
Roles of gyrA Mutations in Resistance of Clinical Isolates and In Vitro Mutants of Bacteroides fragilis to the New Fluoroquinolone Trovafloxacin
Author(s) -
Rafik Bachoual,
L. Dubreuil,
Claude-James Soussy,
Jacques Tankovic
Publication year - 2000
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.44.7.1842-1845.2000
Subject(s) - bacteroides fragilis , trovafloxacin , microbiology and biotechnology , mutant , biology , bacteroidaceae , bacteroides , ciprofloxacin , dna gyrase , minimum inhibitory concentration , antibacterial agent , bacteria , antibiotics , genetics , escherichia coli , gene
We determined whethergyrA mutations were present in fluoroquinolone-resistant laboratory mutants derived from theBacteroides fragilis reference strain ATCC 25285 and in clinical isolates ofB. fragilis . The two first-step mutants selected on ciprofloxacin (CIP) were devoid ofgyrA mutations, whereas two of the three CIP-selected second-step mutants studied presented the samegyrA mutation leading to a Ser82Phe change. Unusual GyrA alterations, Asp81Asn or Ala118Val, were detected in two of the three first-step mutants selected on trovafloxacin (TRO), Mt3 and Mt1, respectively. The Ala118Val change had no effect on the susceptibility of Mt1 to CIP. No second-step mutant could be obtained with TRO as a selector. For the 12 clinical isolates studied, a Ser82Phe change in GyrA was found only in the 3 strains which showed the highest levels of TRO resistance (MIC, 4 μg/ml). Thus, the resistance phenotypes and genotypes observed in fluoroquinolone-resistant clinical isolates ofB. fragilis were similar to those found in CIP-selected laboratory mutants, whereas peculiar mutational events could be selected in vitro with TRO.