Enterococcal Infections¶
Chapter 154 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Enterococci (E. faecalis and E. faecium) are major nosocomial pathogens with increasing resistance to antibiotics, particularly vancomycin (VRE).
- Clinical syndromes include urinary tract infections (UTIs), endocarditis, bacteremia, intra-abdominal infections, and meningitis.
- Treatment regimens depend on species (E. faecalis vs. E. faecium), resistance patterns, and infection severity, often requiring combination therapy.
1. DEFINITION & OVERVIEW¶
Enterococci are gram-positive bacteria that colonize the human gastrointestinal tract. They are significant pathogens in healthcare settings, causing infections such as bacteremia, endocarditis, and urinary tract infections. E. faecalis and E. faecium are the primary species responsible for most infections, with E. faecium increasingly associated with multidrug resistance.
Table 154-1: Suggested Regimens for E. faecalis Infections¶
| CLINICAL SYNDROME | SUGGESTED THERAPEUTIC OPTIONS |
|---|---|
| Endovascular infections (including endocarditis) | Ampicillin (12 g/d IV) + ceftriaxone (2 g IV q12h) |
| Nonendovascular bacteremia | Ampicillin (12 g/d IV) ± aminoglycoside |
| Meningitis | Ampicillin (20–24 g/d IV) + aminoglycoside + ceftriaxone |
| Urinary tract infections | Amoxicillin (500 mg PO q8h) or fosfomycin (3 g PO) |
1.1 Taxonomy and Morphology¶
Enterococci are classified as a distinct genus, not streptococci, due to differences in DNA hybridization and 16S rRNA sequencing. They appear as single cells, diplococci, or short chains in clinical specimens. They are nonhemolytic on sheep blood agar but may lyse human RBCs due to acquired hemolysin/cytolysin genes.
1.2 Pathogenesis¶
Enterococci colonize the gut and can cause infections through mechanisms including adherence to host tissues, biofilm formation, and secretion of virulence factors like cytolysin and aggregation substance. Resistance to antibiotics and colonization resistance disruption by antimicrobial use contribute to pathogenicity.
2. EPIDEMIOLOGY¶
Enterococci are the third most common hospital-associated pathogens in the U.S., with E. faecium increasingly prevalent. Vancomycin resistance (VRE) is common in E. faecium (50–80% in long-term care facilities). Risk factors include prolonged hospitalization, antibiotic use, and immunocompromise.
Table 154-2: Suggested Regimens for E. faecium Infections¶
| CLINICAL SYNDROME | SUGGESTED THERAPEUTIC OPTIONS |
|---|---|
| Endovascular infections (including endocarditis) | High-dose daptomycin + aminoglycoside |
| Nonendovascular bacteremia | High-dose daptomycin ± linezolid |
| Meningitis | Linezolid (600 mg IV q12h) ± CSF-penetrating agent |
| Urinary tract infections | Fosfomycin (3 g PO) or nitrofurantoin |
2.1 Global Trends¶
VRE prevalence has increased globally, with higher rates in Europe (25–50% in southern/ eastern Europe) and Latin America (34% of E. faecium isolates). Use of glycopeptides in animal agriculture contributed to VRE emergence in Europe.
2.2 Transmission¶
VRE spreads via contaminated surfaces, medical equipment, and healthcare workers. Colonized patients remain carriers for >1 year, increasing risk of Enterococcus-related infections.
3. CLINICAL FEATURES¶
Common presentations include UTIs (especially in catheterized patients), endocarditis (especially in IV drug users or post-TAVI), and bacteremia. Intra-abdominal infections are frequent in immunocompromised patients. Meningitis is rare but associated with neurosurgical procedures or hematogenous spread.
3.1 Urinary Tract Infections¶
Enterococci are common causes of catheter-associated UTIs. Diagnosis is challenging due to overlap with colonization. Positive urine cultures (>10^5 CFU/mL) with leukocytes and systemic symptoms suggest infection.
3.2 Endocarditis¶
E. faecalis is the leading cause of infective endocarditis after TAVI. Subacute presentation with fever, weight loss, and cardiac murmurs. Complications include heart failure and embolic events.
4. INVESTIGATIONS & DIAGNOSIS¶
Diagnosis involves blood cultures, urine cultures, and imaging for abscesses. CSF analysis for meningitis shows pleocytosis with PMNs and low glucose. Molecular methods (PCR) and MALDI-TOF MS aid in rapid identification.
4.1 Laboratory Tests¶
Blood cultures are critical for bacteremia. Vancomycin resistance testing (E-test or broth microdilution) is essential for VRE identification. Molecular assays detect resistance genes like vanA.
4.2 Imaging¶
Ultrasound or CT for intra-abdominal abscesses. Echocardiography confirms endocarditis. MRI for CNS infections.
5. MANAGEMENT & TREATMENT¶
Combination therapy is standard for severe infections. Daptomycin, linezolid, and ampicillin/ceftriaxone are first-line for E. faecalis. For VRE, daptomycin + aminoglycoside or linezolid is preferred. Surgical intervention may be needed for abscesses or foreign bodies.
Table 154-1: Suggested Regimens for E. faecalis Infections¶
| CLINICAL SYNDROME | SUGGESTED THERAPEUTIC OPTIONS |
|---|---|
| Endovascular infections (including endocarditis) | Ampicillin (12 g/d IV) + ceftriaxone (2 g IV q12h) |
| Nonendovascular bacteremia | Ampicillin (12 g/d IV) ± aminoglycoside |
| Meningitis | Ampicillin (20–24 g/d IV) + aminoglycoside + ceftriaxone |
| Urinary tract infections | Amoxicillin (500 mg PO q8h) or fosfomycin (3 g PO) |
5.1 Antimicrobial Therapy¶
E. faecalis: Ampicillin + aminoglycoside. E. faecium: Daptomycin + aminoglycoside. Linezolid is an alternative for VRE. Avoid monotherapy due to resistance risks.
5.2 Surgical Intervention¶
Catheter removal for UTIs. Drainage of abscesses. Valve replacement for endocarditis with multidrug-resistant strains.
6. PROGNOSIS & COMPLICATIONS¶
Mortality is higher for E. faecium infections due to resistance. Complications include endocarditis-related heart failure, sepsis, and abscess formation. VRE infections have worse outcomes, especially in immunocompromised patients.
6.1 Risk Factors¶
Prolonged hospitalization, antibiotic use, immunosuppression, and prior VRE colonization increase mortality. E. faecium infections have higher resistance rates and poorer outcomes.
6.2 Long-Term Outcomes¶
Relapse rates for E. faecalis endocarditis are 2–11% with antibiotic-only therapy vs. 0–3% with surgery. Chronic colonization may persist for >1 year.
7. SPECIAL CONSIDERATIONS¶
Pregnancy: Avoid aminoglycosides and vancomycin; use ampicillin. Pediatrics: Enterococci are common in neonatal sepsis; avoid quinupristin-dalfopristin. Elderly: Higher risk of VRE and complications from antibiotic therapy.
7.1 Pregnancy¶
Ampicillin is preferred for UTIs. Avoid aminoglycosides and vancomycin due to fetal risks. Monitor for neonatal sepsis in preterm infants.
7.2 Immunocompromised Patients¶
Higher risk of VRE colonization and severe infections. Daptomycin + aminoglycoside is preferred. Monitor for Strongyloides hyperinfection.
8. KEY POINTS & CLINICAL PEARLS¶
- E. faecalis and E. faecium are the main pathogens; E. faecium is increasingly resistant to vancomycin.
- Combination therapy is essential for severe infections, especially with VRE.
- Daptomycin is effective for VRE but requires monitoring for rhabdomyolysis.
- Catheter removal is critical for UTIs and may reduce the need for prolonged antibiotic therapy.
- Endocarditis caused by E. faecalis is often subacute with cardiac murmurs and embolic complications.