Enterococcus

Etiology

Enterococci are gram-positive, catalase-negative facultative anaerobes that grow in pairs or short chains. Most are nonhemolytic (also called γ-hemolytic) on sheep blood agar, although some isolates have α- or β-hemolytic activity. Enterococci are distinguished from most Lancefield-groupable streptococci by their ability to grow in bile and hydrolyze esculin. They are able to grow in 6.5% NaCl and hydrolyze l -pyrrolidinyl-β-naphthylamide, features used by clinical laboratories to distinguish them from group D streptococcus. Identification at the species level is achieved by differing patterns of carbohydrate fermentation.

Epidemiology

Enterococci are normal inhabitants of the gastrointestinal (GI) tract of humans and organisms throughout the animal kingdom, suggesting they are highly evolved to occupy this niche. Oral secretions and dental plaque, the upper respiratory tract, skin, and vagina may also be colonized by Enterococcus. Enterococcus faecalis is the predominant organism, with colonization usually occurring in the 1st wk of life. By the time of adulthood, E. faecalis colonization is nearly ubiquitous but accounts for a minor fraction of the intestinal microbiota in the normal host. Enterococcus faecium colonization is less consistent, although approximately 25% of adults harbor this organism, generally at very low abundance. Disruption of the normal intestinal microbiota by antibiotic exposure or hematopoietic stem cell transplantation greatly enriches for fecal enterococcal abundance and dramatically increases the risk of subsequent bloodstream infection.

E. faecalis accounts for approximately 80% of enterococcal infections, with almost all the remaining infections caused by E. faecium. Only rarely are other species, such as Enterococcus gallinarum and Enterococcus casseliflavus, associated with invasive infection, but these organisms are notable for their intrinsic low-level vancomycin resistance. Whole genome sequencing suggests that the patient's indigenous flora is the source of enterococcal infection in most cases. However, direct spread from person to person or from contaminated medical devices may occur, particularly within newborn nurseries and intensive care units (NICUs), where nosocomial spread has resulted in hospital outbreaks.

Pathogenesis

Enterococci are not aggressively invasive organisms, usually causing disease only in children with damaged mucosal surfaces or impaired immune response. Their dramatic emergence as a cause of nosocomial infection is predominantly a result of their resistance to antibiotics commonly used in the hospital setting. Hospital-associated enterococci generally lack CRISPR (clustered regularly interspaced short palindromic repeat) elements. Their diverse antimicrobial resistance repertoire is likely related to deficient CRISPR-mediated defense against phage-mediated horizontal gene transfer. Secreted and cell surface molecules are implicated in pathogenesis. Adhesion-promoting factors such as the surface protein Eps likely account for the propensity of these organisms to cause endocarditis and urinary tract infections (UTIs). The ability to form biofilms likely facilitates the colonization of urinary and vascular catheters. Other proposed virulence factors include cytolysin, aggregation substance, gelatinase, and extracellular superoxide.