Yersinia pestis

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This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Yersinia pestis infection.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Esther Lee, M.A.; Rim Halaby, M.D. [2]; João André Alves Silva, M.D. [3]

Overview

Yersinia pestis (Y. pestis), a rod-shaped facultative anaerobe with bipolar staining (giving it a safety pin appearance) causes the infection in mammals and humans.[1] The bacteria maintain their existence in a cycle involving rodents and their fleas. 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.

Taxonomy

Bacteria; Proteobacteria; Gammaproteobacteria; Enterobacteriales; Yersinia; Yersinia pestis

Biology

Yersinia pestis, Direct Fluorescent Antibody Stain (DFA), 200x Magnification Courtesy: Public Health Image Library (PHIL), Centers for Disease Control and Prevention (CDC)[2]
Photomicrograph of Yersinia (Pasteurella) pestis, sometimes referred to as Bacillus pestis. Courtesy: Public Health Image Library (PHIL), Centers for Disease Control and Prevention (CDC)[3]

Yersinia pestis is a nonmotile, non-spore-forming, Gram-negative, non-lactose fermenting, ovoid and "safety-pin-shaped" (bipolar appearance when stained) bacillus. It is an enterobacteriaceae commonly measuring 0.75x1.5 μm. On cell cultures, it grows on sheep-blood agar, as grayish translucent colonies. It also grows on MacConkey and nutrient-rich broths.[4]

Yersinia pestis only survives for a few hours on physical surfaces, being very sensitive to high temperatures, sunlight and disinfectants.[4][5][6]

Yersinia pestis is thought to have evolved from Yersinia pseudotuberculosis about 1500 - 2000 years ago. According to its behavior towards nitrate and glycerol, Yersinia pestis may be classified as:[4]

  • Biovar Antiqua
  • Nitrate reduction: positive
  • Glycerol reduction: positive
  • Biovar Medievalis
  • Nitrate reduction: negative
  • Glycerol use: positive
  • Biovar Orientalis
  • Nitrate reduction: positive
  • Glycerol use: negative

Genome

The complete genomic sequence is available for two of the three sub-species of yersinia pestis:

  • Strain KIM - Biovar Medievalis[7]
  • Strain CO92 - Biovar Orientalis[8]

As of 2006, the genomic sequence of a strain of biovar Antiqua has been completed.[9] Similar to the other pathogenic strains, there are signs of mutations causing loss of function. The chromosome of strain KIM is 4,600,755 base pairs long; the chromosome of strain CO92 is 4,653,728 base pairs long.

Similarly to other enterobacteriaceae (Yersinia pseudotuberculosis and Yersinia enterocolitica), Yersinia pestis is host to the plasmid pCD1. In addition, it also hosts two other plasmids, pPCP1 (also called pPla or pPst) and pMT1 (also called pFra) that are not carried by the other Yersinia species.

Together, these plasmids, and a pathogenicity island called HPI, encode several pathogenic proteins, characteristic of Yersinia pestis. Among other things, these virulence factors are required of:

  • Bacterial adhesion
  • Injection of proteins into the host cell
  • Invasion of the host cell (via a Type III secretion system)
  • Acquisition and binding of iron from red blood cell, via siderophores

A comprehensive and comparative proteomics analysis of Yersinia pestis strain KIM was performed in 2006.[11] The analysis focused on the transition to a growth condition mimicking growth in host cells.

Tropism

Yersinia pestis shows tropism for lymphoid tissue.

Natural Reservoir

Plague is primarily a disease of rodents. The infection is maintained in natural foci of the disease in wild rodent colonies, through transmission between rodents, by their flea ectoparasites.[12]


Gallery

References

  1. 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. "http://phil.cdc.gov/phil/details.asp". 
  3. "http://phil.cdc.gov/phil/details.asp". 
  4. 4.0 4.1 4.2 Koirala, Janak (2006). "Plague: Disease, Management, and Recognition of Act of Terrorism". Infectious Disease Clinics of North America. 20 (2): 273–287. ISSN 0891-5520. doi:10.1016/j.idc.2006.02.004. 
  5. Perry RD, Fetherston JD (1997). "Yersinia pestis--etiologic agent of plague.". Clin Microbiol Rev. 10 (1): 35–66. PMC 172914Freely accessible. PMID 8993858. 
  6. Gage KL, Dennis DT, Orloski KA, Ettestad P, Brown TL, Reynolds PJ; et al. (2000). "Cases of cat-associated human plague in the Western US, 1977-1998.". Clin Infect Dis. 30 (6): 893–900. PMID 10852811. doi:10.1086/313804. 
  7. Deng W; et al. (2002). "Genome Sequence of Yersinia pestis KIM". Journal of Bacteriology. 184 (16): 4601–4611. PMC 135232Freely accessible. PMID 12142430. doi:10.1128/JB.184.16.4601-4611.2002. 
  8. Parkhill J; et al. (2001). "Genome sequence of Yersinia pestis, the causative agent of plague". Nature. 413 (6855): 523–527. PMID 11586360. doi:10.1038/35097083. 
  9. Chain PS; Hu P; Malfatti SA; et al. (2006). "Complete Genome Sequence of Yersinia pestis Strains Antiqua and Nepal516: Evidence of Gene Reduction in an Emerging Pathogen". J. Bacteriol. 188 (12): 4453–63. PMC 1482938Freely accessible. PMID 16740952. doi:10.1128/JB.00124-06. 
  10. Lathem WW, Price PA, Miller VL, Goldman WE (2007). "A plasminogen-activating protease specifically controls the development of primary pneumonic plague.". Science. 315 (5811): 509–13. PMID 17255510. doi:10.1126/science.1137195. 
  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. doi:10.1021/pr060179y. 
  12. "Plague". 
  13. 13.00 13.01 13.02 13.03 13.04 13.05 13.06 13.07 13.08 13.09 13.10 13.11 13.12 13.13 "Public Health Image Library (PHIL)". 


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