The Genus Yersinia pp 55-62

Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 529)

Transmission Factors: Yersinia pestis Genes Required to Infect the Flea Vector of Plague

  • B. Joseph Hinnebusch

Conclusion

Y. pestis Ymt and Hms proteins have complementary but distinct roles. Ymt is required for survival in the midgut compartment, but not the proventriculus compartment, of the flea digestive tract. Conversely, the hms genes are not required to infect the midgut, but are required to infect the proventriculus. In addition to ymt and hms, the outer surface plasminogen activator of Y. pestis is considered to be important for fleaborne transmission, although this role does not occur in the flea (Hinnebusch et al., 1998). Sodeinde et al., (2002) showed that Pla is important for dissemination from a subcutaneous inoculation site in mice. This finding suggested that pla is pertinent to the fleaborne life-cycle of Y. pestis, which demands that the bacteria be able to disseminate from the dermis where they are deposited by a flea. Notably, ymt and pla are located on plasmids that are unique to Y. pestis. Thus, acquisition of these two plasmids by horizontal transfer helps to account for the rapid evolutionary transition of Y. pestis to fleaborne transmission within the last 20,000 years.

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References

  1. Bacot, A.W., and Martin, C.J., 1914, Observations on the mechanism of the transmission of plague by fleas. J. Hygiene Plague Suppl. 3: 423–439.Google Scholar
  2. Bacot, A.W., 1915, Further notes on the mechanism of the transmission of plague by fleas. J. Hygiene Plague Suppl. 4: 774–776.Google Scholar
  3. Brown, S.D., and Montie, T.C., 1977, Beta-adrenergic blocking activity of Yersinia pestis murine toxin. Infect. Immun. 18: 85–93.PubMedGoogle Scholar
  4. Cherepanov, P.A., Mikhailova, T.G., Karimova, G.A., Zakharova, N.M., Ershov, I.V., and Volkovoi, K.I., 1991, [Cloning and detailed mapping of the fra-ymt region of the Yersinia pestis pFra plasmid]. Mol. Gen. Mikrobiol. Virusol. 12: 19–26.PubMedGoogle Scholar
  5. Du, Y., Galyov, E., and Forsberg, A., 1995, Genetic analysis of virulence determinants unique to Yersinia pestis. Contrib Microbiol Immunol 13: 321–324.PubMedGoogle Scholar
  6. Fetherston, J.D., and Perry, R.D., 1994, The pigmentation locus of Yersinia pestis KIM6+ is flanked by an insertion sequence and includes the structural genes for pesticin sensitivity and HMWP2. Mol. Microbiol. 13: 697–708.PubMedGoogle Scholar
  7. Hare, J.M., and McDonough, K.A., 1999, High-frequency RecA-dependent and-independent mechanisms of Congo red binding mutations in Yersinia pestis. J. Bacteriol. 181: 4896–4904.PubMedGoogle Scholar
  8. Hinnebusch, B.J., Perry, R.D., and Schwan, T.G., 1996, Role of the Yersinia pestis hemin storage (hms) locus in the transmission of plague by fleas. Science 273: 367–370.PubMedGoogle Scholar
  9. Hinnebusch, B.J., Fischer, E.R., and Schwan, T.G., 1998, Evaluation of the role of the Yersinia pestis plasminogen activator and other plasmid-encoded factors in temperature-dependent blockage of the flea. J. Infect. Dis. 178: 1406–1415.CrossRefPubMedGoogle Scholar
  10. Hinnebusch, B.J., Rosso, M.-L., Schwan, T.G., and Carniel, E., 2002a, High-frequency conjugative transfer of antibiotic resistance genes to Yersinia pestis in the flea midgut. Mol. Microbiol. 46: 349–354.CrossRefPubMedGoogle Scholar
  11. Hinnebusch, B.J., Rudolph, A.E., Cherepanov, P., Dixon, J.E., Schwan, T.G., and Forsberg, Å., 2002b, Role of Yersinia murine toxin in survival of Yersinia pestis in the midgut of the flea vector. Science 296: 733–735.CrossRefPubMedGoogle Scholar
  12. Hinnebusch, J., Cherepanov, P., Du, Y., Rudolph, A., Dixon, J.D., Schwan, T., and Forsberg, A., 2000, Murine toxin of Yersinia pestis shows phospholipase D activity but is not required for virulence in mice. Int. J. Med. Microbiol. 290: 483–487.PubMedGoogle Scholar
  13. Iwasaki, Y., Nakano, H., and Yamane, T., 1994, Phospholipase D from Streptomyces antibioticus: cloning, sequencing, expression, and relationship to other phospholipases. Appl. Microbiol. Biotechnol. 42: 290–299.PubMedGoogle Scholar
  14. Jackson, S., and Burrows, T.W., 1956, The pigmentation of Pasteurella pestis on a defined medium containing haemin. Br. J. Exp. Pathol. 37: 570–576.PubMedGoogle Scholar
  15. Jones, H.A., Lillard, J.W., Jr., and Perry, R.D., 1999, HmsT, a protein essential for expression of the haemin storage (Hms+) phenotype of Yersinia pestis. Microbiology 145: 2117–2128.PubMedGoogle Scholar
  16. Pollitzer, R., 1954, Plague. World Health Organization, Geneva.Google Scholar
  17. Ponting, C.P., and Kerr, I.D., 1996, A novel family of phospholipase D homologues that includes phospholipid synthases and putative endonucleases: identification of duplicated repeats and potential active site residues. Protein Sci 5: 914–922.PubMedGoogle Scholar
  18. Rudolph, A.E., Stuckey, J.A., Zhao, Y., Matthews, H.R., Patton, W.A., Moss, J., and Dixon, J.E., 1999, Expression, characterization, and mutagenesis of the Yersinia pestis murine toxin, a phospholipase D superfamily member. J. Biol. Chem. 274: 11824–11831.PubMedGoogle Scholar
  19. Schwan, T.G., and Hinnebusch, B.J., 1998, Bloodstream-versus tick-associated variants of a relapsing fever bacterium. Science 280: 1938–1940.CrossRefPubMedGoogle Scholar
  20. Simond, P.-L., 1898, La propagation de la peste. Ann. Inst. Pasteur 12: 662–687.Google Scholar
  21. Sodeinde, O.A., Subrahmanyam, Y.V., Stark, K., Quan, T., Bao, Y., and Goguen, J.D., 1992, A surface protease and the invasive character of plague. Science 258: 1004–1007.PubMedGoogle Scholar
  22. Walker, R.V., 1967, Plague toxins-a critical review. Curr. Top. Microbiol. Immunol. 41: 23–42.PubMedGoogle Scholar

Copyright information

© Kluwer Academic Publishers 2004

Authors and Affiliations

  • B. Joseph Hinnebusch
    • 1
  1. 1.Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious DiseasesNational Institutes of HealthHamiltonUSA

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