1887

Abstract

We investigated antimicrobial susceptibility and the molecular mechanism underlying low-level resistance to fluoroquinolones in 70 non-duplicate clinical isolates of . The isolates were collected in a general hospital in Tokyo, Japan, between January and October 2013 from 38 men and 32 women; most of the isolates (48 out of 70, 68.5 %) were obtained from post-nasal drips of children. The antimicrobial susceptibility of isolates was determined with an Etest, and low-level fluoroquinolone-resistant isolates were subtyped by PFGE. Mutations in the and genes were determined by PCR and sequencing. PCR products of the and genes from the low-level fluoroquinolone-resistant isolates were transformed into a fluoroquinolone-susceptible strain. Among the 70 isolates, five (7.1 %) exhibited elevated fluoroquinolone MICs (levofloxacin, 1.0 mg l; ciprofloxacin, 0.5 mg l) and different PFGE patterns. The patients from whom these five isolates were isolated had not undergone treatment with fluoroquinolones for the past 6 months. Each of the five low-level fluoroquinolone-resistant isolates had a gene mutation resulting in a Thr-to-Ile substitution at aa 80 (T80I) in the GyrA protein, while no changes were detected in the gene. A transformant carrying the gene containing the T80I substitution, which corresponded to Ser83 in , displayed an elevated fluoroquinolone MIC and contained the T80I alteration in GyrA. Thus, our findings reveal that the low-level resistance to fluoroquinolones in is due to an amino acid substitution of Thr80 to Ile in GyrA. This is the first evidence of low-level fluoroquinolone resistance in .

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2014-08-01
2019-09-22
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