Role of topoisomerase mutations and efflux in fluoroquinolone resistance of Bacteroides fragilis clinical isolates and laboratory mutants

Antimicrob Agents Chemother. 2004 Apr;48(4):1344-6. doi: 10.1128/AAC.48.4.1344-1346.2004.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Infective Agents / metabolism*
  • Anti-Infective Agents / pharmacology*
  • Bacteroides Infections / microbiology*
  • Bacteroides fragilis / drug effects*
  • DNA Gyrase / genetics
  • DNA Topoisomerase IV / genetics
  • DNA Topoisomerases, Type I / genetics*
  • Drug Resistance, Bacterial
  • Fluoroquinolones / metabolism*
  • Fluoroquinolones / pharmacology*
  • Microbial Sensitivity Tests
  • Mutation / genetics*

Substances

  • Anti-Infective Agents
  • Fluoroquinolones
  • DNA Topoisomerase IV
  • DNA Topoisomerases, Type I
  • DNA Gyrase