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Yersinia pestisUnlike the other pathogenic yersiniae, and the other bacteria covered by ERIC, Yersinia pestis does not cause a gastroenteric disease. Rather, it is the causative agent of bubonic and pneumonic plague - the disease that has come to stand, in the public imagination, as the exemplar of infectious diseases. Rodents are the main reservoir of Y. pestis, but other animals and humans can also serve as hosts. It is transmitted between hosts by fleas, being contracted from the bite of an infected flea or by scratching the flea's feces present at the bite wound. Although pathogenesis in mammals does not involve the gastrointestinal system, transmission via the flea vector does involve a gastroenteric disease of sorts: in the infected flea the digestive tract is partially obstructed by masses of Y. pestis. As a consequence, the flea is effectively starving, causing it to bite more frequently and regurgitate infected material into the bite wounds. In chronically infected fleas the digestive tract is not obstructed, but Y. pestis is present in their feces. From the bite site the bacteria are carried to the regional lymph nodes where they are taken up by macrophages. The intracellular environment induces transformation of the bacteria to an encapsulated form which elaborates a number of virulence factors. The now fully virulent bacteria break out of the phagocytes and infect the lymph nodes producing the characteristic enlarged 'buboes' of bubonic plague. The bacteria are subsequently released into the bloodstream from necrotic lymph nodes, causing a stage called septicemic plague. Endotoxin release results in shock and disseminated intravascular coagulation (DIC); the mortality rate for persons with untreated bubonic plague is between 50% and 80%. However, if detected in the early stages, plague can be treated successfully with antibiotics. Infection of the lung from the bloodstream also can occur, resulting in secondary pneumonic plague. The bacteria can be transmitted via aerosol from an infected person or animal with the pneumonic form of the disease, in which case they are already fully virulent and highly contagious. Pneumonic plague progresses rapidly, and is nearly always fatal within days. Virulence factors of Y. pestis are encoded both on three plasmids and chromosomally. A small 9.6 kb plasmid (pPCP1) encodes the Pla protease, which activates plasminogen - causing blood clots at the bite wound to dissolve and allowing the initial dissemination of the bacteria to the lymph nodes. A 70 kb plasmid (pCD1; also present in Y. pseudotuberculosis, where it is called pIB1) encodes the Yop system, a type III secretion system essential for virulence. A 100 to 110 kb plasmid (pMT1 or pFra) encodes the murine toxin Ymt and the F1 capsular protein. Three distinct biovars of Y. pestis (Antiqua, Mediaevalis, and Orientalis) have been associated with
the three historically recognized pandemics. They are phylogenetically distinct, as shown by analysis of DNA
restriction fragment polymorphisms and ribotyping. Y. pestis biovar Orientalis is thought to have
emerged most recently.
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