JAC Advance Access published online on August 13, 2003
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkg368
© 2003 by The British Society for Antimicrobial Chemotherapy
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Original article
1 University of Minnesota,
Minneapolis, MN, USA; Antimicrobial
Agents Research Group, Division of Immunity and Infection, School
of Medicine, University of Birmingham, Edgbaston, Birmingham B15
2TT, UK
* Corresponding author. E-mail: l.j.v.piddock{at}bham.ac.uk.
Received 4 April 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 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
Plasmid-mediated complementation of gyrA
and gyrB in fluoroquinolone-resistant Bacteroides
fragilis
2 University of Minnesota,
Minneapolis, MN, USA
3 Antimicrobial
Agents Research Group, Division of Immunity and Infection, School
of Medicine, University of Birmingham, Edgbaston, Birmingham B15
2TT, UK
Phe),
one mutant had a substitution in GyrA (Asp-81Gly),
one mutant had a substitution in GyrB (Glu-478Lys),
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.
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