Enterococcal Infections



Enterococci are part of the normal intestinal flora of humans and animals but are also important pathogens responsible for serious infections. The genus Enterococcus includes more than 17 species, but only a few cause clinical infections in humans. With increasing antibiotic resistance, enterococci are recognized as feared nosocomial pathogens that can be challenging to treat.

Enterococcus species (see the image below) are hardy, facultative anaerobic organisms that can survive and grow in many environments. In the laboratory, enterococci are distinguished by their morphologic appearance on Gram stain and culture (gram-positive cocci that grow in chains) and their ability to (1) hydrolyze esculin in the presence of bile, (2) grow in 6.5% sodium chloride, (3) demonstrate pyrrolidonyl arylamidase and leucine aminopeptidase, and (4) react with group D antiserum. Before they were assigned their own genus, they were known as group D streptococci.

View Image

Enterococcus species.

Enterococcus faecalis and Enterococcus faecium are the most prevalent species cultured from humans, accounting for more than 90% of clinical isolates. Other enterococcal species known to cause human infection include Enterococcus avium, Enterococcus gallinarum, Enterococcus casseliflavus, Enterococcus durans, Enterococcus raffinosus and Enterococcus mundtii.[1] E faecium represents most vancomycin-resistant enterococci (VRE).

Isolation of enterococci resistant to multiple antibiotics has become increasingly common in the hospital setting.[2] According to National Nosocomial Infections Surveillance (NNIS) data from January 2003 through December 2003, more than 28% of enterococcal isolates in ICUs of the more than 300 participating hospitals were vancomycin-resistant. Clonal spread is the dominant factor in the dissemination of multidrug-resistant enterococci in North America and Europe.[3] Virulence and pathogenicity factors have been described using molecular techniques. Several genes isolated from resistant enterococci (agg, gelE, ace, cylLLS, esp, cpd, fsrB) encode virulence factors such as the production of gelatinase and hemolysin, adherence to caco-2 and hep-2 cells, and capacity for biofilm formation.[4, 3]

Enterococci have both an intrinsic and acquired resistance to antibiotics, making them important nosocomial pathogens. Intrinsically, enterococci tolerate or resist beta-lactam antibiotics because they contain penicillin-binding proteins (PBPs); therefore, they are still able to synthesize some cell-wall components. They are intrinsically resistant to penicillinase-susceptible penicillin (low level), penicillinase-resistant penicillins, cephalosporins, nalidixic acid, aztreonam, macrolides, and low levels of clindamycin and aminoglycosides. They use already-formed folic acid, which allows them to bypass the inhibition of folate synthesis, resulting in resistance to trimethoprim-sulfamethoxazole.

Enterococci also have acquired resistance, which includes resistance to penicillin by beta-lactamases, chloramphenicol, tetracyclines, rifampin, fluoroquinolones, aminoglycosides (high levels), and vancomycin. The genes that encode intrinsic or acquired vancomycin resistance result in a peptide to which vancomycin cannot bind; therefore, cell-wall synthesis is still possible.

Unlike streptococcal species, enterococci are relatively resistant to penicillin, with minimum inhibitory concentrations (MICs) that generally range from 1-8 mcg/mL for E faecalis and 16-64 mcg/mL for E faecium. Therefore, exposure to these antibiotic agents inhibits but does not kill these species. Combining a cell wall–active agent such as ampicillin or vancomycin with an aminoglycoside may result in synergistic bactericidal activity against enterococci.

The acquisition of vancomycin resistance by enterococci has seriously affected the treatment and infection control of these organisms. VRE, particularly E faecium strains, are frequently resistant to all antibiotics that are effective treatment for vancomycin-susceptible enterococci, which leaves clinicians treating VRE infections with limited therapeutic options.

Newer antibiotics (eg, quinupristin-dalfopristin, linezolid, daptomycin, tigecycline) with activity against many VRE strains have improved this situation, but resistance to these agents has already been described. A mutation (G2576U) in the domain V of the 23S rRNA is responsible for linezolid resistance,[3] whereas resistance to quinupristin-dalfopristin may be the result of several mechanisms: modification of enzymes, active efflux, and target modification. Resistance of E faecalis and E faecium to daptomycin, a newer cyclic lipopeptide antibiotic that acts on the bacterial cell membrane, has also been reported.[5]

Six phenotypes of vancomycin resistance, termed VanA, VanB, VanC, VanD, VanE, and VanG, have been described. The VanA and VanB phenotypes are clinically significant and mediated by 1-2 acquired transferable operons that consist of 7 genes in 2 clusters termed VANA and VANB operons. In 1988, these gene clusters first were reported in enterococcal strains. VanA is carried on a transposon Tn1546 that is almost always plasmid-mediated.

In the United States and Europe, the 3 major phenotypes include VanA, VanB, and VanD. VanA is the most common, and enterococcal isolates exhibit high-level resistance to both vancomycin and teicoplanin, while VanB isolates have variable resistance to vancomycin and remain susceptible to teicoplanin. The VanC phenotype is mediated by the chromosomal VANC1 and VANC2 genes, which are constitutively present in E gallinarum (VANC1) and E casseliflavus (VANC2). These genes confer relatively low resistance levels to vancomycin and are not transferable. To date, the VanD, VanE, and VanG phenotypes have been described in only a few strains of enterococci.

Three patients infected with vancomycin-resistant Staphylococcus aureus (VRSA) have been reported in the United States.[6, 7] The in vivo conjugative transfer potential of the vanA resistance gene from vancomycin-resistant E faecalis to methicillin-resistant S aureus (MRSA) was confirmed in the first of these cases. This poses an emerging threat to patient safety. E faecium isolates with a complex-17 lineage have also emerged in hospital and community settings in 5 continents over just the past 2 decades. This continued global spread of resistant organisms and the creation of new, highly virulent pathogens from transfer of resistance genes underscore the importance of infection control and prevention, active surveillance, and use of appropriate antibiotics.


Infections commonly caused by enterococci include urinary tract infections, endocarditis, bacteremia, catheter-related infections, wound infections, and intra-abdominal and pelvic infections. Many infecting strains originate from the patient's intestinal flora. From here, they can spread and cause urinary tract infection, intra-abdominal infection, and surgical wound infection. Bacteremia may result with subsequent seeding of more distant sites. For example, genitourinary tract infection or instrumentation often precedes the onset of enterococcal endocarditis. Meningitis, pleural space infections, and skin and soft-tissue infections have also been reported.

Intestinal colonization with resistant enterococcal strains is more common than clinical infection; for example, in Cleveland, VRE stool isolates outnumber clinical isolates by a factor of 10 in hospitals in which active VRE surveillance is performed. If infection occurs, it usually develops in those who are previously colonized. Colonized patients are a potential source for the spread of organisms to the hands of health care workers, the environment, and other patients. Antibiotic-selective pressure facilitates the spread of resistant enterococcal strains by promoting overgrowth of these strains in the intestinal tract. Enterococci can survive for long periods on environmental surfaces, contributing to their transmission. VRE have been isolated from all objects and sites in health care facilities.

For colonization development and infection with VRE, antimicrobial and nonantimicrobial risk factors have been identified. Vancomycin use is associated with VRE colonization and infection, but prior exposure is not required for colonization. Third-generation cephalosporins, aminoglycosides, aztreonam, ciprofloxacin, imipenem, clindamycin, and metronidazole have been associated with VRE colonization. Nonantimicrobial risk factors (eg, increased duration of exposure to individuals colonized with VRE and close proximity to other colonized patients) increase the likelihood of VRE exposure.

Individuals at risk for colonization include critically ill patients who have received lengthy courses of antibiotics (particularly those in long-term care facilities), solid-organ transplant recipients and patients with hematologic malignancies, and health care workers. Unfortunately, spontaneous decolonization is uncommon, and antimicrobials are unlikely to eradicate VRE colonization. Identified risk factors for VRE bacteremia include prior intestinal colonization, prior long-term antibiotic use, increased severity of illness, hematologic malignancy, bone marrow transplant, mucositis, neutropenia, indwelling urinary catheters, corticosteroid treatment, chemotherapy, and parenteral nutrition.



United States

According to recent NNIS surveys, enterococci remain in the top 3 most common pathogens that cause nosocomial infections. Enterococci frequently cause urinary tract infections, bloodstream infections, and wound infections in hospitalized patients. Nosocomial enterococcal infections typically occur in very ill debilitated patients who have been exposed to broad-spectrum antibiotics. They are the fourth most common cause of nosocomial bloodstream infections in the United States.

In 1989, VRE was first reported in New York City; subsequently, VRE has spread rapidly throughout the United States. From 1989-1993, the NNIS surveys reported that the percentage of enterococcal isolates exhibiting vancomycin resistance increased from 0.3% to 7.9%, with a 34-fold rise seen in ICUs. In 2003, the percentage of nosocomial enterococcal isolates exhibiting vancomycin resistance in ICU patients increased to more than 28%—an increase of 12% compared with 1998-2002.

NNIS data reveal the pooled mean for vancomycin-resistant Enterococcus species from all ICUs, non-ICU inpatient areas, and outpatient areas were 13.9%, 12%, and 4.6%, respectively, from 1998 through June 2004. VRE was initially isolated mainly in large university hospitals, but subsequent reports demonstrate the presence of significant VRE epidemics in community hospitals and chronic care facilities, whereby a single clone can easily spread. VRE is isolated almost exclusively from hospitalized (or recently hospitalized) individuals.


In contrast, Europe appears to have a large community reservoir of VRE without as rapid an increase in incidence of hospital-associated infections seen in the United States. In European countries, VanA-type VRE has been isolated from various farm animals, chicken carcasses, other meat products, and wastewater samples from sewage treatment plants. In 1994, a German community screened 100 healthy people for VRE, and 12% were found to be carriers.

In Europe, the use of avoparcin, a glycopeptide antibiotic, as a growth promoter for farm animals has been proposed to explain the epidemiology of VRE. Until banned by the European Union in 1997, avoparcin had been used in several European countries and provided a selective pressure for the emergence and spread of vancomycin-resistant genes. This hypothesis is supported by a Danish study that found VanA-type VRE in chicken stool samples from farms using avoparcin but not in samples from farms not using avoparcin. Among the Saxony-Anhalt region in Germany, the prevalence of VRE fecal colonization in healthy individuals after discontinuing avoparcin use in animal husbandry decreased from 12% to 3%, concurrent with a similar decrease in the prevalence of VRE in German poultry products.

Several outbreaks of VRE colonization[8] and infection have been reported by hospitals in Europe[3] and have been associated with increased mortality rates.[9] A Korean study documented unexpectedly high levels of resistance in VRE isolates to daptomycin, linezolid, and tigecycline despite the rare use of these antibiotics in Korean hospitals.[10]






Physical examination findings in patients with enterococcal infections vary widely and depend on the associated infectious syndrome; therefore, direct the examination according to the patient's symptoms and laboratory findings.

Laboratory Studies

Imaging Studies

Other Tests


Surgical incision and drainage of skin or soft-tissue abscesses or radiology-guided aspiration of abscess material may be required in certain enterococcal infections. In many cases, removal of prosthetic devices, such as vascular catheters, shunts, and prosthetic cardiac valves or orthopedic devices, is necessary to facilitate cure of the infection. Some vascular catheters may be exchanged over a wire and antibiotic lock therapy can be attempted, but the device should be permanently removed if failure occurs.

Medical Care

Surgical Care



In patients who are persistently colonized with VRE, attempts are occasionally made to eradicate the bacteria. Enteral antibiotics such as bacitracin rarely achieve long-term success. In a small recent study, probiotic therapy (Lactobacillus rhamnosus GG in yogurt) was used to successfully clear VRE colonization and infection in renal patients.[30]

Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications.

Ampicillin (Polycillin, Omnipen)

Clinical Context:  DOC if no penicillin allergy. Must be administered in combination with an aminoglycoside if bactericidal activity is required (eg, endocarditis).

Amoxicillin (Trimox, Amoxil)

Clinical Context:  Oral equivalent of ampicillin. PO therapy is appropriate for mild-to-moderate enterococcal infections and for continuing therapy after stabilization of patients with severe infections. PO therapy should not be used for treatment of endocarditis. Interferes with synthesis of cell wall mucopeptides during active multiplication.

Vancomycin (Vancocin, Lyphocin, Vancoled)

Clinical Context:  Used to treat enterococcal infections when ampicillin is contraindicated due to significant penicillin allergy and when strains are resistant to ampicillin but susceptible to vancomycin. Target levels of 30-50 mcg/mL (peak) and 10-15 mcg/mL (trough) for endocarditis and other serious infections.

Gentamicin (Garamycin, Gentacidin)

Clinical Context:  Aminoglycoside antibiotic administered in combination with ampicillin or vancomycin to provide bactericidal activity for treatment of enterococcal endocarditis and other serious enterococcal infections. Target levels of 3 mcg/mL (peak) and < 1 mcg/mL (trough). Drug levels should be drawn with third dose and then prn until target drug levels achieved. Thereafter, levels should be rechecked weekly during therapy or with any significant change in serum creatinine level.

Quinupristin/dalfopristin (Synercid)

Clinical Context:  Belongs to the group that includes macrolide, lincosamide, and streptogramin. Inhibits protein synthesis and is usually bacteriostatic. Effective against E faecium but not E faecalis strains. Option for treatment of vancomycin-resistant E faecium infections.

Linezolid (Zyvox)

Clinical Context:  Oxazolidinone antibiotic effective for treatment of both E faecalis and E faecium vancomycin-resistant enterococci (VRE) strains. Inhibits protein synthesis and is bacteriostatic. Has been effective in treating a variety of infections caused by VRE species, including a few cases of enterococcal endocarditis.

The FDA warns against the concurrent use of linezolid with serotonergic psychiatric drugs, unless indicated for life-threatening or urgent conditions. Linezolid may increase serotonin CNS levels as a result of MAO-A inhibition, increasing the risk of serotonin syndrome.[31]

Nitrofurantoin (Macrodantin)

Clinical Context:  Effective for treatment of VRE urinary tract infections. Synthetic nitrofuran that interferes with bacterial carbohydrate metabolism by inhibiting acetylcoenzyme A. Bacteriostatic at low concentrations (5-10 mcg/mL) and bactericidal at higher concentrations.

Daptomycin (Cubicin)

Clinical Context:  Cyclic lipopeptide antibiotic that binds to components of the cell membrane and inhibits DNA, RNA, and protein synthesis; bactericidal in a concentration-dependent manner. Approved for vancomycin-sensitive E faecalis infections.

Tigecycline (Tygacil)

Clinical Context:  Used to treat complicated skin infections to include methicillin-resistant S aureus and vancomycin-sensitive E faecalis. Inhibits protein synthesis.

Telavancin (Vibativ)

Clinical Context:  Lipoglycopeptide antibiotic that is a synthetic derivative of vancomycin. Inhibits bacterial cell wall synthesis by interfering with polymerization and cross-linking of peptidoglycan. Unlike vancomycin, telavancin also depolarizes the bacterial cell membrane and disrupts its functional integrity. Indicated for complicated skin and skin structure infections caused by susceptible gram-positive bacteria, including Staphylococcus aureus (both methicillin-resistant and methicillin-susceptible strains), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus anginosus group, and Enterococcus faecalis (vancomycin-susceptible isolates only).

Class Summary

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Further Outpatient Care




Endocarditis may occur as a complication of enterococcal infection at a remote site if bacteremia occurs. For example, some cases of endocarditis are preceded by intravascular catheter infections or urinary tract infection or instrumentation.


Enterococcal bacteremia tends to occur in very debilitated patients, making the exact contribution of the bacteremia to mortality difficult to determine. Nevertheless, studies have estimated the attributable mortality rate of enterococcal bacteremia to be 31-37%. Even with current therapeutic regimens, the mortality rate of enterococcal endocarditis remains approximately 20%.


Susan L Fraser, MD, Chief, Infectious Diseases Service, Fort Belvoir Community Hospital; Chairman, Infection Control Committee; Associate Professor of Medicine, Uniformed Services University of the Health Sciences

Disclosure: Nothing to disclose.


Curtis J Donskey, MD, Chairman of Infection Control, Instructor, Department of Internal Medicine, Section of Infectious Diseases, Stokes Cleveland VA Medical Center, Case Western Reserve University

Disclosure: Nothing to disclose.

Julia Lim, MD, Associate Program Director, Internal Medicine Residency Program, Tripler Army Medical Center

Disclosure: Nothing to disclose.

Robert A Salata, MD, Chief and Clinical Program Director of Division of Infectious Diseases, Vice Chair for International Affairs, Professor, Department of Medicine, Case Western Reserve University School of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

David Hall Shepp, MD, Program Director, Fellowship in Infectious Diseases, Department of Medicine, North Shore University Hospital; Associate Professor, New York University School of Medicine

Disclosure: Gilead Sciences Salary Management position

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ronald A Greenfield, MD, Professor, Department of Internal Medicine, University of Oklahoma College of Medicine

Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest Pharmaceuticals Speaking and teaching

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Disclosure: Nothing to disclose.


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Enterococcus species.

Enterococcus species.