Enterococcus faecalis bacteria

Enterococcus faecalis

Enterococcus faecalis picture enterococcus faecalis rotating

Enterococcus faecalis on Columbia agar with 5% sheep blood. Fig. A, B, C: mixture of E. faecalis colonies and Streptococcus pyogenes (from a patient with prosthetic joint infection). Colonies are without hemolysis (gamma-hemolysis, compare with beta-hemolytic colonies of Streptococcus pyogenes) or, in some strains, surrounded by a zone of alpha-hemolysis. Rarely can be beta-hemolytic. Morphologically, the enterococci are often oval and form diplococci or short chains (liquid media).

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 animals (they are found in the intestine of nearly all animals, from cockroaches to humans [1]). E.faecalis has many biochemical and cultural features that reflect its habitat, such as the ability to grow in the presence of high concentrations of bile salts and sodium chloride.

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.
Enterococcus faecalis can cause endocarditis and bacteremia, urinary tract infections (UTI), meningitis, and other infections in humans. In the United States, Enterococcus faecalis is associated with nosocomial infections including catheter-associated UTI, central line-associated bloodstream infection, and surgical site infections. 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.

Abbreviated from Wikipedia.

Vancomycin-resistant enterococci (VRE)

Enterococci, leading causes of nosocomial bacteremia, surgical wound infection, and urinary tract infection, are becoming resistant to many and sometimes all standard therapies. New rapid surveillance methods are highlighting the importance of examining enterococcal isolates at the species level. Most enterococcal infections are caused by Enterococcus faecalis. [1]
Vancomycin-resistant enterococci (VRE), are bacterial strains of the genus Enterococcus that are resistant to the antibiotic vancomycin. VRE can be carried by healthy people who have come into contact with the bacteria, usually in a hospital, although it is thought that a significant percentage of intensively farmed chicken also carry VRE.
Six different types of vancomycin resistance are shown by enterococcus : Van-A, Van-B, Van-C, Van-D, Van-E and Van-G. The significance is that Van-A VRE is resistant to both vancomycin and teicoplanin, Van-B VRE is resistant to vancomycin but susceptible to teicoplanin, and Van-C is only partly resistant to vancomycin, and susceptible to teicoplanin.

[1] Huycke MM, Sahm DF, Gilmore MS. Multiple-Drug Resistant Enterococci: The Nature of the Problem and an Agenda for the Future. Emerg Infect Dis [serial on the Internet]. 1998, Jun.

Are certain people at risk of getting VRE?

The following persons are at increased risk becoming infected with VRE:
  • People who have been previously treated with the antibiotic vancomycin or other antibiotics for long periods of time.
  • People who are hospitalized, particularly when they receive antibiotic treatment for long periods of time.
  • People with weakened immune systems such as patients in intensive care units, or in cancer or transplant wards.
  • People who have undergone surgical procedures such as abdominal or chest surgery.
  • People with medical devices that stay in for some time such as urinary catheters or central intravenous (IV) catheters.
  • People who are colonized with VRE.

Enterococcus faecalis basic characteristics

  • CATALASE: NEGATIVE (a pseudo catalase is sometimes produced and a weak effervescence is observed in the catalase test)

Enterococcus faecalis and Enterococcus faecium tests for identification

  • all strains grow in broth containing 6.5% NaCl
  • hydrolyze esculin in the presence of bile salts (bile-esculin medium)
  • hydrolyze pyrrolidonyl-β-naphthylamide (PYR test; pyrrolidonylarylamidase production)
  • produce a cell-wall associated glycerol teichoic acid antigen that is identified as the streptococcal group D antigen (26 to 74% E.faecium strains are positive).

Growth in
0.04% tellurite
Sorbitol Sorbose Mannitol D-Raffinose
E.faecalis NEG. POS. (-) POS. NEG. POS. NEG.
E.faecium POS. NEG. NEG. NEG. NEG. POS. d
α-Galactosidase Pyrrolidonyl
group D
E.faecalis POS. POS. d POS. NEG. POS. POS.
E.faecium POS. POS. (-) POS. d POS. V

  • POS. 90% or more of the strains of isolates are positive
  • V 26 to 74% are positive
  • (-) 11 to 25% are positive
  • NEG. 10% or less are positive
  • d discrepancies among reference studies

Source: Manero A, Blanch R A. Identification of Enterococcus spp. with a Biochemical Key. Appl Environ Microbiol. 1999.

Antibiotic treatment of Enterococcus faecalis infections

Should be always guided by in vitro susceptibility tests!!
Selection of appropriate antibiotics depends on diagnosis!!

Relative to the streptococci, enterococci are intrinsically resistant to many commonly used antimicrobial agents. All enterococci exhibit decreased susceptibility to penicillin and ampicillin, as well as high-level resistance to most cephalosporins and all semi-synthetic penicillins, as the result of expression of low-affinity penicillin-binding proteins. For many strains, their level of resistance to ampicillin does not preclude the clinical use of this agent. In fact, ampicillin remains the treatment of choice for enterococcal infections that lack other mechanisms for high-level resistance. Enterococci are also intrinsically resistant to clindamycin. Trimethoprimsulfamethoxazole appears to be active against enterococci when tested in vitro on folate-deficient media, but fails in animal models, presumably because enterococci can absorb folate from the environment (Zervos & Schaberg, 1985). Enterococci also have a native resistance to clinically achievable concentrations of aminoglycosides, which precludes their use as single agents. Although E. faecalis is naturally resistant to quinupristin-dalfopristin, this combination is highly active against E. faecium strains that lack specific resistance determinants. [2; p.1]

The majority of enterococcal infections are described in critically ill patients for whom treatment is usually required. The clinical approach to the treatment of susceptible versus resistant enterococal infections differs significantly. For practical purposes, the majority of modern-day "susceptible" enterococcal infections are caused by isolates of E. faecalis that lack resistance to ampicillin (or penicillin) and vancomycin, and do not exhibit high-level resistance (HLR) to aminoglycosides. Nonetheless, although ampicillin resistance continues to be uncommon in clinical isolates of E. faecalis, high-level resistance (HLR) to aminoglycosides has become more common, and vancomycin resistance appears to be increasing. On the other hand, most MDR enterococcal infections are caused by E. faecium, in which both ampicillin and vancomycin have become obsolete, and the isolates often exhibit HLR to aminoglycosides. [2; p.25]

[2] Kristich CJ, Rice LB, Arias CA. Enterococcal Infection-Treatment and Antibiotic Resistance. 2014 Feb 6. In: Gilmore MS, Clewell DB, Ike Y, et al., editors. Enterococci: From Commensals to Leading Causes of Drug Resistant Infection [Internet]. Boston: Massachusetts Eye and Ear Infirmary; 2014-.
Available from: http://www.ncbi.nlm.nih.gov/books/NBK190420/
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
To view a copy of this license, visit https:// creativecommons.org/licenses/by-nc-nd/4.0/

Treatment of ampicillin and vancomycin-susceptible E.faecalis without HLR to aminoglycosides
  • amino-penicillins (such as ampicillin) + aminoglycoside (gentamicin or streptomycin)
  • ureidopenicillins (such as piperacillin) + GEN
  • penicillin G + GEN

  • Ampicillin and vancomycin-susceptible E. faecalis with HLR to aminoglycosides
  • Ampicillin + ceftriaxone
  • Ampicillin + imipenem + vancomycin
  • Ampicillin + fluoroquinolones (ciprofloxacin, ofloxacin)
  • Ampicillin + high-dose daptomycin

  • Penicillinase-producing E. faecalis
  • Ampicillin-sulbactam plus aminoglycosides (gentamicin or streptomycin)

  • Vancomycin-resistant E. faecalis
  • They are usually susceptible to ampicillin, and ampicillin-based regimens are preferred

HLR = high-level resistance

Other antibiotics used in treatment of infections caused by Enterococcus spp.
  • vancomycin
  • quinupristin-dalfopristin
  • linezolid
  • daptomycin
  • tigecycline
  • linezolid
  • More about antibiotic treatment of E.faecalis: [2; page 24-33].

    Enterococcus faecalis colonies on agar cultivation media

    Enterococcus faecalis on blood agar

    enterococcus faecalis culture in Petri dish colonies of Enterococcus faecalis on agar plate Enterococcus faecalis colony morphology and hemolysis E.faecalis on blood agar plate colony appearance and morphology on agar medium with sheep blood Enterococcus faecalis colony morphology with description enterococcus faecalis on cap agar e.faecalis and s.aureus colonies on blood agar blood agar plate with enterococcus faecalis bacteria enterococcus faecalis colony morphology enterococcus faecalis pure culture in Petri dish enterococcus faecalis growth on blood agar enterococcus faecium

    Enterococcus faecalis on Bile Esculin Agar & Bile Esculin Azide Agar

    enterococci faecalis growing on bile esculin agar e.faecalis on bile esculin agar plate enterococcus faecalis colony morphology on bile esculin azide agar colonies on bile esculin azide agar esculin hydrolysis on bile esculin agar esculin hydrolyzing enterococci; e.faecalis a hand holding agar plate with enterococcus faecalis bacteria growing on bile esculin agar

    Enterococcus faecalis on various cultivation agar media

    enterococcus faecalis growing on plate with tryptic soy agar enterococcus faecalis and staphylococcus aureus comparison on tryptic (trypticase) soy agar enterococcus faecalis on CLED agar enterococcus faecalis on TSA, BHI agar, MacConkey No.3 agar and CLED agar enterococcus faecalis and staphylococcus aureus on Endo agar e.faecalis on TSA, bile esculin agar, MacConkey No.1 agar and Endo agar comparison of enterococcus faecalis with klebsiella pneumoniae and escherichia coli on CLED agar comparison of enterococcus faecalis colony morphology with pseudomonas aeruginosa colony morphology of enterococcus faecalis, staphylococcus aureus and staphylococcus epidermidis colony appearance of enterococcus faecalis, staphylococcus aureus and pseudomonas aeruginosa on tsa vancomycin resistant enterococcus faecium, oxoid brilliance chromogenic agar vancomycin resistant enterococcus faecalis on VRE selective agar medium vancomycin resistant enterococcus faecalis culture in Petri dish, VRE colonies on agar

    Enterococcus faecalis identification

    enterococcus faecalis PYR test, PYRase test; positive PYR test result enterococcus faecalis identification with a commercial kit

    Enterococcus faecalis Gram-stain

    enterococcus faecalis under microscope, Gram stain enterococcus faecalis micrograph, Gram stain enterococcus faecalis Gram stain, e.faecalies viewed through the microscope enterococcus sp. in sputum

    Enterococcus faecalis SEM

    Enterococcus faecalis electron microscopy enterococcus faecalis SEM enterococcus faecalis electron micrograph

    Useful Links