Yersinia pestis
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'''Yersinia pestis''' | '''Yersinia pestis''' | ||
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Yersinia pestis (formerly Pasteurella pestis) is a Gram-negative rod-shaped bacterium that can infect humans and other animals. Its closest relative is the gastrointestinal pathogen Yersinia pseudotuberculosis, and more distantly Yersinia enterocolitica. | Yersinia pestis (formerly Pasteurella pestis) is a Gram-negative rod-shaped bacterium that can infect humans and other animals. Its closest relative is the gastrointestinal pathogen Yersinia pseudotuberculosis, and more distantly Yersinia enterocolitica. | ||
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==Transmission== | ==Transmission== | ||
| - | Rat flea (Xenopsylla cheopis), the | + | Initial acquisition of Y. pestis by the vector occurs during feeding on an infected animal. |
| - | + | Rat flea (Xenopsylla cheopis), the classical vector for plague will ingest 0.03 to 0.5 µl of blood. | |
| - | + | Maintenance of the bacteria in the flea digestive tract is contributed by several proteins some of these are | |
| + | hemin storage (Hms) system and Yersinia murine toxin (Ymt). Ymt is important for the survival of Y. pestis in fleas | ||
| + | while Hms system plays an important role in the transmission of Y. pestis back to a mammalian host.he Hms system plays | ||
| + | an important role in the transmission of Y. pestis back to a mammalian host. In the insect vector, proteins encoded by | ||
| + | Hms genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus.Transmission | ||
| + | of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges | ||
| + | bacteria growing there and is regurgitated back into the host circulatory system. | ||
| + | |||
| + | ==Pathogenic Activity== | ||
| + | Y. pestis's most of the spreading occurs between rodents and fleas. Every infected animal can transmit the infection to humans through | ||
| + | contact with skin tissue. Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors including an ability of | ||
| + | these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. It expresses a plasminogen | ||
| + | activator that is an important virulence factor for pneumonic plague and which might degrade on blood clots in order to facilitate systematic | ||
| + | invasion. | ||
| + | ==Virulence== | ||
| + | Two important anti-phagocytic antigens, named F1 (Fraction 1) and V or LcrV, are both important for virulence. Y. pestis survives and produces | ||
| + | F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved | ||
| + | by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils. | ||
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[http://en.wikipedia.org/wiki/Yersinia_pestis Wikipedia] | [http://en.wikipedia.org/wiki/Yersinia_pestis Wikipedia] | ||
| - | [[category: | + | [[category:PolysacDB]] |
Current revision
Yersinia pestis
Yersinia pestis (formerly Pasteurella pestis) is a Gram-negative rod-shaped bacterium that can infect humans and other animals. Its closest relative is the gastrointestinal pathogen Yersinia pseudotuberculosis, and more distantly Yersinia enterocolitica.
| Kingdom | Eubacteria |
|---|---|
| Phylum | Proteobacteria |
| Class | Gammaproteobacteria |
| Order | Enterobacteriales |
| Family | Enterobacteriaceae |
| Genus | Yersinia |
| Species | Y. pestis |
| Binomial | Yersinia pestis |
Contents |
[edit] Surface Characteristics
Y. pestis has typical cell wall and whole-cell lipid compositions and an enterobacterial antigen. Its lipopolysaccharide is characterized as rough, possessing core components but lacking extended O-group side chains; while there is no true capsule, a carbohydrate-protein envelope, termed capsular antigen or fraction 1 (F1), forms during growth above 33 C (14, 32, 215). This facultative anaerobe possesses a constitutive glyoxylate bypass and unregulated L-serine deaminase expression but lacks detectable adenine deaminase, aspartase, glucose 6-phosphate dehydrogenase, ornithine decarboxylase, and urease activities, as well as a possible lesion in -ketoglutarate dehydrogenase (32, 33, 125).
[edit] Transmission
Initial acquisition of Y. pestis by the vector occurs during feeding on an infected animal. Rat flea (Xenopsylla cheopis), the classical vector for plague will ingest 0.03 to 0.5 µl of blood. Maintenance of the bacteria in the flea digestive tract is contributed by several proteins some of these are hemin storage (Hms) system and Yersinia murine toxin (Ymt). Ymt is important for the survival of Y. pestis in fleas while Hms system plays an important role in the transmission of Y. pestis back to a mammalian host.he Hms system plays an important role in the transmission of Y. pestis back to a mammalian host. In the insect vector, proteins encoded by Hms genetic loci induce biofilm formation in the proventriculus, a valve connecting the midgut to the esophagus.Transmission of Y. pestis occurs during the futile attempts of the flea to feed. Ingested blood is pumped into the esophagus, where it dislodges bacteria growing there and is regurgitated back into the host circulatory system.
[edit] Pathogenic Activity
Y. pestis's most of the spreading occurs between rodents and fleas. Every infected animal can transmit the infection to humans through contact with skin tissue. Pathogenesis due to Y. pestis infection of mammalian hosts is due to several factors including an ability of these bacteria to suppress and avoid normal immune system responses such as phagocytosis and antibody production. It expresses a plasminogen activator that is an important virulence factor for pneumonic plague and which might degrade on blood clots in order to facilitate systematic invasion.
[edit] Virulence
Two important anti-phagocytic antigens, named F1 (Fraction 1) and V or LcrV, are both important for virulence. Y. pestis survives and produces F1 and V antigens while it is residing within white blood cells such as monocytes, but not in neutrophils. Natural or induced immunity is achieved by the production of specific opsonic antibodies against F1 and V antigens; antibodies against F1 and V induce phagocytosis by neutrophils.
