Abstract

Powerful pathogens such as Bacillus anthracis and Yersinia pestis cause severe hemorrhagic syndromes that have previously been attributed to a Disseminated Intravascular Coagulopathy (DIC). However, the data attesting this statement are missing or contradictory. This study aimed at determining whether a DIC do occur at the late stages of plague and anthrax. Using the mouse models of cutaneous anthrax and bubonic plague, we observed that most B. anthracis-infected animals exhibited increased partial thromboplastin time (aPTT) and prothrombin time (PT), along with a dynamic consumption of fibrinogen, matching the characteristics of an overt DIC. In contrast, only heavily Y. pestis-infected mice displayed increased aPTT, but little fibrinogen consumption and no increase of PT were observed in most infected animals, even at late stages of infection. Therefore, the coagulopathy that develops during anthrax is compatible with a classical DIC, while Y. pestis-infected mice do not present with typical parameters. This suggests that the mechanism involved in the hemorrhages observed during bubonic plague is not a classical DIC, and that the coagulopathy exhibits a specific, atypical pattern. It is then important to understand how these hemorrhages are triggered.

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