Group A streptococci

GAS ID - The Fiery Chain-Maker

• Morphology: Gram-positive cocci growing in chains ("Strepto-").
• Culture: Shows complete (β) hemolysis on blood agar.
• Key Biochemical Markers:
  • Catalase-negative (all Strep are).
  • PYR positive (pyrrolidonyl arylamidase).
  • Bacitracin susceptible (differentiates from Group B Strep).

⭐ The "A" disk (Bacitracin) is key for presumptive ID. A zone of inhibition suggests S. pyogenes.

📌 Mnemonic: Remember B-BRAS: Bacitracin susceptible, Beta-hemolytic.

Virulence Factors - Weapons of Inflammation

• M Protein: Major virulence factor; antiphagocytic & anti-complement (degrades C3b).
  • Undergoes antigenic variation.
  • Mediates molecular mimicry → rheumatic fever.
• Hyaluronic Acid Capsule: Antiphagocytic; non-immunogenic as it mimics host connective tissue.
• Enzymes (“Spreading Factors”):
  • Streptokinase: Fibrinolytic; converts plasminogen to plasmin.
  • DNase (Streptodornase): Liquefies pus, facilitating spread.
• Toxins:
  • Streptolysin O: Oxygen-labile, antigenic (basis for ASO titer), lyses RBCs.
  • Pyrogenic Exotoxins (SpeA, B, C): Superantigens causing scarlet fever rash & toxic shock syndrome.

⭐ Antibodies against M protein can cross-react with cardiac myosin, leading to rheumatic heart disease-a classic example of molecular mimicry.

Clinical Syndromes - A Nasty Trio

• Pyogenic Inflammation (Local Invasion)

  • Pharyngitis (Strep Throat): Red, swollen tonsils/pharynx; exudates; tender cervical nodes.
  • Skin Infections: Impetigo (honey-crusted lesions), Cellulitis (deeper dermis), Erysipelas (superficial, well-demarcated).

• Toxin-Mediated Syndromes

  • Scarlet Fever: Sandpaper rash, strawberry tongue, Pastia's lines. Follows pharyngitis.
  • Toxic Shock-Like Syndrome (TSLS): Mediated by SpeA/C superantigens. Causes fever, shock, and multi-organ failure.
  • Necrotizing Fasciitis: "Flesh-eating bacteria." Deep subcutaneous infection, rapid tissue destruction.

• Immunologic (Post-Streptococcal) Disease

  • Acute Rheumatic Fever (ARF): 📌 JONES criteria (Joints, ❤️ Carditis, Nodules, Erythema marginatum, Sydenham chorea). Occurs 2-4 weeks post-pharyngitis ONLY.
  • Post-Streptococcal Glomerulonephritis (PSGN): Nephritic syndrome. Occurs after pharyngitis OR skin infection.

⭐ Rheumatic fever is a non-suppurative complication that follows pharyngitis only, not skin infections. PSGN can follow either.

Immunologic Sequelae - Post-Infection Chaos

Two major non-suppurative complications triggered by an adaptive immune response to Group A Strep antigens.

Acute Rheumatic Fever (ARF)

• Mechanism: Type II hypersensitivity. Molecular mimicry between Strep M protein and cardiac myosin.
• Diagnosis: Jones Criteria (major): migratory polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, Sydenham chorea.
• 📌 Mnemonic: JONES criteria.
• Key Finding: Aschoff bodies on heart biopsy.

Post-Streptococcal Glomerulonephritis (PSGN)

• Mechanism: Type III hypersensitivity. Immune complex deposition in glomeruli.
• Presentation: Nephritic syndrome (1-3 weeks post-infection) with edema, hypertension, and cola-colored urine (hematuria).
• Labs: ↓ C3 levels, ↑ ASO/anti-DNase B titers.
• Biopsy: Subepithelial "humps" on EM; granular "lumpy-bumpy" immunofluorescence.

⭐ High-Yield: PSGN can follow pharyngitis or skin infection (impetigo). Rheumatic fever only follows pharyngitis.

High‑Yield Points - ⚡ Biggest Takeaways

• Streptococcus pyogenes is the key pathogen, characterized by β-hemolysis.
• Its primary virulence factor, the M protein, is strongly antiphagocytic.
• Common suppurative infections include pharyngitis, impetigo, and cellulitis.
• Toxin-mediated diseases are scarlet fever, toxic shock syndrome, and necrotizing fasciitis.
• Immune sequelae are Acute Rheumatic Fever (molecular mimicry) and Post-Streptococcal Glomerulonephritis (Type III hypersensitivity).
• Penicillin remains the treatment of choice.