Enterococcus faecalis – formerly classified as part of the Group D Streptococcus system – is a Gram-positive, commensal bacterium inhabiting the gastrointestinal tracts of humans and other mammals. Like other species in the genus Enterococcus, E. faecalis can cause life-threatening infections in humans, especially in the nosocomial (hospital) environment, where the naturally high levels of antibiotic resistance found in E. faecalis contribute to its pathogenicity. E. faecalis has been frequently found in root canal-treated teeth in prevalence values ranging from 30% to 90% of the cases. Root canal-treated teeth are about nine times more likely to harbor E. faecalis than cases of primary infections.
E. faecalis is a nonmotile, facultatively anaerobic microbe; it ferments glucose without gas production, and does not produce a catalase reaction with hydrogen peroxide. It can produce a pseudocatalase reaction if grown on blood agar. The reaction is usually weak. It produces a reduction of litmus milk, but does not liquefy gelatin. Growth on nutrient broth is consistent with being facultatively anaerobic. They catabolize a variety of energy sources including carbohydrates, glycerol, lactate, malate, citrate, arginine, agmatine, and many keto acids. Enterococci survive very harsh environments including extreme alkaline pH (9.6) and salt concentrations. They resist bile salts, detergents, heavy metals, ethanol, azide, and desiccation. They can grow in the range of 10°C to 45°C and survive at temperatures of 60°C for 30 min [Stuart et al. 2006].
E. faecalis can cause endocarditis and bacteremia, urinary tract infections (UTI), meningitis, and other infections in humans. Several virulence factors are thought to contribute to E. faecalis infections. A plasmid-encoded hemolysin, called the cytolysin, is important for pathogenesis in animal models of infection, and the cytolysin in combination with high-level gentamicin resistance is associated with a five-fold increase in risk of death in human bacteremia patients. A plasmid-encoded factor called "aggregation substance" is also important for virulence in animal models of infection.
E. faecalis is resistant to many commonly used antimicrobial agents (aminoglycosides, aztreonam, cephalosporins, clindamycin, the semisynthetic penicillins nafcillin and oxacillin, and trimethoprim-sulfamethoxazole). Resistance to vancomycin in E. faecalis is becoming more common. Treatment options for vancomycin-resistant E. faecalis include nitrofurantoin (in the case of uncomplicated UTIs), linezolid, and daptomycin, although ampicillin is preferred if the bacteria are susceptible. Quinupristin/dalfopristin can be used to treat Enterococcus faecium but not E. faecalis.
In root canal treatments NaOCl and chlorhexidine(CHX) are used to fight E. Faecalis before isolating the canal. However recent studies determined that NaOCl or CHX showed low ability to eliminate E. faecalis.
Survival and Virulence Factors
- Endures prolonged periods of nutritional deprivation
- Binds to dentin and proficiently invades dentinal tubules
- Alters host responses
- Suppresses the action of lymphocytes
- Possesses lytic enzymes, cytolysin, aggregation substance,pheromones, and lipoteichoic acid
- Utilizes serum as a nutritional source
- Resists intracanal medicaments (i.e. Ca(OH)2)
- Maintains pH homeostasis
- Properties of dentin lessen the effect of calcium hydroxide
- Competes with other cells
- Forms a biofilm
[Review Article Stuart et al. JOE 2006]
In 2013 a combination of cold denaturation and NMR spectroscopy was used to show detailed insights into the unfolding of the E. faecalis homodimeric repressor protein CylR2.
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