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J Antimicrob Chemother. 2015 Mar;70(3):899-904. doi: 10.1093/jac/dku468. Epub 2014 Dec 2.

Epidemiology and risk factors for infections due to AmpC β-lactamase-producing Escherichia coli.

Author information

1
Hospital Universitari Mútua de Terrassa, Barcelona, Spain vanesapascual@hotmail.com.
2
Hospital de la Santa Creu i Sant Pau and Institut d'Investigació Biomèdica Sant Pau (IIB Sant Pau), Barcelona, Spain.
3
Catlab, Barcelona, Spain.
4
Hospital de la Santa Creu i Sant Pau and Institut d'Investigació Biomèdica Sant Pau (IIB Sant Pau), Barcelona, Spain Universitat Autònoma de Barcelona, Barcelona, Spain Red Española de Investigación en Patología Infecciosa (REIPI), Instituto de Salud Carlos III, Madrid, Spain.
5
Consorci Sanitari de Terrassa, Barcelona, Spain.
6
Hospital de la Santa Creu i Sant Pau and Institut d'Investigació Biomèdica Sant Pau (IIB Sant Pau), Barcelona, Spain Red Española de Investigación en Patología Infecciosa (REIPI), Instituto de Salud Carlos III, Madrid, Spain.
7
Hospital Universitari Mútua de Terrassa, Barcelona, Spain.
8
Hospital Universitari Mútua de Terrassa, Barcelona, Spain Universitat Internacional de Catalunya, Barcelona, Spain.

Abstract

OBJECTIVES:

To describe the prevalence and risk factors for infection due to AmpC β-lactamase-producing Escherichia coli (AmpC-EC).

METHODS:

For the prevalence study, all clinical isolates of E. coli with reduced susceptibility to third-generation cephalosporins were prospectively included from June 2010 to November 2011. For risk factor analysis, a case-control study was conducted. Cases were patients with an infection due to AmpC-EC. Controls were patients infected with cephalosporin-susceptible E. coli, matched 1 : 2. Detection of blaAmpC genes was done with a multiplex AmpC-PCR, and hyperproduction of E. coli chromosomal blaAmpC by quantitative RT-PCR. Alteration of the blaAmpC promoter was studied by PCR and sequencing.

RESULTS:

We identified 243 (1.1%) AmpC-EC strains out of 21 563 clinical isolates. Three cases with strains carrying ESBLs, 18 strains that were considered due to colonization and 8 cases lost to clinical follow-up were excluded. Finally, 214 cases were included in the analysis. Ninety-one cases (42.5%) and 269 (62.8%) controls were strictly community acquired (P < 0.001). Thirty-five (16.3%) cases and 186 controls (43.5%) did not have any identifiable risk factor (P < 0.001). Among cases, 158 (73.8%) were found to harbour an acquired AmpC (73.4% CMY-2). Previous use of fluoroquinolones [OR 2.6 (95% CI 1.12-3.36); P = 0.008] was independently associated with AmpC-EC in the multivariate analysis.

CONCLUSIONS:

Prevalence of AmpC in E. coli remains low in our area. Plasmid acquisition (CMY type) represents the main mechanism of AmpC production. A high proportion of community-acquired isolates and patients with no identifiable risk factors were found. Previous use of fluoroquinolones was identified as a risk factor.

KEYWORDS:

AmpC β-lactamases; E. coli; cephalosporins resistance

PMID:
25468902
DOI:
10.1093/jac/dku468
[Indexed for MEDLINE]

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