Yersinia pestis

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{{Taxobox | color = lightgrey | name = Yersinia pestis | image = Yersinia_pestis_fluorescent.jpeg | image_width = 240px | image_caption = Yersinia pestis under fluorescent staining, 2000x. Source: CDC | regnum = Eubacteria | phylum = Proteobacteria | classis = Gamma Proteobacteria | ordo = Enterobacteriales | familia = Enterobacteriaceae | genus = Yersinia | species = Y. pestis | binomial = Yersinia pestis | binomial_authority = (Lehmann & Neumann, 1896)
van Loghem 1944 }} Yersinia pestis is a Gram-negative bacterium belonging to the family Enterobacteriaceae. The infectious agent of bubonic plague, it can also cause pneumonic and septicemic plague. All three forms have been responsible for high mortality rates in epidemics throughout human history e.g. the Great Plague and the Black Death, the latter of which accounted for the death of approximately 25% of the European population.

The role of Y. pestis in the Black Death is debated amongst historians and 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, while medieval corpses who died from other causes did not test positive for Y. pestis<ref>Template:Cite journal</ref>^,<ref>Template:Cite journal </ref>. 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.

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.

1 History
2 Pathogenicity and immunity
3 Genome
4 Susceptibility
5 See also
6 References
7 External links

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History

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. Yersin was a member of the Pasteur school of thought. Shibasaburo Kitasato, a Germany-trained Japanese bacteriologist who practiced Koch's methodology was also engaged at the time in finding the causative agent of plague. However, it was Yersin who actually linked plague with Yersinia pestis. Originally named Pasteurella pestis, the organism was renamed in 1967.

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Pathogenicity and immunity

Pathogenicity of Y. pestis is due to two anti-phagocytic antigens, named F1 and VW, both required for virulence. These antigens are produced by the bacterium at 37°C: this is why insects—such as the flea—harbor non-virulent bacteria. Furthermore, Y. pestis survive and produce 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. They induce phagocytosis neutrophils.<ref>Template:Cite book</ref>

There is a formalin-inactivated vaccine available for adults at high risk of contracting the plague, but it is of limited effectiveness and may cause severe inflammatory reactions. Experiments with genetic engineering of a vaccine based on F1 and VW antigens is underway and shows great promise.

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Genome

The genome of the CO92-strain obtained from clinical isolate from the USA was recently sequenced.<ref>Template:Cite journal</ref> The chromosome sequence 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.

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Susceptibility

Y. pestis is highly susceptible to several antibiotics, mainly streptomycin and chloramphenicol. Second-tier aetiotropic drugs include tetracycline-group preparations; the latter are often used together with streptomycin due to synergistic effects. It should be noted that strains resistant to one or two agents specified above have been isolated.

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