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Plasmid-mediated quinolone resistance in Salmonella from South Africa.

Invasive infections with Salmonella species are usually treated with fluoroquinolones or extended-spectrum b-lactams. Quinolone resistance results in reduced susceptibility to fluoroquinolones, leaving health-care professionals with limited resources for treatment of salmonellosis. Several mechanisms contribute to the development of quinolone resistance in Salmonella and these include: mutations in the quinolone resistance-determining region (QRDR) of DNA gyrase (gyrA/gyrB) and/or topoisomerase IV (parC/parE) genes (Eaves et al., 2004); active efflux of antibiotic out of the bacterial cell (Baucheron et al., 2002); and plasmidmediated quinolone resistance encoded by qnr genes A, B and S (Robicsek et al., 2006a). The qnr genes encode pentapeptide repeat proteins that block the action of quinolones on bacterial DNA gyrase and topoisomerase IV, resulting in low-level quinolone resistance (Tran et al., 2005a, b). The first qnr gene was isolated in 1998 from a Klebsiella pneumoniae isolate from Birmingham, Alabama, USA, and was named qnr (later renamed qnrA) (Martinez-Martinez et al., 1998). qnr genes have been identified in various bacterial species worldwide (Robicsek et al., 2006a). More recently, a novel quinoloneresistance mechanism has been identified in K. pneumoniae which involves the modification of certain fluoroquinolones by a specific type of aminoglycoside acetyltransferase (Robicsek et al., 2006b). We report what we believe to be the first discovery of plasmid-mediated quinolone resistance in Salmonella from South Africa, which was identified in a clinical isolate of Salmonella enterica serovar Typhimurium.