Jpn. J. Infect. Dis., 65 (3), 264-267, 2012
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Dhruba Acharya1, Suwanna Trakulsomboon2, Surendra Kumar Madhup3, and Sunee Korbsrisate1*
1Department of Immunology, and 2Division of Infectious Disease and Tropical Medicine, Department of Medicine, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700; and 3Department of Microbiology, Dhulikhel Hospital-Kathmandu University Hospital, Kavre, Nepal
(Received December 28, 2011. Accepted April 4, 2012)
*Corresponding author: Mailing address: Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand. Tel: +662-418-0569, Fax: +662-418-1636, E-mail: このメールアドレスはスパムボットから保護されています。閲覧するにはJavaScriptを有効にする必要があります。
SUMMARY: Monitoring the antibiotic susceptibility pattern of Salmonella enterica serovar Typhi (S. Typhi) is important for efficiently managing cases of typhoid fever. In this study, the antimicrobial susceptibility patterns of 114 S. Typhi isolates, which were collected from a university hospital in Nepal during July 2009–December 2010, were investigated by disc diffusion assays. All of the S. Typhi isolates were sensitive to amoxycillin-clavulanic acid. More than 95% of the isolates were sensitive to chloramphenicol, ceftazidime, ceftriaxone, and cotrimoxazole. In addition, 1.7% of the studied isolates showed multiple drug resistance patterns. Of the 40 S. Typhi isolates, 32 strains (80%) showed nalidixic acid (NA) resistance with decreased susceptibility to ciprofloxacin (CIP). Importantly, we found the simultaneous presence of NA resistance and decreased susceptibility to CIP, suggesting that the resistance to NA is a reliable indicator of decreased CIP susceptibility (sensitivity, 97.5%; specificity, 100.0%). Furthermore, the sequencing of NA-resistant S. Typhi isolates showed a predominant amino acid alteration in the quinolone resistance-determining region (QRDR) of gyrA gene at position 83 from Ser→Phe. Two isolates with resistance to both CIP and NA had a double-mutation (Ser83→Phe and Asp87→Asn) in the QRDR of the gyrA gene, of which one had an additional amino acid mutation (Ser80→Ilu) in the QRDR of the parC gene.