Mutations in the gyrA gene contribute considerably to quinolone resistance
in Escherichia coli. Mechanisms for quinolone resistance in anaerobic bacte
ria are less well studied. The Bacteroides fragilis group are the anaerobic
organisms most frequently isolated from patients with bacteremia and intra
abdominal infections. Forty-four clinafloxacin-resistant and-susceptible fe
cal and clinical isolates of the B. fragilis group (eight Bacteroides fragi
lis, three Bacteroides ovatus, five Bacteroides thetaiotaomicron, six Bacte
roides uniformis, and 22 Bacteroides vulgatus) and six ATCC strains of the
B. fragilis group were analyzed as follows: (i) determination of susceptibi
lity to ciprofloxacin, levofloxacin, moxifloxacin, and clinafloxacin by the
agar dilution method and (ii) sequencing of the gyrA quinolone resistance-
determining region (QRDR) located between amino acid residues equivalent to
Ala-67 through Gln-106 in E. coli. Amino acid substitutions were found at
hotspots at positions 82 (n = 15) and 86 (n = 8). Strains with Ser82Leu sub
stitutions (n = 13) were highly resistant to all quinolones tested. Mutatio
ns in other positions of gyrA were also frequently found in quinolone-resis
tant and -susceptible isolates. Eight clinical strains that lacked mutation
s in their QRDR were susceptible to at least two of the quinolones tested.
Although newer quinolones have good antimicrobial activity against the B. f
ragilis group, quinolone resistance in B. fragilis strains can be readily s
elected in vivo. Mutational events in the QRDR of gyrA seem to contribute t
o quinolone resistance in Bacteroides species.