ALBERT

Description: 〈h3〉Abstract〈/h3〉 〈p〉The aim of this study was to evaluate the contribution of plasmid-mediated genes and efflux to fluoroquinolone resistance in collection of 〈em〉Achromobacter〈/em〉 spp. gathered during a 3-year period. Susceptibility to ciprofloxacin and levofloxacin was tested by disk diffusion and microdilution tests for a collection of 98 〈em〉Achromobacter〈/em〉 spp. clinical isolates. Identification of fluoroquinolone-resistant isolates was performed by sequencing and phylogenetic analyses of the 〈em〉nrdA〈/em〉 gene. Genetic relatedness among resistant isolates was determined by pulsed-field gel electrophoresis (PFGE) analysis. The influence of an H〈sup〉+〈/sup〉 conductor cyanide 〈em〉m〈/em〉-chlorophenyl hydrazone (CCCP) and a resistance-nodulation-division-type efflux pump inhibitor phenylalanine-arginine beta-naphthylamide (PAβN) on minimal inhibitory concentration (MIC) value was evaluated by broth microdilution. The presence of the plasmid-mediated 〈em〉qnrA〈/em〉, 〈em〉qnrB〈/em〉, 〈em〉qnrC〈/em〉, 〈em〉qnrS〈/em〉, and 〈em〉aac-(6′)-Ib-cr〈/em〉 genes was investigated by PCR and sequencing. 〈em〉Achromobacter〈/em〉 spp. isolates that were resistant or intermediately resistant to fluoroquinolones in disk diffusion tests (44/98) were subjected to microdilution. As a result, 20/98 isolates were confirmed to be resistant to ciprofloxacin while 10/98 was resistant to levofloxacin. CCCP decreased twofold MIC value for ciprofloxacin in six isolates and more than 16 times in one isolate, while MIC value for levofloxacin was decreased in all isolates (twofold to more than eightfold). Fluoroquinolone-resistant isolates were identified as 〈em〉A. xylosoxidans〈/em〉 with the 〈em〉nrdA〈/em〉 gene sequencing. PFGE revealed that resistant isolates belonged to seven different genotypes. Ten isolates belonging to four genotypes were positive for the 〈em〉aac-(6′)-Ib-cr〈/em〉 gene. Although resistance to fluoroquinolones was not widespread among analyzed isolates, detected contribution of efflux pumps and the presence of the 〈em〉aac-(6′)-Ib-cr〈/em〉 gene present a platform for emergence of more resistant strains.〈/p〉