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Enterococcus faecalis

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Title: Enterococcus faecalis  
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Enterococcus faecalis

Enterococcus faecalis
Scientific classification
Domain: Bacteria
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Cocci
Order: Lactobacillales
Family: Enterococcaceae
Genus: Enterococcus
Species: E. 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]


Contents

  • Physiology 1
  • Pathogenesis 2
  • Antibacterial resistance 3
  • Survival and virulence factors 4
  • Historical 5
  • Genome structure 6
  • See also 7
  • References 8

Physiology

E. faecalis is a Aerotolerant 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. It shows consistent growth throughout nutrient broth which is consistent with being an aerotolerant anaerobe. They catabolize a variety of energy sources including glycerol, lactate, malate, citrate, arginine, agmatine, and many keto acids. Enterococci survive very harsh environments including extremely 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 to 45°C and survive at temperatures of 60°C for 30 min.[4]

Pathogenesis

E. faecalis can cause endocarditis and bacteremia, urinary tract infections, meningitis, and other infections in humans.[5][6] 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.[7][8][9] A plasmid-encoded factor called "aggregation substance" is also important for virulence in animal models of infection.[8][10]

This is a Gram stain for Enterococcus faecalis under 1000 magnification (bright field microscopy)

Antibacterial resistance

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.[11][12] Treatment options for vancomycin-resistant E. faecalis include nitrofurantoin (in the case of uncomplicated UTIs),[13] linezolid, and daptomycin, although ampicillin is preferred if the bacteria are susceptible.[14] Quinupristin/dalfopristin can be used to treat Enterococcus faecium but not E. faecalis.[14]

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.[15]

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[16]

Historical

Prior to 1984, enterococci were members of the genus Streptococcus; thus, E. faecalis was known as Streptococcus faecalis.[17]

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.[18]

Genome structure

The E. faecalis genome contains 3,22 Mbp with 3,113 protein-coding genes.[19]

See also

References

  1. ^ a b Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed.). McGraw Hill. pp. 294––5.  
  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. ^ Stuart et al. 2006
  5. ^ Murray, BE. (Jan 1990). "Enterococcus"The life and times of the . Clin Microbiol Rev 3 (1): 46–65.  
  6. ^ 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.  
  7. ^ Huycke, MM.; Spiegel, CA.; Gilmore, MS. (Aug 1991). "Enterococcus faecalis"Bacteremia caused by hemolytic, high-level gentamicin-resistant . Antimicrob Agents Chemother 35 (8): 1626–34.  
  8. ^ 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.  
  9. ^ Ike, Y.; Hashimoto, H.; Clewell, DB. (Aug 1984). contributes to virulence in mice"zymogenes subspecies Streptococcus faecalis"Hemolysin of . Infect Immun 45 (2): 528–30.  
  10. ^ Hirt, H.; Schlievert, PM.; Dunny, GM. (Feb 2002). mediated by the sex pheromone-sensing system of pCF10"Enterococcus faecalis"In vivo induction of virulence and antibiotic resistance transfer in . Infect Immun 70 (2): 716–23.  
  11. ^ Amyes SG (May 2007). "Enterococci and streptococci". Int. J. Antimicrob. Agents. 29 Suppl 3: S43–52.  
  12. ^ Courvalin P (January 2006). "Vancomycin resistance in Gram-positive cocci". Clin. Infect. Dis. 42 Suppl 1: S25–34.  
  13. ^ Zhanel GG, Hoban DJ, Karlowsky JA; Hoban; Karlowsky (January 2001). "Nitrofurantoin is active against vancomycin-resistant enterococci". Antimicrob. Agents Chemother. 45 (1): 324–6.  
  14. ^ a b Arias, CA.; Contreras, GA.; Murray, BE. (Jun 2010). "Management of multidrug-resistant enterococcal infections". Clin Microbiol Infect 16 (6): 555–62.  
  15. ^ Estrela, C; Silva, J. A.; De Alencar, A. H.; Leles, C. R.; Decurcio, D. A. (2008). "Efficacy of sodium hypochlorite and chlorhexidine against Enterococcus faecalis--a systematic review". Journal of applied oral science : revista FOB 16 (6): 364–8.  
  16. ^ Review Article Stuart et al. JOE 2006
  17. ^ 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.  
  18. ^ Jaremko, M., Jaremko, L., Kim, H.-Y., Cho, M.-K., Schwieters, C. D., Giller, K., Becker,S., Zweckstetter, M.; Jaremko; Kim; Cho; Schwieters; Giller; Becker; Zweckstetter (2013). "Cold denaturation of a protein dimer monitored at atomicresolution". Nat. Chem. Biol. 9 (4): 264–270.  
  19. ^ Paulsen, IT.; Banerjei, L.; Myers, GS.; Nelson, KE.; Seshadri, R.; Read, TD.; Fouts, DE.; Eisen, JA.; et al. (Mar 2003). "Role of mobile DNA in the evolution of vancomycin-resistant Enterococcus faecalis". Science 299 (5615): 2071–4.  
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