Molecular characterisation of outbreak-related strains of vancomycin-resistant Enterococcus faecium from an intensive care unit in Beijing, China
Introduction
The isolation of vancomycin-resistant enterococci (VRE) was first reported in 1988 in the UK and France, and shortly thereafter, VRE was detected in hospitals in the USA. Since then, VRE have emerged with unanticipated rapidity and are now encountered in most hospitals.1, 2, 3 Patients in intensive care units (ICUs) are frequently affected, mainly because they are severely ill, and heavily exposed to multiple antibiotics and exogenous colonisation pressure.4
To our knowledge this is the first study that has characterised the phenotypic and molecular features of VRE isolated from an intensive care unit in Mainland China.
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Bacterial strains and culture media
Eighteen isolates of vanA type Enterococcus faecium isolated from 15 patients within one year were used in this study (Table I). Enterococci were grown in Todd–Hewitt broth (THB). Type strains E. faecium WHO03 and E. faecalis WHO14 having VanA and VanB phenotypes were used as controls.
Antimicrobial susceptibility testing
Glycopeptide resistance levels were determined by the agar dilution method. An overnight culture of the strains grown in Mueller–Hinton broth was diluted 100-fold with fresh broth. A total of 100 μL of each
Isolation and characterisation of vanA-type vancomycin-resistant E. faecium
During an outbreak affecting 14 patients in a 20-bed ICU (incidence 3.56 cases per 1000 ICU patient-days) between September 2006 and August 2007, 18 strains of vancomycin-resistant E. faecium were isolated. These were the first VRE to be isolated from that ICU. We screened the stool of all patients in the ICU on 7 September 2006 and five of 14 patients carried VRE. One year after the first VRE strain was isolated we screened stool samples on August 6 2007 and four of 16 patients were found
Discussion
Recently, genetic population studies have shown that a majority of vancomycin-resistant E. faecium strains associated with nosocomial infections worldwide are part of the same lineage called CC17.14 CC17 strains are generally resistant to ampicillin and carry genes for putative virulence factors, such as esp.15 Our study supports this observation and the outbreak strains showed an antibiotic resistance profile and virulence genes similar to those described for CC17. It has been argued that
Acknowledgements
We thank H. Grundmann for reviewing the manuscript.
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