•
When a history and physical examination suggest bacterial meningitis, the practitioner should proceed swiftly to lumbar puncture to establish a diagnosis. However, the clinician is faced with the question of whether the procedure will put the patient at risk for herniation and subsequent neurologic deterioration. To assess this risk, physicians often order head computed tomography (CT) scans prior to performing the procedure. In certain populations, provided there is no delay in delivery of empiric antibiotics, this approach may be appropriate.
It is generally accepted that patients with coma, papilledema, or other focal neurologic deficits should undergo neuroimaging prior to lumbar puncture for suspected acute bacterial meningitis. Hasbrun et al have determined that in such patients, head CT scanning should be used in making the decision to perform lumbar puncture.
A recent prospective study has confirmed, however, that clinical features can be used to determine which patients are unlikely to have an abnormal CT scan and can thus undergo lumbar puncture without delay. In this study of 235 patients who underwent a head CT scan prior to lumbar puncture, abnormalities were more often associated with certain historical features and neurologic findings. Patients older than 60 years with known immune deficiency (due to human immunodeficiency virus, immunosuppression, or transplantation), central nervous system disease, or a history of seizure 1 week prior to presentation were more likely to have abnormal head CT scans. Patients with focal neurologic findings were also more likely to have abnormal scans. In the patients with none of these features, only 3% of the CT scans were abnormal, and there was no evidence of mass lesion or herniation risk that precluded subsequent lumbar puncture. Kastenbauer et al retrospectively studied the records of 75 adults with pneumococcal meningitis and similarly determined that patients with focal neurologic deficits, seizures, and reduced level of consciousness (Glasgow coma score <12) were more likely to have head CT abnormalities.
*3/348/5*
•
Anthrax is caused by Bacillus anthracis, a spore-forming gram-positive rod. Naturally acquired infection results from contact with contaminated animals. No human-to-human transmission of the disease has ever been confirmed.
The virulence of B. anthracis is dependent on its capsule and the two toxins it produces. The poly-D-glutamic acid capsule is antiphagocytic and prevents bacterial lysis of the organism by host proteins. The anthrax toxins have been shown to be composed of three entities that act synergistically to produce the clinical effects of anthrax:
- Protective antigen (so named because it is the main protective constituent of the anthrax vaccine) binds to target cell receptors and then cleaves off a portion of its protein, which allows attachment by either edema or lethal factor.
- Edema factor can bind to the exposed region on protective factor and form edema toxin, which can disrupt cellular water balance, causing intracellular edema.
- Lethal factor, a metalloprotease, can bind to the exposed domain on protective antigen and form lethal toxin, which at sufficient concentrations inhibits neutrophil function and can destroy cellular tissues. Lethal toxin also stimulates macrophages to release tumor necrosis factor and interleukin-1, which contribute to sudden death in cases of systemic anthrax.
Clinical disease can occur when endospores of B. anthracis are introduced into the body by abrasion, inhalation, or ingestion. These spores are ingested by local macrophages and transported to regional lymph nodes, where germination to form vegetative bacilli may occur up to 60 days later. These bacteria release themselves from macrophages and multiply within the lymphatic system, elaborating toxins that overwhelm the clearance ability of regional lymph nodes. Bacteremia and the systemic production of toxins can then ensue.
*206/348/5*
ANTHRAX: PATHOGENESISAnthrax is caused by Bacillus anthracis, a spore-forming gram-positive rod. Naturally acquired infection results from contact with contaminated animals. No human-to-human transmission of the disease has ever been confirmed.The virulence of B. anthracis is dependent on its capsule and the two toxins it produces. The poly-D-glutamic acid capsule is antiphagocytic and prevents bacterial lysis of the organism by host proteins. The anthrax toxins have been shown to be composed of three entities that act synergistically to produce the clinical effects of anthrax:- Protective antigen (so named because it is the main protective constituent of the anthrax vaccine) binds to target cell receptors and then cleaves off a portion of its protein, which allows attachment by either edema or lethal factor.- Edema factor can bind to the exposed region on protective factor and form edema toxin, which can disrupt cellular water balance, causing intracellular edema.- Lethal factor, a metalloprotease, can bind to the exposed domain on protective antigen and form lethal toxin, which at sufficient concentrations inhibits neutrophil function and can destroy cellular tissues. Lethal toxin also stimulates macrophages to release tumor necrosis factor and interleukin-1, which contribute to sudden death in cases of systemic anthrax.Clinical disease can occur when endospores of B. anthracis are introduced into the body by abrasion, inhalation, or ingestion. These spores are ingested by local macrophages and transported to regional lymph nodes, where germination to form vegetative bacilli may occur up to 60 days later. These bacteria release themselves from macrophages and multiply within the lymphatic system, elaborating toxins that overwhelm the clearance ability of regional lymph nodes. Bacteremia and the systemic production of toxins can then ensue.*206/348/5*