Genome-based characterization of hospital-adapted Enterococcus faecalis lineages

Abstract

Vancomycin-resistant Enterococcus faecalis (VREfs) is an important nosocomial pathogen1,2. We undertook whole genome sequencing of E. faecalis associated with bloodstream infection in the UK and Ireland over more than a decade to determine the population structure and genetic associations with hospital adaptation. Three lineages predominated in the population, two of which (L1 and L2) were nationally distributed, and one (L3) geographically restricted. Genome comparison with a global collection identified that L1 and L3 were also present in the USA, but were genetically distinct. Over 90% of VREfs belonged to L1-L3, with resistance acquired and lost multiple times in L1 and L2, but only once followed by clonal expansion in L3. Putative virulence and antibiotic resistance genes were over-represented in L1, L2 and L3 isolates combined, versus the remainder. Each of the three main lineages contained a mixture of

Pathogen colonization of the gastrointestinal microbiome at intensive care unit admission and risk for subsequent death or infection

“…For Enterococcus , the pathogen that best predicted death or infection, sequencing results were closely comparable to results from VRE cultures. Gain and loss of resistance is common for hospital E. faecalis lineages and domination may be an important marker even in the absence of vancomycin resistance [27]. …”

Partial Diversity Generates Effector Immunity Specificity of the Bac41-Like Bacteriocins of Enterococcus faecalis Clinical Strains

“…Table S1). Notably, of 100 strains belonging to clonal complex 2 (CC2), which is the major hospital-adapted lineage, containing ST2 and ST6 (44,45), 71 strains (71%) were Bac41 positive. In contrast, for 11 strains of the other major lineage, ST40, there were no Bac41-positive strains.…”

Tracing the Enterococci from Paleozoic Origins to the Hospital

“…Most MDR enterococci belong to highly hospital-adapted lineages (Lebreton et al, 2013a; Raven et al, 2016). MDR enterococci differ from commensals in lacking CRISPR defenses (Palmer et al, 2010), and possess genomes that are often >25% larger than commensals through accretion of mobile elements –phages, pathogenicity islands and resistance genes (Shankar et al, 2002; Paulsen et al, 2003).…”