Enterococcus faecalis vs faecium: Key Clinical Differences
E. faecium is significantly more antibiotic-resistant than E. faecalis, particularly to ampicillin, fluoroquinolones, and vancomycin, and is increasingly responsible for nosocomial infections despite E. faecalis historically being more common.
Infection Frequency and Epidemiological Trends
E. faecalis remains the predominant species overall but E. faecium is rapidly increasing in healthcare settings. Recent surveillance data shows E. faecalis accounts for approximately 46-94% of enterococcal infections, while E. faecium represents 6-54% 1, 2, 3. However, the proportion of E. faecium bacteremia has risen dramatically from 41% in 2015 to 51% in 2021 in hospital settings 4.
Key epidemiological differences:
- E. faecalis: More common in community-acquired infections, UTIs, and mitral valve endocarditis
- E. faecium: Predominantly nosocomial, associated with intra-abdominal infections, tricuspid valve endocarditis, and device-related infections 5, 1
The shift toward E. faecium is concerning as it represents hospital-adapted strains with greater genomic plasticity and resistance acquisition capacity 1.
Antibiotic Susceptibility: Critical Differences
E. faecalis Resistance Profile
- Low resistance to ampicillin (typically <25%), imipenem, and nitrofurantoin 2, 6
- Vancomycin resistance: 7.2% (U.S. CDC data) 5
- Generally susceptible to penicillins and can be treated with ampicillin-based regimens
- High-level aminoglycoside resistance: 54.55% 3
E. faecium Resistance Profile
- High resistance to ampicillin (often >25-100%), fluoroquinolones, and β-lactams 2, 7
- Vancomycin resistance: 82.1% (U.S. CDC data) with increasing prevalence from 8.1% (2012) to 19% (2018) in Europe 5
- Carries significantly more antimicrobial resistance genes than E. faecalis 1
- Multidrug resistance (MDR), extensively drug-resistant (XDR), and pandrug-resistant (PDR) phenotypes are more common 2
The vancomycin resistance mechanism in E. faecium is predominantly mediated by vanHAX gene clusters (35.5% of isolates), while only 3.1% of E. faecalis carry this resistance 1.
Treatment Implications Based on Species
For E. faecalis infections:
- Ampicillin remains effective for most infections including UTIs and bacteremia
- For UTIs: Nitrofurantoin (69.69% sensitive) or fosfomycin (78.79% sensitive) are excellent options 3
- High-dose ampicillin (18-30g IV daily) can overcome resistance even in ampicillin-resistant strains for UTIs due to high urinary concentrations 5
For E. faecium infections (especially VRE):
- Linezolid 600mg IV/PO q12h is the first-line recommendation for serious enterococcal infections (Strong recommendation) 5
- High-dose daptomycin 8-12 mg/kg/day ± β-lactam combination for bacteremia (Weak recommendation) 5
- For intra-abdominal infections: Tigecycline 100mg loading then 50mg q12h 5
- For uncomplicated UTIs: Fosfomycin 3g PO single dose or nitrofurantoin 100mg PO q6h 5
Clinical Outcomes and Risk Factors
E. faecium infections are associated with worse outcomes, including longer hospital stays, higher mortality in endocarditis, and longer duration of bacteremia compared to E. faecalis 5. XDR isolates have the longest hospital stays 2.
Risk factors specifically for E. faecium bacteremia:
- Hospital-acquired infection
- Prior exposure to piperacillin/tazobactam (independent risk factor) 4
- Prior carbapenem exposure 4
- Hemodialysis and liver transplantation 5
- Presence of central venous catheters 5
Critical Clinical Pitfalls
Do not use piperacillin/tazobactam or cephalosporins for E. faecium - these agents select for E. faecium over E. faecalis and are intrinsically ineffective 4
Species identification is mandatory before definitive therapy - the resistance profiles are too divergent to treat empirically without speciation 2
Differentiate colonization from true infection before initiating anti-VRE therapy, especially in ICU settings where VRE colonization prevalence reaches 45% 5
E. faecium has greater genomic plasticity - even clonally related isolates from the same patient show marked genomic diversity and can rapidly acquire resistance plasmids 1