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OVERVIEW: What every practitioner needs to know
Are you sure your patient has bacterial meningitis? What should you expect to find?
Patients usually present with fever (which may be absent in patients receiving immunosuppressive agents) accompanied by meningeal symptoms and the physical findings indicative of meningitis.
Headache. A generalized headache is the rule. A more localized headache should make you worry about brain abscess or brain tumor. Because meningitis is accompanied by severe inflammation, headache should be severe and you would not expect it to be relieved by over-the-counter medications. Little difference in the character of headache has been reported between patients with bacterial versus viral versus fungal meningitis.
Stiff neck. Rigidity of neck muscles (i.e., inability to touch chin to chest) is the rule. Neck stiffness may not be seen in patients receiving corticosteroids or other immunosuppressive agents. Classically, this sign is absent in patients with cryptococcal meningitis. Neck stiffness is often surprisingly severe in patients with viral meningitis. Textbooks often emphasized Kernig's (i.e., bend knee up to chest and then straighten the leg) and Brudzinski's signs (i.e., flex neck and the patient draws up knees).
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However, the signs were more useful in the preantibiotic era. In modern medicine, these findings are most commonly encountered in patients with chronic forms of meningitis (e.g., fungal and tuberculous). Their sensitivity is extremely low (5-9%) in bacterial meningitis. Nuchal rigidity only has a sensitivity of 30% and a positive predictive value of 26%.
Vomiting. Vomiting may accompany headache and probably reflects brainstem irritation. The prognostic importance of vomiting and its frequency have not been fully explored in the literature.
Depressed mental status is the single most important characteristic to evaluate in your initial physical exam. To objectively assess mental status, the Glasgow Coma Score should be applied. Mental status most closely correlates with outcome, and is used to determine whether or not to administer corticosteroids.
No focal neurological deficits. A careful neurological exam is critical. Careful examination of the cranial nerves should be performed. Specific cranial nerve findings may suggest localized infections or increased cranial pressure.
Papilledema should not be seen in acute bacterial meningitis because edema of the retinal area takes 48-72 hours to develop and bacterial meningitis usually develops over 12-24 hours. In early meningitis, elevated cerebrospinal fluid (CSF) pressure is rare and usually develops in the later stages of the illness when inflammation is extreme. The findings of any focal neurological deficits or papilledema raise the possibility of a space occupying lesion and represent a contraindication for lumbar puncture.
How did the patient develop bacterial meningitis? What was the primary source from which the infection spread?
Remember, bacterial meningitis usually arises as a consequence of bacteremia, and bacteremia arises as a consequence of a primary infection at one of six sites (this is sometimes termed portal of entry, because this is the site from which bacteria gain entry into the bloodstream). Therefore, each site needs to be evaluated by physical exam, and if symptoms and signs are suggestive of involvement of any of these sites, imaging studies may be indicated:
Pharyngitis. For patients with erythema of the posterior pharynx and possibly symptoms of sore throat and who subsequently develop signs and symptoms of meningitis, you need to keep in mind the possibility of meningococcal diseases. This infection can be spread from person to person by droplets, and Neisseria meningitidis can be carried asymptomatically by healthy individuals. In early studies in military recruits, those who lacked specific protective antibodies against N. meningitidis had a 33% risk over 3 weeks of developing N. meningitidis bacteremia and/or meningitis. Always worry about this organism in crowded environments, such as dormitories.
Otitis media. In children, otitis media is the leading primary infection associated with bacterial meningitis. Prior to the use of Haemophilus influenzae vaccine, H. influenzae was the most common bacterial cause of pediatric meningitis. Now it is rare. Otitis media is also caused by Streptococcus pneumoniae, and this is now the most common pathogen to result in otitis media associated bacterial meningitis.
Sinusitis. This form of infection less commonly leads to bacteremia and only rarely spreads directly to the meninges. The most feared form of bacterial sinusitis is sphenoid sinusitis and, if the bacteria spread beyond the walls of this sinus, bacterial infection of the large complex of veins called the cavernous sinus can result in their thrombosis. Spread to the cavernous sinuses has also been associated with bacterial meningitis. The most common bacteria to result in sinusitis-associated meningitis are S. pneumoniae and H. influenzae.
Pulmonary infection. Lobar pneumonia due to S. pneumoniae is associated with bacteremia in a significant percentage of cases (10-16%, approximately), and bacteremia can result in meningitis. A depressed mental status in a patient with pneumonia should always raise concerns about the possibility of bacterial meningitis.
Endocarditis. Bacterial endocarditis results in persistent bacteremia. Most pathogens associated with this infection rarely cause bacterial meningitis. One exception is Staphylococcus aureus and this invasive pathogen often results in cerebritis, which results in a para-meningeal CSF formula, but rarely actually infects the meninges. Another exception is S. pneumoniae. This rare infection mostly occurs in patients with liver disease or immunosuppression, and in nearly half of cases is complicated by meningitis.
Gastroenteritis. Listerie monocytogenes is a foodborne pathogen commonly contracted by eating foods refrigerated for prolonged periods (Listeria can grow on foods at 4°C), such as deli meats, soft cheeses, and a variety of other foods. On ingesting Listeria-contaminated food, patients with defects in cell-mediated immunity develop bacteremia. Listeria has a unique propensity to infect the meninges and can also invade the brain stem, causing rhombencephalitis. Less commonly, this pathogen can invade the cerebral cortex.
Which individuals are of greater risk of developing bacterial meningitis?
There are specific conditions that predispose patients to bacterial meningitis, and these conditions need to be explored by history and laboratory examination:
Immunoglobulin deficiency. Specific antibodies are capable of binding to encapsulated organisms such as S. pneumoniae through their variable region and then attaching to the immunoglobulin Fc receptors on neutrophils and macrophages to stimulate phagocytosis (or ingestion) of bacteria; stimuli that induce phagocytosis are termed opsonins. Patients with deficiencies in immunoglobulins or an inability to generate specific antibodies against encapsulated organisms are at risk for developing bacteremia and meningitis from these pathogens.
Splenectomy. The spleen filters 10% of the blood flow and allows the blood to pass by resident macrophages and lymphocytes. Foreign objects such as bacteria, particularly when bound with immunoglobulin, are readily phagocytosed and cleared from the blood stream. Patients without spleens are at higher risk for the development of overwhelming S. pneumoniae, H. influenzae, and N. meningitidis sepsis.
Terminal complement deficiency. The terminal complement components are responsible for forming what is sometimes termed an attack complex capable of lysing the lipid laden outer cell wall of Neisseria species, and patients deficient in the production of these products are at increased risk for systemic N. meningitidis infection. It is estimated that 33% of sporadic cases of meningococcal meningitis have a defect in the production of these terminal complement pathway products.
Head trauma with dural leak. Remember, patients who have had significant head trauma, particularly in association with motor vehicle accidents, are at increased risk for CSF leaks in the area of the cribriform plate, as well as at the base of the skull near the middle ear. Patients with cribriform plate defects may have a history of unexplained clear fluid drainage from the nose. Usually, when meningitis occurs, the inflammation temporarily closes the CSF leak. Any patient who suffers more than one episode of S. pneumoniae should undergo studies to exclude a CSF leak.
Immunocompromised patients. Patients receiving immunosuppressants to prevent solid organ rejection or patients who have undergone hematopoietic cell transplant, as well as patients receiving high-dose corticosteroids and patients with AIDS, have depressed cell-mediated immunity and are at increased risk for L. monocytogenes.
Elderly (older than 55 years of age). These individuals also have reduced cell-mediated immunity and are at increased risk for L. monocytogenes.
Post neurosurgery. Following neurosurgery, patients are at risk for meningitis due to nosocomial pathogens, predominantly Gram-negative bacilli, S. aureus and Enterococcus.
Beware: there are other diseases that can mimic bacterial meningitis
Cerebrovascular accident. In particular, subarachnoid hemorrhage can result in headache and depressed mental status. Fever is uncommon initially, and the headache comes on with extreme suddenness.
Brain abscess. Patients suffering with brain abscess may complain of headaches; however, headache is often localized to the side where the brain abscess is located. These patients can develop a depressed mental status and can also present with seizures. Avoid lumbar puncture in these patients because of the danger of herniation.
Brain tumor. Patients with brain tumors can present identically to brain abscess, and, when their mental status is depressed or they develop seizures, the problem can be mistaken for meningitis. Avoid lumbar puncture in these patients as well because of the risk of herniation.
Drug overdose. Depressed sensorium accompanied by fever can also be the result of a drug overdose combined with an aspiration pneumonia. These patients' symptoms can be difficult to differentiate from bacterial meningitis, and such patients often require lumbar puncture to exclude this diagnosis.
"Chemical" meningitis. Following epidural anesthesia, anesthetics and contaminants can result in an increase in CSF neutrophils and a low CSF glucose. Similar findings can accompany epidermoid tumors or craniopharyngiomas that leak material into the subarachnoid space. Additionally, hypersensitivity reactions to some drugs, especially NSAIDs, several antibiotics and IV immunoglobulin preparations can result in symptoms indistinguishable from those seen with bacterial meningitis.
Elderly patient with fever and confusion. Elderly patients who have had any prior CNS problems may become confused as a consequence of fever or a metabolic imbalance. Because under these circumstances there may be no focal neurological deficits and because many elderly patients may have stiff neck muscles under normal circumstances, it is clinically impossible to differentiate toxic metabolic encephalopathy from meningitis. Therefore, in elderly patients with confusion accompanied by fever, clinicians should have a low threshold to perform a lumbar puncture.
What laboratory studies should you order and what should you expect to find?
Peripheral white blood cell (WBC) with differential. In acute bacterial meningitis, expect an elevated peripheral WBC with increased percentage of bands and polymorphonuclear leukocytes (PMNs). In tuberculous meningitis, rarely there can be a leukemoid reaction (WBC >30,000), but more commonly the percentage of peripheral monocytes is increased. In patients with cryptococcal meningitis, the peripheral lymphocyte count may be decreased, reflecting previously undiagnosed HIV infection that has progressed to AIDS.
Results that confirm the diagnosis
Blood cultures. Blood cultures are very helpful and may be positive, particularly in Listeria, pneumococcal and meningococcal meningitis. Serum cryptococcal antigen is positive in almost all HIV-infected patients with cryptococcal meningitis.
Lumbar puncture. Lumbar puncture (LP) is the critical test for making the diagnosis of meningitis. There is no other diagnostic study capable of diagnosing or ruling out infection of the meninges. If meningitis is part of your differential diagnosis, a lumbar puncture should always be performed if there are no focal neurologic deficits or papilledema to suggest an intracranial mass lesion. The IDSA guidelines have recommended CT scan for all patients with depressed sensorium. A recent review of the Swedish quality registry has revealed that CT significantly delays antibiotic administration, and based on this analysis impaired mental status should no longer be considered a contraindication for lumbar puncture. However, in patients with focal neurological deficits or papilledema, a CT scan with contrast should be performed before lumbar puncture, and, if a space-occupying lesion is found, the lumbar puncture is contraindicated because of an approximately 30% risk of herniation.
CSF profile interpretation (Table I). The cellular response seen in the CSF is very helpful for narrowing the possible etiology. The usual bacterial pathogens induce an acute inflammatory response consisting of neutrophils, although intracellular pathogens, particularly tuberculosis, fungi and to some extent Listeria induce lymphocytic response. A decrease in CSF glucose is thought to be the consequence of impaired blood-brain barrier glucose transport as a consequence of severe inflammation and damage. A normal CSF glucose should be two-thirds the serum glucose. In many patients, a simultaneous blood sugar is not drawn at the time of the lumbar puncture, making interpretation of this value problematic. However, severe cases of bacterial meningitis with markedly depressed mental status are usually accompanied by a very low CSF glucose levels (<25 mg/dL). The elevation in protein is thought to be due to damage to the blood-brain barrier and leakage of serum proteins into the CSF. CSF proteins are usually highest in bacterial meningitis and can reach 1,000 mg/dL.
Table I.
|Type of Infections
|Glucose (nl 2/3 serum)
|Untreated Bacterial
|Low (can be < 25 m/dl)
|High (150-1000 mg%)
|(except Listeria)
|Partially Treated
|Moderately high (80-500 mg%)
|Slight elevation (60-150 mg%)
|Parameningeal (brain abscess)
|Lymphs or PMN
|Normal or slightly elevated
Untreated bacterial. A predominance of neutrophils (usually >90% PMN), a markedly low CSF glucose (also termed hypoglycorrhachia), and an elevated CSF protein are seen almost exclusively in bacterial meningitis. The CSF formula always warrants empiric antibiotic coverage. In patients with greater than 90% PMN and the appropriate risk factors, Listeria meningitis should be suspected and empiric coverage for this pathogen should be added (ampicillin or bactrim if PCN allergic).
Tuberculous, fungal, treated bacterial. A predominance of lymphocytes, a moderately low CSF glucose and a moderately elevated CSF protein are the most common findings. This profile is found in patients with tuberculous meningitis (although PMNs may be seen early), fungal meningitis (Cryptococcus the most common form, particularly in patients with AIDS and solid organ transplant patients), and in patients who have partially treated bacterial meningitis (i.e., have received antibiotics more than 24 hours prior to lumbar puncture). The CSF cryptococcal antigen test is very specific and sensitive. If this test is negative, cryptococcal meningitis is essentially excluded.
Viral. A predominance of lymphocytes, a normal CSF glucose, and a modestly elevated CSF protein (usually not > 200 mg/ml) represent the most typical findings. This profile strongly suggests a viral meningitis. Occasionally, viral meningitis, particularly in children, may fluctuate between 100% lymphocytes and 60-70% lymphocytes with 30-40% PMNs. In these patients, the wisest course of action is to cover with antibiotics for 24-48 hours awaiting the CSF culture results to exclude bacterial meningitis, particularly Listeria. When a patient has both a depressed mental status and a viral CSF profile, viral encephalitis needs to be considered.
Parameningeal. A few PMNs and/or lymphocytes with a normal CSF glucose and a normal or slightly elevated protein are typical. This CSF profile is seen when an infection lies near the meninges (parameningeal) but does not directly involve this area. Examples include brain abscess, otitis media, sphenoid and/or frontal bacterial sinusitis. When this CSF profile is observed, CNS imaging should be performed.
If the CSF profile shows a predominance of PMN, what other CSF tests should be ordered?
CSF Gram Stain. In approximately 80% of bacterial meningitis cases, CSF Gram stain is positive and reveals the pathogen. Because Listeria is an intracellular pathogen, CSF Gram stain reveals this organism in approximately 30% of cases.
Latex agglutination for bacteria has no greater sensitivity or specificity than Gram stain and is generally not recommended.
If the CSF profile shows a lymphocytes and a low glucose, what other CSF tests be ordered?
CSF cryptococcal antigen latex agglutination.
CSF acid fast stain and polymerase chain reaction (PCR) for TB.
Mycobacterial and fungal culture.
Peripheral and CSF Venereal Disease Related Laboratory (VDRL) test, as well as a peripheral FTA-ABS or other specific treponema test (MHA-TP, TP-PA). In some cases of syphilitic meningitis, the peripheral VDRL can be negative; however, the peripheral specific treponemal test should always be positive.
If the CSF profile shows lymphocytes and a normal CSF, are other CSF tests indicated?
Generally, not, but the exception is that recurrent bouts of viral meningitis raise the possibility of herpes simplex type 2 viral meningitis (Mollaret's meningitis). A CSF PCR for herpes simplex should be performed, and if positive, acyclovir treatment should be considered.
What imaging studies will be helpful in making or excluding the diagnosis of bacterial meningitis?
CXR. Particularly in patients with pneumococcal meningitis, CXR may reveal a lobar infiltrate. Other forms of pneumonia are rarely accompanied by meningitis. However, if the individual's sensorium is markedly depressed or he/she has suffered seizure radiologic changes consistent with aspiration, pneumonia may also be observed.
CT scan with contrast or MRI with contrast. This should be performed if there are physical findings or history suggesting the possibility of brain abscess or brain tumor. In these patients, lesions are generally enhanced by contrast. In patients with meningitis, increased contrast uptake may be seen throughout the meninges. However, this finding is nonspecific. If CNS imaging is to be performed, empiric antibiotics should be initiated after blood cultures have been drawn and before the imaging study. The average time required to complete a CT scan is more than 45 minutes, and in cases of bacterial meningitis, this delay in the initiation of antibiotics can result in increased mortality and morbidity.
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What consult service or services would be helpful for making the diagnosis and assisting with treatment?
Neurology consult. This assists in determining the level of coma and finding if there are focal neurological deficits.
Infectious disease consult. This assists in managing many nuances with regard to empiric antibiotic coverage, as well as for the antibiotic treatment of pneumococcal meningitis.
If you decide the patient has bacterial meningitis, what therapies should you initiate immediately?
Antibiotics should be initiated within 30 minutes. Administer the highest dose of each antibiotic allowable. The blood-brain barrier reduces antibiotic penetration into the central nervous system; therefore, to achieve therapeutic levels in the CSF, maximal doses are required and should be administered intravenously (sometimes referred to as meningeal doses).
The duration of therapy depends on the organism and the response to therapy. For most cases, 10-14 days of antibiotics are sufficient for bacterial meningitis. The one exception to this rule is L. monocytogenes, because relapse is common if the duration of therapy is not extended to 3 weeks. Fungal and tuberculous meningitis require months of therapy while viral meningitis is a self-limited infection that generally does not require therapy. The one exception to this rule is meningitis due to herpes simplex. Intravenous acyclovir or valacyclovir is recommended for these cases.
1. Antibacterial agents
If I am not sure what bacteria is causing the infection what antibiotics should I order?
The empiric regimens depend on the patient's age, underlying diseases and whether or not the patient has recently been hospitalized or undergone neurosurgery (Table II).
- Neonates require Gram-negative and Group B streptococcal coverage: Cefepime and ampicillin.
- Older children require coverage for S. pneumoniae, N. meningitidis, and H. infuenzae (rare in children who have received the H. influenzae B vaccine): ceftriaxone and vancomycin (until PCN-resistant S. pneumoniae excluded).
- Otherwise healthy adults younger than 55 years of age require coverage for S. pneumoniae, N. meningitides, and H. influenzae (rare in adults): Ceftriaxone and Vancomycin (until PCN-resistant S. pneumoniae excluded).
- Immunocompromised patients (on corticosteroids or other immunosuppressive drugs) should be treated for L. monocytogenes in addition to S. pneumoniae, N. meningitidis, and H. influenzae: ampicillin, ceftriaxone, and vancomycin (until PCN-resistant S. pneumonia excluded).
- Adults older than 55 years of age should also be empirically covered for L. monocytogenes in addition to S. pneumoniae, N. meningitidis, and H. influenzae: ampicillin, ceftriaxone, and vancomycin (until PCN-resistant S. pneumoniae excluded).
- Post neurosurgery needs to cover for Gram-negative bacilli, S. aureus, including MRSA and Enterococcus: cefepime and vancomycin.
2. Other key therapeutic modalities
Corticosteroids. In adult bacterial meningitis, the beneficial effects of corticosteroids are seen in those with a specific level of mental status depression (Glasgow Coma Scale score 8-11). Although no benefit has been documented for more severe coma scores, many clinicians administer dexamethasone (10 mg Q6H IV x 4 day) in all patients with Glasgow Coma Scale scores of 11 or less.
In developing countries, studies have failed to reveal any benefit from dexamethasone. However, in industrialized countries where patients seek medical attention more promptly, studies do suggest some benefit. No harmful side effects have been documented as a consequence of short course dexamethasone; however, CSF penetration of vancomycin may be impaired as a consequence of improved integrity of the blood-brain barrier, and, in patients with PCN-resistant S. pneumoniae, rifampin should be added to the antibiotic regimen to assure cidal CSF activity.
The major complications associated with meningitis arise as a consequence of excessive inflammation. Multiple studies have demonstrated a reduced incidence of deafness, particularly in children, and improved overall outcome if this inflammatory response in bacterial meningitis can be blunted by the administration of high-dose corticosteroids. The benefits of dexamethasone in adults has been demonstrated for S. pneumoniae, but not for N. meningitidis.
Because the cell walls of the bacteria often break down quickly in response to cidal antibiotics, such as cephalosporin, penicillin and vancomycin, and the release of cell wall products can induce a cascade of inflammatory stimuli, corticosteroids should be given before or simultaneously with anti-infective therapy.
Hydration with normal saline. Because of the association of cerebral edema with bacterial and fungal meningitis, administration of free water should be avoided. To maintain fluid and electrolyte balance, normal saline should always be administered. D5W or D5½ normal saline are contraindicated. Hypertonic saline has been shown to reduce cerebral edema, and may be considered in severely ill patients.
Positioning of the head. The head should be positioned at a 30° angle. This will maximize cerebral venous drainage while not significantly compromising cerebral blood flow. This helps reduce CSF pressure.
Intubation and ventilatory support to reduce PaCO2 to 27-30 mmHg are often required. Reductions in PaCO2 result in cerebral vessel constriction that reduce intracerebral blood volume and reduce CSF pressure.
Mannitol or glycerol. If lumbar puncture reveals a CSF pressure greater than 300 mm H2O, the administration of hypertonic solutions that can draw free water from the central nervous system should be considered, and these products can at least temporarily reduce cerebral edema and elevated CSF pressure. If a high CSF pressure is noted at the time of lumbar puncture (LP), immediately replace the stylet and only use the fluid in the manometer for culture, cell count and Gram stain.
Do not immediately remove the LP needle, because the needle leaves a tear in the dura and will allow CSF to leak from this site. This condition can lead to brain stem herniation. Initiation of intravenous mannitol (20% solution administered at a rate of 200 cc/h) should reduce CSF pressure within 30-45 minutes, and the LP needle can be removed at that time
In pediatric cases, oral glycerol has been shown to reduce deafness, as well as other neurological sequelae; however, in adults, their use is of questionable benefit. The role of hypertonic solutions with regards to improving mortality remains controversial.
Antiseizure medications. Preventive administration of seizure medications is not recommended by most experts because less than one-third of cases of bacterial meningitis develop seizures during their acute illness. Standard grand-mal antiseizure medical regimens are recommended.
What complications could arise as a consequence of bacterial meningitis? What should you tell the family about the patient's prognosis?
- Persistent sensorineural hearing loss occurs in 10% of children but is rare in adults. It is most commonly associated with S. pneumoniae and H. influenzae.
- Seizures (focal or generalized) occur in 20-30% of patients, usually because of cerebral infarction resulting from cerebral arteritis or cortical vein thrombosis. Alcohol withdrawal can be a confounding factor in some cases.
- Elevated CSF pressure due to cerebral edema and/or hydrocephalus can occur and lead to temporal lobe herniation (found in one-fourth of fatal cases).
- Focal neurological deficits, including hemiparesis, dysphasia, and visual field defects caused by arterial or cortical vein occlusions can occur.
- Bacterial meningitis is a very serious infection. If treatment is prompt a rapid recovery can be expected.
- Delays in therapy increase the likelihood of complications and/or death.
- A poor outcome is more likely in patients who are obtunded, elderly, have seizures within the first 24 hours, develop focal neurological deficits, or have an underlying disease (e.g., leukemia, liver disease, alcoholism).
- Overall mortality for bacterial meningitis depends on the organism: 5% for H. influenzae; 10% for N. meningitides; 20% for S. pneumoniae; 20-30% for L. monocytogenes; 20-30% for gram-negative bacillary meningitis (but may be improving with more rapid diagnosis and more effective treatment).
- After recovery, 10-20% of patients have residual neurological deficits. Twenty-five percent of adults who "fully" recovered were subsequently found to have cognitive slowing or other neuropsychological deficits 6-24 months after discharge from the hospital.
- Deafness occurs uncommonly in children.
How do you contract bacterial meningitis and how frequent is the disease?
The World Health Organization (WHO) estimates that there are 1.2 million cases of bacterial meningitis per year worldwide. The incidence of bacterial meningitis in the U.S. has been declining: in 1998-1999 it was 2.00 cases per 100,000, which decreased to 1.38 cases per 100,000 population in 2006-2007.
The epidemiology of bacterial meningitis depends on the etiologic agent:
S. pneumoniae is the most common cause of community acquired bacterial meningitis. It colonizes the nasopharynx of 20% of healthy adults. Colonization is higher during the late fall, winter and early spring. The capsular serotypes that are most likely to cause disease are types 3, 4, 6, 7, 9, 12, 14, 18, 19, and 23. It is spread from person to person by close personal contact. Native Americans and Australian Aboriginal populations are at higher risk of disease, as are patients with immunoglobulin deficiencies or splenectomy.
N. meningitidis is second in prevalence, and is a major problem in developing countries. Rates of meningococcal disease are as high as 5-10 per 100,000 in sub-Saharan Africa. Epidemics in this region are cyclic, occurring every 8-10 years, and can be associated with incidences as high as 1/1000. Local outbreaks also occur in the U.S., Canada, Europe, Japan, Australia and other industrialized countries; however, the overall incidence is lower (0.3-2 per 100,000). The organism colonizes the nasopharynx and is spread from person to person by respiratory droplets. It has an 8-25% colonization rate in adults (highest in adolescents and closed populations (military recruits); higher rates are associated with intimate personal contact and crowding (e.g., dormitories, bars, social events). Infection usually develops within 1-14 days of acquiring the organism. Six serogroups cause disease: A, B, C, W-135, X and Y.
L. monocytogenes is the third to fourth most common cause of community acquired bacterial meningitis. The incidence of listeriosis is only 0.7 cases per 100,000 but is higher in those older than 70 years of age (2.1/100,000), pregnant women (12/100,000), and transplant and HIV patients (100/100,000). It is foodborne (raw milk and cheeses, raw vegetables and fruits, undercooked chicken, hot dogs, and virtually any other processed food product). Prolonged refrigeration is a risk, because the organism is able to grow at 4°C (39°F). Bermudez A, Delicatessen foods are a danger. Microwave reheating usually does not kill this pathogen (>74°C or >165°F required for sterilization).
H. Influenzae is now a rare cause of bacterial meningitis because of widespread H. influenzae B (HIB) vaccination. Adult infections are now 1.7/100,000. H. Influenzae is carried in the nasopharynx 3-5% of children if not vaccinated (much lower following vaccination) and as a consequence a nonimmune household contact of an infected patient is at 600 times higher risk of infection. Patients with HIV are at greater risk (15-79/100,000). Patients with immunoglobulin deficiencies, sickle cell disease, splenectomy, history of recurrent otitis media, Native Americans and attendees of daycare centers are at higher risk.
What pathogens are responsible for this disease?
Table III. Pathogens
Table III.
|Nosocomial %
|S. pneumoniae
|N. meningitidis
|Group B Streptococci
|Listeria monocytogenes
|H. Influenzae
|Staphylococcocus aureus
|Gram-negative Bacilli
How do these pathogens cause bacterial meningitis?
During bacterial meningitis, bacteria generally gain access to the subarachnoid space as a consequence of bacteremia (Table III). Less frequently, bacteria can spread to this space by direct spread as a consequence of a CSF leak following head trauma that damages the cribriform plate or results in a basilar skull fracture. Once bacteria gain entry into the sterile subarachnoid space that lacks complement and immunoglobulins, bacteria can grow rapidly. Because of the rapid progression of this infection, emergent treatment is indicated to prevent irreversible neurological damage.
When bactericidal antibiotics are administered, components of the bacterial cell wall are released, stimulating toll-like receptors that in turn stimulate the release of acute inflammatory cytokines. These bacterial products also serve to attract and activate neutrophils that release toxic proteases and oxygen byproducts. These acute inflammatory responses result in cerebral edema, as well as arterial and venous thrombosis. As a consequence of these events, arterial circulation to the cerebral cortex is impaired, leading to cerebral infarction.
What other clinical manifestations may help me to diagnose and manage bacterial meningitis?
Changes in mental status usually include a loss of orientation and lethargy. Less commonly, patients become manic and their symptoms can mimic a psychiatric illness. Bacterial meningitis needs excluded for any patient with sudden behavioral changes that are accompanied by fever.
What other additional laboratory findings may be ordered?
CSF lactate levels are high in bacterial meningitis and can be helpful in differentiating bacterial from viral meningitis. The cut-off level varies from laboratory to laboratory. A CSF level above 2.1-4.44 strongly suggests bacterial meningitis.
How can bacterial meningitis be prevented?
Conjugate vaccines have proven highly effective for preventing bacterial meningitis. H. influenzae type B conjugate vaccine has virtually eliminated H. influenzae bacterial meningitis in the pediatric population. Recent studies have also demonstrated the efficacy of the meningococcal vaccine in young children and adolescents. A conjugate vaccine directed against meningococcal serotypes A, C, W135, and Y polysaccharides is recommended for all persons 11-18 years of age. More recently, recombinant vaccines against serotype B have become available, however routine administration is not presently recommended, being left up to the discretion of the physician and the family. The recommended age for administration is 16-18 years.
The 23-valent pneumococcal capsular antigen vaccine has been shown to reduce invasive pneumococcal disease in many patient populations, including those over age 65. More recently, a 13-valent conjugate pneumococcal vaccine has become available, and should be administered in addition to the older 23-valent vaccine. The incidence of pneumococcal meningitis has decreased with the increased use of the vaccine; however, disease caused by serotypes not found in the vaccine has been observed. It is hoped that the 13-valent conjugated vaccine will lead to even greater reductions in invasive pneumococcal disease, including meningitis.
H. influenzae. Rifampin 20 mg/kg daily x 4 days is recommended for household or possibly for daycare center contacts younger than 2 years of age. Prophylaxis should be instituted quickly, because secondary cases usually develop within 6 days of the index case.
WHAT'S THE EVIDENCE for specific management and treatment recommendations?
General reviews
Kim, KS.. "Acute bacterial meningitis in infants and children". Lancet Infect Dis. vol. 10. 2010. pp. 32-42. (Emphasizes the importance of rapid institution of antibiotics and coverage for potential antibiotic resistant S. pneumoniae.)
Lin, AL, Safdieh, JE.. "The evaluation and management of bacterial meningitis: current practice and emerging developments". Neurologist. vol. 16. 2010. pp. 143-51. (Emphasizes the poor sensitivity of the classic triad of fever, neck stiffness and altered mental status. Recommends adding headache to this triad to improve sensitivity.)
Large clinical series
van de Beek, D, de Gans, J, Spanjaard, L, Weisfelt, M, Reitsma, JB, Vermeulen, M.. "Clinical features and prognostic factors in adults with bacterial meningitis". N Engl J Med. vol. 351. 2004. pp. 1849-59.
Thomas, KE, Hasbun, R, Jekel, J, Quagliarello, VJ.. "The diagnostic accuracy of Kernig's sign, Brudzinski's sign, and nuchal rigidity in adults with suspected meningitis". Clin Infect Dis. vol. 35. 2002. pp. 46-52.
Durand, ML, Calderwood, SB, Weber, DJ. "Acute bacterial meningitis in adults. A review of 493 episodes". N Engl J Med. vol. 328. 1993. pp. 21-8.
Thigpen, MC, Whitney, CG, Messonnier, NE. "Bacterial meningitis in the United States, 1998-2007". N Engl J Med. vol. 364. 2011. pp. 2016-25.
Huang, CR, Chen, SF, Lu, CH. "Clinical characteristics and therapeutic outcomes of nosocomial super-infection in adult bacterial meningitis". BMC Infect Dis. vol. 11. 2011. pp. 133
Moon, SY, Chung, DR, Kim, SW. "Changing etiology of community-acquired bacterial meningitis in adults: a nationwide multicenter study in Korea". Eur J Clin Microbiol Infect Dis. vol. 29. 2010. pp. 793-800.
Georges, H, Chiche, A, Alfandari, S, Devos, P, Boussekey, N, Leroy, O.. "Adult community-acquired bacterial meningitis requiring ICU admission: epidemiological data, prognosis factors and adherence to IDSA guidelines". Eur J Clin Microbiol Infect Dis. vol. 28. 2009. pp. 1317-25.
Barahona-Garrido, J, Hernandez-Calleros, J, Tellez-Avila, FI, Chavez-Tapia, NC, Remes-Troche, JM, Torre, A.. "Bacterial meningitis in cirrhotic patients: case series and description of the prognostic role of acute renal failure". J Clin Gastroenterol. vol. 44. 2010. pp. e218-23.
Vibha, D, Bhatia, R, Prasad, K, Srivastava, MV, Tripathi, M, Singh, MB.. "Clinical features and independent prognostic factors for acute bacterial meningitis in adults". Neurocrit Care. vol. 13. 2010. pp. 199-204.
Weisfelt, M, de Gans, J, van der Ende, A, van de Beek, D.. "Community-acquired bacterial meningitis in alcoholic patients". PLoS One. vol. 5. 2010. pp. e9102
Kasanmoentalib, ES, Brouwer, MC, van der Ende, A, van de Beek, D.. "Hydrocephalus in adults with community-acquired bacterial meningitis". Neurology. vol. 75. 2010. pp. 918-23.
Gerber, J, Nau, R.. "Mechanisms of injury in bacterial meningitis". Curr Opin Neurol. vol. 23. 2010. pp. 312-8.
Koedel, U, Klein, M, Pfister, HW.. "New understandings on the pathophysiology of bacterial meningitis". Curr Opin Infect Dis. vol. 23. 2010. pp. 217-23.
Kim, BJ, Hancock, BM, Bermudez, A, Del Cid, N. "Bacterial induction of Snail1 contributes to blood-brain barrier disruption". J Clin Invest. vol. 125. 2015. pp. 2473-83. (Bacteria stimulate the induction of Snail1 causing a breakdown in the tight junctions of the blood-brain barrier and prevention of upregulation of Snail 1 prevents this effect.)
Lumbar puncture
Michael, B, Menezes, BF, Cunniffe, J. "Effect of delayed lumbar punctures on the diagnosis of acute bacterial meningitis in adults". Emerg Med J. vol. 27. 2010. pp. 433-8.
Huy, NT, Thao, NT, Diep, DT, Kikuchi, M, Zamora, J, Hirayama, K.. "Cerebrospinal fluid lactate concentration to distinguish bacterial from aseptic meningitis: a systemic review and meta-analysis". Crit Care. vol. 14. 2010. pp. R240
Sakushima, K, Hayashino, Y, Kawaguchi, T, Jackson, JL, Fukuhara, S.. "Diagnostic accuracy of cerebrospinal fluid lactate for differentiating bacterial meningitis from aseptic meningitis: a meta-analysis". J Infect. vol. 62. 2011. pp. 255-62.
Rafi, W, Chandramuki, A, Mani, R, Satishchandra, P, Shankar, SK.. "Rapid diagnosis of acute bacterial meningitis: role of a broad range 16S rRNA polymerase chain reaction". J Emerg Med. vol. 38. 2010. pp. 225-30.
Glimåker, M, Johansson, B, Grindborg, Ö, Bottai, M. "Adult bacterial meningitis: earlier treatment and improved outcome following guideline revision promoting prompt lumbar puncture". Clin Infect. Dis. vol. 60. 2015. pp. 1162-9. (Depressed mental status should not be considered a contraindication for LP.)
Hughes, DC, Raghavan, A, Mordekar, SR, Griffiths, PD, Connolly, DJ.. "Role of imaging in the diagnosis of acute bacterial meningitis and its complications". Postgrad Med J. vol. 86. 2010. pp. 478-85.
Overall guidelines for treatment
Tunkel, AR, Hartman, BJ, Kaplan, SL. "Practice guidelines for the management of bacterial meningitis". Clin Infect Dis. vol. 39. 2004. pp. 1267-84.
Beckham, JD, Tyler, KL.. "Initial management of acute bacterial meningitis in adults: summary of IDSA guidelines". Rev Neurol Dis. vol. 3. 2006. pp. 57-60.
Antibiotic treatment
van de Beek, D, Brouwer, MC.. "No difference between short-course and long-course antibiotics for bacterial meningitis in children, but available evidence limited". Evid Based Med. vol. 15. 2010. pp. 6-7.
Molyneux, E, Nizami, SQ, Saha, S. "5 versus 10 days of treatment with ceftriaxone for bacterial meningitis in children: a double-blind randomised equivalence study". Lancet. vol. 377. 2011. pp. 1837-45.
Laxmi, S, Tunkel, AR.. "Healthcare-Associated Bacterial Meningitis". Curr Infect Dis Rep. 2011.
Sakata, H, Sato, Y, Nonoyama, M. "Results of a multicenter survey of diagnosis and treatment for bacterial meningitis in Japan". J Infect Chemother. vol. 16. 2010. pp. 396-406.
Sakoulas, G, Nonejuie, P, Kullar, R, Pogliano, J. "Examining the use of ceftaroline in the treatment of Streptococcus pneumoniae meningitis with reference to human cathelicidin LL-37". Antimicrob Agents Chemother. vol. 59. 2015. pp. 2428-2431. (When dosed at 600 mg, Q8H IV ceftaroline proved to be effective in the treatment of S. pneumonia and promises to be a helpful alternative to vancomycin when intermediate or high penicillin resistance is a concern.)
Adjunctive therapy
Ajdukiewicz, KM, Cartwright, KE, Scarborough, M. "Glycerol adjuvant therapy in adults with bacterial meningitis in a high HIV seroprevalence setting in Malawi: a double-blind, randomised controlled trial". Lancet Infect Dis. vol. 11. 2011. pp. 293-300.
Liu, S, Li, L, Luo, Z. "Superior effect of hypertonic saline over mannitol to attenuate cerebral edema in a rabbit bacterial meningitis model". Crit Care Med. vol. 39. 2011. pp. 1467-73.
Peterkovic, V, Trkulja, V, Kutlesa, M, Krajinovic, V, Lepur, D.. "Dexamethasone for adult community-acquired bacterial meningitis: 20 years of experience in daily practice". J Neurol. 2011.
Brouwer, MC, McIntyre, P, de Gans, J, Prasad, K, van de Beek, D.. "Corticosteroids for acute bacterial meningitis". Cochrane Database Syst Rev. 2010. pp. CD004405
Quagliarello, V, Scheld, WM.. "Infectious disease: do steroids benefit patients with bacterial meningitis?". Nat Rev Neurol. vol. 6. 2010. pp. 529-30. (Written by 2 renowned experts on bacterial meningitis. Reviews all the current data and concludes that in industrialized countries corticosteroids should be used. However, they recognize that the world-wide impact of such adjunctive therapy will be minimal. Universal vaccination will be the critical intervention.)
van de Beek, D, Farrar, JJ, de Gans, J. "Adjunctive dexamethasone in bacterial meningitis: a meta-analysis of individual patient data". Lancet Neurol. vol. 9. 2010. pp. 254-63.
Glimåker, M, Johansson, B, Halldorsdottir, H, Wanecek, M. "Neuro-intensive treatment targeting intracranial hypertension improves outcome in severe bacterial meningitis: an intervention-control study". Plos 1. vol. 9. 2014: Mar 25. pp. e91976(ICU care with close monitoring of CSF pressure, administration of corticosteroids, osmotherapy, CSF drainage, and cooling reduced mortality by 68%.)
Riordan, A.. "The implications of vaccines for prevention of bacterial meningitis". Curr Opin Neurol. vol. 23. 2010. pp. 319-24.
Leventer-Roberts, M, Feldman, BS, Brufman, I, Cohen-Stavi, CJ. "Effectiveness of 23-valent pneumococcal polysaccharide vaccine against invasive disease and hospital-treated pneumonia among people aged ≥65 years: a retrospective case-control study". Clin Infect Dis. vol. 60. 2015. pp. 1472-80. (A significant reduction in invasive disease was demonstrated, but not a reduction in pneumonia.)
Ratilal, BO, Costa, J, Pappamikail, L, Sampaio, C.. "Antibiotic prophylaxis for preventing meningitis in patients with basilar skull fractures". Cochrane Database Syst Rev. 2015. (Antibiotic prophylaxis is not of proven benefit for preventing meningitis. The effectiveness of antibiotics in patients with basilar skull fractures cannot be determined because studies published to date are flawed by biases.)
Schmand, B, de Bruin, E, de Gans, J, van de Beek, D.. "Cognitive functioning and quality of life nine years after bacterial meningitis". J Infect. vol. 61. 2010. pp. 330-4.
DRG CODES and expected length of stay
The overall length of stay is typically 11-12 days. For staphylococcus meningitis the average length of stay is 21 days, and for Meningococcal meningitis 8 days.
Copyright © 2017, 2013 Decision Support in Medicine, LLC. All rights reserved.
No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC. The Licensed Content is the property of and copyrighted by DSM.
- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has bacterial meningitis? What should you expect to find?
- How did the patient develop bacterial meningitis? What was the primary source from which the infection spread?
- Which individuals are of greater risk of developing bacterial meningitis?
- Beware: there are other diseases that can mimic bacterial meningitis
- What laboratory studies should you order and what should you expect to find?
- Results that confirm the diagnosis
- What imaging studies will be helpful in making or excluding the diagnosis of bacterial meningitis?
- What consult service or services would be helpful for making the diagnosis and assisting with treatment?
- 1. Antibacterial agents
- 2. Other key therapeutic modalities
- What complications could arise as a consequence of bacterial meningitis? What should you tell the family about the patient's prognosis?
- How do you contract bacterial meningitis and how frequent is the disease?
- What pathogens are responsible for this disease?
- How do these pathogens cause bacterial meningitis?
- What other clinical manifestations may help me to diagnose and manage bacterial meningitis?
- What other additional laboratory findings may be ordered?
- How can bacterial meningitis be prevented?
- Vaccination
- Chemoprophylaxis
- WHAT'S THE EVIDENCE for specific management and treatment recommendations?
- DRG CODES and expected length of stay


text:
As an amateur runner who has been jogging for many years, I've had the pleasure (usually!) of participating in a LOT of road races. So I was really happy when the awesome folks at Catalyst Weekly—an amazing event guide and website for Medellín—invited me to write a post on road races in the City of Eternal Spring. If you live in Medellín or are willing to travel to run (it's a thing!), definitely check out this list. Registration dates are coming up fast!
For more running-related posts from me, click on "Browse by subject" in the column to the right, and navigate down to "Running". If I had to choose one old one for you to read, it'd be this one—hopefully you'll get a laugh out of my pain. 😉 Until next time….

subset: commoncrawl


text:
Barack Obama is fond of saying that we are our brothers' and sisters' keepers. I complained about his apparent ignorance of Christian theology here, after Obama said:
I came to my Christian faith later in life, and it was because the precepts of Jesus Christ spoke to me in terms of the kind of life that I would want to lead — being my brothers' and sisters' keeper, treating others as they would treat me.
I grumbled:
Nor did Jesus ever say that we should be our brothers' and sisters' keepers; Obama apparently referred to the story of Cain and Abel.
This is the point I want to make: Biblical precepts are often twisted by liberals to support socialism. Jesus was not a socialist. On the contrary, he explicitly disclaimed any political agenda. And the moral of the story in Genesis is not that we are, or should be, our brothers' keepers. Rather, the phrase comes from Cain's answer when God asks him the whereabouts of his brother Abel, whom Cain has just killed. Cain denies any knowledge, and adds the self-exculpatory question, "Am I my brother's keeper?" The point of the story is not that Cain was responsible for looking after Abel, like an Old Testament Nancy Pelosi. Cain was condemned not for failing to keep watch over his brother, but for killing him.
Of course, when Obama says that we are our brothers' keepers, he is speaking metaphorically. He doesn't mean real brothers, he means people in general. And he doesn't intend that we should "keep" them personally, but rather that we (some of us, anyway) should pay a lot more in taxes so that others can be kept by the government. Obama's words represent narrative, not reality.
We conservatives understand the metaphor and rebel against it. At the same time, it is hard to imagine any conservative failing to help a real brother who is in real need. And with our own time and money, not someone else's. That's reality, not narrative.
We learned in a remarkable news story, a couple of days ago, that Barack Obama has an actual brother, not a figurative one, who is living in poverty in Africa. His name is George Obama. Barack has met his brother George, but has no ongoing contact with him. George Obama is in trouble: he has a young son who is sick and has been hospitalized, and George, a poor man, has no way to pay the hospital bill.
You would naturally assume that George Obama would reach out to his brother Barack for help. After all, Barack is a multimillionaire; not only that, he is the most powerful man in the world and has often spoken of the importance of being one's brother's keeper. So surely Barack would be happy to "keep" his real brother by paying his son's–Barack's nephew's–hospital bill, right?
Wrong. What a silly idea! George Obama exists in the world of reality, not narrative. He is a real brother, not a fictitious "brother" who exists only as an excuse to raise someone else's taxes. George apparently knew better than to call on his real brother, the President of the United States, in a time of need. So where did he turn? To Dinesh D'Souza.
George met D'Souza when Dinesh was in Africa, working on his blockbuster movie 2016, which is harshly critical of Barack Obama. D'Souza interviewed George Obama, and they spent a day together. Here is how Dinesh tells the story:
A few days ago I received a call from a man I recently met named George. He was a bit flustered, and soon informed me that his young son was sick with a chest condition. He pleaded with me to send him $1,000 to cover the medical bills. Since George was at the hospital I asked him to let me speak to a nurse, and she confirmed that George's son was indeed ill. So I agreed to send George the money through Western Union. He was profusely grateful. But before I hung up I asked George, "Why are you coming to me?" He said, "I have no one else to ask." Then he said something that astounded me, "Dinesh, you are like a brother to me."
This is, I think, one of the more stunning stories I have ever read, and if Barack Obama were a Republican, it would dominate the news. George Obama turned to a political opponent of his brother the President for help, because his brother Barack is useful only in the world of narrative, not in the world of reality. If you actually need a thousand bucks, and now, don't go to a liberal: "brotherhood" goes only so far. Even in Africa, it apparently is understood that if you need real help in the real world, you should go to a conservative.
Is Barack Obama embarrassed that George Obama preferred to call Dinesh D'Souza, the president's political critic, for help, rather than contacting his own brother the President? I don't suppose we will ever know, since no reporter with access to the White House is likely to ask the question.


text:
My story, Closing the Door, recently published in Stories That Need to be Told: A Tulip Tree Anthology, tells of the emergence some fifty years ago of cardiac catheterization, artificial heart valves and cardiopulmonary resuscitation and how I, as a young nurse, had to make sense of the advancement of technology versus patient benefit.
This story is especially significant to me because just six months ago my husband had open-heart surgery replacing two valves with biological valves. I witnessed, first hand, the tremendous advances in cardiac surgery and treatment.
I gagged on the alcohol fumes as I carefully measured out sixty milliliters of Black and White Scotch into a medicine glass. Balancing the small plastic tray with a pack of Lucky Strikes and the Scotch on one hand, I locked the door to the tiny medication room with the other. Then I went in search of Charlie Hobbs.
A plume of tobacco smoke drifted from the patients' lounge. A ripped vinyl sofa and two orange bucket-like chairs lined the walls. The sole occupant was a middle-aged man hunched over a jigsaw puzzle on the card table. Charlie Hobbs had been admitted to the research unit on the third floor of the city hospital with just the clothes on his back. Every day he wore the hospital issued striped robe and pajamas. One of other staff nurses had donated slippers.
I gazed down at the top of Charlie's wild red hair. He shuffled jigsaw pieces by day and watched television by night, all a maneuver, I thought, to keep human interaction at bay. No one ever visited him. Did he even have a home to go back to?
"I got to get me another puzzle," he said without looking up. "This here one is almost done."
At twenty-three, and a nurse for just two years, I vacillated between professionalism and irreverence. At times, I imagined myself the airline stewardess I had always wanted to be. Coffee, tea, or me? This day I was a Playboy Bunny as I bent at the knees, stretching to place the drink in front of Charlie, while his blue eyes riveted on my imagined cleavage. But Charlie's eyes fixed solely on the amber liquid. Not once in the past four weeks had he acknowledged me, the young nurse in a starched white uniform with thick support hose, and practical shoes. An unlikely dispenser of booze and butts.
Charlie snuffed out the remnant of his cigarette into an overflowing ashtray and reached for the drink.
Harold Clark's research money supported Charlie's hospital stay. Dr. Clark needed recruits who would agree to have a cardiac catheterization in order to see the effects, if any, that alcohol had on their hearts. Cardiac catheterization was the latest tool of the sixties to measure heart function. This new procedure carried a high risk of injury, and even death.
Dr. Clark had scoured the downtown bars searching for men who drank excessively. On a warm autumn night he had gotten lucky. Charlie seized the carrot: a roof over his head, three squares a day plus free liquor and cigarettes. He agreed to live on the research unit for a month, and then undergo a cardiac catheterization.
I carried the empty medicine glass and the tray back to the nursing station. How could Charlie drink alcohol at nine in the morning? Or all day long, for that matter? What would make a man so desperate that he would consent to undergo a procedure that might kill him?
Even though I didn't particularly like Charlie, there were times when I placed the Scotch in front of him that I wanted to nudge him, and jerk my head towards the exit sign at the end of the hallway. Get out, Charlie. The catheterization isn't worth all the free alcohol and cigarettes. But I didn't have the audacity to undermine Dr. Clark's research, no matter how conflicted I felt.
In the small sink in the medicine room, I rinsed out the glass and turned it upside down to dry on a paper towel that rested on the narrow windowsill. Still thinking of Charlie Hobbs, I started down the hall to check on my other patients.
Nellie Mineo waved to me from the doorway of her husband's room. She looked like the Italian housewife that she was: salt and pepper hair piled in a bun on the top of her head. A well-worn cardigan sweater covered her simple cotton dress. When I walked toward her, she grabbed my hand. Behind her I could just make out her husband's outline under the starched white sheets.
"He seems worse," she said, rubbing my hand in absent-minded distraction. "Promise me you'll stop in before you go off duty today."
The Mineos had known the chances weren't in their favor when they first met with Dr. Clark to discuss replacing Joe's diseased heart valve with an artificial one. He was so short of breath that he could hardly talk, much less continue working in the family grocery store.
In the operating room, Dr. Clark had removed the incompetent valve, and slipped the artificial one, a silastic ball encased in metal cage, into the excavated space. The ball-valve clicked audibly. Not a pleasant side effect.
After my regular tour of duty, I rode the elevator to the fifteenth floor, the surgical unit, and worked overtime as Joe's private nurse. He reminded me of my Uncle Tony with olive skin, dark eyes, and soft smile. At first things looked great, but soon Joe developed a cough and a fever. His legs swelled. He had difficulty breathing. Diuretics worked for a while. Antibiotics failed to prevent an infection. His once muscular body had shriveled into sagging skin covering a bony frame. Although the valve was being rejected, it continued to click on.
"Stop and see me before you go off duty," Nellie repeated. I nodded. Only then did she loosen her grip on my hand.
At the end of the day, as I flung my coat over my arm, I heard a racket from the patients' lounge. Charlie stomped past me, head down, and fists clenched. "I'm outta here."
"What happened?" I asked the nurse who jogged after Charlie.
"Charlie kicked over the card table. For no reason I could see." She shrugged her shoulders, and continued on.
Nellie watched the commotion from the other side of the hall. The Mineo's large, gregarious family resembled my own extended Italian family. Visitors came and went at all hours, but that day only Nellie stood guard. When I approached, she pulled me into her husband's room, grabbed my coat and purse, and clutched them against her body. From behind her I could hear Joe's wet bubbly breaths, which barely muffled the click of the valve. Even in my short stint as a nurse I recognized the rancid smell of impending death. I wanted to escape the hopelessness of Joe's futile struggle, but Nellie moved her face closer to mine.
"He's dying," she whispered.
She swallowed hard as if to stop herself from crying. "I don't want him resuscitated. Please stay with us. Don't let them resuscitate him."
Nellie had witnessed plenty of resuscitation attempts as she lingered outside her husband's hospital room day after day. Cardiopulmonary resuscitation was so new that all patients were candidates. At the first moment a patient stopped breathing, we leapt into action. We flung him to the floor and straddled him. We thumped the sternum with the side of our fist, then breathed frantically into his mouth. Pumped on his chest. We worked until we were exhausted. In most cases the patient died anyway with fractured ribs, and a lacerated liver.
Nellie kept her gaze on me; her dark eyes pleading. What would I want for Uncle Tony? A quiet death, or zealots in white coats beating on his chest? What should I do?
Charlie's voice boomed from down the hall spewing curses. Perfect timing. Charlie would leave the hospital AMA—against medical advice—right before his scheduled catheterization. He wasn't as clueless as I had thought.
Hopefully, Charlie would distract the staff long enough for Joe to die. My heartbeats kicked up a notch. How could I ignore Nelly's plea? I reached over and slowly shut the door.
Nellie's hold on my coat and purse relaxed, and they slid to the floor. Wordlessly, she settled in the chair next to Joe's bed, lifted his limp hand onto her lap. I commandeered the chair by the door: the sentry blocking the enemy from entering.
I had seen dead people before but never lingered for that final breath. The valve and the minutes clicked on. The lapses between Joe's gasps for air stretched farther apart. Just when I thought he had quit breathing, he gulped for air. I silently cheered him on. Die Joe. Come on, get it over with.
I sat knotted tight. How would I explain the closed door to a co-worker who decided to check on Joe? Or the fact I was still there after my shift had ended?
Finally, Joe's noisy breathing ceased. Then the mechanical valve stopped clicking. The silence sounded thunderous as I grappled with the fact Joe had actually died. I walked to the bed to see his torturous face frozen, his dark hair matted with sweat, his mouth agape. His open eyes stared at nothing. I placed my hand over Joe's clammy hospital gown. No movement in his chest. No heart thumping against my palm. As I smoothed down his lids, Nellie gripped her husband's hand to her breast and sobbed softly.
While I felt relief that Joe had died with his wife by his side, each footstep by the door made my heart flip.
"I really need to leave, Nellie."
Tears trickled down her cheeks. She placed Joe's hand over his chest before she rose from the chair to embrace me.
"Thank you," she said, her voice cracking. She cried on my shoulder as my own tears fell. Then she pulled away, and sat back down next to Joe, taking his hand again.
Grabbing my coat and purse from the floor, I wiped the moisture off my face with the coat sleeve. I cracked open the door, and glanced up and down the empty hallway. I forced myself to walk leisurely toward the exit.
Nellie waited for the evening nurse to discover Joe dead in the bed.
The floor was unusually quiet. The medication door stood ajar in the nursing station. I had no intention of poking my head inside, and saying so long to the evening nurse. Just a few more steps and I would be in the clear.
I turned the corner of the white tiled hallway, my thoughts back in the room with Nellie and Joe. My body jerked as Charlie Hobbs blocked my way.
"Hi," he said as if we were old friends. "I'm leaving."
He sported a bright green jacket that covered the rumpled clothes he had worn when first admitted. "Borrowed this from the guy in the next room," he said, noticing my eyes on the jacket. "I'll return it." I nodded even though I knew the coat would never make it back to its owner.
"I ain't got no money on me. Can ya spare a buck? I'll pay ya back." He shifted his feet nervously waiting for my answer. For a fleeting moment, I thought to try to persuade him to stay. But that would have been hypocritical. I reached into my purse knowing he would head for the nearest tavern, and never give a second thought to repaying me.
"Thanks," Charlie mumbled, shoving the dollar bill into the pocket of the purloined jacket. He turned abruptly, and disappeared though the doorway under the exit sign.
While I jogged down the three flights of stairs following behind Charlie's footfalls, I attempted to justify my behavior. Frightening to me was how quickly I intervened for my patients without foresight into the repercussions.
However, I felt positive that Charlie had planned all along to leave the hospital before the catheterization. Not giving him the dollar wouldn't have made a difference. And who would question that my closing the door to Joe's room to allow him to die naturally had violated any ethical rule? Even if I didn't intervene, the chances that anyone would get past Nellie Mineo to resuscitate Joe seemed unlikely.
How could I have realized that over the years I would continue to struggle with knowing when to step back, and when to dig deeper into my patients' psyche. How to be empathic and not sympathetic? How to balance cool detachment with overbearing involvement? It was just the beginning. There would be many choices throughout my long nursing career that would test my allegiance, and strain my conscience.
Before I reached the last flight of stairs, Charlie had flung open the door to the street, and let it crash behind him.


text:
Matthieu's Playbook: Tried and True Patterns for Kickstarting Scrum Teams New and Old
You recently completed a two-day training, and you are now a Certified ScrumMaster. There's only one problem: what do you actually do next? Or maybe you feel like your team's adoption of Scrum is sluggish and somewhat ineffective. How do you breathe new life into your practices?
Part of the genius of the Agile Manifesto is that it doesn't tell you exactly what to do. It gives you a resilient foundation of values and principles that is grounded in discovered truths, and then lets you figure out how to apply it. Scrum describes process a bit more, but still leaves a lot of open questions. Again, this room to adapt is incredibly powerful. However, at the outset it can be quite daunting. Even after going through Certified ScrumMaster training, new practitioners may be a little lost as to what exactly to do next.
Over the years, I've built up a set of simple, concrete practices that I use both to get teams started and to help existing teams that are having trouble. Recently, I helped three teams get up to speed in quick succession. I wrote down these practices as a playbook. While I look forward to the day when these teams grow beyond my playbook and throw it in the trash, I have seen great results from starting with a small set of concrete practices. Come to this session and walk out with simple, specific things you can do to get your team flying.
Outline/Structure of the Talk
- Understanding the Basic Dynamics of Scrum
- A frame for the rest of the talk.
- Start with the Ending
- The value of finish lines
- Story writing is an art to be perfected; for now, start by writing a clear ending
- Set Yourselves Up To Succeed
- During Sprint Planning, build your sprint one story at a time to avoid overcommitment
- Cycle through four questions to build a reasonable sprint well understood by the whole team
- The Daily Question
- Learn a simple question you can ask the team every day to increase their chances of completing their goals.
- To Point or Not to Point
- Ideally: Build the team's "gut sense" of the size of stories through relative estimation
- At the very least: use count of stories as a way to measure completion
- "Just Enough" Refinement
- 9 times out of 10, backlog refinement is the Product Owner and Tech Lead talking while everyone else looks at their phones
- Learn a small-group exercise that rapidly advances team understanding of stories while keeping everyone engaged from start to finish
- Put On Your Lab Coats
- Learn simple habits for your retrospective to drive more meaningful improvement
Learning Outcome
Participants will leave with knowledge of how to use basic, concrete steps that can be used alone or in combination to drive strong improvement of their team. Includes steps for jumping to greater effectiveness in each of the following areas:
- Story Writing
- Sprint Planning
- Daily Stand-Up
- Estimation
- Backlog Refinement
- Sprint Retrospective
Target Audience
Agile Coaches, ScrumMasters, anyone curious about concrete techniques for invigorating Scrum teams
Prerequisites for Attendees
The practices I recommend are aimed at giving you practical steps to take right away. If you have a team and want to get things off the ground, you have everything you need to take advantage of this practical session.
- Growing Truffles: Ramblings of a Learning Agile Coach
My blog!
- Matthieu's Playbook: Tried and True Patterns for Kickstarting Scrum Teams New and Old
Talk given at AgileDC 2018 and NYC XP & Agile Meetup November 2018
Some feedback from those sessions:
- "I've been an SM for years and found this helpful. Love the tip about the daily question!"
- "Excellent! Such useful info--I can't wait to download the playbook and use it"
- "Great talk! Like a master class in 45 minutes."
- Focusing Your Flow: OKRs and Outcomes Thinking
Talk given at NYC Lean/Kanban Meetup 2018
- The Lean Grownup: Applying Lean Startup on Established Teams
Talk given at AgileCamp NY 2017
- How Amplify Connected OKR and Agile
Text interview at Perdoo blog
- Agile & OKRs: Achieving Harmony
Talk given at AgileDC 2016 and AgileCamp Dallas 2016
- Amplify's Model for Team Member ScrumMaster
Video interview on hybrid ScrumMaster model
- The Myth of Fixed Scope: Why Goals Matter
Talk given at AgileDC 2015 and Agile Philly 2015
- A Spoonful of Sugar
Workshop run at Agile Games 2015.
- Elephant Carpaccio
Alistair Cockburn-designed workshop run for New York City meet-up.
schedule Submitted 4 years ago
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It's inevitable, and almost unavoidable, that Professionals of all skill-sets and experience will encounter "coaching up" situations. In this session, I will review three coaching techniques that can be used in Sr Leader and "coaching up" scenarios. These techniques will provide participants with new/alternative ways to prepare for, engage, follow up, and reflect with Sr Leaders. These techniques are heavily based in the core values of openness, courage, and respect and rooted in the fundamentals of cultural and human interaction.
Colleen Johnson - Why WIP Matters.Colleen JohnsonScatterSpoke
schedule 4 years agoSold Out!
60 Mins
We prize our ability to multitask yet we rarely acknowledge the impact this has on our ability to get work done. As a team we look to process to create efficiencies but ignore one simple tool that has the ability to transform the amount, the speed, and the quality of their work: Limiting the amount of Work In Progress. In this talk I will share my stories and experiences of the power that limiting WIP has to bring a team focus, flexibility and follow through. Learn where to start, what to look for over time and how to optimize the amount of things you are working on so that you can get more done!
Alex Sloley - The Product Owner and Scrum Master Brain Transplant! Mwuhahahaha!!!Alex SloleyAgile Coach Facilitator Teacher MentorAlex Sloley
schedule 4 years agoSold Out!
60 Mins
Imagine you are a Mad Agile Scientist and have a diabolical experiment to conduct - what would happen if you exchanged the brains of a Product Owner and Scrum Master? Mwuhahahaha!!! How would the body of a Product Owner with the brain of a Scrum Master act? And vice versa?
Perhaps the Scrum Master would now treat the team like a backlog? This Scrum Master would be focused on value and maintaining a coaching backlog of team and person improvements. This Scrum Master is refining the team, crafting a group that delivers value.
And perhaps the Product Owner might treat the backlog like a team? Rather than backlog refining, they coach the backlog. They would be focused on nurturing, protecting, and empowering the backlog. The backlog might transform from an irritation into a labor of love.
Although this experiment sounds terrible, this change of perspective might be what you need to reanimate your dead team or backlog.
Join the fun and come learn what horrifying results await!
Billie Schuttpelz - Want fierce Business Agility? Kick out the Imposter!Billie SchuttpelzSolutionsIQ/Accenture
schedule 4 years agoSold Out!
180 Mins
AdvancedWith Business Agility, we talk about innovation and failure. What we don't talk about are the head games that keep us from innovating. We don't talk about the internal dialogues that hold us back from taking risks. Imposter Syndrome is stealing too many of our innovative ideas.What if the key to fierce business agility is embracing the concept that people are more innovative when operating in their authentic voice? If that's the case, then we should strive to create a psychologically safe space for them to uncover their authentic voice. This will naturally unleash the innovative ideas already within them.Let's break open the conversation around Imposter Syndrome and Business Agility. It could be the key to unlocking innovation.
David Bernstein - Five Development Practices Essential for Agile TeamsDavid BernsteinTo Be Agile
schedule 4 years agoSold Out!
60 Mins
This session focuses on the five development practices that are often overlooked but are essential to iterative software development. These five practices include automating the build for continuously integrating software as it is written, collaborating with team members through pair programming, practicing agile design skills that enable testability, using test-first development to drive design, and refactoring code to reduce technical debt. Together, these five technical areas are proving to be essential for sustained success with Scrum development. But many teams have not been exposed to the benefits of these practices or how to use them effectively.
In this session, we explore why these engineering practices are essential for Scrum software development and how to use them to reduce risk and build in quality at every level of the development process. We make the business case for these technical practices by showing how they address the inherent risks and challenges in building software. We then look at how these practices help mitigate the core issues of software development and help us drop the cost of maintaining and extending software in the future.
Faye Thompson - Cultivating Space for LearningFaye ThompsonAnnalect
schedule 4 years agoSold Out!
120 Mins
Our understanding of how humans learn has grown tremendously in the last 20 years. Providing an environment in which people have room to think, and the safety to experiment and adapt is key. We will review fundamental concepts of neuroscience and how they intersect with organizational behavior. We will also review how the agile mindset takes advantage of these concepts. From there, we can begin to envision the conditions that will provide the greatest opportunity for learning and continuous improvement. Together, we will share ideas on how we can start to transform our environments into safe spaces where teams can grow and thrive.
James Gifford - 5 Metrics to Create Safety and High Performing TeamsJames GiffordEPAM Systems
schedule 4 years agoSold Out!
60 Mins
I see that a lot of organizations use metrics in inappropriate ways to measure teams. At the heart of these metrics, nine times out of ten, are velocity and story points. These metrics lead to a lot of mistrust, fear, and bad technical practices. This talk will focus on shifting the focus to diagnostic metrics.
Before shifting focus to diagnostic metrics, we need to understand what inappropriate metrics are. When questioning teams about why their velocity was lower from one sprint to another, teams are more likely to inflate their estimates to avoid questions in the future. This is one of my scenarios. We will explore this case and my other top-ten based on the 165 teams I have interacted with. Focusing on one metric does not provide a balanced view of the team.
For balance, I promote five metrics. The combination of metrics balances each other. These five metrics are lead time, quality, happiness, agile maturity, and business value. Focusing on these five metric areas can be used as a diagnostic tool to help teams grow and support coaching. During the session, we will use my Excel-based tool and visual model to simulate this balance.
When you push shorter lead times (how fast) on a team with a lower agile maturity, the first thing to change is quality, followed by happiness and then the delivery of value. Conversely, if a team focuses on TDD, the first thing to change is quality, followed by agile maturity, reduction in lead time, and increased delivery of value.
Teaching teams to harness data in a positive way will help them to flourish.
Mark Kilby - Facilitating Distributed TeamsMark KilbySonatype
schedule 4 years agoSold Out!
60 Mins
Facilitating distributed team meetings can feel like having one arm tied behind your back and one eye covered, but you can free yourself of these virtual constraints using other agile practices. We struggle with meeting tools and keeping people engaged online, but what if we collaborate with our teams to get the most value out of their meetings? If we leverage pairing, mobbing and other practices, we can co-facilitate successful outcomes with our teams.
Adam Weisbart - Agile Jesters, Magicians, and Clowns: Using the unexpected to move mountains (and your retrospectives)Adam WeisbartRecess!
schedule 4 years agoSold Out!
120 Mins
Scrum is excellent at helping surface team and organizational dysfunction, but dealing with dysfunction can be uncomfortable. As an agilist, how do you help your team work through these newly voiced challenges?
Court jesters have a long history of helping give voice to uncomfortable truths, often speaking words that would have others killed. In the 1300's when the French fleet was destroyed by the English at the Battle of Sluys, the French king's jester told him that the English sailors "don't even have the guts to jump into the water like our brave French". This session will help you become an agile jester - speaking difficult truths through humor.
During this workshop you'll get hands-on experience using practical tools drawn from improvisational comedy, the art of magic, and clowning. Every agilist should have these tools in their bag of tricks.
Steve Ropa - Career growth, recognition and continuous learning for software craftspeopleSteve RopaMaster CraftsmanRocky Mountain Programmers Guild
schedule 4 years agoSold Out!
60 Mins
Over the years, we've talked quite a bit about how to become a craftsman, exploring deeply how to progress from Apprentice to Master. What is often missing is any detail beyond the general thoughts that this is a Good Idea. Steve will share an approach, based on his experience of many years and many development organizations, to learning and career development for your team. This approach goes beyond the general ideas around Craftsmanship, but provides actual concrete areas of development. Unlike a formalized "skills checklist" we will apply a pattern language to help identify a continuum of growth for anyone's long term development.
We will discuss building understanding and building skills in the following areas:
Professional Skills
Process and Technical Ecosystems
Claire Moss - Everything You Wanted To Know About DevOps But Were Afraid To AskClaire Mossaclairefication
schedule 4 years agoSold Out!
60 Mins
As a career software tester, I've heard rumors DevOps culture will put me out of a job, so I took a job testing for a DevOps team. I'm new to DevOps, but aren't we all? What matters most is our teams' intentional decisions to grow our DevOps practices along with our development community.
Join me as I share my experiences blending disciplines, companies, levels of experience, and differing expectations as a member of efficient and effective delivery teams. I'll describe common cultural and interpersonal problems I experienced while transforming a cross-functional agile team dogfooding a DevOps implementation.
Whether you're into development, operations, testing, customer support, or product ownership, you'll leave with concrete strategies for improving your DevOps working relationships to keep the technology running smoothly. People factors strongly affect your DevOps technical outcomes, so optimizing your flow includes improving your people practices.
Don't feel afraid to ask about DevOps anymore!
Thomas Perry - Agile Management: Dealing with ImpedimentsThomas PerryThomas Perry LLC
schedule 4 years agoSold Out!
60 Mins
When not uncovered and resolved, impediments can do harm to an otherwise well run project in ways that are often subtle and easy to miss. If impediments undermine the success of our teams, then we as project managers, leaders, and stakeholders should all be very passionate about removing impediments. In order to accomplish this we need to do three things: we need to give impediments the proper attention, we need to become experts at uncovering them, and we need to integrate them into the process of continuous improvement within the team.
In this session Tom makes a passionate appeal for the importance of the lowly impediment - often ignored, but never missed.
Rachel Weston Rowell - Advanced Facilitation: Creating and holding space in conflictRachel Weston RowellManaging PartnerTrail Ridge
schedule 4 years agoSold Out!
120 Mins
You've worked with the meeting leader, designed a great purpose and agenda, and invited all the right people. Then the meeting goes sideways. Someone comes in angry and drops a bombshell that has everyone fighting. A team clearly has a second agenda but won't be honest about what they want and need. A leader came in angry and threatening and now nobody will say what needs to be said. You're trying to help the group make a decision, but they are off on tangents and going down ratholes with no end in sight.
When meetings get challenging, standard facilitation techniques won't cut it. It's time to pull out the stops and apply some advanced techniques to create a safe, action-oriented space to help get your meeting attendees where they need to be.
Allison Matlack - "Boss" is a four-letter word: Managing people in the age of digital transformationAllison MatlackRed Hat
schedule 4 years agoSold Out!
60 Mins
One of the foundational principles of the Agile Manifesto is that the best solutions "emerge from self-organizing teams," yet most of us are still locked in hierarchical organizational structures better suited for the factory floors where they originated. What should become of the role of people manager in the age of digital transformation?
In this session, we'll explore different ways that managers can become the catalysts that their teams need, as well as some things Agile practitioners can do to cultivate these important behaviors in the teams they work with. Come ready to learn practical tips for how to navigate the tricky space between ensuring that business needs are met and that the individuals on your team reach their full potential.
Adam Anderson - Delivering Business Value Faster for Data Focused TeamsAdam AndersonAmerican AgCredit
schedule 4 years agoSold Out!
60 Mins
Every team's goal is to deliver business value faster, the question is how do you do that? Using continuous integration (CI) and deployment techniques a team can increase velocity, improve transparency, and reduce risks. During this session, you will also learn the differences between CI/CD for applications development and data focused teams. Working with databases and especially data warehouses can be challenging, but there are simple techniques to help alleviate the pain.
Kimberly Andrikaitis - Distributed Scrum Teams Whack-a-Mole: Creative Solutions to Common ObstaclesKimberly AndrikaitisVaco
schedule 4 years agoSold Out!
60 Mins
Let's be honest. Distributed Agile teams are here to stay, but not without considerable stumbling blocks. It's easy to lose focus or feel disconnected, misunderstood or disengaged due to language barriers, limited time overlap and communication mishaps. For new teams, it's even more challenging establishing relationships, since we lack face to face interaction.
This talk focuses on shifting a distributed team from stunted to high performing despite language / cultural / time zone differences, misunderstanding of Scrum, and the "us" vs. "them" mentality (all bothersome moles we will whack).
Using a true case study, we'll journey through the challenges of relationship building, the anti-agile mindset, lack of focus, and lifeless ceremonies. You will walk away from this presentation with a toolbox full of proven, creative, and innovative ideas for successfully overcoming these obstacles.
Tomo Watanabe - "You might be a great Scrum Master if…" --- A brief guide to Scrum MasteryTomo WatanabeAgile CoachA Fortune 500 financial service company
schedule 4 years agoSold Out!
60 Mins
This session is not only for current and aspiring Scrum Masters but also for People Managers, Development Team Members, Product Owners, Project Managers, and Leaders.
The Scrum Guide defines what is expected of a Scrum Master. When you read it, I bet you react like "that's a piece of cake!" But when you actually do it, many of us come to a realization that it's really, really hard. (That's what happened to me!) The Scrum Master job is hard because much of it has to do with humans, one of the most complex beings in the universe. Humans are intelligent; humans have emotions; and humans are unpredictable. Just going through the motions does not cut it. Even if you approach with the best of your intention, matters could backfire on you anytime. Borrowing "You might be a redneck if..." from a comedian, Jeff Foxworthy, Tomo will present behaviors of a great Scrum Master and those of a "not so good" Scrum Master. Then, he will take you through why the great Scrum Master's behaviors make her great and how they contribute to building a high performing team and helping the organization be more effective and productive. Finally, he will share tips and tricks that help Scrum Masters grow into greatness (for example, powerful questions, 3 levels of listening, facilitation tools & techniques, etc.)!
This session will give current and aspiring Scrum Masters what to focus on for career development and people in other roles a concrete idea on what qualities to look for in a Scrum Master.
There will be a handout for participants to take home with.
HENRY C DITTMER - Leadership Framework Mash-upHENRY C DITTMERAgile For All, LLC
schedule 4 years agoSold Out!
60 Mins
There are many leadership frameworks that one might use to help with growth in leadership skills, approaches, and methods. As you begin to review various frameworks, there emerge similarities that when exposed can provide further insight into your own learning. This session explores several of these frameworks, 'mashing them up' into a cohesive bigger picture. Explore MindSET to MindSIGHT to MindFULNESS!
Christen McLemore - Building a Leadership BacklogChristen McLemoreFounderHeyMac Consulting
schedule 4 years agoSold Out!
60 Mins
Getting leaders to adopt an Agile Mindset doesn't happen by sending them to training. It won't happen simply because they approved the funding to do a transformation. Many leaders need your experience and appreciation for how Agile works differently than what they may have seen in the past. Helping them build, own and progress through a backlog of system wide challenges is key to their success and the success of the teams. We will walk through some examples, create backlog items of your own and create an actionable plan to take back to our office during this workshop style session.


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"Do not spoil what you have by desiring what you have not;
remember that what you now have was once among the things you only hoped for."
(a basket of wild "wood" pears / Julie Cook / 2017)
Late September, here in Georgia, is no more reminiscent of what Fall should be
than that of a palm tree currently living and thriving in Alaska.
It just isn't happening.
Granted the weather gods are telling us that "it's going to feel like Fall
come tomorrow, yet they preface that with,
but we are still well above the typical highs and lows this time of year….
Throw in the recent sightings of rabid foxes in our county,
the continued proliferation of the fire ants,
this being the most active time of year for yellow jackets, along with the increased chances of running into a copperhead or rattlesnake while working in the yard and most
sane folks would continue hunkering down indoors hoping that
October may be more of a welcoming month for outdoor adventure.
My husband, I know, would have told me "no, don't do it."
He would have said stay out of those woods, especially wearing those sandals,
not unless you want to be covered in ticks and bit by a snake.
But he wasn't home to say those things so it was an out of sight out of mind sort
of moment.
I had to get outside and start the process of digging up and removing the dead,
dried up remnants of summer.
I had to cut back, dead head, and just rid my visible world of the reminders
of what was once vibrancy and color…all of which is now just hot dried up death.
Living on what was once mostly pasture land surrounded by woods, I usually haul my
"debris," aka cut back dead things, to the woods….to a "compost" pile that never
composts like it should. My husband calls it a brush pile. I like to be cutting edge…
hence, a compost pile…
I also happen to know that there is a lone pear tree deep in those woods
that, this time of year, usually bears pears…albeit every other year—
but I was pretty certain this was the year.
Leaving the safety of my yellow wheelbarrow perched along the edge of the woods,
I gingerly picked my way into the woods….very conscious of the recent tale of
rabid foxes, active snakes and hungry ticks.
As my shorts, tank top and chaco sandals would be no match for the briars let alone
rabies, deadly venom or Lyme disease.
Did I mention the giant spiders?
Spiders who seem to think fall is the season to built profuse webs spanning the entire
expanse of woods so you can walk right into a web and have a full web and spider
stuck on your face.
The sun was cutting down through the trees, light glaring down upon the wood's
floor, as I turned my head upward searching the overhead branches.
Squinting with my hand held over my eyes, I scanned the heavens
for the objects of my desire.
And there they were.
Giant heavy brown orbs hanging low amongst the leaves.
The tree was ladened with "wood" pears.
I've written about wood pears before.
They are wild pears that grow obviously, in the woods….
hence why I call them wood pears.
That is not a scientific name mind you, just an observational name.
They are as hard as rocks, never ripening like a normal pear would
and even the deer and squirrels won't eat the wood pears.
I did read once that some folks will stew them down in an attempt to make jam,
but my husband has minced no words when quickly telling me not to bother
because he's not about to eat something that even the wild animals find
disdain over.
Yet the pears beckoned.
I looked around on the wood's thick debris covered floor, careful as I pushed aside accumulated leaves with my mostly exposed feet as I searched for any early
fallen pears.
The remnants of an old barbed wire fence sinisterly peeked out here and there as
I was careful to avoid adding tetanus to my list of wood worries.
A few pears had indeed fallen as the ants had also found those pears.
Finding a stick I attempted hitting at some of the lower branches,
knocking a few pears to the ground—being very careful that they didn't hit me
on the head as they would probably have knocked me out as they are that hard.
I gathered about 10.
But the tree was loaded.
I knew I was going to have to find something else that was both long and tall in which
to knock down those low hanging pears on the branches closest to my reach, yet frustratingly out of reach for my stick.
Obviously not satisfied with a bucket of 10 or so pears,
I trapsed back to the house to gather a long rake.
I kept hearing the admonishment of my husband ringing in my head,
as I was wondering what I would do if a copperhead bit my foot while my cell phone
was back at the house.
But the tree was loaded, beckoning for me to get more.
Decorative purposes only, yet I wanted more pears.
And that's the thing…
These pears serve absolutely no purpose other than being decorative.
And here I was willing to risk life and limb in order to gather them up.
Yet what of a quest of faith?
What lengths would we go to seek God?
Would we risk life or limb to seek Him who has called us by name?
Would we strategize and scrutinize what was needed in order to procure
Him as our own?
Perhaps it's time we all rethink our desires….
"Behold, days are coming," declares the Lord GOD,
"When I will send a famine on the land, Not a famine for bread or a thirst for water,
But rather for hearing the words of the LORD.
Amos 8:11


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