Infectious Disease Compendium



Gram positive cocci, often in pairs. E. faecalis and E. faecium are the big two, as well as E. avium, E. casseliflavus, E. durans, E. gallinarum, E. hira, E. raffinosus.

Epidemiologic Risks

Normal bowel flora.


UTI and blood stream infections are most common.

ICU line related bacteremias have a high incidence (almost 50%) of both MOSF and death (PubMed), although patients may be dying with it rather than of it (PubMed).

But i'ts only one positive blood culture, you say. Doesn't matter. One or many, enterococcus does not belong in the blood (PubMed). Treat it.

Often a part of mixed intra-abdominal infections; it does not increase mortality or need for re-operation, but may increase the rate of abscess formation (PubMed).

Worst disease is endocarditis and always suspect it when there are positive blood cultures, even if you have a source (PubMed). The risks for endocarditis are monomicrobial E. faecalis bacteremia, community acquisition, prosthetic heart valve, and males (Pubmed).

Half of Enterococcal endocarditis patients will have a colonic neoplasm so they require a colonoscopy (PubMed). The patient not the enterococcus.


E. faecalis, E. faecium: usually ampicillin, vancomycin, linezolid, daptomycin, or quinupristin/dalfopristin.

If vancomycin resistant (VRE) use linezolid, daptomycin, or quinupristin/daptomycin; I use them in that order.

What data there is suggests linezolid is better than daptomycin for bacteremia VRE (PubMed). Although a retrospective analysis shows little difference between linezolid and daptomycin for VRE blood stream infections (PubMed)(PubMed), others show superiority of linezolid (PubMed) and others the superiority of daptomycin (PubMed).  If Newton had been a doctor, he would say that for every study there is an equal and opposite study.

If you are going to give daptomycin go with higher dose 9 mg/kg or even 10 mg/kg (PubMed)(PubMed) for blood stream infections, although daptomycin should probably not be used for endocarditis (PubMed).

For VRE, 9 mg/kg daptomycin had better outcomes (PubMed) (PubMed).

Failure may occur depending on genotype, even if it appears sensitive in the lab (PubMed). Sometimes I wish I could somehow safely autoclave the patient to get rid of some of these bugs.

Endocarditis: For high level gentamicin resistance and gentamicin susceptible, ampicillin 12 grams a day PLUS ceftriaxone 2 gm q 12 for 6 to 8 weeks works (PubMed) and is the treatment of choice (PubMed).

There was a case of high level gentamicin resistant endocarditis treated with daptomycin plus ceftaroline (PubMed).

The old school treatment is 6 weeks of ampicillin (preferred; 12 grams a day) PLUS an aminoglycoside OR vancomycin PLUS an aminoglycoside no matter what it does to the ears or kidneys (although the risk for gentamicin toxicity may be genetic). If patients have been ill less than three months, 4 week may be enough. Beware of high level gentamicin resistance (MIC > 500).

Maybe, for VRE, use daptomycin PLUS ampicillin for 8 to 10 weeks or quinupristin/dalfopristin for 6 weeks or linezolid or daptomycin (high dose) WITH tigecycline. Best bet may be to go right to valve replacement.

Other combinations of antibiotics have been tried for endocarditis, reviewed in 2018 (PubMed).

UTI: amoxicillin OR a quinolone po will usually suffice. And fosfomycin should also work (PubMed). For all other common infections single drug usually suffices as long as the pus is drained.

When part of mixed flora I tend to ignore it as when you treat and debride the other infections, the enterococcus tends to go away (although, being resistant to ALL cephalosporins, over growth with occasional bacteremia is a known complication of cephalosporin based therapies).

Arthritis: If the prosthetic joint is infected with Enterococcus, monotherapy is equal to combination (PubMed). If you have VRE, there is no difference between linezolid or quinupristin/dalfopristin in terms of outcome (PubMed). Other enterococci have variable resistance and need to be checked for antibiotic susceptibility.


The big problem with the enterococcus is not that it is very virulent buty it tends to be found in dead tissues or people who are soon to become dead tissue.

The other big problem is resistance, and no one expects the Spanish inquisition: no single antibiotic can kill it, which is why you have to give combination therapy to cure endocarditis. Vancomycin resistance (VRE), which occurs in at least four forms, is a bigger worry, again, not because it is all that virulent, but because the organism serves as a reservoir for resistance from S. aureus; these genes have jumped from Enterococcus to S. aureus at least twice and will do so again.

Evolution progresses apace: E. faecium has acquired beta-lactamases (PubMed). Crap.

A curiosity: stool transplants for C. difficile gets rid of VRE (Pubmed). I am sure that has some profound consequences in understanding the bowel biome.

Enterococci are old: "enterococci first emerged 425–500 million years ago from ancestral Vagococcus lutrae—more than 200 million years before the appearance of dinosaurs, but about the same time that land-adapted animals appeared" and there was a "rapid emergence of new enterococcal species following the End Permian Extinction" (PubMed). Blame VRE on the asteroids.

Curious Cases

Relevant links to my Medscape blog

Old mans disease in a young mans body

Five Months Qualifies for Sustained

Small Things I Thought Were True

Late Relapse


Last Update: 07/15/18.