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. 2013 Oct 9;11:217.
doi: 10.1186/1741-7015-11-217.

B. Anthracis Associated Cardiovascular Dysfunction and Shock: The Potential Contribution of Both Non-Toxin and Toxin Components

Free PMC article

B. Anthracis Associated Cardiovascular Dysfunction and Shock: The Potential Contribution of Both Non-Toxin and Toxin Components

Kenneth E Remy et al. BMC Med. .
Free PMC article


The development of cardiovascular dysfunction and shock in patients with invasive Bacillus anthracis infection has a particularly poor prognosis. Growing evidence indicates that several bacterial components likely play important pathogenic roles in this injury. As with other pathogenic Gram-positive bacteria, the B. anthracis cell wall and its peptidoglycan constituent produce a robust inflammatory response with its attendant tissue injury, disseminated intravascular coagulation and shock. However, B. anthracis also produces lethal and edema toxins that both contribute to shock. Growing evidence suggests that lethal toxin, a metalloprotease, can interfere with endothelial barrier function as well as produce myocardial dysfunction. Edema toxin has potent adenyl cyclase activity and may alter endothelial function, as well as produce direct arterial and venous relaxation. Furthermore, both toxins can weaken host defense and promote infection. Finally, B. anthracis produces non-toxin metalloproteases which new studies show can contribute to tissue injury, coagulopathy and shock. In the future, an understanding of the individual pathogenic effects of these different components and their interactions will be important for improving the management of B. anthracis infection and shock.


Figure 1
Figure 1
Overview of basic pathways potentially leading to shock, organ injury and death during B. anthracis infection. A. As Gram-positive bacteria, B. anthracis and its products (for example, cell wall and peptidoglycan) activate host defenses and inflammatory mediator release which are necessary for microbial clearance. However, if this response is excessive it may result in the development of shock, organ failure and death. B. B. anthracis also produces two exotoxins, lethal and edema toxins, which are capable of contributing directly to shock, organ injury and death via diverse mechanisms. C. Lethal and edema toxin also appear capable of subverting critical host defense systems and contributing to the pathogenesis of shock, organ injury and death by limiting microbial clearance. Other mechanisms not depicted in this figure, such as the activation of metalloproteases other than lethal factor, may contribute to shock and organ injury with B. anthracis as well (see text).

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