Abstract
Yersinia pestis, the causative agent of bubonic plague, is one of the most virulent bacterial pathogens known to mankind. This gram-negative bacterium is usually transmitted to humans by an infected rodent flea. After infection, the pathogen invades lymphatic tissue and proliferates in the lymph nodes. The two other human pathogenic species of Yersinia , Y. enterocolitic a and Y. pseudotuberculosis , cause enteric infections that usually are self-limiting. These orally transmitted pathogens also proliferate in lymphatic tissue, and their primary site of infection is the lymphoid follicles of the small intestine. For a long time, Yersinia was considered to be an intracellular pathogen, but recent findings have shown that the pathogen proliferates in the extracellular fluid during infection and prevents its uptake process by professional phagocytes, a mechanism termed antiphagocytosis (1). This is a major virulence mechanism that is
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