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Journal of Clinical Microbiology, July 2005, p. 3373-3379, Vol. 43, No. 7
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.7.3373-3379.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Differential Distribution and Expression of Panton-Valentine Leucocidin among Community-Acquired Methicillin-Resistant Staphylococcus aureus Strains

Battouli Saïd-Salim,1 Barun Mathema,1 Kevin Braughton,2 Stacy Davis,1 Daniel Sinsimer,1,3 William Eisner,1 Yekaterina Likhoshvay,1 Frank R. DeLeo,2 and Barry N. Kreiswirth1*

TB Center, Public Health Research Institute, Newark, New Jersey 07103,1 Laboratory of Human Bacterial Pathogenesis, Rocky Mountain Laboratories, and National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840,2 and Department of Microbiology and Molecular Genetics, University of Medicine and Dentistry of New Jersey, Newark, New Jersey 071033

Received 2 November 2004/ Returned for modification 23 December 2004/ Accepted 25 February 2005

Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is an emerging threat worldwide. CA-MRSA strains differ from hospital-acquired MRSA strains in their antibiotic susceptibilities and genetic backgrounds. Using several genotyping methods, we clearly define CA-MRSA at the genetic level and demonstrate that the prototypic CA-MRSA strain, MW2, has spread as a homogeneous clonal strain family that is distinct from other CA-MRSA strains. The Panton-Valentine leucocidin (PVL)-encoding genes, lukF and lukS, are prevalent among CA-MRSA strains and have previously been associated with CA-MRSA infections. To better elucidate the role of PVL in the pathogenesis of CA-MRSA, we first analyzed the distribution and expression of PVL among different CA-MRSA strains. Our data demonstrate that PVL genes are differentially distributed among CA-MRSA strains and, when they are present, are always transcribed, albeit with strain-to-strain variability of transcript levels. To directly test whether PVL is critical for the pathogenesis of CA-MRSA, we evaluated the lysis of human polymorphonuclear leukocytes (PMNs) during phagocytic interaction with PVL-positive and PVL-negative CA-MRSA strains. Unexpectedly, there was no correlation between PVL expression and PMN lysis, suggesting that additional virulence factors underlie leukotoxicity and, thus, the pathogenesis of CA-MRSA.


* Corresponding author. Mailing address: TB Center, Public Health Research Institute, 225 Warren Street, Newark, NJ, 07103. Phone: (973) 854-3240. Fax: (973) 854-3241. E-mail: barry{at}phri.org.


Journal of Clinical Microbiology, July 2005, p. 3373-3379, Vol. 43, No. 7
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.7.3373-3379.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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