Korean J Lab Med.
2005 Feb;25(1):39-45.
Antimicrobial Susceptibities and PFGE Patterns of Vancomycin-Resistant Enterococcus isolated from Clinical Specimens and Chickens
- Affiliations
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- 1Department of Laboratory Medicine and Research Institute of Bacterial Resistance, Yonsei University College of Medicine, Seoul, Korea. leekcp@yumc.yonsei.ac.kr
- 2Department of Laboratory Medicine, Ajou University School of Medicine, Suwon, Korea.
- 3Division of Infectious Disease, Department of Internal Medicine, The Catholic University of Korea, Seoul, Korea.
Abstract
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BACKGROUND: Enterococcal infections have become extremely difficult to manage because of an increase in antibiotic resistance among enterococci. In Europe, the use of avoparcin in animals was reported to be the cause of vancomycin-resistant enterococci (VRE) transmission to humans. In this study, we performed antimicrobial susceptibility testing and pulsed-field gel electrophoresis (PFGE) to characterize the genetic relatedness of VRE of human and chicken.
METHODS
Ninety strains of VRE were isolated from clinical specimens in three University hospitals located in Seoul and Kyungi province in 2001-2002. Thirty isolates of VRE were collected from four chicken farms located in areas remotely distanced from each other. The isolates were identified to the species level by conventional biochemical tests and commercial kits. Antimicrobial susceptibilities were tested by the NCCLS disk diffusion and agar dilution methods. For a molecular epidemiologic analysis, PFGE was performed.
RESULTS
Among the 90 clinical isolates were 73 vancomycin-resistant Enterococcus faecium (VREFM) and 17 vancomycin-resistant E. faecalis (VREFA). The resistant rates of VREFA to ampicillin, levofloxacin and tetracycline were 0%, 100%, and 100%, respectively, and for VREFM, 100%, 96%, and 26%, respectively. However, the resistant rates of VREFM isolated from chicken were 19% to ampicillin, 0% to levofloxacin, and 100% to tetracycline. The PFGE patterns of genomic DNA of the clinical isolates were very diverse, suggesting a polyclonal spread of VRE, although some isolates had an identical PFGE pattern, indicating a mini-outbreak due to a clonal spread. The PFGE patterns of genomic DNA of the chicken isolates were very different from those of the human isolates.
CONCLUSIONS
VRE isolates from human and chicken showed very different antimicrobial susceptibilities and PFGE patterns. These results suggest that VRE isolated from human and chicken are not closely related genetically.
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