A 50 year old man presented with painful swelling in his feet, knees and right wrist 14 days after a throat infection (below). An ECG at the onset of symptoms had shown first degree heart block (ECG 1). His ESR was 108 mm/hr, CRP 336 mg/ml, WBC at 14.3×10⁹/l. ECG was normal (ECG 2). Treatment was started with ciprofloxacin, clarithromycin (he is penicillin sensitive) and tinzaparin for presumed cellulitis.

He developed chest pain and became pyrexial (38.5°C). ECG showed saddle shaped ST elevation in the anterior chest leads (ECG 3). Creatinine kinase was 19 and 20 iu/l (25–175), possibly low because of inactivation by low tissue glutathione (convalescent creatinine kinase was 114 iu/l). Troponin T was <0.01 μg/ml (<0.1). He was treated with aspirin 300 mg and pain relief. Echocardiogram was normal. Chest pain persisted and he went into atrial fibrillation (ECG 4); anticoagulation was initiated. Antistreptolysin O titres were raised at >800units/ml (<200), anti DNAse B 3840 units/ml (<240) and these subsequently fell indicating evidence of recent group A streptococcus infection. Throat swab showed scanty candida only.

At outpatient review he was in sinus rhythm (ECG 5) and there were no audible murmurs. He was commenced on clarithromycin 250 mg twice daily as prophylaxis and the warfarin was stopped.

As doctors in the UK are persuaded not to prescribe antibiotics for viral sore throats this will inevitably mean that more group A streptococcal throat infections go untreated. Can we expect to see a resurgence of rheumatic fever, a condition that many doctors trained in the developed world will never have seen, or will other host and organism related factors keep it at bay?