Enterococcus faecalis

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Not to be confused with Enterococcus faecium.
This is a Gram stain for Enterococcus faecalis under 1000 magnification (bright field microscopy)
Enterococcus faecalis
Enterococcus faecalis20023-300.jpg
Scientific classification
Domain: Bacteria
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Bacilli
Order: Lactobacillales
Family: Enterococcaceae
Genus: Enterococcus
Species: faecalis
Binomial name
Enterococcus faecalis

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.[1] 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.[1] E. faecalis has been frequently found in root canal-treated teeth in prevalence values ranging from 30% to 90% of the cases.[2] Root canal-treated teeth are about nine times more likely to harbor E. faecalis than cases of primary infections.[3]

Physiology[edit]

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].

Pathogenesis[edit]

E. faecalis can cause endocarditis and bacteremia, urinary tract infections (UTI), meningitis, and other infections in humans.[4][5] 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.[6][7][8] A plasmid-encoded factor called "aggregation substance" is also important for virulence in animal models of infection.[7][9]

Antibacterial resistance[edit]

E. faecalis is resistant to many commonly used antimicrobial agents (aminoglycosides, aztreonam, cephalosporins, clindamycin, the semisynthetic penicillins nafcillin and oxacillin, and trimethoprim-sulfamethoxazole).[citation needed] Resistance to vancomycin in E. faecalis is becoming more common.[10][11] Treatment options for vancomycin-resistant E. faecalis include nitrofurantoin (in the case of uncomplicated UTIs),[12] linezolid, and daptomycin, although ampicillin is preferred if the bacteria are susceptible.[13] Quinupristin/dalfopristin can be used to treat Enterococcus faecium but not E. faecalis.[13]

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.[14]

Survival and Virulence Factors[edit]

  • 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]

Historical[edit]

Prior to 1984, enterococci were members of the genus Streptococcus: thus E. faecalis was known as Streptococcus faecalis.[15]

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.[16]

See also[edit]

References[edit]

  1. ^ a b Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 294––5. ISBN 0-8385-8529-9. 
  2. ^ Molander A, Reit C, Dahlen G, Kvist T: Microbiological status of root-filled teeth with apical periodontitis, Int Endod J 31:1, 1998
  3. ^ Rocas, IN, Siquiera JF, Jr., Santos KR: Association of Enterococcus faecalis with different forms of periradicular diseases, J Endod 30:315, 2004.
  4. ^ Murray, BE. (Jan 1990). "The life and times of the Enterococcus.". Clin Microbiol Rev 3 (1): 46–65. PMC 358140. PMID 2404568. 
  5. ^ Hidron AI, Edwards JR, Patel J, et al. (November 2008). "NHSN annual update: antimicrobial-resistant pathogens associated with healthcare-associated infections: annual summary of data reported to the National Healthcare Safety Network at the Centers for Disease Control and Prevention, 2006-2007". Infect Control Hosp Epidemiol 29 (11): 996–1011. doi:10.1086/591861. PMID 18947320. 
  6. ^ Huycke, MM.; Spiegel, CA.; Gilmore, MS. (Aug 1991). "Bacteremia caused by hemolytic, high-level gentamicin-resistant Enterococcus faecalis.". Antimicrob Agents Chemother 35 (8): 1626–34. doi:10.1128/aac.35.8.1626. PMC 245231. PMID 1929336. 
  7. ^ a b Chow, JW.; Thal, LA.; Perri, MB.; Vazquez, JA.; Donabedian, SM.; Clewell, DB.; Zervos, MJ. (Nov 1993). "Plasmid-associated hemolysin and aggregation substance production contribute to virulence in experimental enterococcal endocarditis.". Antimicrob Agents Chemother 37 (11): 2474–7. doi:10.1128/aac.37.11.2474. PMC 192412. PMID 8285637. 
  8. ^ Ike, Y.; Hashimoto, H.; Clewell, DB. (Aug 1984). "Hemolysin of Streptococcus faecalis subspecies zymogenes contributes to virulence in mice.". Infect Immun 45 (2): 528–30. PMC 263283. PMID 6086531. 
  9. ^ Hirt, H.; Schlievert, PM.; Dunny, GM. (Feb 2002). "In vivo induction of virulence and antibiotic resistance transfer in Enterococcus faecalis mediated by the sex pheromone-sensing system of pCF10.". Infect Immun 70 (2): 716–23. doi:10.1128/iai.70.2.716-723.2002. PMC 127697. PMID 11796604. 
  10. ^ Amyes SG (May 2007). "Enterococci and streptococci". Int. J. Antimicrob. Agents. 29 Suppl 3: S43–52. doi:10.1016/S0924-8579(07)72177-5. PMID 17659211. 
  11. ^ Courvalin P (January 2006). "Vancomycin resistance in gram-positive cocci". Clin. Infect. Dis. 42 Suppl 1: S25–34. doi:10.1086/491711. PMID 16323116. 
  12. ^ Zhanel GG, Hoban DJ, Karlowsky JA (January 2001). "Nitrofurantoin is active against vancomycin-resistant enterococci". Antimicrob. Agents Chemother. 45 (1): 324–6. doi:10.1128/AAC.45.1.324-326.2001. PMC 90284. PMID 11120989. 
  13. ^ a b Arias, CA.; Contreras, GA.; Murray, BE. (Jun 2010). "Management of multidrug-resistant enterococcal infections.". Clin Microbiol Infect 16 (6): 555–62. doi:10.1111/j.1469-0691.2010.03214.x. PMID 20569266. 
  14. ^ Estrela C1, Silva JA, de Alencar AH, Leles CR, Decurcio DA. 2008) Efficacy of sodium hypochlorite and chlorhexidine against Enterococcus faecalis--a systematic review http://www.ncbi.nlm.nih.gov/pubmed/19082392
  15. ^ Schleifer KH; Kilpper-Balz R (1984). "Transfer of Streptococcus faecalis and Streptococcus faecium to the genus Enterococcus nom. rev. as Enterococcus faecalis comb. nov. and Enterococcus faecium comb. nov". Int. J. Sys. Bacteriol. 34: 31–34. doi:10.1099/00207713-34-1-31. 
  16. ^ Jaremko, M., Jaremko, L., Kim, H.-Y., Cho, M.-K., Schwieters, C. D., Giller, K., Becker,S., Zweckstetter, M. (2013). "Cold denaturation of a protein dimer monitored at atomicresolution". Nat. Chem. Biol. 9: 264–270. doi:10.1038/nchembio.1181. PMID 23396077.