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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.


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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