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15 December 2006

Volume 194, Number 12
The Journal of Infectious Diseases 2006;194:1761–1770
© 2006 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2006/19412-0020$15.00
DOI: 10.1086/509506
MAJOR ARTICLE

Is Panton‐Valentine Leukocidin the Major Virulence Determinant in Community‐Associated Methicillin‐Resistant Staphylococcus aureus Disease?

Jovanka M. Voyich,1,a

Michael Otto,1

Barun Mathema,4

Kevin R. Braughton,1

Adeline R. Whitney,1

Diane Welty,2

R. Daniel Long,2

David W. Dorward,3

Donald J. Gardner,2

Gérard Lina,5

Barry N. Kreiswirth,4 and

Frank R. DeLeo1

1Laboratory of Human Bacterial Pathogenesis, 2Rocky Mountain Veterinary Branch, and 3RTB Research Technologies Section, Microscopy Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana; 4Public Health Research Institute Tuberculosis Center, International Center for Public Health, Newark, New Jersey; 5Université Claude Bernard, INSERM E230, Institut Fédératif de Recherche 62, Faculte de Médecine Laennec, Lyon, France

Methicillin‐resistant Staphylococcus aureus (MRSA) remains a major problem in hospitals, and it is now spreading in the community. A single toxin, Panton‐Valentine leukocidin (PVL), has been linked by epidemiological studies to community‐associated MRSA (CA‐MRSA) disease. However, the role that PVL plays in the pathogenesis of CA‐MRSA has not been tested directly. To that end, we used mouse infection models to compare the virulence of PVL‐positive with that of PVL‐negative CA‐MRSA representing the leading disease‐causing strains. Unexpectedly, strains lacking PVL were as virulent in mouse sepsis and abscess models as those containing the leukotoxin. Isogenic PVL‐negative (lukS/F‐PV knockout) strains of USA300 and USA400 were as lethal as wild‐type strains in a sepsis model, and they caused comparable skin disease. Moreover, lysis of human neutrophils and pathogen survival after phagocytosis were similar between wild‐type and mutant strains. Although the toxin may be a highly linked epidemiological marker for CA‐MRSA strains, we conclude that PVL is not the major virulence determinant of CA‐MRSA.

Received 28 March 2006; accepted 15 August 2006; electronically published 2 November 2006.

Reprints or correspondence: Dr. Frank R. DeLeo, Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840 ().

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  • Potential conflicts of interest: none reported.

    Financial support: Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health (support to F.R.D.); Johnson & Johnson, L.L.C. (research grant to B.N.K.).

  • Present affiliation: Department of Veterinary Molecular Biology, Montana State University, Bozeman.

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