Options
Clonal spread of CC17 vancomycin-resistant Enterococcus faecium with multilocus sequence type 78 (ST78) and a novel ST444 in Taiwan
Type
article
Resource
European Journal of Clinical Microbiology and Infectious Diseases. 29(2010): 25-30.
Date Issued
2009
2012-02-01
Author(s)
Hsieh,Yu-Chia; Lee,Wen-Sen; Ou,Tsong-Yih; Hsueh,Po-Ren
Subjects
內科學科
Abstract
From May 2007 to January 2008, 30 isolates of
vancomycin-resistant enterococci (VRE), including 29 Enterococcus faecium (96.7%) and 1 E. faecalis (3.3%) were obtained from various clinical specimens of 30 patients treated at a university hospital in Taiwan. Among these patients, 27 had VRE infections, including urinary tract infection (n=16), bacteremia (n=5), wound infection (n=5), and central nervous system infection (n=1). Three
patients had VRE colonization. All of these isolates belonged to the vanA genotype with vancomycin minimum inhibitory concentrations of 64≥128 μg/ml. The isolate of E. faecalis had VanB phenotype-vanA genotype. All these isolates were susceptible to linezolid and were inhibited by tigecycline at 0.25 μg/ml. Multilocus sequence typing (MLST) analysis of the E. faecium isolates showed that 82.8% were ST78, which belongs to lineage C1. Transposon typing classified the 30 isolates of VRE into three types and most of the Tn1546-like elements contained an IS1251-
like insertion sequence. Mating experiments showed that the vanA gene clusters were transferable at a frequency of about 10−6 to 10−7. Our findings indicate that nosocomial
spread of VRE resulted from dissemination of lineage C1 E. faecium clones, including a novel E. faecium MLST type(ST444), and the horizontal transfer of Tn1546 elements among enterococci.
vancomycin-resistant enterococci (VRE), including 29 Enterococcus faecium (96.7%) and 1 E. faecalis (3.3%) were obtained from various clinical specimens of 30 patients treated at a university hospital in Taiwan. Among these patients, 27 had VRE infections, including urinary tract infection (n=16), bacteremia (n=5), wound infection (n=5), and central nervous system infection (n=1). Three
patients had VRE colonization. All of these isolates belonged to the vanA genotype with vancomycin minimum inhibitory concentrations of 64≥128 μg/ml. The isolate of E. faecalis had VanB phenotype-vanA genotype. All these isolates were susceptible to linezolid and were inhibited by tigecycline at 0.25 μg/ml. Multilocus sequence typing (MLST) analysis of the E. faecium isolates showed that 82.8% were ST78, which belongs to lineage C1. Transposon typing classified the 30 isolates of VRE into three types and most of the Tn1546-like elements contained an IS1251-
like insertion sequence. Mating experiments showed that the vanA gene clusters were transferable at a frequency of about 10−6 to 10−7. Our findings indicate that nosocomial
spread of VRE resulted from dissemination of lineage C1 E. faecium clones, including a novel E. faecium MLST type(ST444), and the horizontal transfer of Tn1546 elements among enterococci.