Quinolone Resistance Determinants of Clinical Salmonella Enteritidis in Thailand

Utrarachkij, Fuangfa; Nakajima, Chie; Changkwanyeun, Ruchirada et al.

Microbial drug resistance, 2017, 23(7), 885-894

Permalink : https://hdl.handle.net/2115/71609

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論文情報

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アクセス権
open access
URI
https://hdl.handle.net/2115/71609
タイトル
Quinolone Resistance Determinants of Clinical Salmonella Enteritidis in Thailand
著者
Utrarachkij, Fuangfa ; Nakajima, Chie ; Changkwanyeun, Ruchirada ; Siripanichgon, Kanokrat ; Kongsoi, Siriporn ; Pornruangwong, Srirat ; Changkaew, Kanjana ; Tsunoda, Risa ; Tamura, Yutaka ; Suthienkul, Orasa ; Suzuki, Yasuhiko
著者名
Utrarachkij, Fuangfa
e-Rad_Researcher
60435964
著者名
Nakajima, Chie
著者名
Changkwanyeun, Ruchirada
著者名
Siripanichgon, Kanokrat
著者名
Kongsoi, Siriporn
著者名
Pornruangwong, Srirat
著者名
Changkaew, Kanjana
著者名
Tsunoda, Risa
e-Rad_Researcher
50382487
著者名
Tamura, Yutaka
著者名
Suthienkul, Orasa
e-Rad_Researcher
90206540
著者名
Suzuki, Yasuhiko
言語
英語
キーワード
Salmonella Enteritidis
quinolone resistance
gyrA
qnrS1
MLVA
発行日
2017-10-01
出版者
Mary Ann Liebert
収録物名
Microbial drug resistance
巻(号)
23(7)
ページ
885-894
抄録
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.
資源タイプ
学術雑誌論文
出版タイプ
Accepted Manuscript
権利情報
Final publication is available from Mary Ann Liebert, Inc., publishers https://doi.org/10.1089/mdr.2015.0234
PISSN
1076-6294
関連情報
PMID
28437229
関連情報 (isVersionOf)
出版社版DOI
https://doi.org/10.1089/mdr.2015.0234