title: Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations in quinolone-resistant Escherichia coli isolated from humans and swine in Denmark.
abstract: Prevalence of quinolone resistance mechanisms and associations to minimum inhibitory concentrations (MICs) of nalidixic acid (NAL) and ciprofloxacin (CIP) were investigated in 124 Escherichia coli isolated from humans (n=85) and swine (n=39) in Denmark. The collection included 59 high-level CIP-resistant isolates (MIC >or= 4) from human (n=51) and pig origin (n=8) and 65 low-level CIP-resistant isolates (MIC >or= 0.125) from human (n=34) and pig origin (n=31). Resistance by target modification was screened by PCR amplification and sequencing of the quinolone resistance determining regions (QRDRs) of gyrA, gyrB, parC, and parE. QRDR mutations occurred in all except two isolates (98%). All high-level CIP-resistant E. coli had one or two mutations in gyrA in combination with mutations in parC or parE. Mutations in parC and parE were only found in combination with gyrA mutations, and no mutations were observed in gyrB. Efflux pump mechanisms were detected in 10 human (11.8%) and 29 porcine (74.4%) isolates by an efflux pump inhibitor (EPI) agar dilution assay. The aac(6')-Ib-cr gene mediating resistance by enzymatic modification was found in 12 high-level CIP-resistant human isolates. The qnrA and qnrS genes conferring quinolone resistance by target protection were detected in two human low-level CIP-resistant isolates that did not display NAL resistance. As expected, target mutation in QRDRs was the most prevalent mechanism of quinolone resistance. This mechanism was complemented by efflux mechanisms in most porcine isolates. Transferable resistance by target protection or enzymatic modification was less common (10%) and restricted to human isolates.
authors.affiliation: Research Group for Antimicrobial Resistance and Molecular Epidemiology, Department for Microbiology and Risk Assessment, National Food Institute, Technical University of Denmark, Copenhagen V, Denmark. licav@food.dtu.dk
authors.forename: Lina Maria
authors.initials: LM
authors.lastname: Cavaco
authors.forename: Niels
authors.initials: N
authors.lastname: Frimodt-Møller
authors.forename: Henrik
authors.initials: H
authors.lastname: Hasman
authors.forename: Luca
authors.initials: L
authors.lastname: Guardabassi
authors.forename: Lene
authors.initials: L
authors.lastname: Nielsen
authors.forename: Frank Møller
authors.initials: FM
authors.lastname: Aarestrup
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D001426:Bacterial Proteins / Q000235:genetics; D002939:Ciprofloxacin / Q000494:pharmacology; D003718:Denmark / Q000453:epidemiology; D024881:Drug Resistance, Bacterial / Q000235:genetics; D004926:Escherichia coli / Q000187:drug effects* / Q000302:isolation & purification; D004927:Escherichia coli Infections / Q000453:epidemiology* / Q000382:microbiology / Q000662:veterinary; D006801:Humans; D008826:Microbial Sensitivity Tests / Q000706:statistics & numerical data; D009154:Mutation; D009268:Nalidixic Acid / Q000494:pharmacology; D015995:Prevalence; D015363:Quinolones / Q000494:pharmacology*; D013552:Swine / Q000382:microbiology*; D013553:Swine Diseases / Q000453:epidemiology* / Q000382:microbiology
chemical_list: D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D015363:Quinolones; D009268:Nalidixic Acid; D002939:Ciprofloxacin