Emergence of CC17Enterococcus faecium: from commensal to hospital-adapted pathogen

Abstract

For many years, Enterococcus faecium was considered to be a commensal of the digestive tract, which only sporadically caused opportunistic infections in severely ill patients. Over the last two decades, vancomycin-resistant E. faecium (VREF) has emerged worldwide as an important cause of nosocomial infections, especially in immunocompromised patients. The global Vancomycin-resistant enterococci (VRE) epidemic was preceded by the emergence of ampicillin-resistant E. faecium (AREfm) in the United States in the early 1980s, followed by the rapid emergence of VRE in the 1990s. A similar increase of VRE may occur in countries with still low levels of VRE in hospitals (such as The Netherlands), but increasing incidence of AREfm infections. Molecular epidemiological studies of both human- and animal-derived E. faecium isolates using multilocus sequence typing revealed the existence of host-specific genogroups, including a specific genetic lineage designated CC17, associated with hospital-related isolates. These strains were characterized by ampicillin and quinolone resistance. In addition, the majority of these CC17 isolates contain over hundred hospital-clade-specific genes, including mobile elements, phage genes and plasmid sequences, hypothetical and membrane proteins and antibiotic and regulatory genes and a putative pathogenicity island including the esp gene.

Screening municipal wastewater effluent and surface water used for drinking water production for the presence of ampicillin and vancomycin resistant enterococci

“…This natural resistance was mainly found in E. faecium and E. faecalis, but was also described in E. raffinosus strains (Facklam et al, 2002). On top of the intrinsically present resistance to beta-lactams and aminoglycosides, hospital-derived E. faecium has acquired resistance to high levels of aminoglycosides and beta-lactams (including ampicillin) through a combination of mutations and horizontal gene transfer (Top et al, 2008a). VRE infections are caused mostly by E. faecalis and E. faecium (Cetinkaya et al, 2000;Jett et al, 1994;Marothi et al, 2005).…”

Multidrug-resistant enterococci in the hospital environment: detection of novel vancomycin-resistant E. faecium clone ST910

“…The expansion of E. faecium isolates belonging to clonal complex (CC17) is remarkable [9]. This epidemic clonal complex is characterized by ampicillin and vancomycin resistance, as well as by the presence of virulence determinants such as hylEfm (encoding a hyaluronidase-like protein) and a putative pathogenicity island that includes espEfm (enterococcal surface protein in E. faecium), and is responsible for severe nosocomial infections and hospital outbreaks [10,11].…”

Vancomycin-resistant Enterococcus faecium high-resolution typing by core genome multilocus sequence typing

“…This is mainly due to high genome plasticity, which allows E. faecium to acquire, by horizontal gene transfer, virulence genes and clusters, as well as antibiotic resistance determinants. Notably, the acquisition of the vancomycin resistance operons gives rise to the more worrisome vancomycin-resistant E. faecium (VREf), which is able to prompt wounds, urinary tract infections, and bacteraemia, especially in severely ill and immune-compromised patients [2], increasing length of patients' hospital stays, mortality, and healthcare costs [3].…”