Streptococci & Enterococci: Species, Virulence & Lab ID
Bench tests, virulence factors, and the diseases they predict
Sorting the catalase-negative cocci
Shared traits. Streptococci and enterococci are gram-positive, catalase-negative cocci in chains or pairs; staphylococci are catalase-positive and grow in clusters. The general identification algorithm is in the Gram-Positive Cocci lesson; this chapter works species by species.
Hemolysis and Lancefield groups. On blood agar, α-hemolysis is partial (green zone), β-hemolysis complete (clear zone), and γ means none. Lancefield groups (A, B, D…) are cell-wall carbohydrate antigens; pneumococcus and most viridans streptococci are non-groupable, so bench tests identify them.
| Organism | Hemolysis | Key tests | Classic diseases |
|---|---|---|---|
| S. pneumoniae | α | Optochin-sensitive, bile-soluble, quellung-positive; lancet diplococci | Pneumonia, meningitis, otitis media, sinusitis |
| Viridans group | α (anginosus variable) | Optochin-resistant, bile-insoluble | Caries, subacute endocarditis, abscesses (anginosus) |
| S. pyogenes (A) | β | Bacitracin-sensitive, PYR-positive | Pharyngitis, skin infection, scarlet fever, TSS, ARF, PSGN |
| S. agalactiae (B) | β | Bacitracin-resistant, CAMP-positive, hippurate-positive | Neonatal sepsis, pneumonia, meningitis |
| S. gallolyticus (D) | Usually α or γ | Bile esculin-positive; no growth in 6.5% NaCl | Bacteremia/endocarditis with colorectal neoplasia |
| Enterococcus (D) | Usually γ (variable) | Bile esculin-positive, grows in 6.5% NaCl, PYR-positive | UTI, biliary/intra-abdominal infection, endocarditis |
α-Hemolytic streptococci: pneumococcus and the viridans group
Identifying S. pneumoniae. Pneumococci are lancet-shaped diplococci, optochin-sensitive (clear zone around the disk), and bile-soluble — bile salts activate the LytA autolysin. In the quellung reaction the capsule swells with type-specific antiserum. Pneumococci are naturally competent for transformation, the basis of Griffith's experiment.
Virulence. The polysaccharide capsule (more than 90 serotypes) is the key virulence factor: it blocks complement opsonization and phagocytosis, and unencapsulated strains are avirulent. IgA protease cleaves secretory IgA to allow nasopharyngeal colonization (also made by H. influenzae and Neisseria). Pneumolysin, a cholesterol-binding pore-forming toxin, injures epithelium and activates complement.
Disease (MOPS). Pneumococcus is the leading cause of community-acquired pneumonia (lobar consolidation, rust-colored sputum) and adult bacterial meningitis, and a top cause of otitis media and sinusitis; bacteremia is common. It often follows influenza or another viral infection. Its penicillin resistance comes from altered penicillin-binding proteins, not β-lactamase.
Asplenia and vaccines. Splenic macrophages, with IgM and complement, clear encapsulated bacteria. After splenectomy or with sickle cell autosplenectomy, patients risk overwhelming sepsis from S. pneumoniae, H. influenzae type b, and N. meningitidis; Howell-Jolly bodies mark absent splenic function. Conjugate vaccines (PCV15, PCV20, PCV21) link capsular polysaccharide to a carrier protein that recruits helper T cells, giving class switching and memory even in infants. PPSV23, a plain polysaccharide, is T-independent, poorly immunogenic under age 2, and lacks booster memory. Vaccinate at least 2 weeks before elective splenectomy.
Viridans streptococci. These optochin-resistant, bile-insoluble mouth commensals include S. mutans and S. sanguinis, which make dextran from sucrose. Dextran builds plaque (caries) and binds fibrin-platelet aggregates on previously damaged valves, causing subacute endocarditis, classically after dental work.
S. anginosus group. S. anginosus, S. intermedius, and S. constellatus (formerly the "milleri" group) form pus: brain, liver, and lung abscesses and empyema. Bacteremia with them should prompt a search for a hidden abscess. Hemolysis varies, and some carry Lancefield A, C, F, or G antigens, mimicking S. pyogenes.
Group A streptococcus (S. pyogenes)
Identification and pharyngitis. S. pyogenes is β-hemolytic, bacitracin-sensitive, and PYR-positive — the leading bacterial cause of pharyngitis (fever, tonsillar exudate, tender anterior cervical nodes, no cough). A rapid antigen test or throat culture confirms it (a negative rapid test in a child is backed up by culture). Penicillin or amoxicillin started within 9 days of onset prevents rheumatic fever.
| Factor | Action | Clinical tie-in |
|---|---|---|
| M protein | Blocks complement deposition and phagocytosis | Anti-M antibody gives type-specific immunity; mimics cardiac myosin |
| Hyaluronic acid capsule | Antiphagocytic; looks like host connective tissue | Nonimmunogenic |
| Streptolysin O | Oxygen-labile, immunogenic hemolysin | ASO titer marks recent infection |
| Streptolysin S | Oxygen-stable, nonimmunogenic hemolysin | β-hemolysis on the agar surface |
| Streptokinase | Converts plasminogen to plasmin | Dissolves clots, aiding spread |
| DNase B, hyaluronidase | Degrade DNA and ground substance | Anti-DNase B titer; tissue spread |
| SpeA, SpeC | Superantigen pyrogenic exotoxins | Scarlet fever, streptococcal TSS |
M protein and mimicry. Antibodies against M protein cross-react with cardiac myosin (molecular mimicry, type II hypersensitivity) — the basis of rheumatic fever, whose pathology is covered in the cardiovascular lesson.
Superantigens. SpeA and SpeC bridge MHC class II and the TCR Vβ chain outside the peptide groove, activating up to about 20% of T cells and releasing IL-2, TNF-α, and IFN-γ.
- Scarlet fever — pharyngitis plus a sandpaper rash starting on the neck and trunk, strawberry tongue, circumoral pallor, Pastia lines in skin folds, and later desquamation.
- Streptococcal TSS — shock and multiorgan failure, usually from an invasive focus such as necrotizing fasciitis; unlike staphylococcal TSS, blood cultures are usually positive.
- ImpetigoEpidermis; honey-crusted lesions around a child's nose and mouth (S. aureus also common)
- ErysipelasUpper dermis and lymphatics; raised, sharply demarcated, fiery-red plaque
- CellulitisDeep dermis and subcutaneous fat; spreading erythema with ill-defined borders
- Necrotizing fasciitisFascia; pain out of proportion, rapid spread, bullae, toxicity
Necrotizing fasciitis needs urgent surgical debridement plus penicillin and clindamycin; clindamycin halts toxin synthesis even in large, slow-growing inocula where penicillin falters (Eagle effect).
Nonsuppurative sequelae. Nephritogenic strains cause PSGN: cola-colored urine, hypertension, periorbital edema, and low C3, usually resolving fully in children.
| Feature | Acute rheumatic fever | PSGN |
|---|---|---|
| Preceding infection | Pharyngitis only | Pharyngitis or skin infection |
| Latency | About 2–4 weeks | ~1–2 weeks (throat); ~3–6 weeks (skin) |
| Mechanism | Type II (M-protein mimicry) | Type III immune complexes; low C3 |
| Prevented by antibiotics? | Yes — penicillin within 9 days | No |
Group B streptococcus and S. gallolyticus
Identifying GBS. S. agalactiae is β-hemolytic, bacitracin-resistant, and hippurate-positive; its CAMP factor enlarges S. aureus hemolysis into an arrowhead. A sialic acid-rich capsule is its main virulence factor.
Neonatal disease. GBS is a leading cause of neonatal sepsis and meningitis. Early-onset disease (first week, usually within 24–48 hours) follows vertical transmission and presents as sepsis, pneumonia, or meningitis; late-onset disease (1 week to 3 months) is usually bacteremia, with meningitis more frequent than in early-onset disease. Empiric neonatal therapy is ampicillin plus gentamicin. In mothers GBS causes chorioamnionitis, endometritis, and UTI.
- ScreenRectovaginal culture at 36 0/7 to 37 6/7 weeks
- Treat without screeningGBS bacteriuria in this pregnancy or a previous infant with GBS disease
- Unknown status in laborTreat if <37 weeks, membranes ruptured ≥18 hours, or intrapartum fever ≥38.0 °C
- IV penicillin G in labor≥4 hours before delivery; ampicillin alternative; cefazolin, clindamycin, or vancomycin for penicillin allergy
Intrapartum prophylaxis prevents early-onset disease only; late-onset GBS disease is unaffected.
S. gallolyticus. Formerly S. bovis biotype I, this non-enterococcal group D streptococcus hydrolyzes bile esculin but cannot grow in 6.5% NaCl. Its bacteremia or endocarditis is strongly linked to colorectal adenoma and carcinoma, so colonoscopy is required.
Enterococci and vancomycin resistance
Biology and disease. E. faecalis causes most enterococcal infections; E. faecium is more drug-resistant. These group D gut commensals grow in 6.5% NaCl and 40% bile (blackening bile esculin agar) and are PYR-positive; hemolysis is variable, usually γ. They cause UTIs (especially catheter-associated), biliary and intra-abdominal infections, and subacute endocarditis, classically in older men after GU or GI procedures.
Enterococci are intrinsically resistant to all cephalosporins (low-affinity PBPs); clindamycin and TMP-SMX are unreliable, and E. faecium is often ampicillin-resistant.
Synergy. Aminoglycosides alone barely enter enterococci (intrinsic low-level resistance). For endocarditis give ampicillin plus gentamicin — the β-lactam lets the aminoglycoside in — or, for E. faecalis, ampicillin plus ceftriaxone, which saturate complementary PBPs without nephrotoxicity. High-level aminoglycoside resistance abolishes gentamicin synergy.
VRE. The vanA cluster, on a transposon often carried by a plasmid, changes the peptidoglycan precursor terminus from D-Ala-D-Ala to D-Ala-D-Lac, lowering vancomycin binding about 1000-fold and giving high-level resistance to vancomycin and teicoplanin (vanB strains stay teicoplanin-susceptible). Most VRE are E. faecium; use contact precautions.
- Linezolid — binds 23S rRNA of the 50S subunit, blocking initiation complex formation; penetrates lung. Causes thrombocytopenia, serotonin syndrome with SSRIs, and optic or peripheral neuropathy.
- Daptomycin — calcium-dependent lipopeptide that depolarizes the membrane; inactivated by surfactant, so it fails in pneumonia; causes CK elevation and myopathy.