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Antimicrob. Agents Chemother. doi:10.1128/AAC.00328-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Genetic and phenotypic identification of fusidic acid-resistant mutants with the small colony variant (SCV) phenotype in Staphylococcus aureus

Programme for Microbiology, Department of Cell and Molecular Biology, Box 596, Biomedical Center, Uppsala University, 751 24 Uppsala, Sweden

^* To whom correspondence should be addressed. Email: diarmaid.hughes{at}icm.uu.se.

	Abstract

Small colony variants (SCV's) of Staphylococcus aureus are a slow-growing sub-population whose phenotypes can include resistance to aminoglycosides, defects in electron transport, and enhanced persistence in mammalian cells. Here we show that a sub-set of mutants selected as SCV's by reduced susceptibility to aminoglycosides are resistant to the antibiotic fusidic acid (FA), and conversely that a sub-set of mutants selected for resistance to FA are SCV's. Mutation analysis reveals different genetic classes of FA-resistant SCV's. One class, FusA-SCV's have amino acid substitution mutations in the ribosomal translocase EF-G different from those found in classic FusA mutants. Most of these mutations are located in structural domain V of EF-G, but some are in domains I or III. FusA-SCV's are auxotrophic for hemin. A second class of FA-resistant SCV's carry mutations in rplF, coding for ribosomal protein L6 and are designated as FusE mutants. FusE mutants fall into two phenotypic groups: one auxotrophic for hemin, the other auxotrophic for menadione. Accordingly, we have identified new genetic and phenotypic classes of FA-resistant mutants, and clarified the genetic basis of a sub-set of S. aureus SCV mutants. A clinical implication of this data is that FA-resistance could be selected by antimicrobial agents other than fusidic acid.

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