Plasmid-mediated complementation of gyrA and gyrB in fluoroquinolone-resistant Bacteroides fragilis

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Objectives: To identify whether mutations in gyrA and gyrB confer fluoroquinolone resistance in Bacteroides fragilis.

Methods: Eight fluoroquinolone-resistant (FQR) strains were complemented with plasmid-mediated B. fragilis wild-type gyrA (pMP1) and gyrB (pMP2), and MICs determined. Sequence analysis of the gyrA and gyrB quinolone resistance determining region (QRDR) was performed for all strains.

Results: MICs of fluoroquinolones were two- to 32-fold higher than wild-type for all mutants. Five mutants had a substitution in GyrA (Ser-82→Phe), one mutant had a substitution in GyrA (Asp-81→Gly), one mutant had a substitution in GyrB (Glu-478→Lys), and one resistant strain did not contain mutations in the QRDR of gyrA or gyrB. Following complementation with pMP1 or pMP2, the MICs of fluoroquinolones were reduced two- to 32-fold for the mutants.

Conclusion: These studies verify that substitutions in GyrA and GyrB confer resistance in B. fragilis. Other mechanisms are also responsible for resistance since not all resistant strains fully complemented to the wild-type phenotype.


Original languageEnglish
Pages (from-to)481-4
Number of pages4
JournalJournal of Antimicrobial Chemotherapy
Issue number3
Early online date13 Aug 2003
Publication statusPublished - Sep 2003


  • Anti-Bacterial Agents, Bacteroides fragilis, DNA Gyrase, Drug Resistance, Bacterial, Fluoroquinolones, Genetic Complementation Test, Microbial Sensitivity Tests, Mutation, Phenotype, Plasmids, Reverse Transcriptase Polymerase Chain Reaction