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Yersinia pestis

Yersinia pestis bacterium, belonging to the family Enterobacteriaceae. It is the infectious agent of bubonic plague, and can also cause pneumonic plague and septicemic plague. All forms have been responsible for enormous mortality in many fearsome epidemics throughout the history of mankind (without treatment, patients with the bubonic form die, and almost 100% with the pneumonic form), such as 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. more...

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Pestis in the Black Death is today highly debated amongst historians, as scientific evidence is pointing away from it as the cause.

The genus Yersinia is Gram negative, bipolar staining coccobacilli, and, similarly to other Enterobacteriaceae, it has a fermentative metabolism. Yersinia pestis produces a antiphagocytic slime. The organism is motile when isolated, but becomes nonmotile in the mammalian host.

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. This was originally called Pasteurella pestis, and was renamed after Yersin in 1967.

Pathogenicity and immunity

Pathogenicity is due to two antiphagocytic antigens, named F1 and VW, both required for virulence. They are produced by the bacterium at the temperature of 37°C, so this explains 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.

There is a formalin-inactivated vaccine available for adults at high risk, but it is not very effective 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.

Genome

The genome of the CO92 strain obtained from clinical isolate from the USA was recently sequenced. The chromosome sequence is 4,653,728 base pairs long. Like its cousins Yersinia pseudotuberculosis and Yersinia 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 Yersinia pseudotuberculosis, and is different only because of the presence of the virulence plasmids.hi

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Bubonic blockage - genetics of bubonic-plague causing bacteria Yersinia pestis - Break Throughs
From Discover, 11/1/96

Bubonic Plague, we've long known, is transmitted by fleas infected with the bacteria Yersinia pestis. The bacteria form large masses in the fleas, digestive tracts and eventually starve them to death; but before they die, during their increasingly persistent and frustrated attempts to feed, the fleas regurgitate infected blood into their victims. All that is clear. What has puzzled researchers, however, is just how Y pestis manages to survive inside fleas in the first place. "The fleas digestive tract is very in hospitable for bacteria," says Joe Hinnebusch, a microbiologist at the National Institutes of Healths Rocky Mountain Laboratories in Montana. "Fleas are frequent blood feeders and they excrete often, so its hard for bacteria to stick around."

Hinnebusch hasn't found a way to control the spread of the plague (the disease is readily treatable with antibiotics if diagnosed early enough), but he may have discovered how Y. pestis manages to thrive where other bacteria cannot. He started with the suspicion that the solution must somehow involve the bacteria's interaction with blood. Eventually that led him to focus on a stretch of DNA in the bacteria called the hermin storage, or hms, locus, which contains genes that code for proteins that bind hemin, an iron-carrying molecule found in blood. Hinnebusch knew from earlier studies that these genes don't function at the relatively high temperatures found in mammalian bodies. They become active only at lower temperatures - about 78 degrees - suggesting that their job in the plague scenario is performed in the cold-blooded flea and not the hot human.

Hinnebusch found that Y pestis bacteria missing the hms genes could indeed infect fleas, but they did not block their digestive tracts - the mutants lived peacefully in the midgut, allowing the fleas to feed normally. The fleas also excreted normally, though, and many of the mutants got flushed out in the process.

Bacteria with hms genes, however, not only colonize the midgut but clump together in a mass in the passageway leading from the esophagus to the midgut. The hms proteins somehow make a bacterium's cell surface hydrophobic, or water fearing, says Hinnebusch, so the bacteria clump to avoid contact with blood. The bacteria clog the works, drive the flea into a feeding frenzy, and kill it - but not before they've moved on.

COPYRIGHT 1996 Discover
COPYRIGHT 2004 Gale Group

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