Gram-positiveCocciCatalase-negative

Enterococcus faecium

Gram-positive, catalase-negative coccus found in chains, notable for intrinsic vancomycin resistance (VRE) and as a leading cause of nosocomial urinary tract infections, bacteremia, and endocarditis.

Organism Card

DomainMust know
Identity
  • G+ve cocci in chains/pairs; facultative anaerobe
  • Formerly classified as Group D streptococci (Lancefield D) [1][2]
  • Now genus Enterococcus; E. faecium is the more resistant species vs E. faecalis
  • Commensal of GI and GU tract
Lab discriminator
  • Catalase −ve (vs staphylococci catalase +ve)
  • PYR +ve (shared with GAS; but enterococci are bile-esculin +ve, GAS is not)
  • Bile-esculin +ve + growth in 6.5% NaCl → distinguishes enterococci from other streptococci
  • E. faecium vs E. faecalis: faecium is ampicillin-resistant (MIC usually high); faecium more likely VRE
Reservoir / transmission
  • Normal flora of human GI tract and female genital tract [1][2]
  • Source: GI/GU tract; enters by pathologies/manipulations [2]
  • Nosocomial spread via contaminated hands, devices (Foley catheters, IV lines) [3]
  • Survives on environmental surfaces; resistant to drying and disinfectants
Key virulence
  • Intrinsic low-level resistance to multiple antibiotics → survival advantage in hospital
  • Biofilm formation on indwelling devices (catheters, prosthetic valves) [3]
  • Intrinsically resistant to cephalosporins and aminoglycosides (as monotherapy) [4][5]
  • Acquired vancomycin resistance (VanA, VanB operons) → defines VRE, major nosocomial threat
Clinical syndromes
  • UTI: 2nd most common cause in complicated/nosocomial UTI (Enterococcus spp 11%) [6][7]
  • Infective endocarditis: subacute; source GI/GU manipulation; native or prosthetic valve [1][2]
  • Nosocomial bacteraemia (esp catheter-related, post-abdominal surgery) [3]
  • Intra-abdominal/pelvic infections (often polymicrobial)
  • PD-related peritonitis (G+ve organism in CAPD patients) [8]
  • Neonatal sepsis (less common than GBS; E. faecalis more common than faecium in neonates)
Diagnosis
  • Blood culture (≥2 sets), urine C/ST, PD fluid culture as appropriate
  • Gram stain: G+ve cocci in chains (may mimic streptococci)
  • Species ID + susceptibility testing essential (ampicillin, vancomycin, high-level gentamicin)
  • High-level aminoglycoside resistance (HLAR) screen: if HLAR +ve → synergy with ampicillin lost
Treatment
  • Ampicillin (IV) or amoxicillin-clavulanate (PO, Augmentin) for susceptible Enterococcus [4][5]
  • E. faecium is usually ampicillin-resistant → use vancomycin [4][5]
  • 3rd-gen cephalosporins are NOT effective (intrinsic resistance) [4][5]
  • Aminoglycosides NOT effective as monotherapy (intrinsic low-level resistance); used for synergy with ampicillin/vancomycin in IE [1][2]
  • For VRE E. faecium: linezolid or daptomycin (last resort agents)
  • IE regimen: IV ampicillin + gentamicin for 4–6 wks (if susceptible); vancomycin if ampicillin-R [2]
Prevention
  • Contact precautions for VRE in hospital; hand hygiene paramount [3]
  • Antibiotic stewardship to limit selection pressure (restrict broad-spectrum cephalosporins/carbapenems)
  • No vaccine available
  • IE prophylaxis: amoxicillin before high-risk dental procedures in high-risk cardiac patients
Classic traps
  • Do NOT use cephalosporins for Enterococcus — a classic exam trap [4][5]
  • E. faeciumE. faecalis: faecium is more drug-resistant (ampicillin-R, more VRE)
  • Neonatal meningitis G+ve cocci in chains → think GBS first, not E. faecalis [9][10]
  • S. bovis IE → think colonic neoplasm; Enterococcal IE → think GU/GI manipulation [2]
  • Nitrofurantoin can treat enterococcal lower UTI (but not upper tract — poor tissue levels) [4]

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