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Pathogenesis of Anthrax
Anthrax infection begins when the spores enter through non-intact skin,
inhalation or via mucosal membranes. The bacteria proliferate and produce
the edema (swelling) and lethal toxins that impair the person's white blood cell
function and lead to the distinctive pathological findings: edema, hemorrhage
(bleeding), tissue death (necrosis), and a relative lack of white blood cells.
In inhalational anthrax, the spores are absorbed in the alveolar membrane,
which transports them to the regional tracheobronchial lymph nodes, where
germination occurs1.
Once in the tracheobronchial lymph nodes, the local production of toxins by
the bacilli gives rise to the characteristic pathological picture: massive
bleeding, swelling and tissue death in the lymph nodes; and mediastinitis
(inflammation in the thoracic cavity, which is a defining characteristic of this
disease)2. The bacilli can then spread to the blood, leading to
septicemia (blood poisoning) with seeding of other organs and frequently causing
hemorrhagic meningitis. In the final stages of disease, toxin is present
in high concentrations in the blood3, however, scientists still don't
understand the actual mechanism by which the toxin causes death. Death is
the result of respiratory failure associated with pulmonary edema, overwhelming
quantities of bacteria in the blood, and, often, meningitis.
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1. Ross JM. The pathogenesis of anthrax following the administration of
spores by the respiratory route. J Pathol Bacteriol. 1957;73:485–494.
2. Dutz W, Kohout E. Anthrax. Pathol Annu. 1971;209–248.
3. Lincoln RE, Fish DC. Anthrax toxin. In: Montie TC, Kadis S, Ajl SJ,
eds. Microbial Toxins. Vol 3. New York, NY: Academic Press; 1970: 361–414.
(This material has been derived from the Virtual Naval Hospital web site
www.vnh.org)
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