriptors: birds microbiology, brain diseases
veterinary, chickens microbiology, fowl plague microbiology, influenza A virus
avian pathogenicity, brain diseases microbiology, fowl plague transmission, influenza A virus
avian isolation and purification, seasons, virulence.
Padilla, N.R., F.E. Aburto, C.M. Fraire, and N.L.
Padilla (2004). Influenza aviar: histopatologia y deteccion viral por rt-pcr
en tejidos fijados con formalina e incluidos en parafina. [Avian influenza:
histopathology and viral detection in formalin-fixed, paraffin-embedded tissues
by RT-PCR]. Veterinaria Mexico 35(1): 1-19. ISSN: 0301-5092.
Call Number: SF604.V485
Descriptors: infection, acute renal tubular necrosis,
avian influenza, non suppurative encephalitis, vasculitis, reverse transcription
polymerase chain reaction, clinical techniques, diagnostic techniques, viral
replication, chickens.
Perdue, M.L. (2000). How can a virus suddenly
become very pathogenic? World Poultry (Special): 9-10. ISSN: 1388-3119.
Call Number: SF481.M54
Descriptors: avian influenza virus, highly pathogenic,
mutations, poultry.
Perkins, L.E. and D.E. Swayne (2001). Pathobiology
of A/chicken/Hong Kong/220/97 (H5N1) avian influenza virus in seven
gallinaceous species. Veterinary Pathology 38(2): 149-64. ISSN: 0300-9858.
Call Number: 41.8 P27
Abstract: Direct bird-to-human transmission, with the
production of severe respiratory disease and human mortality, is unique to the
Hong Kong-origin H5N1 highly pathogenic avian influenza (HPAI) virus, which was
originally isolated from a disease outbreak in chickens. The pathobiology of
the A/chicken/Hong Kong/220/97 (H5N1) (HK/220) HPAI virus was investigated in
chickens, turkeys, Japanese and Bobwhite quail, guinea fowl, pheasants, and
partridges, where it produced 75-100% mortality within 10 days. Depression,
mucoid diarrhea, and neurologic dysfunction were common clinical manifestations
of disease. Grossly, the most severe and consistent lesions included
splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric
lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions
were observed in multiple organs and were characterized by exudation,
hemorrhage, necrosis, inflammation, or a combination of these features. The
lung, heart, brain, spleen, and adrenal glands were the most consistently
affected, and viral antigen was most often detected by immunohistochemistry in
the parenchyma of these organs. The pathogenesis of infection with the HK/220
HPAI virus in these species was twofold. Early mortality occurring at 1-2 days
postinoculation (DPI) corresponded to severe pulmonary edema and congestion and
virus localization within the vascular endothelium. Mortality occurring after 2
DPI was related to systemic biochemical imbalance, multiorgan failure, or a
combination of these factors. The pathobiologic features were analogous to
those experimentally induced with other HPAI viruses in domestic poultry.
Descriptors: birds virology, fowl plague pathology,
influenza A virus avian pathogenicity, poultry diseases virology, adrenal
glands pathology, antigens, viral blood, brain pathology, chick embryo, fowl
plague virology, hemorrhage veterinary, immunohistochemistry veterinary, lung
pathology, poultry diseases pathology, pulmonary edema veterinary, specific
pathogen free organisms, splenomegaly veterinary.
Perkins, L.E.L. and D.E. Swayne (2003). Varied
pathogenicity of a Hong Kong-origin H5N1 avian influenza virus in four
Passerine species and budgerigars. Veterinary Pathology 40(1):
Call Number: 41.8 P27
Descriptors: avian influenza virus, experimental
infections, lesions, pathogenicity, species differences, wild birds,
budgerigars, Passer domesticus, Carpodacus mexicanus, Sternus
vulgaris, Taeniopygia guttata.
Perkins, L.E.L. and D.E. Swayne (2002). Pathogenicity
of a Hong Kong-origin H5N1 highly pathogenic avian influenza virus for emus,
geese, ducks, and pigeons. Avian Diseases 46(1): 53-63. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: The H5N1 type A influenza viruses that
emerged in Hong Kong in 1997 are a unique lineage of type A influenza viruses
with the capacity to transmit directly from chickens to humans and produce
significant disease and mortality in-both of these hosts. The objective of this
study was to ascertain the susceptibility of emus (Dramaius novaehollandiae),
domestic geese (Anser anser domesticus), domestic ducks (Anas
platyrhynchos), and pigeons (Columba livia) to intranasal (i.n.)
inoculation with the A/chicken/Hong Kong/220/97 (H5N1) highly pathogenic avian
influenza virus. No mortality occurred within 10 days postinoculation (DPI) in
the four species investigated, and clinical disease, evident as neurologic
dysfunction, was observed exclusively in emus and geese. Grossly, pancreatic
mottling and splenomegaly were identified in these two species. In addition,
the geese had cerebral malacia and thymic and bursal atrophy. Histologically,
both the emus and geese developed pancreatitis, meningoencephalitis, and mild myocarditis.
Influenza viral antigen was demonstrated in areas with histologic lesions up to
10 DPI in the geese. Virus was reisolated from oropharyngeal and cloacal swabs
and from the lung, brain, and kidney of the emus and geese. Moderate
splenomegaly was observed grossly in the ducks. Viral infection of the ducks
was pneumotropic, as evidenced by mild inflammatory lesions in the respiratory
tract and virus reisolation from oropharyngeal swabs and from a lung. Pigeons
were resistant to HK/220 infection, lacking gross and histologic lesions, viral
antigen, and reisolation of virus. These results imply that emus and geese are
susceptible to i.n. inoculation with the HK/220 virus, whereas ducks and
pigeons are more resistant. These latter two species probably played a minimal
epidemiologic role in the perpetuation of the H5N1 Hong Kong-origin influenza
Descriptors: infection, veterinary medicine, H5N1 avian
influenza virus infection, etiology, mortality, viral disease, bursal atrophy,
joint disease, cerebral malacia, nervous system disease, meningoencephalitis,
nervous system disease, myocarditis, heart disease, neurologic dysfunction,
nervous system disease, pancreatic mottling, digestive system disease,
endocrine disease, pancreas, pancreatitis, digestive system disease,
respiratory tract inflammation, respiratory system disease, splenomegaly, blood
and lymphatic disease, thymic atrophy, endocrine disease, thymus.
Pysina, T.V. and A.S. Gorbunova (1970). Sootnosheniia
mezhdu patogennost'iu virusov grippa ptits dlia laboratornykh zhivotnykh i
infitsirovaniem avifauny. [Relation between the pathogenicity of avian
influenza viruses for laboratory animals and infection of avifauna]. Voprosy
Virusologii 15(3): 298-301. ISSN:
Call Number: 448.8 P942
Descriptors: bird diseases microbiology, orthomyxoviridae
pathogenicity, bird diseases epidemiology, chickens, Czechoslovakia, ducks,
England, influenza epidemiology,
influenza microbiology, mice, Scotland, Siberia, South Africa, tissue culture,
virus cultivation.
Ranck, F.M.J., L.C. Grumbles, C.F. Hall, and J.E.
Grimes (1970). Serology and gross lesions of turkeys inoculated with an
avian influenza A virus, a paramyxovirus, and Mycoplasma gallisepticum.
Avian Diseases 14(1): 54-65.
Call Number: 41.8 Av5
Descriptors: Mycoplasma infections pathology,
orthomyxoviridae infections pathology, poultry diseases, antibody formation,
hemagglutination inhibition tests, immune sera analysis, lung diseases
pathology, lung diseases veterinary, mycoplasma pathogenicity, Mycoplasma
infections immunology, orthomyxoviridae pathogenicity, orthomyxoviridae
infections immunology, pulmonary alveoli immunology, pulmonary alveoli
microbiology, pulmonary alveoli pathology, turkeys.
Reinacher, M., J. Bonin, O. Narayan, and C.
Scholtissek (1983). Pathogenesis of neurovirulent influenza A virus
infection in mice. Route of entry of virus into brain determines infection of
different populations of cells. Laboratory Investigation a Journal of
Technical Methods and Pathology 49(6): 686-92. ISSN: 0023-6837.
Call Number: 448.8 L11
Abstract: Coinfection of a cell culture with a human
and avian influenza A virus had yielded a recombinant virus with high
neurovirulence for mice. This study reports on the comparative pathogenesis of
central nervous system infection in mice between the parental human and the
recombinant virus using the immunohistologic peroxidase-antiperoxidase method
and virus assay of tissue suspensions. The human virus replicated poorly in
mice and did not replicate in the brain even after intracerebral inoculation.
In contrast, the recombinant virus replicated to high titer in the lung and
brain with resulting viremia after inoculation of young mice by the intracerebral,
intraperitoneal, or intranasal routes. Different populations of cells in the
brain became infected after inoculation by each of the three routes: choroid
plexus, and ependymal and subependymal cells after intracerebral inoculation;
cells in perivenous areas, neurons in the olfactory bulbs and trigeminal
ganglia and nuclear groups in the brainstem and midbrain after intranasal
inoculation. Intraperitoneal inoculation resulted almost exclusively in the
perivenous spread of the virus. The intranasal inoculation suggested that virus
entry into the brain both by spread along nerve cell processes from the nasal
mucosa to the brain and trigeminal ganglia and subsequent perivenous spread
after viremia developed following virus replication in the lung. To dissect
these two mechanisms we inoculated neonatal mice that had acquired high levels
of serum antibody by nursing from actively immunized mothers. Intraperitoneal
inoculation of these mice failed to cause infection, whereas intranasal
inoculation resulted in the same pattern of cellular spread through the
olfactory and trigeminal pathways as noted previously. This proved that this
recombinant influenza virus could invade the central nervous system after
infection via a natural route of infection. This highly neuroinvasive agent
provides one example of the extent of virulence which can be acquired by
recombination of apathogenic influenza viruses and raises a note of caution for
adequate control of those agents generated in the laboratory.
Descriptors: brain diseases microbiology, influenza
microbiology, influenza A virus avian pathogenicity, influenza A virus human
pathogenicity, antigens, viral analysis, birds, brain microbiology, brain
pathology, brain diseases immunology, brain diseases pathology, immunization,
influenza immunology, influenza pathology, influenza A virus avian genetics,
influenza A virus avian immunology, influenza A virus human genetics, influenza
A virus human immunology, lung microbiology, lung pathology, mice, plaque
assay, recombination, genetic, virulence, virus replication.
Resende, M. (1981). Comparative pathogenesis of
virulent and avirulent avian influenza viruses in turkeys. Dissertation
Abstracts International, B 41(10): 3706.
Call Number: Z5055.U49D53
Descriptors: avian influenza virus, turkeys, pathogenesis.
Rimmelzwaan, G.F., T. Kuiken, A.G. van, T.M.
Bestebroer, R.A.M. Fouchier, and A.D.M.E. Osterhaus (2003). A primate model
to study the pathogenesis of influenza A (H5N1) virus infection. Avian
Diseases 47(Special Issue): 931-933.
Call Number: 41.8 Av5
Abstract: Cynomolgus macaques (Macaca fascicularis)
infected with influenza virus A/HongKong/156/97 (H5N1) developed acute
respiratory distress syndrome (ARDS) with fever. Reverse transcriptase/polymerase
chain reaction (RT/PCR) and virus isolation showed that the respiratory tract
is the major target of the virus. The main lesion observed upon necropsy,
performed 4 or 7 days postinfection, was a necrotizing bronchointerstitial
pneumonia, similar to that found in primary influenza pneumonia in human
beings. By immunohistochemistry, influenza virus antigen proved to be limited
to pulmonary tissue and tonsils. The data indicate that ARDS and multiple organ
dysfunction syndrome (MODS), observed in both humans and monkeys infected with
this virus, are caused by diffuse alveolar damage from virus replication in the
lungs alone.
Descriptors: infection, acute respiratory distress
syndrome (ARDS), respiratory system disease, avian influenza, infectious
disease, respiratory system disease, viral disease, bronchointerstitial
pneumonia, respiratory system disease, multiple organ dysfunction syndrome
(MODS), disease miscellaneous, immunohistochemistry immunologic techniques,
laboratory techniques, necropsy clinical techniques, reverse transcriptase
polymerase chain reaction (RT PCR) genetic techniques, laboratory techniques,
viral isolation laboratory techniques, influenza pathogenesis viral
Rott, R. (1982). Determinants of influenza virus
pathogenicity. Lecture held on the occasion of the reception of the reception
of the Otto-Warburg-Medaille on September 27, 1982. Hoppe Seyler's
Zeitschrift Fur Physiologische Chemie 363(11): 1273-82. ISSN: 0018-4888.
Call Number: 384 Z38
Descriptors: orthomyxoviridae pathogenicity, amino acid
sequence, cell transformation, viral, hemagglutinins, influenza A virus avian
genetics, avian pathogenicity, orthomyxoviridae genetics, plaque assay, RNA
viral genetics, species specificity, viral proteins genetics.
Rott, R. (1985). In vitro Differenzierung von
pathogenen und apathogenen aviaren Influenzaviren. [In vitro differentiation of
pathogenic and nonpathogenic avian influenza viruses]. Berliner Und
Munchener Tierarztliche Wochenschrift 98(2): 37-9. ISSN: 0005-9366.
Call Number: 41.8 B45
Descriptors: influenza A virus avian classification,
microbiological techniques veterinary, chick embryo, fibroblasts,
hemagglutination tests, avian pathogenicity, plaque assay veterinary, tissue
culture, virulence, virus cultivation.
Rott, R. (1981). The role of the hemagglutinin in
infectivity and pathogenicity of avian influenza viruses. In: Proceedings
of the First International Symposium on Avian Influenza, Beltsville, Maryland,
USA, p. 116-133.
Call Number:
aSF995.6.I6I5 1981a
Descriptors: avian influenza viruses,
pathogenicity, infectivity, hemagglutinins, symposium.
Rott, R., H.D. Klenk, Y. Nagai, and M. Tashiro
(1995). Influenza viruses, cell enzymes, and pathogenicity. American
Journal of Respiratory and Critical Care Medicine 152(4, Pt. 2):
Abstract: Proteolytic cleavage of the influenza virus
hemagglutinin glycoprotein (HA) by cellular proteases is a prerequisite for
virus infectivity, spread of the virus in the infected organism, tissue
tropism, and viral pathogenicity. Production of infectious virus depends upon
the structure at the HA cleavage site as well as the substrate specificity and
the distribution of appropriate enzymes. Differences exist in the specificities
of the endoproteases that recognize the different sequence motifs at the cleavage
site. With avian influenza viruses that cause lethal systemic infections, the
cleavage site consists of multibasic amino acids. Furin, which activates this
type of HA, is a member of the subtilisin family and represents the prototype
of ubiquitously occurring membrane-bound proteases. On the other hand, serine
proteases secreted from a restricted number of cell types and some bacterial
enzymes recognize a monobasic cleavage signal at HA of the mammalian and the
apathogenic avian influenza viruses. The limited occurrence of these proteases
results in only localized infection. Implementation of these defined conditions
for virus activation may represent a novel type of disease control.
Descriptors: hemagglutinins viral physiology,
orthomyxoviridae enzymology, orthomyxoviridae pathogenicity, serine
endopeptidases physiology, subtilisins physiology, furin, hemagglutinins viral
chemistry, substrate specificity.
Rott, R., H.D. Klenk, and C. Scholtissek (1984). Bedeutung
des Hamagglutinins fur die Pathogenitat aviarer Influenzaviren. [Significance
of hemagglutinins for the pathogenicity of avian influenza viruses]. Zentralblatt
Fur Bakteriologie, Mikrobiologie, Und Hygiene. Series A, Medical Microbiology,
Infectious Diseases, Virology, Parasitology 258(2-3): 337-49. ISSN: 0176-6724.
Call Number: 448.3 C33 (1)
Abstract: In addition to acute viral diseases,
persistent infections have attained considerable interest in recent years. Such
persistent infections are characterized by extended time periods in which the
infecting virus remains within the organism before the eventual appearance of
manifest symptoms. These infections may be evoked by a variety of virus species
resulting in a diversity of pathogenic reactions and clinical manifestations.
The mechanisms of viral persistence, where known, also appear to be quite
diverse. As far as space permits, some examples of persistent infections will
be presented and the mechanisms of the pathogenesis of the resulting diseases
will be discussed.
Descriptors: hemagglutinins viral analysis, hemagglutinins
viral genetics, hemagglutinins viral immunology, influenza A virus avian
pathogenicity, amino acid sequence, cell membrane microbiology, chick embryo,
fetal membranes microbiology, genes viral, avian genetics, avian growth and
development, avian ultrastructure, models, molecular, mutation, virulence.
Rott, R., H.D. Klenk, C. Scholtissek, A Kohn (ed.),
and P Fuchs (ed.). (1984). On the pathogenicity of avian influenza viruses.
In: Mechanisms of viral pathogenesis: from gene to pathogen - Proceedings of
the 28th OHOLO Conference, p. 246-256.
Call Number:
Descriptors: avian influenza viruses,
Rott, R., M. Orlich, and C. Scholtissek (1979). Correlation
of pathogenicity and gene constellation of influenza A viruses. III.
Non-pathogenic recombinants derived from highly pathogenic parent strains. Journal
of General Virology 44(2): 471-7.
Call Number: QR360.A1J6
Abstract: We have demonstrated by recombination of two
highly pathogenic avian influenza viruses [A/FPV/Rostock (Hav1N1) x
A/turkey/England/63 (Hav1Nav3)] that recombinants can be isolated which are
pathogenic as well as non-pathogenic for chickens. They carried the
glycoproteins of either parent strains, and all are produced in infectious form
in chick embryo cells. Genetic analysis revealed that the non-pathogenic
recombinants possess a mixed RNA polymerase complex, consisting of pol 1, pol
2, ptra and NP gene products, while, with one exception, the pathogenic
recombinants have the genes coding for the polymerase activity from one or
other parent virus. The biological properties of the recombinant viruses did
not correlate with their pathogenicity for chickens.
Descriptors: genes viral, influenza A virus avian
genetics, recombination, genetic, chickens, DNA directed RNA polymerases
genetics, fowl plague microbiology, avian pathogenicity, neuraminidase
genetics, turkeys.
Samadieh, B. (1975). Cytopathogenic effect of
avian influenza-A viruses upon different cell lines. In: 20th World
Veterinary Congress. Summaries, Volume 2, p. 1059-1060.
Descriptors: avian influenza A viruses,
cytopathogenicity, cell lines.
Scholtissek, C. and R. Rott (1984). Correlation
between loss of the temperature-sensitive phenotype and pathogenicity of fowl
plague virus mutants in the chicken. Virus Research 1(2):
Call Number: QR375.V6
Abstract: The reversion of temperature-sensitive (ts)
mutants of fowl plague virus to the ts+ phenotype was correlated with
pathogenicity for chicken. Two types of ts mutants were investigated: those
obtained by mutagenesis with 5-fluorouracil and those obtained by undiluted
passages at 33 degrees C. The reversion frequency of the former mutants
depended on the RNA segment in which the ts defect was located, mutations in
RNA segments 1 and 2 having the highest reversion frequency, those in the RNA
segments coding for the glycoproteins the lowest. ts mutants obtained by
undiluted passages behaved differently in this respect. There was an
approximate correlation between frequency of reversion and pathogenicity for
chicken. Double mutants induced by 5-fluorouracil, having one tight and one
leaky mutation, reverted easily without loss of the leaky mutation. These
double mutants were still to a limited extent pathogenic for the chicken. Only
one double mutant with two tight mutations (ts 293) was completely
nonpathogenic after intramuscular inoculation. Two ts mutants with multiple
tight defects (ts 1/1 and ts 3/18) obtained by undiluted passage did not revert
to wild-type after injection into embryonated eggs and incubation at 33 degrees
C, but they were still slightly pathogenic for the chicken. There was no
obvious correlation between the shut-off temperature and pathogenicity of
mutants carrying a single ts defect. However, for mutants with multiple tight
mutations a high shut-off temperature seemed to be essential for reversion
during serial passages as well as for pathogenicity in the chicken, when
different routes of inoculation were examined. ts mutants seem to be safe as
live vaccines only, (1) if they carry at least two tight ts defects, (2) if
they have a relatively low shut-off temperature, and (3) if they could be
administered other than via the respiratory tract.
Descriptors: influenza A virus avian genetics, mutation,
temperature, chickens microbiology, fluorouracil pharmacology, avian
Scholtissek, C., A. Vallbracht, B. Flehmig, and R.
Rott (1979). Correlation of pathogenicity and gene constellation of
influenza A viruses. II. Highly neurovirulent recombinants derived from
non-neurovirulent or weakly neurovirulent parent virus strains. Virology
Call Number: 448.8 V81
Descriptors: genes viral, influenza A virus pathogenicity,
recombination, genetic, brain microbiology, chickens, influenza A virus avian
genetics, human genetics, influenza A virus genetics, lung microbiology, mice,
tissue culture, virulence.
Selleck, P.W., G. Arzey, P.D. Kirkland, R.L. Reece,
A.R. Gould, P.W. Daniels, and H.A. Westbury (2003). An outbreak of highly
pathogenic avian influenza in Australia in 1997 caused by an H7N4 virus. Avian
Diseases 47(Special Issue): 806-811.
Call Number: 41.8 Av5
Abstract: In November of 1997 an outbreak of highly
pathogenic avian influenza occurred near the town of Tamworth, in northern New
South Wales, Australia. The viruses isolated from chickens on two commercial
chicken farms were identified as H7N4 viruses, with hemagglutinin cleavage site
amino acid sequences of RKRKRG and intravenous pathogenicity indices of 2.52
and 2.90, respectively. A virus with an identical nucleotide sequence, but with
an intravenous pathogenicity index of 1.30, was also isolated from cloacal
swabs collected from asymptomatic emus kept on a third property.
Descriptors: animal husbandry, epidemiology, infection,
avian influenza, infectious disease, respiratory system disease, viral disease,
commercial chicken farms, disease outbreaks.
Shalaby, A.A., R.D. Slemons, and D.E. Swayne (1994). Pathological
studies of A/chicken/Alabama/7395/75 (H4N8) influenza virus in
specific-pathogen-free laying hens. Avian Diseases 38(1):
Call Number: 41.8 Av5
Abstract: Specific-pathogen-free laying hens were
inoculated with avian influenza virus (AIV) A/chicken/Alabama/7395/75 (H4N8)
either intratracheally (IT) or intravenously (IV). IT inoculation produced a
localized infection of the upper and lower respiratory tracts with lesions of
tracheitis, bronchitis, airsacculitis, and pneumonia around the secondary
bronchi. IV inoculation produced a systemic infection with major lesions of
nephritis, interstitial pneumonia, salpingitis, and splenic and hepatic
necrosis. In IV-inoculated hens, AIV nucleo-protein was demonstrated within
renal tubule epithelium, in luminal surface and glandular oviduct epithelium,
and in mononuclear cells within pulmonary blood capillaries. However, no virus
was recovered from internal contents of eggs laid between days 1.5 and 5
postinfection. These data indicate that A/chicken/Alabama/7395/75 has tissue
tropism and pathogenicity for the respiratory and urogenital systems of
reproductively active laying hens. Site and severity of lesion development are
determined by the localized or systemic nature of AIV infection.
Descriptors: fowl plague pathology, influenza A virus
avian isolation and purification, chickens, kidney microbiology, kidney
pathology, lung microbiology, lung pathology, ovary microbiology, ovary
pathology, oviducts microbiology, oviducts pathology, oviposition, specific
pathogen free organisms.
Shinya, K., T. Awakura, A. Shimada, F.D. Silvano, T.
Umemura, and K. Otsuki (1995). Pathogenesis of pancreatic atrophy by avian
influenza A virus infection. Avian Pathology 24(4): 623-632. ISSN: 0307-9457.
Call Number: SF995.A1A9
Abstract: Specific-pathogen-free (SPF), 2-day-old
chicks were inoculated with type A influenza virus (A/whistling
swan/Shimane/499/83/(H5N3)) into their caudal thoracic air sac. The original
isolate of the virus was of low virulence (ICPI 0.20 to 0.40), and was passaged
10 times through the respiratory organs of SPF chicks. Most of the chicks
inoculated with the passaged virus (strain 499) showed respiratory and
alimentary signs. Three of 30 chicks died on days 2, 6 and 7 post-inoculation
(p.i.). Almost half of the infected chicks showed poor growth, and the
variation of body size in the flock became prominent from day 10 p.i. Infected
chicks consistently had pathological changes in the pancreas, liver, kidneys
and respiratory tracts, and occasionally in the brain, duodenum and bone marrow.
Positive immunoreaction to avian influenza virus (AIV) antigen and recovery of
the virus persisted for longer period in the pancreas than in other organs. The
pancreatic lesions were caused by a direct, lytic virus infection of the acinar
cells and contributed to poor growth of the chicks.
Descriptors: chicks, avian influenza virus, pancreas,
atrophy, pathogenesis, virulence, symptoms, histopathology, growth retardation,
acinar cells.
Silvano, F.D., M. Yoshikawa, A. Shimada, K. Otsuki,
and T. Umemura (1997). Enhanced neuropathogenicity of avian influenza A
virus by passages through air sac and brain of chicks. Journal of
Veterinary Medical Science the Japanese Society of Veterinary Science
Call Number: SF604.J342
Abstract: Three-day-old, specific-pathogen-free (SPF)
chicks were inoculated with the strains of influenza A/whistling swan/Shimane/
499/83 (H5N3) via the air sac route. The strains had been passaged through air
sacs or air sacs and brains of SPF chicks. Two experiments were undertaken to
examine the pathogenicity of these strains and the development of brain lesions
based on time-interval changes. In experiment 1, original strain (4e) showed
low pathogenicity with mild respiratory signs and zero mortality. Air sac
passaged strains (18a and 24a) of 4e demonstrated mortalities of 50% and 67%,
respectively, and inoculated chicks showed hemorrhages and necrotic lesions in
major organs. Air sac-brain passaged strain (24a5b) of 4e produced 100%
mortality and severe nervous signs. Severe circulatory disturbance with
multiple foci of necrosis in major organs including the brain was found in
chicks inoculated with 24a5b. The 24a5b was analogous to highly pathogenic
avian influenza virus in regard to its pathogenicity to chicks. Hence, low
pathogenic influenza virus (4e) gradually aggravated its pathogenicity to
highly pathogenic virus (24a5b) by air sac and brain passages. In experiment 2,
chicks were inoculated with 24a5b, and the earliest histological lesion was the
enlargement of the vascular endothelial cells at 18 hr post-inoculation (PI)
followed by necrotizing encephalitis at 24 to 48 hr PI. Immunohistological
staining revealed avian influenza virus antigen initially in the vascular
endothelial cells and then in the astrocytes, neurons and ependyma.
Descriptors: air sacs virology, brain virology, chickens,
fowl plague pathology, influenza A virus pathogenicity, air sacs pathology,
antigens, viral analysis, brain immunology, brain pathology, endothelium, vascular
pathology, influenza A virus immunology, microscopy, electron methods,
microscopy, electron veterinary, necrosis, neurons ultrastructure, serial
passage, specific pathogen free organisms, time factors.
Slemons, R.D., P.K. Condobery, and D.E. Swayne (
1991). Assessing pathogenicity potentical of waterfowl-origin type A
influenza viruses in chickens. Avian Diseases 35(1): 210-215. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: Intravenous pathogenicity index (IVPI) tests
on 29 wild duck-origin type A influenza viruses, two turkey-origin type A
influenza viruses, and one chicken-origin type A influenza virus resulted in
indices ranging from 0.0 to 0.49. Most of the wild duck-origin viruses and the
two turkey-origin viruses had indices of 0.0, indicating they are not
pathogenic. Six of the duck-origin viruses had indices ranging from 0.25 to
0.49, and the IVPI for A/chicken/Alabama/75 (H4N8) was 0.49, indicating they
had low pathogenic potential. An IVPI of 1.25 up to the maximum score of 3.0 is
necessary for a type A influenza virus to be classified as highly pathogenic.
Gross lesions observed in chickens dying following intravenous viral challenge
included kidney swelling with more prominent lobular patterns, but visceral
urate deposits were not present. The usefulness of the IVPI test in evaluating
the pathogenicity potential of nonpathogenic and low-pathogenic strains of
avian influenza virus may be limited.
Descriptors: fowls, avian influenza virus, waterfowl,
ducks, pathogenicity, kidneys, lesions, mortality, Ohio.
Slemons, R.D., L.N. Locke, M.G. Sheerar, R.M. Duncan,
V.S. Hinshaw, and B.C. Easterday (1990). Kidney lesions associated with
mortality in chickens inoculated with waterfowl influenza viruses. Avian
Diseases 34(1): 120-8. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: Seventy-six type A influenza viruses
recovered from waterfowl in Wisconsin, California, South Dakota, Florida,
Texas, Alabama, and Nebraska were tested for virulence in chickens. The
challenge to chickens was intravenous inoculation of first-, second-, or
third-egg-passage virus. Each of the virus strains was tested separately in
three or four chickens. Eighteen of the 76 viruses caused the death of one or
more chickens following inoculation. Postmortem lesions were similar in all
dead birds. In decreasing order of frequency, gross lesions included: swollen
kidneys evident as accentuated lobular patterns, urates in the pericardial sac,
and urates on the surface of the liver. Microscopic lesions present in kidneys
were consistent with visceral gout. Mortality was associated with inoculations
having higher concentrations of infectious virus. These results indicate that
the influenza A viruses circulating in duck populations may include strains
potentially pathogenic for chickens.
Descriptors: chickens, fowl plague pathology, influenza A
virus avian pathogenicity, kidney pathology, animals, wild, antibodies, viral
biosynthesis, birds, ducks, fowl plague microbiology, fowl plague mortality,
geese, avian immunology, avian isolation and purification, virulence.
Smolenskii, V.I. (1976). Izuchenie patogeneza
estestvennogo grippa kur. [Pathogenesis of spontaneous influenza of fowls].
Sbornik Nauchnykh Trudov, Moskovskaya Veterinarnaya Akademiya 87: 73-77.
Descriptors: avian influenza virus, immunofluorescence
technique, pathogenesis.
Swayne, D.E. (1997). Pathobiology of H5N2 Mexican
avian influenza virus infections of chickens. Veterinary Pathology
Call Number: 41.8 P27
Abstract: To determine the association between specific
structural changes in the hemagglutinin gene and pathogenicity of avian
influenza viruses (AIVs), groups of 4-week-old White Plymouth Rock chickens
were inoculated intravenously or intranasally with AIVs of varying
pathogenicities isolated from chickens in central Mexico during 1994-1995.
Mildly pathogenic (MP) viruses had a common hemagglutinin-connecting peptide
sequence of Pro-Gln-Arg-Glu-Thr-Arg decreases Gly and had restricted capability
for replication and production of lesions in tissues. The principle targets for
virus replication or lesion production were the lungs, lymphoid organs, and
visceral organs containing epithelial cells, such as kidney and pancreas. Death
was associated with respiratory and/or renal failure. By contrast, highly
pathogenic (HP) AIVs had one substitution and the addition of two basic amino
acids in the hemagglutinin connecting peptide, for a sequence of
Pro-Gln-Arg-Lys-Arg-Lys-Thr-Arg decreases Gly. The HP AIVs were pantropic in
virus replication and lesion production ability. However, the most severe
histologic lesions were produced in the brain, heart, adrenal glands, and
pancreas, and failure of multiple critical organs was responsible for disease
pathogenesis and death. No differences in lesion distribution patterns or in
sites of AIV replication were evident to explain the variation in mortality
rates for different HP AIVs, but HP AIVs that produced the highest mortality
rates had more severe necrosis in heart and pancreas. The ability of individual
HP AIVs to produce low or high mortality rates could not be explained by
changes in sequence of the hemagglutinin-connecting peptide alone, but probably
required the addition of other undetermined genomic changes.
Descriptors: chickens, fowl plague pathology, influenza A
virus avian genetics, avian pathogenicity, avian physiology, adrenal glands
chemistry, adrenal glands pathology, adrenal glands virology, brain pathology,
brain virology, brain chemistry, fowl plague epidemiology, fowl plague
mortality, hemagglutinins viral chemistry, hemagglutinins viral genetics,
immunohistochemistry, kidney chemistry, kidney pathology, kidney virology,
Mexico epidemiology, myocardium chemistry, myocardium pathology, pancreas chemistry,
pancreas pathology, pancreas virology, specific pathogen free organisms, spleen
chemistry, spleen pathology, spleen virology, viral proteins analysis, viral
proteins metabolism, virus replication.
Swayne, D.E., M.L. Perdue, M. Garcia, E. Rivera Cruz,
and M. Brugh (1997). Pathogenicity and diagnosis of H5N2 Mexican avian
influenza viruses in chickens. Avian Diseases 41(2): 335-346. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: Chickens were inoculated with one of five
H5N2 Mexican-origin avian influenza virus (AIV) isolates to determine their
pathogenicity for chickens and to determine the ability of routine virologic
and serologic tests to detect infections. In laboratory infections, three AIVs,
H5/94, M5/94, and J12/94, produced sporadic illness and death and were
categorized as mildly pathogenic. Q1/95 produced illness and death in all
inoculated chickens and was categorized as highly lethal and highly pathogenic
(HP). P11/94B commonly produced clinical illness, but deaths were infrequent.
During the presence of clinical signs, oropharyngeal swabs were superior for
isolation of AIV; but cloacal swabs were more successful after disappearance of
clinical signs. Agar gel precipitin (AGP) serologic test was superior for
detecting AIV infection during the clinical phase, but AGP and hemagglutinin
inhibition tests were equally effective in detecting infections after recovery
from clinical illness. Passage of P11/94B parent stock and selected
14-day-embryo-passed AIVs in adult hens resulted in emergence of some HP AIV
derivatives. The hemagglutinin of Q1/95 and P11/94B parent stock and derivative
AIVs had an identical proteolytic cleavage site of....Pro-
Gln-Arg-Lys-Arg-Lys-Thr-Arg decreased Gly, consistent with AIVs of high
pathogenicity. However, no consistent differences were identified in the
sequence of the hemagglutinin gene to explain the discrepancy in lethality
patterns of the P11/94B AIVs. This suggests that genes other than the
hemagglutinin impact the full expression of high lethality of Mexican-origin
AIV infections in chickens.
Descriptors: Mexico, chickens, avian influenza virus,
pathogenicity, diagnosis, immunodiffusion tests, hemagglutination tests,
chemical composition, agglutination tests, America, biological properties,
birds, domestic animals, domesticated birds, Galliformes, immunological
techniques, immunoprecipitation tests, influenza virus, Latin America,
livestock, microbial properties, North America, orthomyxoviridae, poultry,
useful animals, viruses, oropharyngeal swabs, cloacal swabs, molecular sequence
data, hemagglutination inhibition test,
amino acid sequences.
Swayne, D.E. and R.D. Slemons (1994). Comparative
pathology of a chicken-origin and two duck-origin influenza virus isolates in
chickens: the effect of route of inoculation. Veterinary Pathology
Call Number: 41.8 P27
Abstract: Forty-nine 5-week-old chickens were
inoculated by the intravenous (i.v.), intratracheal (IT), or intranasal (IN)
routes with either a chicken-origin or one of two duck-origin type A influenza
virus isolates. Twelve control chickens were inoculated with sterile
chorioallantoic fluid. For all viruses, i.v. inoculation produced predominate
lesions of renal tubule necrosis (nephrosis) and nephritis, and influenza virus
nucleoprotein was localized in nuclei and cytoplasm of necrotic renal tubule
epithelium. Chickens inoculated by the IT route, and to a lesser extent the IN
route, had mild to severe tracheitis, bronchitis, and ventromedial pneumonia
associated with secondary bronchi but lacked renal tubule necrosis and
nephritis. These data indicate low-virulence avian-origin influenza viruses
were nephrotropic during simulated systemic infection (i.v. inoculation) and
pneumotropic during simulated local infection (IT and IN inoculation). Gross
and histologic kidney lesions produced by i.v. inoculation of the
chicken-origin influenza virus were similar to changes reported in outbreaks of
low-virulence influenza virus in laying chickens.
Descriptors: chickens microbiology, ducks microbiology,
fowl plague pathology, influenza A virus avian pathogenicity, poultry diseases
pathology, acute disease, administration, intranasal, immunohistochemistry,
injections, intravenous, intubation, intratracheal, virulence.
Swayne, D.E. and R.D. Slemons (1995). Comparative
pathology of intravenously inoculated wild duck- and turkey-origin type A
influenza viruses in chickens. Avian Diseases 39(1): 74-84. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: Five-week-old specific-pathogen-free chickens
were inoculated intravenously with one of 16 low-pathogenicity type A influenza
virus isolates; 14 were of wild duck origin, and two were of turkey origin.
Tubulointerstitial nephritis was the most frequent specific histopathologic
change. The frequency and severity of kidney lesions were independent of the
virus hemagglutinin-neuraminidase subtype or titer of the challenge virus.
Influenza nucleoprotein was most frequently demonstrated in the kidney and was
consistently localized to necrotic proximal and/or distal renal tubule
epithelium. Common nonspecific histopathologic changes were lymphoid
hyperplasia of the spleen and cecal tonsils, as well as lymphocyte depletion in
the cloacal bursa. Uncommon histopathologic changes, in decreasing order of
frequency, were interstitial pneumonia, lymphoid follicular hyperplasia in the
myocardium, and lymphocytic tracheitis. Histopathologic changes were rare or
absent in the jejunum, duodenum, pancreas, and brain. The low-pathogenicity
avian-origin type A influenza virus isolates were epitheliotropic in chickens,
primarily nephrotropic. Such findings were dissimilar from findings with highly
pathogenic avian-origin type A influenza virus isolates both in severity and in
tissue distribution of histopathologic changes and influenza viral antigen.
Descriptors: fowl plague pathology, influenza A virus
avian pathogenicity, antigens, viral analysis, chickens, ducks,
immunohistochemistry, avian isolation and purification, nephritis pathology,
nephritis virology, organ specificity, species specificity, turkeys.
Tashiro, M., M. Reinacher, and R. Rott (1987). Aggravation
of pathogenicity of an avian influenza virus by adaptation to quails. Archives
of Virology 93(1-2): 81-95. ISSN:
Call Number: 448.3 Ar23
Abstract: Influenza virus A/turkey/Ontario/7732/66 (H 5
N 9), which is highly pathogenic to chickens, is nonpathogenic to quails. After
intratracheal or intramuscular inoculation of quails, virus replication was
limited to the respiratory tract, genital organs, and pancreas. However,
aggravation of the pathogenicity was achieved through adaptation only by
several passages of lung homogenates in quails. The adapted virus caused a
fatal generalized infection in quails as well as in chickens. The pathogenic
change of the virus could not be explained by a change in the proteolytic
cleavability of the hemagglutinin, because no difference was found in the
cleavability between the original and the adapted viruses. The adapted virus
formed larger plaques and grew a little faster than the original one in both
chicken embryo and quail embryo cells. The faster multiplication of the adapted
virus at the site of infection might be the reason for its change in
pathogenicity. The original virus could circulate among quails by a direct
contact transmission without causing disease. The shed virus, however, caused a
fatal infection in chickens when they were kept in contact with the infected
quails. The epidemiological significance of this observation is discussed.
Descriptors: Coturnix microbiology, fowl plague
microbiology, influenza A virus avian pathogenicity, quail microbiology,
adaptation, physiological, antibodies, viral analysis, antigens, viral
analysis, central nervous system microbiology, chickens microbiology,
hemagglutinins viral analysis, avian immunology, ribonucleoproteins analysis,
turkeys microbiology, virus replication.
To, K.F., P.K. Chan, K.F. Chan, W.K. Lee, W.Y. Lam,
K.F. Wong, N.L. Tang, D.N. Tsang, R.Y. Sung, T.A. Buckley, J.S. Tam, and A.F.
Cheng (2001). Pathology of fatal human infection associated with avian
influenza A H5N1 virus. Journal of Medical Virology 63(3): 242-6
Abstract: Eighteen cases of human influenza A H5N1
infection were identified in Hong Kong from May to December 1997. Two of the
six fatal cases had undergone a full post-mortem which showed reactive
hemophagocytic syndrome as the most prominent feature. Other findings included
organizing diffuse alveolar damage with interstitial fibrosis, extensive
hepatic central lobular necrosis, acute renal tubular necrosis and lymphoid
depletion. Elevation of soluble interleukin-2 receptor, interleukin-6 and
interferon-gamma was demonstrated in both patients, whereas secondary bacterial
pneumonia was not observed. Virus detection using isolation, reverse
transcription-polymerase chain reaction and immunostaining were all negative.
It is postulated that in fatal human infections with this avian subtype,
initial virus replication in the respiratory tract triggers hypercytokinemia
complicated by the reactive hemophagocytic syndrome. These findings suggest
that the pathogenesis of influenza A H5N1 infection might be different from
that of the usual human subtypes H1-H3.
Descriptors: influenza pathology, influenza virology,
influenza A virus avian isolation and purification, adolescent, adult, bone
marrow pathology, cytokines blood, disease outbreaks, fatal outcome, Hong Kong
epidemiology, influenza epidemiology, lung pathology, lymphoid tissue
pathology, postmortem changes.
Tumpey, T.M., D.L. Suarez, L.E.L. Perkins, D.A.
Senne, J. Lee, Y.J. Lee, I.P. Mo, H.W. Sung, and D.E. Swayne (2003 ). Evaluation
of a high-pathogenicity H5N1 avian influenza A virus isolated from duck meat.
Avian Diseases 47(Special Issue): 951-955. ISSN: 0005-2086.
Call Number: 41.8 Av5
Abstract: The introduction of an influenza A virus
possessing a novel hemagglutinin (HA) into an immunologically naive human
population has the potential to cause severe disease and death. Such was the
case in 1997 in Hong Kong, where H5N1 influenza was transmitted to humans from
infected poultry. Because H5N1 viruses are still isolated from domestic poultry
in southern China, there needs to be continued surveillance of poultry and characterization
of virus subtypes and variants. This study provides molecular characterization
and evaluation of pathogenesis of a recent H5N1 virus isolated from duck meat
that had been imported to South Korea from China. The HA gene of
A/Duck/Anyang/AVL-1/01 (H5N1) isolate was found to be closely related to the
Hong Kong/97 H5N1 viruses. This virus also contained multiple basic amino acids
adjacent to the cleavage site between HA1 and HA2, characteristic of
high-pathogenicity avian influenza viruses (HPAI). The pathogenesis of this
virus was characterized in chickens, ducks, and mice. The DK/Anyang/AVL-1/01
isolate replicated well in all species and resulted in 100% and 22% lethality
for chickens and mice, respectively. No clinical signs of disease were observed
in DK/Anyang/AVL-1/01-inoculated ducks, but high titers of infectious virus
could be detected in multiple tissues and oropharyngeal swabs. The presence of
an H5N1 influenza virus in ducks bearing a HA gene that is highly similar to
those of the pathogenic 1997 human/poultry H5N1 viruses raises the possibility
of reintroduction of HPAI to chickens and humans.
Descriptors: epidemiology, infection, duck meat,
contamination, poultry product, immunologically naive populations,
pathogenesis, viral introduction, viral transmission.
United States. Animal and Plant Health Inspection
Service. (2001). Highly Pathogenic Avian Influenza: a Threat to U.S.
Poultry, Program Aid, Vol. 1704,
United States. Dept. of Agriculture: [Washington, DC]: The Service, 1 folded
sheet 8 p.
Call Number: 1 Ag84Pro no. 1704
Descriptors: nonindigenous pests control, United States,
avian influenza, threat, poultry.
van der Goot, J.A., G. Koch, M.C.M. de Jong, and M.
Van Boven (2003). Transmission dynamics of low- and high-pathogenicity
A/Chicken/Pennsylvania/83 avian influenza viruses. Avian Diseases
47(Special Issue): 939-941. ISSN:
Call Number: 41.8 Av5
Abstract: High-pathogenicity avian influenza (HPAI)
viruses emerged from low-pathogenicity avian influenza (LPAI) viruses in
Pennsylvania (1983-84), Mexico (1994-95), and Italy (1999-2000). Here we focus
on the question of why the HPAI virus supersedes the LPAI virus, once it has
appeared during the epidemic. To study this, we used an experimental model in
chickens that enabled us to estimate the reproduction ratio (R0). Using this
model, we determined the R0 of the A/Chicken/Pennsylvania/21525/83 (LPAI) and
of the A/Chicken/Pennsylvania/1370/83 (HPAI). Comparing the R0 of both viruses,
we concluded that the R0 of the HPAI virus is significantly higher than the R0
of the LPAI.
Descriptors: epidemiology, infection, avian influenza,
infectious disease, respiratory system disease, viral disease, transmission
Vertinskii, K.I. and A.P. Strel' nikov (1974). Gripp
kur. [Avian influenza: pathological studies]. Sbornik Nauchnykh Trudov
Moskovskaya Veterinarnaya Akademiya 73(Pt. 1): 122-125.
Descriptors: pathology, fowl, lesions, symptoms, Moscow
region, avian influenza.
Yamagiwa, A. and C. Itakura (1970). [Fowl plague
prevailing in Manchuria. 4. Central nervous system lesions in chickens
inoculated experimentally with fowl plague virus through serial passage]. Nippon
Juigaku Zasshi Japanese Journal of Veterinary Science 32(5): 251-6. ISSN: 0021-5295.
Call Number: 41.8 J27
Descriptors: central nervous system pathology, fowl plague
pathology, chickens, China, influenza A virus avian, virus cultivation.
Zambon, M.C. (1999). Epidemiology and pathogenesis
of influenza. Journal of Antimicrobial Chemotherapy 44(Suppl. B):
Call Number: RM260.J6
Abstract: Influenza A, B and C all have a segmented
genome, although only certain influenza A subtypes and influenza B cause severe
disease in humans. The two major proteins of influenza are the surface
glycoproteins-haemagglutinin (HA) and neuraminidase (NA). HA is the major
antigen for neutralizing antibodies and is involved in the binding of virus
particles to receptors on host cells. Pandemics are a result of novel virus
subtypes of influenza A, created by reassortment of the segmented genome
(antigenic shift), whereas annual epidemics are a result of evolution of the
surface antigens of influenza A and B virus (antigenic drift). The rapid
evolution of influenza viruses highlights the importance of surveillance in
identifying novel circulating strains. Infectivity of influenza depends on the
cleavage of HA by specific host proteases, whereas NA is involved in the
release of progeny virions from the cell surface and prevents clumping of newly
formed virus. In birds, the natural hosts of influenza, the virus causes
gastrointestinal infection and is transmitted via the faeco-oral route.
Virulent avian influenza strains, which cause systemic disease, have an HA that
is cleaved by proteases present in all cells of the body, rather than by
proteases restricted to the intestinal tract. In mammals, replication of
influenza subtypes appears restricted to respiratory epithelial cells. Most
symptoms and complications, therefore, involve the respiratory tract. However,
systemic complications are sometimes observed and other viral genes besides the
HA, including the NA, may be involved in determination of virulence of
influenza strains in mammals.
Descriptors: antigenic variation physiology, hemagglutinin
glycoproteins, influenza virus physiology, influenza epidemiology,
neuraminidase physiology, antiviral agents therapeutic use, influenza drug
therapy, influenza virology, influenza A virus human pathogenicity,
neuraminidase antagonists and inhibitors, sialic acids therapeutic use.
Zambon, M.C. (2001). The pathogenesis of influenza
in humans. Reviews in Medical Virology 11(4): 227-41. ISSN: 1052-9276.
Descriptors: antigenic variation physiology, influenza
virology, orthomyxoviridae pathogenicity, orthomyxoviridae physiology,
antigenic variation genetics, birds virology, disease reservoirs, evolution,
molecular, hemagglutinin glycoproteins, influenza virus chemistry,
hemagglutinin glycoproteins, influenza virus genetics, hemagglutinin
glycoproteins, influenza virus metabolism, influenza epidemiology, influenza
transmission, neuraminidase genetics, neuraminidase metabolism,
orthomyxoviridae enzymology, orthomyxoviridae genetics.
Zitzow, L.A., T. Rowe, T. Morken, W.J. Shieh, S.
Zaki, and J.M. Katz (2002). Pathogenesis of avian influenza A (H5N1) viruses
in ferrets. Journal of Virology 76(9): 4420-9. ISSN: 0022-538X.
Call Number: QR360.J6
Abstract: Highly pathogenic avian influenza A H5N1
viruses caused outbreaks of disease in domestic poultry and humans in Hong Kong
in 1997. Direct transmission of the H5N1 viruses from birds to humans resulted
in 18 documented cases of respiratory illness, including six deaths. Here we
evaluated two of the avian H5N1 viruses isolated from humans for their ability
to replicate and cause disease in outbred ferrets. A/Hong Kong/483/97 virus was
isolated from a fatal case and was highly pathogenic in the BALB/c mouse model,
whereas A/Hong Kong/486/97 virus was isolated from a case with mild illness and
exhibited a low-pathogenicity phenotype in mice. Ferrets infected intranasally
with 10(7) 50% egg infectious doses (EID(50)) of either H5N1 virus exhibited
severe lethargy, fever, weight loss, transient lymphopenia, and replication in
the upper and lower respiratory tract, as well as multiple systemic organs,
including the brain. Gastrointestinal symptoms were seen in some animals. In
contrast, weight loss and severe lethargy were not noted in ferrets infected
with 10(7) EID(50) of two recent human H3N2 viruses, although these viruses
were also isolated from the brains, but not other extrapulmonary organs, of
infected animals. The results demonstrate that both H5N1 viruses were highly
virulent in the outbred ferret model, unlike the differential pathogenicity
documented in inbred BALB/c mice. We propose the ferret as an alternative model
system for the study of these highly pathogenic avian viruses.
Descriptors: disease models, animal, ferrets, influenza
physiopathology, influenza A virus avian pathogenicity, adolescent, child,
preschool, influenza pathology, influenza virology, lung pathology, lung virology, virulence,
virus replication.