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15 January 2008

Volume 197, Number 2
The Journal of Infectious Diseases 2008;197:195–204
© 2008 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2008/19702-0005$15.00
DOI: 10.1086/523763
MAJOR ARTICLE

Coexistence of Panton‐Valentine Leukocidin–Positive and –Negative Community‐Associated Methicillin‐Resistant Staphylococcus aureus USA400 Sibling Strains in a Large Canadian Health‐Care Region

Kunyan Zhang,1,2,3,4,5,6

Jo‐Ann McClure,1

Sameer Elsayed,3,5

Jonathan Tan,1 and

John M. Conly1,2,3,4,5,6

1Centre for Antimicrobial Resistance, Calgary Health Region/Calgary Laboratory Services/University of Calgary, Departments of 2Pathology and Laboratory Medicine, 3Microbiology and Infectious Diseases, and 4Medicine, and 5Institute of Infection, Immunity and Inflammation, University of Calgary, and 6Calgary Laboratory Services, Calgary, Alberta, Canada

Community‐associated methicillin‐resistant Staphylococcus aureus (CA‐MRSA) strains often carry the Panton‐Valentine leukocidin (PVL) genes. However, the specific role that PVL plays in the epidemiological features and pathogenesis of CA‐MRSA infections has remained undefined and controversial. Conducting a retrospective study on a natural population of MRSA clinical isolates recovered from community and hospital patients in a large Canadian health‐care region during a 6‐year period, we identified the coexistence of 2 USA400 (a major clonal group of CA‐MRSA) sibling strains with and without PVL genes. Polymerase chain reaction and sequence analysis indicated that the PVL‐carrying prophage Sa2mw was present in PVL+ but absent in PVL− USA400 isolates. These strains shared identical genotypic and phenotypic properties and similar clinical characteristics. This study provides direct evidence that PVL genes are not necessarily the key determinants associated with the increasing dissemination of CA‐MRSA strains, suggesting that the genomic milieu may play a greater role in this regard.

Received 3 April 2007; accepted 15 May 2007; electronically published 9 January 2008.

Reprints or correspondence: Dr. Kunyan Zhang, Dept. of Pathology and Laboratory Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1 ().

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  • Potential conflicts of interest: none reported.

    Presented in part: 106th general meeting of American Society for Microbiology, Orlando, Florida, 21–25 May 2006 (abstract C‐224).

    Financial support: The Banting Research Foundation (grant 2005/6 to K.Z.); CHR/CLS Research (grant 17975 to K.Z.); Centre for Antimicrobial Resistance, Calgary Health Region (operating funds to K.Z.). J.T. was a 2005 Alberta Heritage Foundation for Medical Research Summer Student.

  • (See the editorial commentary by Gorwitz, on pages 179–82.)

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