B. anthracis associated cardiovascular dysfunction and shock: the potential contribution of both non-toxin and toxin components

BMC Medicine

Peter Q Eichacker¹  Xizhong Cui¹  Yan Li¹  Ping Qiu¹  Kenneth E Remy¹ 

[1] Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD 20892, USA

关键词: Shock;    Cardiovascular dysfunction;    Metalloproteases;    Lethal and edema toxins;    Cell wall components;    Anthrax;    Bacillus anthracis;   

Others  :  855628
DOI  :  10.1186/1741-7015-11-217

 received in 2012-12-11, accepted in 2013-09-13,  发布年份 2013

【 摘 要 】

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.

【 授权许可】

   
2013 Remy et al.; licensee BioMed Central Ltd.

【 图 表 】

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