JAC Advance Access published online on December 4, 2003
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkh020
© 2003 by The British Society for Antimicrobial Chemotherapy
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Brief report
1 Antimicrobial Research Centre and Division of Microbiology,
School of Biochemistry and Molecular Biology, University of Leeds,
Leeds LS2 9JT, UK
* Corresponding author. E-mail: i.chopra{at}leeds.ac.uk.
Received 31 July 2003
; revised 29 September 2003
; accepted 13 October 2003
Objectives and methods: Failure to
eradicate nasal carriage of a glycopeptide-intermediate Staphylococcus aureus (strain
GISA-2) with mupirocin was recently attributed to a mutation that
confers low-level mupirocin resistance. To identify this mutation
the ileS genes of GISA-2 and its mupirocin-susceptible
progenitor GISA-1 were sequenced. For comparison, the ileS genes
of 10 laboratory-derived mupirocin-resistant mutants of the GISA
strain Mu50 were also examined. The fitness of GISA-2 and mupirocin-susceptible GISA-1,
as well as Mu50 and its mupirocin-resistant derivatives, were compared
by evaluation of growth rates and performance in mixed-culture competition
assays. Results: The point mutation V588F in the isoleucyl-tRNA
synthetase was identified from the ileS sequences of
GISA-2 and mupirocin-resistant mutants of Mu50. The V588F mutation
was not associated with a significant fitness burden. Conclusions: The low fitness cost of the V588F
substitution in isoleucyl-tRNA synthetase is consistent with the
frequent appearance and maintenance of this mutation in mupirocin-resistant
clinical isolates, including GISA-2.
Keywords: GISA, mupirocin-resistant Staphylococcus
aureus
The isoleucyl-tRNA synthetase mutation V588F conferring
mupirocin resistance in glycopeptide-intermediate Staphylococcus
aureus is not associated with a significant fitness burden
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