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Review
. 2009 Jan 1;14(12):4516-24.
doi: 10.2741/3544.

Pathophysiology of anthrax

Arthur E Frankel  1 , Shu-Ru Kuo, David Dostal, Linley Watson, Nicholas S Duesbery, Che-Ping Cheng, Heng Jie Cheng, Stephen H Leppla
Affiliations
Review

Pathophysiology of anthrax

Arthur E Frankel et al. Front Biosci (Landmark Ed). .

Abstract

Infection by Bacillus anthracis in animals and humans results from accidental or intentional exposure, by oral, cutaneous or pulmonary routes, to spores, which are normally present in the soil. Treatment includes administration of antibiotics, vaccination or treatment with antibody to the toxin. A better understanding of the molecular basis of the processes involved in the pathogenesis of anthrax namely, spore germination in macrophages and biological effects of the secreted toxins on heart and blood vessels will lead to improved management of infected animals and patients. Controlling germination will be feasible by inhibiting macrophage paralysis and cell death. On the other hand, the control of terminal hypotension might be achieved by inhibition of cardiomyocyte mitogen-activated protein kinase and stimulation of vessel cAMP.

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Figures

Figure 1
Figure 1
Schematic diagram of domain organization of anthrax toxin molecules. The amino acid (a.a.) boundary is indicated above each domain. (a) protective antigen (PA). (b) lethal factor (LF) (c) edema factor (EF).
Figure 2
Figure 2
Plot of macrophage IC50 (pM) vs. spore tolerance based on experiments above and spore data from Young (39).
Figure 3
Figure 3
Effect of bolus anthrax toxins on mean arterial pressure (MAP). MAP in rats was recorded continuously via telemetry before and after toxin injection.
Figure 4
Figure 4
Rat echocardiography studies performed as described (41). A. Ejection fraction of lethal toxin treated rats; B. Left ventricular end-diastolic area of edema toxin treated rats.
Figure 5
Figure 5
Lung pathology of control, anthrax lethal toxin and anthrax edema toxin treated rats. Arrows point to interstitial protein/fluid with lethal toxin and vascular disruption/hemorrhage with edema toxin.
Figure 6
Figure 6
Dog left ventricle pressure-volume loops after anthrax lethal toxin infusion
Figure 7
Figure 7
Isolated dog cardiomyocyte in vitro contractility parameters. Cells were from anthrax toxin treated or control dogs.
See this image and copyright information in PMC

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