How the structural gene products of Yersinia pestis relate to virulence.
Bubonic plague is the most devastating acute infectious disease known to man. The causative agent, Yersinia pestis, is now more firmly entrenched in sylvatic reservoirs throughout the world than at any time in the past. Consequently, the organism increasingly causes casual human disease and is readily available for use as a bioweapon. Recent attempts to understand the severe nature of plague have focused upon its very recent divergence from Yersinia pseudotuberculosis, an etiological instrument of chronic enteropathogenic infection. This review emphasizes that the invasive nature of plague and its dissemination by fleabite is mediated by plasmids not shared by enteropathogenic yersiniae. The basis for high lethality is considered within the context of chromosomal degeneration causing loss of normal metabolic functions and modification of virulence factors, permitting a terminal anti-inflammatory phase associated with pronounced septicemia.
The University of Chicago, Department of Microbiology, Cummings Life Sciences Center, Chicago, IL 60637, USA. t-rbruba@bsd.uchicago.edu
Robert R
RR
Brubaker
D000818:Animals; D014644:Genetic Variation; D016680:Genome, Bacterial; D006801:Humans; D010930:Plague / Q000382:microbiology* / Q000635:transmission; D014774:Virulence / Q000235:genetics; D015010:Yersinia pestis / Q000235:genetics* / Q000378:metabolism / Q000472:pathogenicity