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15 November 2004

Volume 190, Number 10
The Journal of Infectious Diseases 2004;190:1730–1738
© 2004 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2004/19010-0002$15.00
DOI: 10.1086/425019
MAJOR ARTICLE

Community‐Adapted Methicillin‐Resistant Staphylococcus aureus (MRSA): Population Dynamics of an Expanding Community Reservoir of MRSA

Heather A. Carleton,1,a

Binh An Diep,1,3,a

Edwin D. Charlebois,2

George F. Sensabaugh,3 and

Françoise Perdreau‐Remington1

1Department of Medicine, Division of Infectious Diseases, and 2AIDS Research Institute, University of California, San Francisco, San Francisco, and 3Program in Infectious Diseases and Immunity, School of Public Health, University of California, Berkeley, Berkeley

To define methicillin‐resistant Staphylococcus aureus (MRSA) reservoirs in the community and their population dynamics, we studied the molecular epidemiology of a random sample ( ) from a collection of 2154 inpatient and outpatient MRSA isolates during a 7‐year period in San Francisco. We noted a progressive replacement of type II staphylococcal chromosomal cassette (SCC)mec–bearing isolates with type IV SCCmec–bearing isolates, which coincided with >4‐fold increase in methicillin resistance between 1998 and 2002. Type IV SCCmec–bearing isolates involved in the increase in methicillin resistance belonged to 4 molecular genotypes. These 4 genotypes were associated predominantly with community‐onset disease, rather than hospital‐ or long‐term‐care facility–onset disease (76.9% vs. 19.4% vs. 3.7%; ), suggesting that they are not feral descendants of hospital isolates. The longitudinal results linked the dramatic increase in MRSA infections to an expanding community reservoir of MRSA genotypes with intrinsic community survival advantage.

Received 19 April 2004; accepted 26 May 2004; electronically published 18 October 2004.

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

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  • Presented in part: 43rd Interscience Conference on Antimicrobial Agents and Chemotherapy, Chicago, 14–17 September 2003 (abstract C2‐1983).

    Financial support: Pfizer Corp. (grant to F.P‐R.); University of California, Berkeley (Eugene Cota‐Robles Predoctoral Fellowship to B.A.D.).

    Potential conflict of interest: F.P.‐R. is a consultant for Pfizer Corp.

  • H.A.C. and B.A.D. contributed equally to this manuscript.

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