Affiliation:
1. University of Zurich, Institute of Medical Microbiology, Gloriastrasse 30/32, CH-8006 Zurich, Switzerland
Abstract
ABSTRACT
Two mechanisms account for AmpC activity in
Escherichia coli
, namely, mutations in the
ampC
promoter and attenuator regions resulting in
ampC
overexpression and acquisition of plasmid-carried
ampC
genes. In this study, we analyzed 51 clinical
E. coli
isolates with reduced susceptibility to amoxicillin-clavulanic acid, piperacillin-tazobactam, or extended-spectrum cephalosporins for the presence of AmpC production. Three phenotypic AmpC confirmation assays (cefoxitin-cloxacillin disk diffusion test, cefoxitin-EDTA disk diffusion test, and AmpC Etest) were compared for the detection of AmpC activity. All 51 isolates were characterized genetically by mutational analysis of the chromosomal
ampC
promoter/attenuator region and by PCR detection of plasmid-carried
ampC
genes. Altogether, 21/51 (41%)
E. coli
isolates were considered true AmpC producers. AmpC activity due to chromosomal
ampC
promoter/attenuator mutations was found in 12/21 strains, and plasmid-carried
ampC
genes were detected in 8/21 isolates. One strain contained both
ampC
promoter mutations and a plasmid-carried
ampC
gene. All three phenotypic tests were able to detect the majority (>90%) of AmpC-positive strains correctly. Cefoxitin resistance was found to be a discriminative parameter, detecting 20/21 AmpC-producing strains. Susceptibility to extended-spectrum cephalosporins, e.g., ceftriaxone, ceftazidime, and cefotaxime, was found in 9 of the 21 AmpC-positive strains. Considering the elevated zone diameter breakpoints of the 2010 CLSI guidelines, 2/21 AmpC-positive strains were categorized as susceptible to extended-spectrum cephalosporins.
Publisher
American Society for Microbiology
Cited by
114 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献