JAC Advance Access originally published online on June 26, 2008
Journal of Antimicrobial Chemotherapy 2008 62(4):694-702; doi:10.1093/jac/dkn257
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Original research |
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
1 Reference Centre for Detection of Antimicrobial Resistance, Department of Microbiology and Infection Control, University Hospital of North-Norway, Tromsø, Norway 2 Department of Microbiology and Virology, University of Tromsø, Tromsø, Norway 3 Division of Infection Control, Norwegian Institute of Public Health, Oslo, Norway 4 University of Cardiff, Cardiff, UK
Received 31 March 2008; returned 22 April 2008; revised 25 May 2008; accepted 29 May 2008
* Correspondence address. Department of Microbiology and Virology, Institute of Medical Biology, Faculty of Medicine, University of Tromsø, 9038 Tromsø, Norway. Tel: +47-90616118; Fax: +47-77645350; E-mail: arnfinn.sundsfjord{at}fagmed.uit.no
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
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