Plasmid-mediated quinolone resistance in nalidixic-acid-susceptible strains of Salmonella enterica isolated in Scotland

Sir, Chromosomal mutations in the topoisomerase II gene gyrA and altered drug accumulation were considered to be the only mechanisms of quinolone resistance until 1998, when the plasmid-mediated quinolone resistance gene, qnrA, was described in an isolate of Klebsiella pneumoniae.1 Since then, other plasmid-borne resistance genes, qnrB, qnrS (and their variants), aac(6′)-Ib-cr and qepA, have been identified.2,3 The clinical importance of these qnr genes is that, although not conferring detectable resistance according to the criteria set by the CLSI or BSAC (currently ≥4 mg/L for ciprofloxacin), their presence facilitates the recovery of mutants with elevated levels of resistance to quinolones.2 The presence of qnr has frequently been detected in strains producing extended-spectrum β-lactamases (ESBLs).2 We investigated a total of 70 isolates of Salmonella enterica that were selected based on reduced susceptibility to ciprofloxacin (≥0.125 mg/L) for the presence of qnr genes. Duplicate samples were excluded, and only a single representative isolate from each outbreak was included. Of these 70 isolates, 53 were susceptible to nalidixic acid (<40 mg/L). The remaining 17 isolates exhibited additional resistance to cefotaxime (1 mg/L).