Abstract
We looked for the presence of
gyrA
mutations in seven fluoroquinolone-resistant French clinical isolates of
Campylobacter jejuni
and
Campylobacter coli
. Three of the five isolates of
C. jejuni
and the two isolates of
C. coli
had high-level resistance to nalidixic acid (MICs 128-256
μ
g/ml) and ciprofloxacin (MICs 32
μ
g/ml). A
gyrA
mutation was
found in all these isolates leading to the following substitutions: Thr86-Ile in four cases and Asp90-Tyr for one
C. coli
strain. One isolate had high-level resistance to nalidixic acid (MIC 64
μ
g/ml)
but low-level resistance to ciprofloxacin (MIC 2
μ
g/ml) and also carried a
gyrA
mutation leading to a Thr86-Ala substitution. The last isolate of
C. jejuni
studied displayed an atypical
resistance phenotype: It was resistant to high levels of ciprofloxacin (MIC 64
μ
g/ml) but remained fully susceptible to nalidixic acid (MIC 2
μ
g/ml). This phenotype was not explained
by the presence of peculiar mutations in
gyrA
or
gyrB
. It carried a
gyrA
mutation leading to a Thr86-Ile substitution and was devoid of
gyrB
mutation. Despite numerous attempts
with various degenerate oligonucleotide primers deduced from conserved regions of known
parC
genes, we were unable to amplify a corresponding sequence in
C. jejuni
or
C. coli
. First-step
and second-step
in vitro
mutants, derived from reference strain
C. coli
ATCC 33559 with ciprofloxacin or moxifloxacin as selecting agents, were found to carry one and two mutations in
gyrA
,
respectively. In contrast with the results obtained with clinical isolates, a variety of
gyrA
mutations were obtained
in vitro
.