A potential virulence gene, hylEfm, predominates in Enterococcus faecium of clinical origin

被引：195

作者：

Rice, LB

Carias, L

Rudin, S

Vael, C

Goossens, H

Konstabel, C

Klare, I

Nallapareddy, SR

Huang, WX

Murray, BE

机构：

[1] Case Western Reserve Univ, Louis Stokes Cleveland Vet Affairs Med Ctr, Res Serv, Cleveland, OH USA

[2] Case Western Reserve Univ, Louis Stokes Cleveland Vet Affairs Med Ctr, Med Serv, Cleveland, OH USA

[3] Univ Texas, Sch Med, Dept Internal Med,Div Infect Dis, Ctr Study Emerging & Reemerging Pathogens, Houston, TX USA

[4] Univ Texas, Sch Med, Dept Microbiol,Div Infect Dis, Ctr Study Emerging & Reemerging Pathogens, Houston, TX USA

[5] Univ Texas, Sch Med, Dept Mol Genet,Div Infect Dis, Ctr Study Emerging & Reemerging Pathogens, Houston, TX USA

[6] Univ Antwerp Hosp, Dept Microbiol, Belgian Reference Ctr Enterococci, Antwerp, Belgium

[7] Robert Koch Inst, Wernigerode Branch, Wernigerode, Germany

来源：

JOURNAL OF INFECTIOUS DISEASES | 2003年 / 187卷 / 03期

关键词：

D O I：

10.1086/367711

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

An open reading frame (hyl(Efm)) with homologies to previously described hyaluronidase genes has been identified in nonstool isolates of Enterococcus faecium. E. faecium isolates (n = p) from diverse sources were screened for the presence of 577 hyl(Efm) and esp(Efm), a putative virulence gene associated with epidemic E. faecium strains. The presence of esp(Efm) was roughly twice that of hyl(Efm), but both were found primarily in vancomycin-resistant E. faecium isolates in nonstool cultures obtained from patients hospitalized in the United States. These data suggest that specific E. faecium strains may be enriched in determinants that make them more likely to cause clinical infections. Differences in the prevalence of these strains may help explain variations in the clinical importance of multi-resistant E. faecium across different continents.

引用

页码：508 / 512

页数：5

共 15 条

[1] Additive attenuation of virulence of Streptococcus pneumoniae by mutation of the genes encoding pneumolysin and other putative pneumococcal virulence proteins [J].