| Title: | Quinolone Resistance Determinants of Clinical Salmonella Enteritidis in Thailand |
| Authors: | Utrarachkij, Fuangfa Browse this author |
| Nakajima, Chie Browse this author →KAKEN DB |
| Changkwanyeun, Ruchirada Browse this author |
| Siripanichgon, Kanokrat Browse this author |
| Kongsoi, Siriporn Browse this author |
| Pornruangwong, Srirat Browse this author |
| Changkaew, Kanjana Browse this author |
| Tsunoda, Risa Browse this author |
| Tamura, Yutaka Browse this author →KAKEN DB |
| Suthienkul, Orasa Browse this author |
| Suzuki, Yasuhiko Browse this author →KAKEN DB |
| Keywords: | Salmonella Enteritidis |
| quinolone resistance |
| gyrA |
| qnrS1 |
| MLVA |
| Issue Date: | 1-Oct-2017 |
| Publisher: | Mary Ann Liebert |
| Journal Title: | Microbial drug resistance |
| Volume: | 23 |
| Issue: | 7 |
| Start Page: | 885 |
| End Page: | 894 |
| Publisher DOI: | 10.1089/mdr.2015.0234 |
| PMID: | 28437229 |
| Abstract: | Salmonella Enteritidis has emerged as a global concern regarding quinolone resistance and invasive potential. Although quinolone-resistant S. Enteritidis has been observed with high frequency in Thailand, information on the mechanism of resistance acquisition is limited. To elucidate the mechanism, a total of 158 clinical isolates of nalidixic acid (NAL)-resistant S. Enteritidis were collected throughout Thailand, and the quinolone resistance determinants were investigated in the context of resistance levels to NAL, norfloxacin (NOR), and ciprofloxacin (CIP). The analysis of point mutations in type II topoisomerase genes and the detection of plasmid-mediated quinolone resistance genes showed that all but two harbored a gyrA mutation, the qnrS1 gene, or both. The most commonly affected codon in mutant gyrA was 87, followed by 83. Double codon mutation in gyrA was found in an isolate with high-level resistance to NAL, NOR, and CIP. A new mutation causing serine to isoleucine substitution at codon 83 was identified in eight isolates. In addition to eighteen qnrS1-carrying isolates showing nontypical quinolone resistance, one carrying both the qnrS1 gene and a gyrA mutation also showed a high level of resistance. Genotyping by multilocus variable number of tandem repeat analysis suggested a possible clonal expansion of NAL-resistant strains nationwide. Our data suggested that NAL-resistant isolates with single quinolone resistance determinant may potentially become fluoroquinolone resistant by acquiring secondary determinants. Restricted therapeutic and farming usage of quinolones is strongly recommended to prevent the emergence of fluoroquinolone-resistant isolates. |
| Rights: | Final publication is available from Mary Ann Liebert, Inc., publishers https://doi.org/10.1089/mdr.2015.0234 |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/71609 |
| Appears in Collections: | 国際連携研究教育局 : GI-CoRE (Global Institution for Collaborative Research and Education : GI-CoRE) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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