Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6117942 | International Journal of Antimicrobial Agents | 2013 | 6 Pages |
Abstract
The aim of this study was to uncover the mechanisms underlying Shigella flexneri resistance to cefalothin. In this study, a resistance-related S. flexneri isolate, S. flexneri YDC, was obtained from S. flexneri mel-1998023/zz pre-incubated with cefalothin at a dose of 0.5à the minimum inhibitory concentration. The ISEcp1 coding element was identified upstream of blaCTX-M-55 in S. flexneri YDC. To further determine the role of ISEcp1 in S. flexneri resistance, plasmids containing blaCTX-M-55 recombinant with or without the ISEcp1 sequence were constructed and named as pCTX and pISECTX, respectively. It was shown that Escherichia coli DH5α(pISECTX) was resistant to all β-lactams tested. In contrast, E. coli DH5α(pCTX) was sensitive to all except β-lactams cefazolin and cefalothin. In addition, reverse transcription PCR showed that expression levels of blaCTX-M-55 were higher in E. coli DH5α(pISECTX). The Clinical and Laboratory Standards Institute (CLSI) assay demonstrated that extended-spectrum β-lactamase was only positively detected in E. coli DH5α(pISECTX) but not in E. coli DH5α(pCTX). Taken together, these results suggest that the translocated ISEcp1 element upstream of blaCTX-M-55 is required for overexpression of blaCTX-M-55, leading to cephalosporin resistance.
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Authors
Yingfang Wang, Chunhua Song, Guangcai Duan, Jingyuan Zhu, Haiyan Yang, Yuanlin Xi, Qingtang Fan,