JAC Advance Access originally published online on October 13, 2005
Journal of Antimicrobial Chemotherapy 2005 56(6):1179-1180; doi:10.1093/jac/dki378
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© The Author 2005. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Correspondence |
Resistance to telithromycin is conferred by msr(A), msrC and msr(D) in Staphylococcus aureus
School of Biochemistry and Microbiology, University of Leeds, Leeds LS2 9JT, UK
* Corresponding author. Tel: +44-113-3435630; Fax: + 44-113-3435638; E-mail: J.H.Cove@leeds.ac.uk
Keywords: ABC transporters , macrolide resistance , ketolide resistance , staphylococci
| The first 10% of the full text of this article appears below. |
Sir,
The antibiotic resistance determinants Msr(A), MsrC and Msr(D) are all members of a group of incomplete or Class 2 ABC transporters, characterized by the presence of two fused nucleotide-binding domains but lacking any identifiable transmembrane domains, and are typically involved in cellular processes other than transport.1
The msr(A) gene is carried on large staphylococcal plasmids, and has been shown to confer high-level inducible resistance to 14- and 15-membered ring macrolides and type B streptogramins (MSB antibiotics) in Staphylococcus aureus in the absence of any additional plasmid-encoded determinants.2 A single copy of msrC is found on the chromosome of Enterococcus faecium. Insertional inactivation of msrC in this species resulted in increased susceptibility to MSB antibiotics.3 We
Transparency declarations