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15 January 2008

Volume 197, Number 2
The Journal of Infectious Diseases 2008;197:187–194
© 2007 by the Infectious Diseases Society of America. All rights reserved.
0022-1899/2008/19702-0004$15.00
DOI: 10.1086/524684
MAJOR ARTICLE

A Geographic Variant of the Staphylococcus aureus Panton‐Valentine Leukocidin Toxin and the Origin of Community‐Associated Methicillin‐Resistant S. aureus USA300

F. Patrick O’Hara,1

Nicolas Guex,4

J. Michael Word,4

Linda A. Miller,2

Julie A. Becker,1

Stacey L. Walsh,1

Nicole E. Scangarella,3

Joshua M. West,3

Ribhi M. Shawar,3 and

Heather Amrine‐Madsen4

1Evolutionary and Structural Bioinformatics, 2Infectious Diseases Medicine Development Center, and 3Department of Microbiology, GlaxoSmithKline, Collegeville, Pennsylvania; 4Evolutionary and Structural Bioinformatics, GlaxoSmithKline, Research Triangle Park, North Carolina

Background.The majority of recent community‐associated methicillin‐resistant Staphylococcus aureus (MRSA) infections in the United States have been caused by a single clone, USA300. USA300 secretes Panton‐Valentine leukocidin (PVL) toxin, which is associated with highly virulent infections.

Methods.We sequenced the PVL genes of 174 S. aureus isolates from a global clinical sample. We combined phylogenetic reconstruction and protein modeling methods to analyze genetic variation in PVL.

Results.Nucleotide variation was detected at 12 of 1726 sites. Two PVL sequence variants, the R variant and the H variant, were identified on the basis of a substitution at nt 527. Of sequences obtained in the United States, 96.7% harbor the R variant, whereas 95.6% of sequences obtained outside the United States harbor the H variant; 91.3% of MRSA isolates harbor the R variant, and 91.3% of methicillin‐susceptible strains harbor the H variant. A molecular model of PVL shows 3 mechanisms by which the amino acid substitution may affect PVL function.

Conclusions.All sampled PVL genes appear to share a recent common ancestor and spread via a combination of clonal expansion and horizontal transfer. US isolates harbor a variant of PVL that is strongly associated with MRSA infections. Protein modeling reveals that this variant may have functional significance. We propose a hypothesis for the origin of USA300.

Received 25 January 2007; accepted 22 May 2007; electronically published 4 January 2008.

Reprints or correspondence: Dr. Heather Amrine‐Madsen, Evolutionary and Structural Bioinformatics, GlaxoSmithKline, 5 Moore Dr., MAI‐C2357, Research Triangle Park, NC 27709 ().

Cited by

S. Monecke, R. Ehricht, P. Slickers, H.-L. Tan, G. Coombs. (2009) The molecular epidemiology and evolution of the Panton-Valentine leukocidin-positive, methicillin-resistant Staphylococcus aureus strain USA300 in Western Australia. Clinical Microbiology and Infection
Online publication date: 1-Jul-2009.
CrossRef
R. V. Goering, A. R. Larsen, R. Skov, F. C. Tenover, K. L. Anderson, P. M. Dunman. (2009) Comparative genomic analysis of European and Middle Eastern community-associated methicillin-resistant Staphylococcus aureus (CC80:ST80-IV) isolates by high-density microarray. Clinical Microbiology and Infection
Online publication date: 1-Jul-2009.
CrossRef
Oana Dumitrescu, Anne Tristan, Hélène Meugnier, Michèle Bes, Manolo Gouy, Jerome Etienne, Gérard Lina, and François Vandenesch. (2008) Polymorphism of the Staphylococcus aureus Panton‐Valentine Leukocidin Genes and Its Possible Link with the Fitness of Community‐Associated Methicillin‐Resistant S. aureus. The Journal of Infectious Diseases 198:5, 792-794
Online publication date: 1-Sep-2008.
Citation-Full Text-PDF Version (143 kB)
Joseph F. John, Jr., and Jodi A. Lindsay. (2008) Clones and Drones: Do Variants of Panton‐Valentine Leukocidin Extend the Reach of Community‐Associated Methicillin‐Resistant Staphylococcus aureus?. The Journal of Infectious Diseases 197:2, 175-178
Online publication date: 15-Jan-2008.
Citation-Full Text-PDF Version (57 kB)

  • Potential conflicts of interest: none reported.

    Financial support: GlaxoSmithKline.

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