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15 January 2008

Volume 197, Number 2
The Journal of Infectious Diseases 2008;197:205–213
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2008/19702-0006$15.00
DOI: 10.1086/524689
MAJOR ARTICLE

Pathogenomic Analysis of the Common Bovine Staphylococcus aureus Clone (ET3): Emergence of a Virulent Subtype with Potential Risk to Public Health

Caitriona M. Guinane,1

Daniel E. Sturdevant,4

Lisa Herron‐Olson,6

Michael Otto,5

Davida S. Smyth,3,a

Amer E. Villaruz,5

Vivek Kapur,6

Patrick J. Hartigan,2

Cyril J. Smyth,3 and

J. Ross Fitzgerald1

1Centre for Infectious Diseases, The Chancellor’s Building, New Royal Infirmary, University of Edinburgh, Edinburgh, Scotland, United Kingdom; Departments of 2Physiology and 3Microbiology, Moyne Institute of Preventive Medicine, Trinity College, Dublin, Ireland; 4Research Technologies Branch and 5Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana; 6Department of Veterinary Pathobiology and Biomedical Genomics Center, University of Minnesota, St. Paul, Minnesota

A common clone (ET3) of Staphylococcus aureus is responsible for a large proportion of cases of bovine mastitis and occasionally causes zoonotic infections of humans. In the present study, we report the identification of a virulent clonal subtype (ST151) of ET3, which resulted in increased tissue damage and mortality in a mouse model of mastitis. ST151 has undergone extensive diversification in virulence and regulatory‐gene content, including the acquisition of genetic elements encoding toxins not made by other ET3 strains. Furthermore, ST151 had elevated levels of RNAIII and cytolytic toxin–gene expression, consistent with the enhanced virulence observed during experimental infection. Previously, the ST151 clone was shown to be hypersusceptible to the acquisition of vancomycin‐resistance genes from Enterococcus spp. Taken together, these data indicate the emergence of a virulent subtype of the common ET3 clone, which could present an enhanced risk to public health.

Received 2 May 2007; accepted 19 July 2007; electronically published 4 January 2008.

Reprints or correspondence: Dr. Ross Fitzgerald, Centre for Infectious Diseases, The Chancellor’s Bldg., New Royal Infirmary, University of Edinburgh, Edinburgh EH16 4SB, Scotland, United Kingdom ().

  • Potential conflicts of interest: none reported.

    Financial support: Biotechnology and Biological Sciences Research Council (grant BB/D521222/1 to J.R.F.); Teagasc, the Irish Agriculture and Food Development Authority.

  • Present affiliation: Department of Microbiology and Immunology, Basic Sciences Building, New York Medical College, Valhalla, New York.

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