F McLaws1, I Chopra, A J O'Neill. 1. Antimicrobial Research Centre and Institute of Molecular and Cellular Biology, University of Leeds, Leeds LS2 9JT, UK.
Abstract
OBJECTIVES: To determine the prevalence and mechanisms of resistance to fusidic acid in clinical isolates of Staphylococcus epidermidis. METHODS: MICs of fusidic acid were determined for S. epidermidis isolates collected from the Leeds General Infirmary and from around Europe. Fusidic acid-resistant isolates were probed for the presence of the horizontally acquired resistance determinants fusB and fusC by a novel multiplex PCR assay. Mutations in the gene encoding the drug target (fusA) were detected by PCR and DNA sequencing. Resistant isolates were subjected to typing using the repeat region of the aap gene. RESULTS: Of 50 S. epidermidis isolates screened, 23 (46%) exhibited resistance to fusidic acid. The most common resistance determinant was fusB, found in 18 of the 23 isolates. Of the remaining isolates, two harboured fusC and three carried an identical mutation in fusA, leading to the substitution L(461)K in the target protein, elongation factor G. Molecular typing showed that this collection of isolates was genetically diverse. CONCLUSIONS: This study suggests a high prevalence of resistance to fusidic acid in clinical isolates of S. epidermidis. As in Staphylococcus aureus, resistance to fusidic acid in S. epidermidis is commonly associated with the fusB determinant.
OBJECTIVES: To determine the prevalence and mechanisms of resistance to fusidic acid in clinical isolates of Staphylococcus epidermidis. METHODS: MICs of fusidic acid were determined for S. epidermidis isolates collected from the Leeds General Infirmary and from around Europe. Fusidic acid-resistant isolates were probed for the presence of the horizontally acquired resistance determinants fusB and fusC by a novel multiplex PCR assay. Mutations in the gene encoding the drug target (fusA) were detected by PCR and DNA sequencing. Resistant isolates were subjected to typing using the repeat region of the aap gene. RESULTS: Of 50 S. epidermidis isolates screened, 23 (46%) exhibited resistance to fusidic acid. The most common resistance determinant was fusB, found in 18 of the 23 isolates. Of the remaining isolates, two harboured fusC and three carried an identical mutation in fusA, leading to the substitution L(461)K in the target protein, elongation factor G. Molecular typing showed that this collection of isolates was genetically diverse. CONCLUSIONS: This study suggests a high prevalence of resistance to fusidic acid in clinical isolates of S. epidermidis. As in Staphylococcus aureus, resistance to fusidic acid in S. epidermidis is commonly associated with the fusB determinant.
Authors: Mariana Castanheira; Amy A Watters; Jan M Bell; John D Turnidge; Ronald N Jones Journal: Antimicrob Agents Chemother Date: 2010-06-21 Impact factor: 5.191
Authors: David J Farrell; Rodrigo E Mendes; Mariana Castanheira; Ronald N Jones Journal: Antimicrob Agents Chemother Date: 2016-05-23 Impact factor: 5.191