JAC Advance Access originally published online on September 12, 2005
Journal of Antimicrobial Chemotherapy 2005 56(5):944-947; doi:10.1093/jac/dki289
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Published by Oxford University Press 2005
Reduced expression of the atl autolysin gene and susceptibility to autolysis in clinical heterogeneous glycopeptide-intermediate Staphylococcus aureus (hGISA) and GISA strains
Bristol Centre for Antimicrobial Research and Evaluation, 1 Department of Cellular and Molecular Medicine, Medical Sciences, University of Bristol, Bristol BS1 8TD, UK; and 2 North Bristol Healthcare Trust, Southmead Hospital, Bristol BS10 5NB, UK
Received 24 May 2005; returned 3 June 2005; revised 25 July 2005; accepted 26 July 2005
* Corresponding author. Tel: +44-117-928-7526; Fax: +44-117-928-7896; E-mail: mandy.wootton{at}bristol.ac.uk
Objectives: To assess a link between resistance to Triton X-100 induced autolysis (TIA) and lowered atl expression in a collection of clinical glycopeptide-intermediate Staphylococcus aureus (GISA) and heterogeneous GISA (hGISA).
Methods: Nine clinical GISA, 11 hGISA and 11 glycopeptide-susceptible S. aureus (GSSA), including three pairs of related isolates, were analysed using TIA assays. Lysostaphin MICs were determined by a broth microdilution technique and reverse transcriptase PCR was used to compare atl expression levels in all isolates.
Results: Eight of nine clinical GISA and six of 11 hGISA exhibited lower susceptibility to TIA and higher MICs of lysostaphin than GSSA. Eight of nine GISA and all hGISA strains had lowered atl expression levels compared with GSSA.
Conclusions: The majority of GISA and hGISA isolates exhibited lowered susceptibility to TIA and lysostaphin and reduced atl expression when compared with GSSA isolates. These factors could contribute to, or predispose to the development of, a thickened cell wall and glycopeptide-intermediate resistance.
Keywords: antibiotic resistance , cell wall , mechanism of resistance
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