Transposition of IS Ecp1 modulates blaCTX-M-55 -mediated Shigella flexneri resistance to cefalothin

• Published in: International journal of antimicrobial agents 2013, Vol.42 (6), p.507-512
• Main Authors: Wang, Yingfang, Song, Chunhua, Duan, Guangcai, Zhu, Jingyuan, Yang, Haiyan, Xi, Yuanlin, Fan, Qingtang
• Format: Article
• Language: English
• Subjects: Infectious Disease
• ISSN: 0924-8579
• DOI: 10.1016/j.ijantimicag.2013.08.009

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 0.5× the minimum inhibitory concentration. The IS Ecp1 coding element was identified upstream of blaCTX-M-55 in S. flexneri YDC. To further determine the role of IS Ecp1 in S. flexneri resistance, plasmids containing blaCTX-M-55 recombinant with or without the IS Ecp1 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 IS Ecp1 element upstream of blaCTX-M-55 is required for overexpression of blaCTX-M-55 , leading to cephalosporin resistance.