Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 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

Affiliations
Free PMC article
Review

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

Abstract

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.

Figures

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).

Similar articles

See all similar articles

Cited by 11 articles

See all "Cited by" articles

References

    1. Booth MG, Hood J, Brooks TJ, Hart A. Anthrax infection in drug users. Lancet. 2010;11:1345–1346. - PubMed
    1. Hicks CW, Sweeney DA, Cui X, Li Y, Eichacker PQ. An overview of anthrax infection including the recently identified form of disease in injection drug users. Intensive Care Med. 2012;11:1092–1104. doi: 10.1007/s00134-012-2541-0. - DOI - PMC - PubMed
    1. Booth M, Donaldson L, Xizhong C, Junfeng S, Eichacker P. Comparison of survivors and nonsurvivors in 27 confirmed injectional anthrax cases from the 2009 outbreak in scotland. Crit Care. 2013;11:668.
    1. National Anthrax Outbreak Control Team. An Outbreak of Anthrax among Drug Users in Scotland, December 2009 to December 2010. Glasgow: Health Protection Scotland; 2011.
    1. Jernigan JA, Stephens DS, Ashford DA, Omenaca C, Topiel MS, Galbraith M, Tapper M, Fisk TL, Zaki S, Popovic T, Meyer RF, Quinn CP, Harper SA, Fridkin SK, Sejvar JJ, Shepard CW, McConnell M, Guarner J, Shieh WJ, Malecki JM, Gerberding JL, Hughes JM, Perkins BA. Bioterrorism-related inhalational anthrax: the first 10 cases reported in the United States. Emerg Infect Dis. 2001;11:933–944. doi: 10.3201/eid0706.010604. - DOI - PMC - PubMed

Publication types

MeSH terms

Feedback