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JAC Advance Access originally published online on August 13, 2003
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Journal of Antimicrobial Chemotherapy (2003) 52, 481-484
© 2003 The British Society for Antimicrobial Chemotherapy

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

M. L. Peterson1,2, J. C. Rotschafer1 and L. J. V. Piddock2,*

1 University of Minnesota, Minneapolis, MN, USA; 2 Antimicrobial Agents Research Group, Division of Immunity and Infection, School of Medicine, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

Received 4 April 2003; returned 1 May 2003; revised 12 June 2003; accepted 12 June 2003

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.

Keywords: anaerobe, quinolone, antibiotic resistance

* Corresponding author. Tel: +44-121-414 6966; Fax: +44-121-414 3454; E-mail: l.j.v.piddock{at}bham.ac.uk


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