Journal Article

The AmpC phenotype in Norwegian clinical isolates of <i>Escherichia coli</i> is associated with an acquired IS<i>Ecp1</i>-like <i>ampC</i> element or hyperproduction of the endogenous AmpC

Bjørg Haldorsen, Bettina Aasnaes, Kristin H. Dahl, Anne-Merethe Hanssen, Gunnar S. Simonsen, Timothy R. Walsh, Arnfinn Sundsfjord and Eirik W. Lundblad

in Journal of Antimicrobial Chemotherapy

Published on behalf of British Society for Antimicrobial Chemotherapy

Volume 62, issue 4, pages 694-702
Published in print October 2008 | ISSN: 0305-7453
Published online June 2008 | e-ISSN: 1460-2091 | DOI: http://dx.doi.org/10.1093/jac/dkn257
The AmpC phenotype in Norwegian clinical isolates of Escherichia coli is associated with an acquired ISEcp1-like ampC element or hyperproduction of the endogenous AmpC

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Objectives

The aim of the study was to examine resistance mechanisms associated with an AmpC phenotype in Norwegian clinical isolates of Escherichia coli.

Methods

Clinical E. coli isolates (n = 106) with reduced susceptibility to third-generation cephalosporins without clavulanic acid synergy were collected from 12 Norwegian laboratories from 2003 to 2005. Twenty-two isolates with an AmpC phenotype were selected for further characterization by PFGE, isoelectric focusing, different PCR-based techniques, DNA sequencing, AmpC qRT–PCR, transfer studies and plasmid analyses.

Results

The 22 isolates were not clonally related by the PFGE analysis. All isolates expressed a β-lactamase with a pI of 9.0–9.2. Ten isolates contained a blaCMY gene, which was linked to an ISEcp1-like element in all cases. Twelve isolates had mutations or insertions in the promoter or the attenuator regions, leading to increased expression of the chromosomal ampC gene. One of these isolates had an ISEc10 element inserted upstream of the chromosomal ampC gene.

Conclusions

This is the first molecular study of Norwegian clinical E. coli isolates with an AmpC phenotype. Resistance was mediated either by expression of blaCMY from acquired ISEcp1-like-blaCMY elements, or by mutations or insertions in the chromosomal ampC gene control region leading to hyperproduction of the endogenous AmpC enzyme. There was no correlation between the level of ampC mRNA and the MICs of cephalosporins.

Keywords: β-lactamases; cephalosporin resistance; insertion sequences; promoter mutations

Journal Article.  5335 words.  Illustrated.

Subjects: Medical Oncology ; Critical Care

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