Detection of the plasmid-mediated quinolone resistance determinant qnr among clinical isolates of Klebsiella pneumoniae producing AmpC-type β-lactamase

被引:62
|
作者
Rodríguez-Martínez, JM
Pascual, A
García, I
Martínez-Martínez, L
机构
[1] Univ Seville, Sch Med, Dept Microbiol, E-41009 Seville, Spain
[2] Univ Seville, Univ Hosp Virgen Macarena, Seville, Spain
关键词
Escherichia coli; fluoroquinolones; cephamycinase; molecular epidemiology;
D O I
10.1093/jac/dkg388
中图分类号
R51 [传染病];
学科分类号
100401 ;
摘要
Objectives: Plasmid pMG252 contains the qnr locus, which is responsible for low-level resistance to quinolones by protecting the DNA gyrase. pMG252 also encodes the AmpC-type beta-lactamase (pACBL), FOX-5. The aim of this study was to determine the prevalence of qnr in strains from different geographical locations in America and Europe. Methods: Four hundred and twenty-five (159 Klebsiella pneumoniae and 266 Escherichia coli) clinical isolates were studied. The detection of qnr was by PCR using specific primers for an internal fragment of 543 bp. Results: qnr was detected in three cefoxitin-resistant K. pneumoniae strains, which also produced a pACBL. None of the E. coli isolates tested contained qnr. The three qnr-positive K. pneumoniae came from the USA, and all transferred a conjugative plasmid coding for cefoxitin resistance to E. coli J53. qnr was also transferred by the same plasmid in two out of the three strains. The sequences of amplified qnr fragments from the three strains were identical to the qnr sequence from pMG252. Conclusions: The qnr determinant is uncommon among clinical isolates of K. pneumoniae and E. coli, but its identification in three pACBL(+) K. pneumoniae from the USA indicates the emergence of this quinolone resistance mechanism.
引用
收藏
页码:703 / 706
页数:4
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