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1 March 2008

Volume 46, Number 5
Clinical Infectious Diseases 2008;46:752–760
© 2008 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2008/4605-0018$15.00
DOI: 10.1086/526773
CLINICAL PRACTICE INVITED ARTICLE

Colonization, Fomites, and Virulence: Rethinking the Pathogenesis of Community‐Associated Methicillin‐Resistant Staphylococcus aureus Infection

Loren G. Miller1,2,3 and

Binh An Diep4

1Division of Infectious Diseases, 2Los Angeles Biomedical Research Institute, and 3David Geffen School of Medicine, Harbor–University of California–Los Angeles, Torrance, and 4Division of Infectious Diseases, Department of Medicine, University of California, San Francisco

Community‐associated methicillin‐resistant Staphylococcus aureus (MRSA) infection is increasingly common worldwide and causes considerable morbidity and mortality. Of concern, community‐associated MRSA infections are often recurrent and are highly transmissible to close contacts. The traditional tenet of pathogenesis is that MRSA colonization precedes infection. This has prompted persons involved in efforts to prevent community‐associated MRSA infection to incorporate the use of intranasal topical antibiotics for nasal decolonization. However, data from outbreaks of community‐associated MRSA infection suggest that skin‐skin and skin‐fomite contact represent important and common alternative routes of acquisition of the infecting strain. Furthermore, strain characteristics of the most successful community‐associated MRSA strain, USA300, may contribute to a distinct pathogenesis. As we develop strategies to prevent community‐associated MRSA infection, we must reconsider the pathogenesis of S. aureus. Reliance on models of health care–associated MRSA transmission for prevention of community‐associated MRSA infection may result in the development of flawed strategies that attenuate our ability to prevent this serious and potentially deadly infection.

Received 31 May 2007; accepted 24 October 2007; electronically published 23 January 2008.

Reprints or correspondence: Dr. Loren G. Miller, David Geffen School of Medicine, Harbor‐UCLA Medical Center, 1000 W. Carson St., Box 466, Torrance, CA 90509 ().

Ellie J. C. Goldstein, Section Editor

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