Enterococcus faecalis and Enterococcus faecium

Heather Clauss, MD

Enterococci are gram-positive cocci that can occur in singles, pairs, and short chains. The cells are sometimes coccobacilli if the Gram stain is prepared from agar plate growth. Until recently they were classified as group D streptococci, a group which includes Streptococcus bovis and Streptococcus equinus. Enterococci are facultative anaerobes that are able to grow under extreme conditions including 6.5% NaCl, high pH, 40% bile salts, and a temperature range of 10°C - 45°C. The most accurate way to presumptively identify a catalase-negative gram positive coccus as an Enterococcus sp. is to demonstrate that the unknown is PYR (an abbreviation for L-pyrrolidonyl-β-naphthylamide) and LAP (leucine-beta-naththylamide) positive, grows in 6.5% NaCl and grows at 45°C. Though it does not prove anything about them, most do not produce hemolysis on blood agar (rare strains are alpha- or beta-hemolytic).

 

 

Enterococci are not fastidious organisms and as such, can be found in soil, food, water, plants, animals, birds and insects. The major habitat in humans is the GI tract, where they make up a significant portion of normal aerobic gut flora. Small numbers can also be found in oropharyngeal secretions, vaginal secretions, and on the perineal skin. Enterococcal infections were traditionally considered to be acquired from the patient’s own normal flora. Recently enterococci have emerged as nosocomial pathogens, causing increased interest in their epidemiology. In most cases these nosocomial strains are also found in the gut of infected patients.

The most common clinical infections caused by these bacteria are urinary tract infections, bacteremia, endocarditis, intra-abdominal, and pelvic infections. Much less commonly, E. faecalis and E. faecium can cause wound and soft tissue infections, meningitis (most commonly post-neurosurgical procedure), and respiratory infections. Enterococci in general are much less intrinsically virulent than Staphylococcus aureus and Streptococcus pyogenes; they do not secrete exotoxins or produce superantigens. However, the resistance of enterococci to multiple antibiotics allows them to survive and proliferate in patients receiving multiple antimicrobials, causing superinfection. Enterococci have an intrinsic resistance to many antibiotics, and also have the ability to acquire new mechanisms of resistance. The most clinically significant of this resistance is the development of vancomycin-resistant enterococci (VRE), first described in the late 1980’s. Multiple antimicrobial agents have been developed to treat VRE including quinupristin/dalfopristin, linezolid, and daptomycin. Of note, quinupristin/dalfopristin is useful only for infections caused by E. faecium, as E. faecalis is intrinsically resistant to this combination.

E. faecalis used to account for 80-90% of the clinical isolates of enterococcus, with E. faecium accounting for only 5-10% and various minor species making up the rest. More recent evidence suggests that the prevalence of E. faecium is increasing, particularly the vancomycin-resistant strain. The resistance to vancomycin, as well as ampicillin, is far more commonly associated with E. faecium (52% of all isolates were VRE) than with E. faecalis (1.9% of isolates were VRE). In one study of E. faecalis vs. E. faecium bacteremia, risk factors favoring E. faecium were: hematologic malignancies, neutropenia, and the previous use of aminoglycosides, carbapenems, cephalosporins, or clindamycin. Urinary catheterization was found to be a risk factor for E. faecalis bacteremia. However, there was no difference in mortality between E. faecalis and E. faecium bacteremia (27% and 29% respectively at 30 days). Other papers have suggested that patients with E. faecium infection tend to be sicker and die at a higher rate -- not necessarily attributable to the enterococcal infection but hard to sort out in individual cases.

 

References:

1. Mandell, Bennett, & Dolin. Principles and Practice of Infectious Disease, 6th edition. 2005.

2. Murray, P et al. Manual of Clinical Microbiology. 7th edition. 1999.

3. Suppola, JP. et al. “Comparison of risk factors and outcome in patients with Enterococcus faecalis vs. Enterococcus faecium bacteraemia.” Scandinavian Journal of Infectious Disease. 1998; 30(2):153-157.