title: Association of fluoroquinolone resistance, virulence genes, and IncF plasmids with extended-spectrum-β-lactamase-producing Escherichia coli sequence type 131 (ST131) and ST405 clonal groups.
abstract: The global increase of extended-spectrum-β-lactamase (ESBL)-producing Escherichia coli is associated with the specific clonal group sequence type 131 (ST131). In order to understand the successful spread of ESBL-producing E. coli clonal groups, we characterized fluoroquinolone resistance determinants, virulence genotypes, and plasmid replicons of ST131 and another global clonal group, ST405. We investigated 41 ST131-O25b, 26 ST131-O16, 41 ST405, and 41 other ST (OST) ESBL-producing isolates, which were collected at seven acute care hospitals in Japan. The detection of ESBL types, fluoroquinolone resistance-associated mutations (including quinolone resistance-determining regions [QRDRs]), virulence genotypes, plasmid replicon types, and IncF replicon sequence types was performed using PCR and sequencing. blaCTX-M, specifically blaCTX-M-14, was the most common ESBL gene type among the four groups. Ciprofloxacin resistance was found in 90% of ST131-O25b, 19% of ST131-O16, 100% of ST405, and 54% of OST isolates. Multidrug resistance was more common in the ST405 group than in the ST131-O25 group (56% versus 32%; P = 0.045). All ST131-O25b isolates except one had four characteristic mutations in QRDRs, but most of the isolates from the other three groups had three mutations in common. The ST131-O25b and ST405 groups had larger numbers of virulence genes than the OST group. All of the ST131-O25b and ST405 isolates and most of the ST131-O16 and OST isolates carried IncF replicons. The most prevalent IncF replicon sequence types differed between the four clonal groups. Both the ST131-O25b and ST405 clonal groups had a fluoroquinolone resistance mechanism in QRDRs, multidrug resistance, high virulence, and IncF plasmids, suggesting the potential for further global expansion and a need for measures against these clonal groups.
authors.affiliation: Department of Clinical Laboratory Medicine, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan.
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Matsumura
authors.forename: Masaki
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Miki
authors.initials: M
authors.lastname: Nagao
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Ito
authors.forename: Shunji
authors.initials: S
authors.lastname: Takakura
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ichiyama
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D024881:Drug Resistance, Bacterial / Q000235:genetics / Q000502:physiology; D004926:Escherichia coli / Q000187:drug effects* / Q000201:enzymology* / Q000235:genetics; D029968:Escherichia coli Proteins / Q000235:genetics / Q000378:metabolism*; D024841:Fluoroquinolones / Q000494:pharmacology*; D010957:Plasmids / Q000235:genetics; D014774:Virulence / Q000235:genetics; D001618:beta-Lactamases / Q000235:genetics / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D029968:Escherichia coli Proteins; D024841:Fluoroquinolones; D001618:beta-Lactamases