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Gram-positiveCocciCatalase-negative

Enterococcus faecalis

Gram-positive, catalase-negative coccus found in chains, a leading cause of nosocomial urinary tract infections, endocarditis, and biliary tract infections, notable for intrinsic resistance to cephalosporins and low-level aminoglycosides.

Organism Card

DomainMust know
Identity
  • G+ve cocci in chains/pairs; facultative anaerobe
  • Formerly classified as "Group D streptococci" (Lancefield D); now genus Enterococcus
  • **E. faecalis & E. faecium are the two most clinically important species** [1]
  • Normal gut flora; mainly opportunistic pathogen [1]
Lab discriminator
  • Catalase −ve (like streptococci), but PYR +ve (vs viridans strep PYR −ve)
  • Grows in 6.5% NaCl and bile-esculin +ve (both distinguish from streptococci)
  • Grows on MacConkey agar (unusual for G+ve cocci)
  • γ-haemolytic (non-haemolytic) on blood agar (some strains α-haemolytic)
  • Lancefield group D antigen (shared with S. bovis, but S. bovis is bile-esculin +ve / 6.5% NaCl −ve)
Reservoir / transmission
  • Normal flora of GI and GU tracts [1][2]
  • Source in IE: GI/GU pathologies or manipulations [2][3]
  • Nosocomial spread via healthcare workers' hands and contaminated devices [4]
  • Common in hospitalized/catheterized patients; biofilm formation on devices [4]
Key virulence
  • Biofilm formation on catheters and prosthetic devices → persistent infection [4]
  • Aggregation substance → adherence to cardiac valves
  • Gelatinase, cytolysin → tissue damage
  • Intrinsic resistance to multiple antibiotic classes is itself a major virulence advantage [1]
Clinical syndromes
  • Catheter-associated UTI — 2nd most common cause of complicated/nosocomial UTI [1][5]
  • Infective endocarditis — subacute; source GI/GU tract; part of VASH mnemonic [2][3]
  • Component of polymicrobial intra-abdominal / biliary infections (e.g. cholecystitis, SBP, liver abscess) [1][6][7]
  • Line sepsis / catheter-related bloodstream infection [1][4]
  • PD-related peritonitis (G+ve cause in CAPD patients) [8]
  • Wound / surgical site infections (mixed flora)
Diagnosis
  • Blood C/ST (≥3 sets for IE); urine C/ST for UTI; peritoneal fluid C/ST for peritonitis
  • Grows readily on standard media; identified by bile-esculin, 6.5% NaCl, PYR
  • In IE: community-acquired enterococcal bacteraemia without primary focus = Duke major criterion [9]
  • Pitfall: must specify species (faecalis vs faecium) — affects resistance profile
Treatment
  • Intrinsically resistant to cephalosporins and aminoglycosides as monotherapy [1][10]
  • 3rd-gen cephalosporins NOT effective against Enterococcus — major exam trap [10]
  • First-line: ampicillin (IV) or amoxicillin-clavulanate (PO/IV) for susceptible strains [10]
  • IE Rx: IV ampicillin + gentamicin (synergistic combination) for 4–6 weeks [2][3]
  • If ampicillin-resistant → vancomycin [10]
  • **VRE (usually E. faecium): daptomycin / linezolid / tigecycline** [1]
  • UTI: augmentin or nitrofurantoin (avoid cephalosporins) [10]
  • Fluoroquinolones have limited role due to marginal potency / acquired resistance [11]
Prevention
  • Strict hand hygiene and contact precautions for VRE
  • Remove/replace unnecessary urinary catheters and IV lines early
  • Antibiotic stewardship: avoid unnecessary cephalosporin/broad-spectrum use (selects for VRE)
  • IE prophylaxis: amoxicillin before high-risk dental procedures in susceptible cardiac patients [2]
Classic traps
  • **E. faecalis vs S. bovis: both are former "Group D strep" and cause IE — but S. bovis is penicillin-sensitive and a/w colonic neoplasia; Enterococcus is penicillin-resistant** [2]
  • **E. faecalis vs E. faecium: faecium more likely VRE; faecalis more common overall** [1]
  • *Neonatal meningitis stem (day 2 of life, G+ve cocci in CSF) → answer is GBS, NOT E. faecalis*** [12][13]
  • Do NOT treat Enterococcal UTI/IE with cephalosporins alone — intrinsic resistance [10]

Exam Intelligence

  1. GC 105 slide explicitly lists Enterococcus diseases as: catheter-associated UTI, endocarditis, component of polymicrobial intra-abdominal/biliary infections, line sepsis — this is the exact HKUMed-examinable disease list [1].

  2. "Resistant to many antibiotics, e.g. cephalosporins" — GC 105 flags this as the key pharmacological point. Cephalosporin resistance is intrinsic and absolute; this is the single most tested treatment trap for Enterococcus [1].

  3. VRE = usually E. faecium, not E. faecalis; treatment options are daptomycin / linezolid / tigecycline — directly from GC 105 [1].

  4. GC 102 (immunocompromised host): Enterococcus listed alongside aerobic G−ve bacilli as a Foley's catheter-associated UTI pathogen — reinforces the catheter-associated UTI angle [4].

  5. Felix Lai notes (Medicine/Paeds/Surgery) all independently emphasise: "Enterococcus is intrinsically resistant to cephalosporins and aminoglycoside monotherapy — use Augmentin or nitrofurantoin" — this exact phrasing appears three times across senior notes and is clearly a favourite teaching point [10].

  6. AOS Microbio Q3 (neonatal meningitis stem): E. faecalis is a distractor; correct answer is GBS — know the neonatal sepsis organisms (GBS, E. coli) and do not confuse with Enterococcus [12].

  • Enterococcus vs S. bovis in IE vignette: Both are "Group D." If the stem mentions colonic pathology (CA colon, ulcerative colitis) → S. bovis. If the stem mentions GU manipulation, catheterisation, or resistant organism → Enterococcus. S. bovis responds to penicillin alone; Enterococcus requires combination therapy (ampicillin + gentamicin) [2][3].

  • Empirical subacute IE regimen: IV ampicillin + IV gentamicin covers viridans strep, HACEK, and enterococci simultaneously. If cultures grow HACEK → switch to ceftriaxone. If Enterococcus confirmed → continue ampicillin + gentamicin [3].

  • Aminoglycoside "synergy" concept: Aminoglycosides alone do NOT kill enterococci (intrinsic low-level resistance). They are added for synergistic bactericidal activity with a cell-wall-active agent (ampicillin or vancomycin). High-level aminoglycoside resistance (HLAR) abolishes this synergy — a potential exam question angle.

  • Carbapenems: Felix Lai notes list E. faecalis and Listeria as G+ve organisms covered by carbapenems (imipenem > meropenem for E. faecalis). However, E. faecium is intrinsically resistant to carbapenems [11].

  • UTI treatment trap: If a complicated UTI question grows Enterococcus → do NOT choose ceftriaxone or gentamicin alone. Choose augmentin (oral) or ampicillin (IV). Nitrofurantoin is an alternative for lower UTI only [10].

2023 Fourth Summative MCQ Q83 [13]:

"A neonate (day 2 of life) develops high fever, lethargy and feeding difficulty. Sepsis workup is performed including lumbar puncture. [Gram stain image of CSF provided.] Which of the following microorganisms is MOST LIKELY to be grown in culture from the cerebrospinal fluid? A. Enterococcus faecalis B. Group B streptococcus C. Staphylococcus aureus D. Streptococcus pneumoniae"

  • Correct answer: B. Group B streptococcus
  • Rationale: Neonatal sepsis/meningitis at day 2 = early-onset neonatal sepsis. The two key organisms are GBS (S. agalactiae) and E. coli. The Gram stain showing G+ve cocci in chains/pairs points to GBS. E. faecalis (option A) is a distractor — it is G+ve cocci in chains but is NOT a classic cause of early-onset neonatal meningitis. S. pneumoniae causes meningitis in older infants/children, not neonates. This question also appears in the AOS Microbio practice set with identical stem [12][13].

No other past paper questions in the indexed context directly test Enterococcus faecalis as the primary organism. However, Enterococcus features as part of empirical IE therapy discussions and UTI microbiology in multiple minicase/SAQ stems across years (e.g. cholecystitis minicases where "Strep faecalis" is listed among secondary biliary infection organisms [7]).

[1] Lecture slides: GC 105. Medically important microbes what every doctor should know.pdf, p17 [2] Senior notes: Adrian Lui Pediatrics Notes.pdf, p237 (IE microbiology) [3] Senior notes: Ryan Ho Cardiology.pdf, p147–150 (IE management) [4] Lecture slides: GC 102. Fever after chemotherapy infections in immunocompromised hosts [Handout].pdf, p5 [5] Senior notes: Ryan Ho Urogenital.pdf, p123 (UTI microbiology table) [6] Senior notes: Ryan Ho GI.pdf, p237 (pyogenic liver abscess microbiology) [7] Senior notes: Maksim Surgery Notes.pdf, p132 (acute cholecystitis – "Strep faecalis") [8] Senior notes: Ryan Ho Urogenital.pdf, p114 (PD peritonitis) [9] Senior notes: Ryan Ho Cardiology.pdf, p149 (Modified Duke Criteria) [10] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf, p993 (UTI treatment – Enterococcus resistance) [11] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf, p22 (antibiotic tables – carbapenems, fluoroquinolones) [12] AOS material: AOS - Microbio.pdf, p3 (neonatal meningitis MCQ) [13] Past papers: 2023 Fourth Summative MCQ.pdf, p32, Q83

Streptococcus agalactiae

Encapsulated beta-hemolytic Group B Streptococcus (Gram-positive coccus in chains) that is a leading cause of neonatal meningitis, sepsis, and pneumonia, as well as invasive infections in pregnant women and immunocompromised adults.

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.

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