Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise post-streptococcal inflammatory disease, prevent recurrence and manage chronic valve damage in a UK pathway.
ARF is rare in the UK, so diagnostic delay is common, particularly in migrants or people with prior disease. Diagnosis is clinical and syndromic: no single ASO titre, ECG change or murmur is definitive.
The major preventable harm is recurrence, because repeated inflammatory episodes compound valve injury. Chronic disease then follows standard lesion-specific valve and anticoagulation pathways, with additional attention to prophylaxis adherence and family/social barriers.
Acute rheumatic fever follows an immune response to group A streptococcal throat or skin infection after a latent interval, rather than direct bacterial invasion of the heart.
Host susceptibility, crowding, repeated streptococcal exposure and barriers to prompt diagnosis or treatment increase risk, including for people arriving from higher-prevalence regions.
A previous episode creates vulnerability to further immune attacks. Missed secondary prophylaxis permits reinfection, and each recurrence can add cumulative valve inflammation and scarring.
The immune system generates antibodies and T-cell responses against streptococcal antigens during the antecedent infection, usually after pharyngeal or cutaneous exposure.
Cross-reactive immune responses recognise structurally similar host tissues, producing sterile inflammation in joints, heart, skin and the nervous system after infection has subsided.
Inflammation may involve endocardium, myocardium and pericardium. Mitral or aortic valvulitis causes regurgitation, and severe acute valve dysfunction can precipitate heart failure.
Acute and especially recurrent valvulitis can heal through fibrosis, causing leaflet thickening, commissural fusion and chordal shortening. These changes may produce stenosis, regurgitation or mixed multivalve disease.
Rheumatic valve obstruction or leakage can enlarge affected atria and ventricles, raise pulmonary pressure and promote atrial fibrillation, congestion and heart failure.
Painful swelling moving between knees, ankles, elbows or wrists after recent streptococcal infection is a typical major manifestation.
Tachycardia, new MR/AR murmur, cardiomegaly, pericarditic features or heart failure indicates pancardial involvement; Doppler-only valvulitis also counts.
Delayed, purposeless movements, emotional lability, hypotonia and deteriorating handwriting may be the sole presentation.
Erythema marginatum is an evanescent non-pruritic serpiginous rash; firm painless subcutaneous nodules are uncommon but specific clues.
Exertional dyspnoea, haemoptysis, AF, opening snap/mid-diastolic murmur or multivalve murmurs years later suggest rheumatic heart disease.
Pulmonary oedema, embolic neurology, pregnancy-related deterioration or fast AF with mitral stenosis needs urgent admission.
Persistent fever, positive blood cultures, destructive valve lesions or embolic phenomena favour active infection; acute rheumatic carditis is sterile and follows a compatible post-streptococcal syndrome.
A single intensely inflamed joint, systemic toxicity and positive synovial culture favour infection; rheumatic arthritis more often migrates between large joints.
Prominent ventricular dysfunction, arrhythmia and myocardial injury without Jones-criteria manifestations or preceding streptococcal evidence support myocarditis rather than rheumatic fever.
Persistent, additive joint inflammation, often with a less marked response to anti-inflammatory treatment and without other rheumatic-fever features, suggests post-streptococcal reactive arthritis.
Medication exposure, autoimmune disease and inherited or metabolic disorders can cause involuntary movements; Sydenham chorea has a compatible delayed post-streptococcal phenotype and neurological examination.
Cumulative valvulitis produces mitral stenosis or regurgitation and often multivalve disease, creating a lifelong need for surveillance and sometimes catheter or surgical intervention.
Elevated left-atrial pressure from mitral disease is transmitted to the pulmonary circulation, while valve overload eventually causes ventricular dysfunction and systemic congestion.
Chronic pressure and volume loading enlarge the left atrium, creating an arrhythmic substrate. Rapid ventricular response may abruptly worsen symptoms or precipitate pulmonary oedema.
Atrial fibrillation and blood stasis within an enlarged left atrium promote thrombus formation, particularly with moderate-to-severe mitral stenosis, allowing embolisation to the brain or other organs.
Increased circulating volume and cardiac output during pregnancy can expose limited reserve in mitral stenosis or pulmonary hypertension, causing congestion and haemodynamic deterioration.
Because it occurs months after infection, inflammatory markers and streptococcal serology can be normal; the neurological phenotype and exclusion of alternatives matter.
PR prolongation is not added as a minor Jones criterion when carditis is already used as a major criterion.
Pathological Doppler regurgitation can establish subclinical carditis even without an audible murmur.
Secondary prophylaxis is disease-modifying public-health treatment, not an optional add-on after joint symptoms resolve.
AF with moderate-to-severe rheumatic mitral stenosis remains a VKA indication; it is not the usual non-valvular AF DOAC pathway.
Diagnosing ARF from an ASO titre alone without a compatible syndrome.
Excluding carditis because there is no murmur or excluding chorea because serology is negative.
Stopping secondary prophylaxis when arthritis resolves without considering residual cardiac disease and age.
Using a DOAC for AF with moderate-to-severe rheumatic mitral stenosis.
Offering routine dental antibiotic prophylaxis solely for rheumatic valve disease despite NICE CG64.
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A 17-year-old has migratory ankle and knee arthritis three weeks after a sore throat, raised CRP and elevated streptococcal antibodies. No murmur is heard. What investigation is still required to look for a major Jones manifestation?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
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Check immediate beta-lactam allergy; administer strictly IM with aspiration and emergency anaphylaxis capability. Long-term therapy needs periodic renal, hepatic and blood-count review.
Adherence is less reliable than depot injection; check penicillin allergy and renal function, and do not use an abbreviated course for active GAS eradication.