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Yersinia pestis

Yersinia pestis

Yersinia pestis under fluorescent staining, 2000x. cheese: CDC
Scientific classification
Kingdom: Eubacteria
Phylum: Proteobacteria
Class: Gamma Proteobacteria
Order: Enterobacteriales
Family: Enterobacteriaceae
Genus: Yersinia
Species: Y. pestis
Binomial name
Yersinia pestis
(Lehmann & Neumann, 1896)
van Loghem 1944

Yersinia pestis (Pasteurella pestis) is a Gram-negative facultative anaerobic bipolar-staining (giving it a safety pin appearance) bacillus 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 Black Death that 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.



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 (Fraction 1) and V, both important for virulence.[1] 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.[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 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[8].


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 comprehensive and 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.


The traditional first line treatment for Y. pestis has been streptomycin,[12][13] chloramphenicol, tetracycline,[14] and fluoroquinolones. 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, ventilatory, 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 is alleged to have been found in the teeth of an individual who supposedly 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.


  1. ^ a b Collins FM (1996). Pasteurella, Yersinia, and Francisella. In: Baron's Medical Microbiology (Baron S et al, eds.), 4th ed., Univ of Texas Medical Branch. ISBN 0-9631172-1-1. 
  2. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill, pp. 484-8. ISBN 0-8385852-9-9. 
  3. ^ Bockemühl J (1994). "[100 years after the discovery of the plague-causing agent--importance and veneration of Alexandre Yersin in Vietnam today]". Immun Infekt 22 (2): 72-5. PMID 7959865.
  4. ^ {cite journal |author=Howard-Jones N |title=Was Shibasaburo Kitasato the discoverer of the plague bacillus? | journal=Perspect Biol Med |volume=16 |issue=2 |pages=292-307 |year=1973 |pmid = 4570035}}
  5. ^ Zhou D, Tong Z, Song Y, Han Y, Pei D, Pang X, Zhai J, Li M, Cui B, Qi Z, Jin L, Dai R, Du Z, Wang J, Guo Z, Wang J, Huang P, Yang R (2004). "Genetics of metabolic variations between Yersinia pestis biovars and the proposal of a new biovar, microtus". J Bacteriol 186 (15): 5147-52. PMID 15262951.
  6. ^ Guiyoule A, Grimont F, Iteman I, Grimont P, Lefèvre M, Carniel E (1994). "Plague pandemics investigated by ribotyping of Yersinia pestis strains". J Clin Microbiol 32 (3): 634-41. PMID 8195371.
  7. ^ Salyers AA, Whitt DD (2002). Bacterial Pathogenesis: A Molecular Approach, 2nd ed., ASM Press. pp. 207-12. 
  8. ^ Welkos S et al.. (2002). "Determination of the virulence of the pigmentation-deficient and pigmentation-/plasminogen activator-deficient strains of Yersinia pestis in non-human primate and mouse models of pneumonic plague". Vaccine 20: 2206–2214. PMID 12009274.
  9. ^ Deng W et al.. (2002). "Genome Sequence of Yersinia pestis KIM". Journal of Bacteriology 184 (16): 4601–4611. PMID 12142430.
  10. ^ Parkhill J et al.. (2001). "Genome sequence of Yersinia pestis, the causative agent of plague". Nature 413: 523–527. PMID 11586360.
  11. ^ Hixson K et al.. (2006). "Biomarker candidate identification in Yersinia pestis using organism-wide semiquantitative proteomics.". Journal of Proteome Research 5 (11): 3008-3017. PMID 16684765.
  12. ^ Wagle PM. (1948). "Recent advances in the treatment of bubonic plague". Indian J Med Sci 2: 489–94.
  13. ^ Meyer KF. (1950). "Modern therapy of plague". JAMA 144: 982–5. PMID 14774219.
  14. ^ Kilonzo BS, Makundi RH, Mbise TJ. (1992). "A decade of plague epidemiology and control in the Western Usambara mountains, north-east Tanzania". Acta Tropica 50: 323–9. PMID 1356303.
  15. ^ Mwengee W, Butler T, Mgema S, et al. (2006). "Treatment of plague with gentamicin or doxycycline in a randomized clinical trial in Tanzania". Clin Infect Dis 42: 614–21. PMID 16447105.
  16. ^ Drancourt M, Aboudharam G, Signolidagger M, Dutourdagger O, Raoult D. (1998). "Detection of 400-year-old Yersinia pestis DNA in human dental pulp: An approach to the diagnosis of ancient septicemia". PNAS 95 (21): 12637–12640. PMID 9770538.
  17. ^ Drancourt M; Raoult D. (2002). "Molecular insights into the history of plague.". Microbes Infect. 4: 105–9. PMID 11825781.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Yersinia_pestis". A list of authors is available in Wikipedia.
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