AAC Accepts, published online ahead of print on 26 February 2007

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Antimicrob. Agents Chemother. doi:10.1128/AAC.01542-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Genetic basis of resistance to fusidic acid in staphylococci

A. J. O'Neill, F. McLaws, G. Kahlmeter, A. S. Henriksen, and I. Chopra^*

Antimicrobial Research Centre and Institute of Molecular & Cellular Biology, University of Leeds, Leeds LS2 9JT, United Kingdom; Department of Clinical Microbiology, Central Hospital, S-351 85 Växjö, Sweden; LEO Pharma, Industriparken 55, DK-2750 Ballerup, Copenhagen, Denmark

^* To whom correspondence should be addressed. Email: i.chopra{at}leeds.ac.uk.

Resistance to fusidic acid in Staphylococcus aureus often results from acquisition of the fusB determinant, or from mutations in the gene (fusA) that encodes the drug target (elongation factor G). We now report further studies on the genetic basis of resistance to this antibiotic in the staphylococci. Two staphylococcal genes that encode proteins exhibiting c. 45% identity with FusB conferred resistance to fusidic acid in S. aureus. One of these genes (designated fusC) was subsequently detected in all fusidic acid-resistant clinical strains of S. aureus tested that did not carry fusB or mutations in fusA, and in strains of S. intermedius. The other gene (designated fusD) is carried by S. saprophyticus, explaining the inherent resistance of this species to fusidic acid. Fusidic acid resistant strains of S. lugdunensis harbored fusB. Thus, resistance to fusidic acid in clinical isolates of S. aureus and other staphylococcal species frequently results from expression of FusB-type proteins.

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