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Antimicrob. Agents Chemother. doi:10.1128/AAC.01164-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Spontaneous Deletion of the Methicillin Resistance Determinant, mecA, Partially Compensates for the Fitness Cost Associated with High Level Vancomycin Resistance in Staphylococcus aureus

Department of Microbiology and Immunology and Internal Medicine, Virginia Commonwealth University School of Medicine, McGuire Hall Room 103, 1112 East Clay Street, Richmond, Virginia

^* To whom correspondence should be addressed. Email: garcher{at}vcu.edu.

	Abstract

Treatment of infections caused by Staphylococcus aureus is often confounded by the bacterium's ability to develop resistance to chemotherapeutic agents. Methicillin-resistant S. aureus (MRSA) arise through the acquisition of Staphylococcal Chromosome Cassette mec (SCCmec), a genomic island containing the resistance determinant mecA. In contrast, resistance to vancomycin can result from exposure to the drug, a mechanism that is not dependent upon a gene acquisition event. Here we describe three MRSA strains that became resistant to vancomycin during passage on increasing concentrations of the drug. In each case two derivative strains were isolated, one that had lost mecA, and one that retained mecA during passage. Strain 5836VR lost mecA by the site-specific chromosomal excision of SCCmec while the other two strains (3130VR and VP32) deleted portions of their SCCmec elements in a manner that appears to involve IS431. Conversion to vancomycin resistance caused a decrease in growth rate that was partially compensated for by deletion of mecA. In mixed culture competition experiments, vancomycin-resistant strains that lacked mecA readily out-competed their mecA-containing counterparts, suggesting that the loss of mecA during conversion to vancomycin resistance was advantageous to the organism.