Histopathological effects of anthrax lethal factor on rat liver

Abstract

Bacillus anthracis, the causative agent of anthrax, has become an increasingly important scientific topic due to its potential role in bioterrorism. The lethal toxin (LT) of B. anthracis consists of lethal factor (LF) and a protective antigen (PA). This study investigated whether only lethal factor was efficient as a hepatotoxin in the absence of the PA. To achieve this aim, LF (100 mg/kg body weight, dissolved in sterile distilled water) or distilled water vehicle were intraperitoneally injected once into adult rats. At 24 h post-injection, the hosts were euthanized and their livers removed and tissue samples examined under light and electron microscopes. As a result of LF application, hepatic injury -including cytoplasmic and nuclear damage in hepatocytes, sinusoidal dilatation, and hepatocellular lysis -became apparent. Further, light microscopic analyses of liver sections from the LF-injected rats revealed ballooning degeneration and cytoplasmic loss within hepatocytes, as well as peri-sinusoidal inflammation. Additionally, an increase in the numbers of Kupffer cells was evident. Common vascular injuries were also found in the liver samples; these injuries caused hypoxia and pathological changes. In addition, some cytoplasmic and nuclear changes were detected within the liver ultrastructure. The results of these studies allow one to suggest that LF could be an effective toxicant alone and that PA might act in situ to modify the effect of this agent (or the reverse situation wherein LF modifies effects of PA) such that lethality results.

Acquired coagulant factor VIII deficiency induced byBacillus anthracislethal toxin in mice

“…19 Previous studies have revealed that anthrax induces liver damage; invasions of bacterium B. anthracis have been observed frequently in the liver of infected patients [20][21][22] and animals. 15,23,24 These results prompted us to investigate whether coagulant factor defects are associated with LT-induced liver damage. Herein, we determined that LT challenges induce toxicity toward hepatic cells in vitro and in vivo.…”