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The Changing Molecular Epidemiology and Establishment of Endemicity of Vancomycin Resistance in Enterococci at One Hospital over a 6‐Year Period
Author(s) -
Woo Joo Kim,
Robert A. Weinstein,
Mary K. Hayden
Publication year - 1999
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/314564
Subject(s) - enterococcus faecium , vancomycin resistant enterococci , pulsed field gel electrophoresis , genotype , molecular epidemiology , microbiology and biotechnology , biology , enterococcus , plasmid , polymerase chain reaction , strain (injury) , vancomycin , epidemiology , streptococcaceae , virology , genetics , bacteria , antibiotics , staphylococcus aureus , medicine , dna , gene , anatomy
The contributions of clonal spread, transfer of genetic elements, and introduction of new strains to the establishment of endemicity of vancomycin-resistant enterococci (VRE) were determined. The study took place at one hospital between 1990, when VRE were first detected, and 1996, when endemicity had become established. Isolates from 183 patients were categorized into 24 strain types by pulsed-field gel electrophoresis; the resistance genotype was determined by polymerase chain reaction. Between 1990 and 1993, 69% of patients were infected with the same vanB Enterococcus faecium strain. VanA resistance was not detected until 1993, but in 1996, the ratio of vanA to vanB was 2.2:1. Over time, 8 vanA strains were detected; a 35- or 40-kb conjugative vanA plasmid was found in 4 of the 8 strains. Clonal spread was a major factor in the establishment of endemicity. Transfer of genetic elements and introduction of new strain types were detected less often. However, these events may have been equally important evolutionarily.

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