Objectives: Vancomycin-resistant enterococci (VRE) are reported to increase in numbers in European hospitals. Vancomycin resistance can be encoded by seven different genes but only vanA and to a lesser extent vanB are widely prevalent among clinical isolates of enterococci. The E. faecium clonal complex 17 (CC17) has been associated with nosocomial outbreaks in five continents. The aim of the present study was to elucidate the molecular epidemiology of VRE in Denmark. Methods: From January 2005 through October 2008, 61 vancomycin resistant enterococcal isolates causing invasive as well as non-invasive infections were referred by seven of the 15 Danish departments of clinical microbiology to Statens Serum Institut. All isolates were identified to species level by PCR, MICs of vancomycin were determined (Trek Diagnostic Systems, UK), and the presence of vanA, vanB and vanC genes were detected by PCR. Multi locus sequence typing (MLST) was performed on the vancomycin-resistant E. faecium isolates. Results: The collection consisted of 45 E. faecium and 16 E. faecalis isolates which originated from 12 different hospitals. Thirty three of 45 E. faecium isolates were vanA positive and the remaining 12 isolates were vanB positive. All but one of the E. faecalis isolates contained the vanB gene (n = 15) and the remaining isolate contained the vanA gene. MLST of the 45 E. faecium isolates revealed 10 different sequence types (ST). The STs were ST18 (n = 21), ST203 (n = 8), ST78 (n = 3), ST192 (n = 3), ST412 (n = 3), ST16 (n = 2), ST17 (n = 2), ST65 (n = 1), ST80 (n = 1), and ST306 (n = 1). Forty four (98%) of the 45 tested isolates belonged to CC17. The 45 E. faecium isolates originated from nine different hospitals. Each hospital was mainly dominated by one specific ST; however, ST18 was present in three of the nine hospitals. Conclusion: The vanA gene was the most common in E. faecium isolates whereas vanB was predominant in E. faecalis isolates. Most of the vancomycin-resistant E. faecium isolates belonged to the hospital-acquired clonal complex 17.
Clinical Microbiology and Infection, 2009, Issue Suppl 4
Main Research Area:
19th Congress of Clinical Microbiology and Infectious Diseases, 2009