Characterisation of Salmonella paratyphi A strains with reduced susceptibility to quinolone isolated from an outbreak in Korea
Abstract number: 902_p1695
Infections with Salmonella paratyphi possessing reduced susceptibility to quinolone may compromise the effectiveness of ciprofloxacin therapy that has been regarded as the drug of choice for paratyphoid fever in Korea before. The purpose of this study was to examine the antibiotic susceptibility and to characterise the resistance mechanism of the S. paratyphi A isolates with decreased susceptibility to quinolone isolated from an outbreak in Korea, and to determine if the isolates were genetically similar or clonal.
A total of 10 clinical isolates of S. paratyphi A, nine from an outbreak and one as control were used. Antibiotic susceptibility of S. paratyphi A to ampicillin, cephalothin, ceftriaxone, gentamicin, tetracycline, chloramphenicol, nalidixic acid, ofloxacin, ciprofloxacin and moxifloxacin were determined by microdilution broth test. The mutations that are responsible for quinolone resistance in gyrA, gyrB, parC, and parE genes of S. paratyphi A were investigated using PCR amplification and DNA sequencing of the quinolone resistance determining regions. Reserpine, a known efflux pump inhibitor, was used to determine whether an efflux-mediated mechanism contributed to reduced susceptibility to quinolone. Pulsed-field gel electrophoresis were performed to examine the clonal relatedness of the isolates.
Among seven patients, three with ciprofloxacin therapy showed no clinical responses and required retreatment with ceftriaxone. Four patients treated with ceftriaxone as initial empirical therapy had successful clinical reponses. All isolates were sensitive to ampicillin, cephalothin, ceftriaxone, gentamicin, tetracycline, chloramphenicol. The MICs of the quinolones of the clinical isolates with reduced susceptibility to quinolone exhibited as follows: nalidixic acid >1024 mg/L, ofloxacin 2 mg/L, ciprofloxacin 2 mg/L, moxifloxacin 2 mg/L. The sequence of QRDR of the gyrA gene had a single mutation at position 83 (from TCC to TTC:from Ser to Phe), but no mutations were found in the gyrB, parC, and parE genes. Reserpine did not effect the MICs for ciprofloxacin, nalidixic acid, ofloxacin and moxifloxacin. PFGE analysis revealed identical patterns in all isolates.
The sequence of the QRDR of gyrA in S. paratyphi A strains with reduced susceptibility to quinolone which were isolated from an outbreak had a single mutation at the Ser-83, and no mutations were found in the gyrB, parC and parE genes."
|Session name:||XXIst ISTH Congress|
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