Yersinia pestis and Bubonic Plague
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CHAPTER 3.3.14 a i n i s reY
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Yersinia pestis and Bubonic Plague BOB BRUBAKER
Introduction Caused by Yersinia pestis, bubonic plague (also known as “the pestilence” or “Black Death”) is the most devastating epidemic bacterial disease known to humankind. This appraisal is based upon the terrifying manifestations of plague (Butler, 1983; Pollitzer, 1954), which include death within 1–3 days following the onset of symptoms (Butler, 1983). Up to 200 million people have succumbed to this disease over the course of history (Duplais, 1988). On the other hand, the closely related Yersinia pseudotuberculosis or the more divergent Yersinia enterocolitica (termed “enteropathogenic” yersiniae because they typically produce gastrointestinal afflictions) do not have the ability of plague bacilli to cause comparable acute lethal disease in rodents and primates. Nevertheless, these three human parasites exhibit a similar basic pattern of pathogenicity mediated by a shared –70-kb plasmid termed “pCD” in Y. pestis, “pYV,” “pCad” or “pIB” in Y. pseudotuberculosis, and “pYV” in Y. enterocolitica (Ben-Gurion and Shafferman, 1981; Cornelis and Wolf-Watz, 1997; Ferber and Brubaker, 1981; Goguen et al., 1984; Hu et al., 1998; Iriate and Cornelis, 1996; Perry and Fetherston, 1997; Perry et al., 1998). Hereafter, the term pCD will apply to the –70-kb plasmid of Y. pestis and pYV will designate its analog in both Y. pseudotuberculosis and Y. enterocolitica. Cells of wild-type Y. pestis, most but not all serotypes of Y. pseudotuberculosis, and invasive isolates of Y. enterocolitica also possess an –35-kb chromosomally encoded high-pathogenicity island (Bearden et al., 1997; Buchrieser et al., 1998a; Buchrieser et al., 1998b; Buchrieser et al., 1999; Carniel et al., 1996; Fetherston et al., 1995; Fetherston and Perry, 1994; Fetherston et al., 1992). The shared plasmid encodes a battery of cytotoxins termed “Yops” and at least three anti-inflammatory activities, whereas the highpathogenicity island contains genes required for the siderophore (yersiniabactin)-dependent assimilation of iron. Superimposed on this common theme are two unique plasmids in Y. pestis that facilitate invasion of tissues and colonization of the flea vector. In addition, plague bacilli have
lost central enzymes of intermediary metabolism and host cell adhesin and invasin activities required by the enteropathogenic yersiniae to express chronic infection (Achtman et al., 1999; Brubaker, 1991; Brubaker, 2000; Hinnebusch, 1997). As a consequence of this genomic finetuning, plague has become the yardstick by which all other acute infectious diseases are measured. Yersinia pestis is now more firmly entrenched in endemic foci throughout the world than at any previous time (Baltazard, 1960; Perry and Fetherston, 1997). Although controllable by antibiotics, the emergence of drug-resistant isolates has been reported (Galimand et al., 1997). The probability of acquiring the disease from natural reservoirs (sylvatic plague) will increase as the human po
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