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Yersinia pestis |
Yersinia pestis under fluorescent staining, 2000x. Source: CDC
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| Scientific classification |
| Kingdom: |
Eubacteria
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| Phylum: |
Proteobacteria
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| Class: |
Gamma Proteobacteria
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| Order: |
Enterobacteriales
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| Genus: |
Yersinia
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| Species: |
Y. pestis
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Binomial name
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Yersinia pestis
(Lehmann & Neumann, 1896)
van Loghem 1944 |
Yersinia pestis is a Gram-negative bacterium belonging to the family Enterobacteriaceae.[1] The infectious agent of bubonic plague, Y. pestis infection can also cause pneumonic and septicemic plague.[2] All three forms have been responsible for high mortality rates in epidemics throughout human history, including the Great Plague and the Black Death, the latter of which accounted for the death of approximately one-third of the European population in 1347 to 1353.
The genus Yersinia is Gram-negative, bipolar staining coccobacilli, and, similarly to other Enterobacteriaceae, it has a fermentative metabolism. Y. pestis produces an antiphagocytic slime. The organism is motile when isolated, but becomes nonmotile in the mammalian host.
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Contents
- 1 Discovery
- 2 Pathogenicity and immunity
- 3 Genome
- 4 Susceptibility
- 5 Historical impact
- 6 References
- 7 External links
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Discovery
Y. pestis was discovered in 1894 by Swiss/French physician and bacteriologist from the Pasteur Institute, Alexandre Yersin, during an epidemic of plague in Hong-Kong.[3] Yersin was a member of the Pasteur school of thought. Shibasaburo Kitasato, a German-trained Japanese bacteriologist who practiced Koch's methodology was also engaged at the time in finding the causative agent of plague.[4] However, it was Yersin who actually linked plague with Yersinia pestis. Originally named Pasteurella pestis, the organism was renamed in 1967.
Three biovars of Y. pestis are known, each thought to correspond to one of the historical pandemics of bubonic plague.[5] Biovar Antiqua is thought to correspond to the Plague of Justinian; it is not known whether this biovar also corresponds to earlier, smaller epidemics of bubonic plague, or whether these were even truly bubonic plague.[6] Biovar Medievalis is thought to correspond to the Black Death. Biovar Orientalis is thought to correspond to the Third Pandemic and the majority of modern outbreaks of plague.
Pathogenicity and immunity
Pathogenicity of Y. pestis is in part due to two anti-phagocytic antigens, named F1 and VW, both important for virulence.[1] These antigens are produced by the bacterium at 37°C. Furthermore, Y. pestis survives and produces F1 and VW antigens within blood cells such as monocytes, but not in polymorphonuclear neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and VW antigens; antibodies against F1 and VW induce phagocytosis by neutrophils.[7]
A formalin-inactivated vaccine once was available for adults at high risk of contracting the plague until removal from the market by the FDA. It was of limited effectiveness and may cause severe inflammation. Experiments with genetic engineering of a vaccine based on F1 and VW antigens are underway and show promise; however, bacteria lacking antigen F1 retain enough virulence, and the V antigens are sufficiently variable, that vaccines composed of these antigens may not be fully protective[8].
Genome
The complete genomic sequence is available for two of the three sub-species of Y. pestis: strain KIM (of biovar Medievalis)[9], and strain CO92 (of biovar Orientalis, obtained from a clinical isolate in the United States)[10]; as of 2006, the genomic sequence of a strain of biovar Antiqua has not yet been completed. The chromosome of strain KIM is 4,600,755 base pairs long; the chromosome of strain CO92 is 4,653,728 base pairs long. Like its cousins Y. pseudotuberculosis and Y. enterocolitica, Y. pestis is host to the plasmid pCD1. In addition, it also hosts two other plasmids, pPCP1 and pMT1 which are not carried by the other Yersinia species. Together, these plasmids, and a pathogenicity island called HPI, encode several proteins which cause the pathogenicity for which Y. pestis is famous. Among other things, these virulence factors are required for bacterial adhesion and injection of proteins into the host cell, invasion of bacteria into the host cell, and acquisition and binding of iron harvested from red blood cells. Y. pestis is thought to be descendant from Y. pseudotuberculosis, differing only in the presence of specific virulence plasmids.
A recent comprensive comparative proteomics analysis of Y. pestis: strain KIM was recently performed [11] , this analysis focused on the transition to a growth condition mimicking growth in host cells.
Susceptibility
The traditional first line treatment for Y. pestis has been streptomycin,[12][13] chloramphenicol or tetracycline.[14] There is also good evidence to support the use of doxycycline or gentamicin.[15]
It should be noted that strains resistant to one or two agents specified above have been isolated: treatment should be guided by antibiotic sensitivities where available. Antibiotic treatment alone is insufficient for some patients, who may also require circulatory support, ventilatory support, or renal support.
Historical impact
The role of Y. pestis in the Black Death is debated among historians; some have suggested that the Black Death spread far too rapidly to be caused by Y. pestis. DNA from Y. pestis has been found in the teeth of those who died from the Black Death, however, and medieval corpses who died from other causes did not test positive for Y. pestis.[16],[17] This suggests that Y. pestis was, at the very least, a contributing factor in some (though possibly not all) of the European plagues. It's possible that the selective pressures induced by the plague might have changed how the pathogen manifests in humans, selecting against the individuals or populations which were the most susceptible.
