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Journal of Clinical Microbiology, February 2008, p. 707-712, Vol. 46, No. 2
0095-1137/08/$08.00+0     doi:10.1128/JCM.01943-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Molecular Epidemiology of Extended-Spectrum β-Lactamases among Escherichia coli Isolates Collected in a Swedish Hospital and Its Associated Health Care Facilities from 2001 to 2006{triangledown}

Hong Fang,* Ferda Ataker, Göran Hedin, and Kathrine Dornbusch

Department of Clinical Microbiology, Karolinska University Hospital Huddinge, Karolinska Institute, SE-141 86 Stockholm, Sweden

Received 2 October 2007/ Returned for modification 1 November 2007/ Accepted 5 December 2007

The genetic characteristics and molecular epidemiology of extended-spectrum β-lactamases (ESBLs) among Escherichia coli isolates were investigated at a general hospital and its associated health care facilities in Stockholm, Sweden, during the period from 2001 to 2006. Of 87 consecutive nonduplicate ESBL-positive isolates, 80 isolates encoded CTX-M-type ESBLs, 64 of which were group 1 enzymes. TEM-type and OXA-type β-lactamases were encoded in 63 and 59% of the ESBL isolates, respectively. Pulsed-field gel electrophoresis (PFGE) analysis revealed 40 different pulsotypes, consisting of 11 clones accounting for 66% of all isolates, and 29 unique patterns. Moreover, of the 11 clones, clones 1 and 4 comprised half of the clonally related isolates (28 of 57). Clone 1 was a persistent endemic clone in the area throughout the years, and clone 4 emerged in 2003. However, in recent years, clone 1 isolates were no longer predominant and were gradually replaced by new emerging strains. Concerning β-lactamase gene profiles in relation to PFGE pulsotypes, clone-related bla profiles were observed in certain clones, while in most cases different bla profiles could be observed in the same clone, and the same bla profile could be present in different clones. The molecular epidemiology of ESBL-positive E. coli in the area shows shifts in predominant strains and increased clonal diversity over time. The study also indicated that both clonal spread of epidemic strains and transfer of transposable genetic elements might contribute to the proliferation of ESBLs.

* Corresponding author. Mailing address: Department of Clinical Microbiology, F68, Karolinska University Hospital Huddinge, SE-141 86 Stockholm, Sweden. Phone: 46 8 58581357. Fax: 46 8 58581080. E-mail: hong.fang{at}karolinska.se

{triangledown} Published ahead of print on 19 December 2007.

Journal of Clinical Microbiology, February 2008, p. 707-712, Vol. 46, No. 2
0095-1137/08/$08.00+0     doi:10.1128/JCM.01943-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



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