Role of topoisomerase mutations and efflux in fluoroquinolone resistance of Bacteroides fragilis clinical isolates and laboratory mutants.
Twelve laboratory mutants and 32 ciprofloxacin-resistant isolates of Bacteroides fragilis were examined for the mechanism(s) of fluoroquinolone resistance. Five mutants had mutations in gyrA. One mutant and two clinical isolates contained a mutation in gyrB. Eight mutants and five clinical isolates accumulated significantly less ciprofloxacin than did wild-type isolates; the mutants and clinical isolates were restored to wild-type characteristics when carbonyl cyanide m-chlorophenylhydrazone was used.
Ricci
Vito
V
Antimicrobial Agents Research Group, Division of Immunity and Infection, University of Birmingham, Birmingham B15 2TT, United Kingdom.
Peterson
Marnie L
ML
Rotschafer
John C
JC
Wexler
Hannah
H
Piddock
Laura J V
LJ
D000890:Anti-Infective Agents / Q000378:metabolism* / Q000494:pharmacology*; D001442:Bacteroides Infections / Q000382:microbiology*; D001441:Bacteroides fragilis / Q000187:drug effects*; D027081:DNA Gyrase / Q000235:genetics; D027101:DNA Topoisomerase IV / Q000235:genetics; D004264:DNA Topoisomerases, Type I / Q000235:genetics*; D024881:Drug Resistance, Bacterial; D024841:Fluoroquinolones / Q000378:metabolism* / Q000494:pharmacology*; D008826:Microbial Sensitivity Tests; D009154:Mutation / Q000235:genetics*
D000890:Anti-Infective Agents; D024841:Fluoroquinolones; D027101:DNA Topoisomerase IV; D004264:DNA Topoisomerases, Type I; D027081:DNA Gyrase