Abstract
PurposeThe purpose of this study was to investigate the molecular mechanisms of fluoroquinolone resistance in Moraxella catarrhalis clinical strains isolated in Lublin, Poland.Materials and methodsA total of 150 non-duplicate clinical strains of M. catarrhalis were obtained from individuals with signs of upper respiratory tract infection. Bacterial identification was corroborated on the basis of phenotypic and biochemical characteristics as well as with the use of molecular tests. The antimicrobial susceptibility of M. catarrhalis isolates was determined using the disk diffusion method and Etest. Mutations in the gyrase (gyrA and gyrB) and topoisomerase (parC and parE) genes were determined by polymerase chain reaction and sequencing.ResultsIt was observed that 16.7% of the studied isolates were drug resistant. Resistance to tetracycline was detected for 12% of the strains. Resistance to nalidixic acid, moxifloxacin, and levofloxacin was exhibited by 2.7% of the strains; 1.3% of the strains were resistant to trimethoprim/sulfamethoxazole and 0.7% to erythromycin. Minimum inhibitory concentration values of the four strains demonstrating fluoroquinolone resistance were: 6–12 mg/L for nalidixic acid, 1–1.5 mg/L for levofloxacin, 1 mg/L for moxifloxacin, and 0.25–0.5 mg/L for ciprofloxacin. The research resulted in the detection of mutations in 4 strains, in gyrase gyrA and gyrB genes. In gyrA gene, there occurred mutation G412C as well as four silent transition mutations. Within gyrB gene, there occurred mutation, substitution A1481G, as well as two identical silent mutations.ConclusionOur findings reveal that resistance to fluoroquinolones in M. catarrhalis is connected with amino acid substitutions in gyrA and gyrB genes. To our knowledge, this work is the first description of fluoroquinolone-resistant clinical strains of M. catarrhalis with described mutations in gyrA and gyrB genes isolated in Poland and in Europe.
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