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JAC Advance Access published online on March 4, 2008

Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkn066
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© The Author 2008. 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

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

Ayla Ergani-Ozcan1, Thierry Naas2,*, Betil Ozhak Baysan1, Dilara Ogunc1, Dilara Inan3, Dilek Colak1 and Patrice Nordmann2

1 Medical Microbiology Department, Akdeniz University School of Medicine, Antalya, Turkey; 2 Service de Bactériologie-Virologie, INSERM U914: Emerging Resistance to Antibiotics, Hôpital de Bicêtre, Assistance Publique—Hôpitaux de Paris, K.-Bicêtre, France; 3 Infectious Diseases and Clinical Microbiology Department, Akdeniz University School of Medicine, Antalya, Turkey

Received 6 November 2007; returned 25 January 2008; revised 30 November 2007; accepted 26 January 2008


* Corresponding author. Tel: +33-1-45-21-29-86; Fax: +33-1-45-21-63-40; E-mail: thierry.naas{at}bct.ap-hop-paris.fr

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.

Key Words: VRE , vanA , Tn1546 , MLST


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