Rapid Review·Cardiovascular
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PATHOLOGY
T2High yieldRheumatic Fever & Rheumatic Heart Disease
FA P319
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Molecular mimicry after strep throat, and the valve that pays for it decades later.
Key takeaways
Molecular mimicry after strep throat
Rheumatic fever
a nonsuppurative consequence of pharyngeal infection with group A beta-hemolytic streptococci. Its late sequela is rheumatic heart disease, hitting mitral > aortic >> tricuspid, i.e. the highest-pressure valves worst.Mechanism
immune mediated, a type II hypersensitivity, and not a direct bacterial effect. Antibodies against streptococcal M protein cross-react with self antigens in nerve and myocardium, most often myosin. This is molecular mimicry.The Jones criteria
| Letter | Criterion |
|---|---|
| J | Joint: migratory polyarthritis |
| ♥ | Carditis, i.e. pancarditis, the main cause of morbidity |
| N | Nodules, subcutaneous |
| E | Erythema marginatum, an evanescent rash with a ring margin |
| S | Sydenham chorea: involuntary irregular movements of limbs and face |
Confirming it
raised anti-streptolysin O and anti-DNase B titers.Histology
Aschoff bodies (granulomas with giant cells) containing Anitschkow cells (enlarged macrophages with an ovoid, wavy, rod-like "caterpillar" nucleus).| Finding | Description |
|---|---|
| Aschoff body | Granuloma with giant cells |
| Anitschkow cell | Enlarged macrophage with an ovoid, wavy, rod-like ("caterpillar") nucleus |
The valve that pays for it
Early regurgitation, late stenosis
that single rule explains why a child presents with mitral regurgitation and the same patient as an adult has mitral stenosis.| Timing | Lesion | Why |
|---|---|---|
| Early | Regurgitation | Acute inflammation of the leaflets |
| Late, years on | Stenosis | Scarring and fusion at the leaflet tips |
| Valve order | Mitral > aortic >> tricuspid | The highest-pressure valves are hit hardest |
Treatment and prophylaxis
penicillin.Why does penicillin prevent rheumatic carditis but not treat it?
The damage is immune, not infectious: antibodies to M protein cross-react with cardiac myosin (type II hypersensitivity). Killing the streptococcus stops the trigger; it does not undo the cross-reaction.
How it's tested
Rheumatic fever is a type II hypersensitivity driven by molecular mimicry: antibodies against streptococcal M protein cross-react with cardiac myosin, so the damage is immune rather than infectious, which is why penicillin is prophylaxis rather than treatment for the carditis. The mitral valve is hit first and hardest because it is the highest-pressure valve, and the lesion evolves from regurgitation in childhood to stenosis decades later, so the same disease gives two different murmurs depending on the patient's age.
Go deeper
First Aid 2026 — CV/Pathology (p.319) · B&B — Rheumatic fever · Mehlman — HY Cardio (Jones criteria, Aschoff bodies, mitral stenosis is 99% rheumatic)
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