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. 2008 May;61(5):1033-9.
doi: 10.1093/jac/dkn066. Epub 2008 Mar 4.

Nosocomial outbreak of vancomycin-resistant Enterococcus faecium in a paediatric unit at a Turkish university hospital

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Nosocomial outbreak of vancomycin-resistant Enterococcus faecium in a paediatric unit at a Turkish university hospital

Ayla Ergani-Ozcan et al. J Antimicrob Chemother. 2008 May.

Abstract

Background: Despite growing concern about vancomycin-resistant enterococci (VRE) as nosocomial pathogens, especially in the USA, they have been rarely isolated in Turkish hospitals. After initial description in 2001 of unrelated VRE isolates, we report now the molecular characterization of a nosocomial outbreak at the Akdeniz University Hospital, Antalya, Turkey.

Methods: VRE isolates were from either clinical or rectal swab specimens. Identification, susceptibility testing and molecular characterization were performed according to standard techniques. Virulence genes (encoding aggregation substance, gelatinase, cytolysin, enterococcal surface protein and hyaluronidase) were sought by PCR.

Results: Thirty-six VRE were isolated from 10 patients between June and October 2005 in the Department of Paediatrics. Six patients were only carriers, two had urinary tract infections and two had bloodstream infections. All isolates were Enterococcus faecium, of vanA genotype and belonged either to a main pulsotype (A) or to three minor pulsotypes (B, C and D). The epidemic strain A, found in eight patients, expressed high-level glycopeptide resistance (MIC of vancomycin 256 mg/L and MIC of teicoplanin 64 mg/L) and was of multilocus sequence typing sequence type (ST) 31, whereas the minor strain D, found in two patients, expressed heterogeneous glycopeptide resistance (MIC of vancomycin 8 to 256 mg/L) and was ST18. Strains B and C were only found in single patients either with strain A or alone. The two epidemic strains A and D were esp gene-positive. Their vanA genes were located on transposons similar to Tn1546, except for deletion of the transposition genes and the presence of IS1542, inserted upstream of the vanA operon, and IS1216, inserted at the 3' end of the vanX gene. VRE outbreak was contained by early identification and implementation of measures for patient isolation and of stringent hand and environmental disinfection policies.

Conclusions: This work underlines the emergence in Turkey of epidemic VRE clones that belong to the clonal complex-17 (CC-17) and that are esp-positive.

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