Bubonic plague causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

The major forms of plague are caused by yersinia pestis living in rodents. The disease is then transferred to humans from the fleas that originally bit the infected rodent.

Causes

Plague is caused by the organism yersinia pestis. Rodents, such as rats, spread the disease to humans. People can get the plague when they are bitten by a flea that carries the plague bacteria from an infected rodent. In rare cases, you may get the disease when handling an infected animal. Certain forms of the plague can be spread from human to human. When someone with pneumonic plague coughs, microscopic droplets carrying the infection move through the air. Anyone who breathes in these particles may catch the disease. An epidemic may be started this way. In the middle ages, massive plague epidemics killed millions of people.

Pathophysiology

A scanning electron micrograph depicting a mass of Yersinia pestis bacteria

• Pathogenicity of Y. pestis is in part due to two anti-phagocytic antigens, named F1 (Fraction 1) and V, both important for virulence. These antigens are produced by the bacterium at 37°C.
• Furthermore, Y. pestis survives and produces F1 and V 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 V antigens; antibodies against F1 and V induce phagocytosis by neutrophils.
• 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 V antigens are underway and show promise; however, bacteria lacking antigen F1 are still virulent, and the V antigens are sufficiently variable, that vaccines composed of these antigens may not be fully protective.

Genetics

• The complete genomic sequence is available for two of the three sub-species of Y. pestis: strain KIM (of biovar Medievalis), and strain CO92 (of biovar Orientalis, obtained from a clinical isolate in the United States); 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 comprehensive and comparative proteomics analysis of Y. pestis: strain KIM was recently performed , 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, chloramphenicol, tetracycline, and fluoroquinolones.
• There is also good evidence to support the use of doxycycline or gentamicin.
• 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.

Images

Male Xenopsylla cheopis (oriental rat flea) engorged with blood. This flea is the primary vector of plague in most large plague epidemics in Asia, Africa, and South America. Both male and female fleas can transmit the infection.

References

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