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Journal of Antimicrobial Chemotherapy (2003) 52, 162-167
© 2003 The British Society for Antimicrobial Chemotherapy

Genetic relatedness among Enterococcus faecalis with transposon-mediated high-level gentamicin resistance in Swedish intensive care units

Anita Hällgren1,*, Baharak Saeedi1, Maud Nilsson1, Hans-Jürg Monstein2, Barbro Isaksson1, Håkan Hanberger3 and Lennart E. Nilsson1

Divisions of 1 Clinical Microbiology and 3 Infectious Diseases, Department of Molecular and Clinical Medicine and 2 Department of Biomedicine and Surgery, Faculty of Health Sciences, S-581 85 Linköping, Sweden

Received 3 May 2002; returned 30 May 2002, revised 24 April 2003; accepted 2 May 2003

We studied 45 isolates of Enterococcus faecalis with high-level gentamicin resistance (HLGR), all but one concomitantly resistant to ciprofloxacin, and 25 ciprofloxacin-resistant isolates without HLGR for genetic relatedness using pulsed-field gel electrophoresis (PFGE). E. faecalis were isolated from patients admitted to intensive care units at eight hospitals in southern Sweden from December 1996 through December 1998. Genomic analysis by PFGE resulted in three clusters of genetically related isolates (designated clusters I, II and III) and 23 unique clones. Cluster I was found predominantly in the eastern and central parts of southern Sweden and clusters II and III in south-western Sweden. Among the 45 isolates with HLGR, 69% belonged to cluster I, 20% to cluster II, and 11% had unique PFGE patterns, which suggests that the majority of isolates with HLGR are closely related. Among the 25 ciprofloxacin-resistant isolates without HLGR, 68% had unique PFGE patterns, 12% belonged to cluster I and 20% to cluster III, which suggests the ciprofloxacin-resistant isolates are not related. All isolates with HLGR contained the aac(6')Ie-aph(2'')Ia gene, which was carried on a Tn5281-like transposon in all isolates except one. We conclude that HLGR in E. faecalis was mainly due to dissemination of genetically related clones during the time studied, and that HLGR in these isolates was due to the presence of the aac(6')Ie-aph(2'')Ia gene.

Keywords: enterococcus, high-level gentamicin resistance, pulsed-field gel electrophoresis, transposon

* Corresponding author. Tel: +46-13-222000; Fax: +46-13-224596; E-mail: aniha{at}imk.liu.se


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