JAC Advance Access published online on December 12, 2002
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkg033
© 2002 by The British Society for Antimicrobial Chemotherapy
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In Brief
1 Antimicrobial Agents Research Group, Department of Infection,
The Medical School, University of Birmingham, Birmingham B15 2TT,
UK
* Corresponding author. E-mail: l.j.v.piddock{at}bham.ac.uk.
Received 27 June 2002
; revised 5 September 2002
; accepted 3 October 2002
Consecutive isolates of quinolone-resistant campylobacter
isolated over a 5 year period (1990-1995) from the
faeces of patients with enteritis in Plymouth, UK, were examined
for the epidemiology of mutations in gyrA (n = 127).
In addition, clinical isolates and poultry isolates from Germany,
The Netherlands and other regions of the UK collected before 1995
were examined for mutations in the quinolone resistance-determining
region of gyrA by single-stranded conformational
polymorphism analysis and direct sequencing of a 270 bp fragment
of PCR-generated DNA. The majority of isolates (173/208) carried
a mutation at codon 86 in gyrA resulting in substitution
of Ile for Thr; all of these were resistant to ciprofloxacin (MIC
Keywords: fluoroquinolone, resistance, Campylobacter
Fluoroquinolone resistance in Campylobacter species
from man and animals: detection of mutations in topoisomerase genes
2 mg/L). One isolate of Campylobacter
jejuni had a mutation at Asp-90, and another had a double mutation
at Thr-86 and Pro-104. Only two resistant isolates showed no mutation
in gyrA. A novel gyrA sequence
was amplified from two Campylobacter lari and one C. jejuni, which exhibited a valine at codon 86.
Only 8/192 isolates had changes in gyrB; all were
shown to relate to silent mutations in gyrB and
presumably reflect natural polymorphisms in the gene.
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