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1 June 2006

Volume 193, Number 11
The Journal of Infectious Diseases 2006;193:1495–1503
© 2006 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2006/19311-0004$15.00
DOI: 10.1086/503777
MAJOR ARTICLE

Roles of 34 Virulence Genes in the Evolution of Hospital‐ and Community‐Associated Strains of Methicillin‐Resistant Staphylococcus aureus

Binh An Diep,1,2

Heather A. Carleton,1

Richard F. Chang,3

George F. Sensabaugh,2 and

Françoise Perdreau‐Remington1

1Division of Infectious Diseases, Department of Medicine, University of California, San Francisco, 2Program in Infectious Diseases and Immunity, School of Public Health, and 3Undergraduate Program in Molecular Cell Biology, College of Letters and Science, University of California, Berkeley

Background.The extent to which the horizontal transfer of virulence genes has contributed to the emergence of contemporary virulent strains of methicillin‐resistant Staphylococcus aureus (MRSA) in hospital and community settings is poorly understood.

Methods.Epidemiologically well‐characterized MRSA isolates collected over 8.5 years were genotyped and tested for the presence of 34 virulence genes.

Results.Six strain types accounted for 88.2% of all MRSA infections. The evolution of contemporary hospital and community phenotypes within the CC8 and CC30 lineages—2 background genomes that produced historical pandemic MRSA clones—were associated with multiple horizontal acquisitions of virulence genes. The epidemic community phenotype of a CC8 strain, designated ST8:USA300, was linked to the acquisition of staphylococcal cassette chromosome (SCC)mec type IV, the genes for Panton‐Valentine leukocidin (PVL), and the enterotoxin Q and K genes. Similarly, the epidemic community phenotype of a CC30 strain, ST30:USA1100, was linked to the acquisition of SCCmec type IV and the pvl genes. In contrast, the epidemic hospital phenotype of another CC30 strain, ST36:USA200, was associated with the acquisition of SCCmec type II, the enterotoxin A gene, and the toxic shock syndrome toxin 1 gene. The pvl genes appear not to be essential for the evolution of other community‐associated strains of MRSA, including ST8:USA500 and ST59:USA1000.

Conclusions.The horizontal transfer of virulence genes, although infrequent, is epidemiologically associated with the emergence of new virulent strains of MRSA.

Received 28 September 2005; accepted 27 December 2005; electronically published 21 April 2006.

Reprints or correspondence: Dr. Françoise Perdreau‐Remington, University of California, San Francisco, Div. of Infectious Diseases, San Francisco General Hospital, 1001 Potrero Ave. UCSF 1372, Bldg. 100, Rm. 301, San Francisco, CA 94110 ().

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  • Presented in part: International Staphylococci and Staphylococcal Infections Meeting, 24–27 October 2004, Charleston, South Carolina.

    Potential conflicts of interest: F.P.‐R. is a consultant for Pfizer Corporation.

    Financial support: Pfizer Corporation (unrestricted grant to F.P.‐R.); Eugene Cota‐Robles Predoctoral Fellowship and a Genetics Training Grant (5‐T32‐GM07127‐29‐30), University of California, Berkeley, to B.A.D.

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