Navigation
Open Access
Review
Molecular determinants for a cardiovascular collapse in anthrax
Jurgen Brojatsch1,Arturo Casadevall1,David L. Goldman1,2,*
1
Department of Microbiology and Immunology, Albert Einstein College of Medicine, USA
2
Department of Pediatrics, Children's Hospital at Montefiore/ Albert Einstein College of Medicine, Bronx, NY, USA
DOI: 10.2741/E697 Volume 6 Issue 1, pp.139-147
Published: 01 January 2014
(This article belongs to the Special Issue Infectious diseases of the myocardium)
*Corresponding Author(s):  
David L. Goldman
E-mail:  
david.goldman@einstein.yu.edu
Abstract

Bacillus anthracis releases two bipartite proteins, lethal toxin and edema factor, that contribute significantly to the progression of anthrax-associated shock. As blocking the anthrax toxins prevents disease, the toxins are considered the main virulence factors of the bacterium. The anthrax bacterium and the anthrax toxins trigger multi-organ failure associated with enhanced vascular permeability, hemorrhage and cardiac dysfunction in animal challenge models. A recent study using mice that either lacked the anthrax toxin receptor in specific cells and corresponding mice expressing the receptor in specific cell types demonstrated that cardiovascular cells are critical for disease mediated by anthrax lethal toxin. These studies are consistent with involvement of the cardiovascular system, and with an increase of cardiac failure markers observed in human anthrax and in animal models using B. anthracis and anthrax toxins. This review discusses the current state of knowledge regarding the pathophysiology of anthrax and tries to provide a mechanistic model and molecular determinants for the circulatory shock in anthrax.


Key words

Anthrax, shock, MAPK, Nod-like receptor, apoptosis, Review

Share and Cite
Jurgen Brojatsch, Arturo Casadevall, David L. Goldman. Molecular determinants for a cardiovascular collapse in anthrax. Frontiers in Bioscience-Elite. 2014. 6(1); 139-147.