Letters to the Editor Uncommon Occurrence of Mutations in the gyrB Gene Associated with Quinolone Resistance in Clinical Isolates of Neisseria gonorrhoeae

Several mechanisms of quinolone resistance have been iden-tified in Neisseria gonorrhoeae strains with decreased suscepti-bilities to quinolones (1, 2, 5). Initially, a mutation was found in the gyrB gene of a laboratory mutant with low-level nalidixic acid resistance (5). Subsequently, mutations in the gyrA and parC genes were found in laboratory strains and clinical iso-lates with high-level resistance to nalidixic acid and decreased susceptibilities to fluoroquinolones (1, 3, 4). However, the data regarding gyrB mutations in quinolone-resistant clinical iso-lates are lacking. We have extended our investigation to char-acterize mechanisms of quinolone resistance in clinical isolates of N. gonorrhoeae by further analyzing the isolates, which we described previously (3, 4), for gyrB mutations. The 55 clinical isolates studied consisted of 24 quinolone-susceptible isolates without mutations in either the quinolone resistance-determining region (QRDR) of the gyrA gene or the analogous region of the parC gene (MICs of ciprofloxacin, 0.004 to 0.015 mg/ml), 20 moderately fluoroquinolone-resistant isolates with mutations in the gyrA gene alone (MICs of cip-rofloxacin, 0.06 to 0.5 mg/ml), and 11 highly fluoroquinolone-resistant isolates with mutations in both the gyrA and parC genes (MICs of ciprofloxacin, 0.25 to 8.0 mg/ml) (3, 4). To analyze gyrB mutations in the region corresponding to the QRDR of the Escherichia coli gyrB gene (8), DNA fragments of the gyrB gene were amplified from chromosomal DNAs of the isolates by PCR with two primers, NG-GYRB-A, 59-AC