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JAC Advance Access originally published online on August 11, 2009
Journal of Antimicrobial Chemotherapy 2009 64(4):712-717; doi:10.1093/jac/dkp288
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© The Author 2009. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

CTX-M-15-producing urinary Escherichia coli O25b-ST131-phylogroup B2 has acquired resistance to fosfomycin

Jesús Oteo1, Beatriz Orden2, Verónica Bautista1, Oscar Cuevas1, Margarita Arroyo1, Rocío Martínez-Ruiz2, María Pérez-Vázquez1, Marta Alcaraz3, Silvia García-Cobos1 and José Campos1,4,*

1 Antibiotic Laboratory, Bacteriology, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Majadahonda, Madrid, Spain 2 Microbiology Department, Centro de Especialidades Argüelles, Hospital Puerta de Hierro, Majadahonda, Madrid, Spain 3 Servicio de Farmacia del Área Sanitaria 6 de la Comunidad de Madrid, Spain 4 Consejo Superior de Investigaciones Científicas, Madrid, Spain

Received 7 May 2009; returned 8 June 2009; revised 15 July 2009; accepted 15 July 2009

* Corresponding author. Centro Nacional de Microbiología, Instituto de Salud Carlos III, Carretera Pozuelo a Majadahonda, 28220 Majadahonda, Madrid, Spain. Tel: +34-918-22-3650; Fax: +34-915-09-7966; E-mail: jcampos{at}isciii.es

Objectives: To describe trends in fosfomycin resistance in urinary isolates of Escherichia coli producing extended-spectrum β-lactamases (ESBLs) in relation to fosfomycin consumption and to characterize representative fosfomycin-resistant isolates.

Methods: In 2007–08, an unexpected increase in fosfomycin resistance in ESBL-producing urinary E. coli was observed. Laboratory records were reviewed and a prospective surveillance study was initiated on all urinary tract infections caused by ESBL-producing, fosfomycin-resistant E. coli. blaESBL types, phylogroups, genetic environment and afa/dra operon were determined by PCR and sequencing. Molecular epidemiology was analysed by PFGE and multilocus sequence typing. To elucidate possible mechanisms of fosfomycin resistance, uhpT, glpT, uhpA, ptsI, cyaA and murA genes were analysed. Fosfomycin consumption was determined as recommended by WHO.

Results: From 2004 to 2008, fosfomycin consumption increased by 50%, while fosfomycin resistance in ESBL producers increased from 2.2% to 21.7%. Of 26 isolates studied, 24 produced CTX-M-15 and belonged to the O25b-ST131-phylogroup B2 clonal strain. PFGE revealed two clusters. Cluster I included 18 isolates, 16 of them indistinguishable from strains producing CTX-M-15 previously described in Madrid. The five isolates of Cluster II had the IS26 linked to blaCTX-M-15 and the afa/dra operon. In Cluster I isolates, no mutations in glpT, uhpT, uhpA, ptsI, cyaA and murA were detected. Cluster II isolates showed a 15 bp deletion (A169–C183) in uhpA.

Conclusions: Fosfomycin resistance in urinary E. coli has increased due to the acquisition of this resistance by a previously circulating CTX-M-15-producing E. coli O25b-ST131-phylogroup B2 strain. This happened during a period when the use of fosfomycin increased by 50%.

Keywords: urinary tract infections , antibiotic consumption , extended-spectrum β-lactamases


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