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Infection and Immunity, June 2003, p. 3512-3520, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3512-3520.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

The rovA Mutant of Yersinia enterocolitica Displays Differential Degrees of Virulence Depending on the Route of Infection

Peter H. Dube, Scott A. Handley, Paula A. Revell,{dagger} and Virginia L. Miller*

Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110

Received 30 September 2002/ Returned for modification 20 January 2003/ Accepted 25 February 2003

Yersinia enterocolitica is an invasive enteric pathogen that causes significant inflammatory disease. Recently, we identified and characterized a global regulator of virulence (rovA). When mice are infected orally with the rovA mutant they are attenuated by 50% lethal dose (LD50) analysis and have altered kinetics of infection. Most significantly, mice orally infected with the rovA mutant have greatly reduced inflammation in the Peyer's patches compared to those infected with wild-type Y. enterocolitica. However, we present data here indicating that when the rovA mutant bacteria are delivered intraperitoneally (i.p.), they are significantly more virulent than when delivered orally. The i.p. LD50 for the rovA mutant is only 10-fold higher than that of the wild-type Y. enterocolitica, and there are significant inflammatory responses to the rovA mutant that are evident in the liver and spleen. Altogether, these data suggest that the RovA regulon may be required for the early events of the infection that occur in the Peyer's patches. Furthermore, these data suggest that the RovA regulon may be dispensable for Y. enterocolitica systemic disease and inflammatory responses if the Peyer's patches are bypassed.

* Corresponding author. Mailing address: Washington University School of Medicine, Department of Molecular Microbiology, 660 S. Euclid Ave., Campus Box 8230, St. Louis, MO 63110. Phone: (314) 286-2891. Fax: (314) 286-2896. E-mail: virginia{at}borcim.wustl.edu.

Editor: V. J. DiRita

{dagger} Present address: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110.

Infection and Immunity, June 2003, p. 3512-3520, Vol. 71, No. 6
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.6.3512-3520.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Kim, T.-J., Young, B. M., Young, G. M. (2008). Effect of Flagellar Mutations on Yersinia enterocolitica Biofilm Formation. Appl. Environ. Microbiol. 74: 5466-5474 [Abstract] [Full Text]  
  • Lawrenz, M. B., Miller, V. L. (2007). Comparative Analysis of the Regulation of rovA from the Pathogenic Yersiniae. J. Bacteriol. 189: 5963-5975 [Abstract] [Full Text]  
  • Cathelyn, J. S., Crosby, S. D., Lathem, W. W., Goldman, W. E., Miller, V. L. (2006). RovA, a global regulator of Yersinia pestis, specifically required for bubonic plague. Proc. Natl. Acad. Sci. USA 103: 13514-13519 [Abstract] [Full Text]  
  • Handley, S. A., Dube, P. H., Miller, V. L. (2006). From the Cover: Histamine signaling through the H2 receptor in the Peyer's patch is important for controlling Yersinia enterocolitica infection. Proc. Natl. Acad. Sci. USA 103: 9268-9273 [Abstract] [Full Text]  
  • Handley, S. A., Dube, P. H., Revell, P. A., Miller, V. L. (2004). Characterization of Oral Yersinia enterocolitica Infection in Three Different Strains of Inbred Mice. Infect. Immun. 72: 1645-1656 [Abstract] [Full Text]  


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