Infectious disease · USMLE Step 1 and Step 2

Streptococcus pyogenes - Group A song

Group A Strep - Sequelae & Toxins, as a song. Hear the short teaser here. The full song is on YouTube and Spotify.

Streptococcus pyogenes - Group A

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Key points in this song10

Streptococcus pyogenes is a gram-positive, beta-hemolytic, catalase-negative coccus that is bacitracin-sensitive and PYR-positive, distinguishing it from other streptococci.
M protein is the major virulence factor, inhibiting complement activation and phagocytosis by binding factor H; antibodies against M protein are type-specific and protective.
Streptolysin O is oxygen-labile and immunogenic, forming the basis of the ASO titer used to confirm recent GAS infection in rheumatic fever workup.
Pharyngitis caused by GAS must be treated with penicillin (first-line) or amoxicillin to prevent acute rheumatic fever; treatment does NOT prevent post-streptococcal glomerulonephritis.
Rheumatic fever follows pharyngitis (never skin infection) and is diagnosed using Jones Criteria: major criteria include carditis, polyarthritis, Sydenham chorea, erythema marginatum, and subcutaneous nodules.
Post-streptococcal glomerulonephritis presents 1–3 weeks after pharyngitis or 3–6 weeks after impetigo with hematuria, hypertension, and low complement (C3); ASO titer is elevated after throat infection, anti-DNase B after skin infection.
Scarlet fever results from erythrogenic exotoxin (superantigen); presents with pharyngitis, strawberry tongue, and a sandpaper rash that blanches, sparing the palms and soles.
Toxic shock-like syndrome from GAS is caused by exotoxin A (superantigen), which cross-links MHC II and T-cell receptor, causing massive cytokine release without prior antigen processing.
Necrotizing fasciitis ("flesh-eating" infection) is a surgical emergency caused by GAS spreading along fascial planes; characterized by pain out of proportion to exam, requires immediate surgical debridement plus IV penicillin and clindamycin.
Clindamycin is added in severe GAS infections to inhibit toxin production by halting ribosomal protein synthesis, even though GAS is uniformly penicillin-sensitive.