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Journal of Clinical Microbiology, May 2005, p. 2380-2383, Vol. 43, No. 5
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.5.2380-2383.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Genetic Background Affects Stability of mecA in Staphylococcus aureus

Yuki Katayama,1 D. Ashley Robinson,2 Mark C. Enright,2 and Henry F. Chambers3*

Department of Bacteriology, Faculty of Medicine, Juntendo University, Tokyo, Japan,1 Department of Biology and Biochemistry, University of Bath, Bath, United Kingdom,2 Division of Infectious Diseases, San Francisco General Hospital, University of California San Francisco, San Francisco, California3

Received 30 August 2004/ Returned for modification 2 September 2004/ Accepted 28 December 2004

The staphylococcal methicillin resistance determinant, mecA, resides on a mobile genetic element, staphylococcus chromosomal cassette mec (SCCmec). The distribution of SCCmec in nature is limited to relatively few clonal complexes of related methicillin-resistant Staphylococcus aureus (MRSA). We have previously reported that some genetic backgrounds are restrictive of mecA and penicillin-binding protein 2a expression, which could account for the restricted clonal distribution of SCCmec in nature. In this study, we investigate the potential role of the host chromosome in the transformability and expression of mecA in 103 naturally occurring methicillin-susceptible S. aureus clinical isolates. The isolates, which had been genotyped previously by multilocus sequence typing, were classified into one of two mutually exclusive categories based on whether the isolates belonged to "major" MRSA lineages or to "other" lineages that are never or occasionally MRSA. We introduced mecA expressed on the low-copy-number plasmid pYK20 into each MSSA strain and assayed the phenotype of resistance to nafcillin by population analysis to assess the relationship between the stability of mecA expression and genetic background. Strains from the major MRSA lineages were more transformable with pYK20 and better able to maintain the plasmid and express resistance in comparison to strains from other lineages. These data support the hypothesis that the presence of mecA within relatively few clonal complexes is partly due to genetic factors that are permissive of mecA and its gene product.

* Corresponding author. Mailing address: Division of Infectious Diseases, Building 30, Room 3400, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94110. Phone: (415) 206-5437. Fax: (415) 648-8425. E-mail: chipc{at}itsa.ucsf.edu.

Journal of Clinical Microbiology, May 2005, p. 2380-2383, Vol. 43, No. 5
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.5.2380-2383.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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