A 20-year-old develops acute rheumatic fever 3 weeks after untreated streptococcal pharyngitis. The mechanism of cardiac damage in rheumatic fever is best explained by:

• A Direct invasion of cardiac muscle by the bacteria
• B Molecular mimicry between M protein and cardiac myosin ✓
• C Streptolysin O directly damaging cardiac cell membranes
• D Immune complex deposition in cardiac endothelium

Explanation

Rheumatic carditis occurs through molecular mimicry: Group A Streptococcus M protein shares antigenic epitopes with human cardiac myosin, valvular endothelium, and sarcolemmal membrane proteins. Antibodies produced against M protein cross-react with these cardiac antigens, causing valvular inflammation and progressive scarring. The mitral valve is most commonly affected, followed by aortic, tricuspid, and pulmonary valves (descending order). Secondary prophylaxis with long-acting benzathine penicillin G prevents recurrences and further valve damage.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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