Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6123612 | Journal of Infection and Chemotherapy | 2014 | 6 Pages |
Abstract
The spread of plasmid-mediated quinolone resistance (PMQR) determinants was evaluated in 150 ceftazidime or cefotaxime-resistant clinical isolates of Klebsiella pneumoniae and Escherichia coli from Tokai, Japan between 2008 and 2011. In this study, qnrB, qnrS, and aac(6â²)-Ib-cr genes were detected in 12 (50.0%), 4 (16.7%), and 1 (4.2%) of 24 K. pneumoniae isolates, respectively, while qnrA, aac(6â²)-Ib-cr, and qepA genes were detected in 1 (0.8%), 11 (8.7%), and 2 (1.6%) of 126 E. coli isolates, respectively. qnr genes were mainly found in K. pneumoniae (66.7%) and to a lesser extent in E. coli (0.8%). We determined the genetic environment of the qnrB4 gene in 24.6 kb class 1 integron structure, including aar-2, cmlA, blaOXA-10, aadA1, qacEdelta1, sul1, and blaDHA-1. In a time-kill assay, introduction of the qnrB4 or qnrS1 plasmid to the recipient E. coli strain decreased the bactericidal activities of fluoroquinolones such as ciprofloxacin, levofloxacin, and pazufloxacin.
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Authors
Hayato Okade, Satoshi Nakagawa, Toru Sakagami, Harumi Hisada, Nobuhiko Nomura, Junichi Mitsuyama, Yuka Yamagishi, Hiroshige Mikamo,