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J Infect Chemother. 2008 Oct;14(5):342-8. doi: 10.1007/s10156-008-0631-2. Epub 2008 Oct 21.

Antimicrobial susceptibility and mechanism of quinolone resistance in Campylobacter jejuni strains isolated from diarrheal patients in a hospital in Tokyo.

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Department of Microbiology and Immunology, Graduate School of Health Sciences, Tokyo Medical and Dental University, Tokyo, 113-8510, Japan.


We determined the minimum inhibitory concentrations of six types of antimicrobial agents for 523 strains of Campylobacter jejuni that were isolated from diarrheal patients in a general hospital in Tokyo during the period between 2003 and 2005. It was revealed that 20.2%, 22.9%, 6.7%, and 0.6% of all the C. jejuni strains tested were resistant to ciprofloxacin (CPFX), nalidixic acid, ampicillin, and fosfomycin, respectively. All the strains were susceptible to clarithromycin and erythromycin. To elucidate the mechanism of quinolone resistance, in a total of 55 strains selected randomly, we carried out sequence determination and analysis of the quinolone-resistance determining regions (QRDRs) of their gyrA and gyrB genes. Amino-acid substitution at codon 86 (Thr --> IIe) of GyrA was found in all the 37 CPFX-resistant strains. There was no amino-acid substitution in the QRDR of the gyrB gene. All of the genomic DNAs of these 55 strains showed distinct pulsed-field gel electrophoresis patterns. Taken together, these results suggested that the quinolone resistance of C. jejuni was attributable mainly to the mutation at codon 86 (Thr --> IIe) in the QRDR of GyrA, and that this particular mutation and other silent mutations could be found not only in a certain clone of C. jejuni but also universally in a wide variety of strains.

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