In June, 2006, a 44-year-old previously healthy woman from a poor socio-economic background presented to us with a 5-day history of fever, dyspnoea, tight chest pain, and postural dizziness. This was preceded by an episode of diarrhoea over a week. On admission, respiratory rate was 40 breaths per min, radial pulse was regular at 130 beats per min, and blood pressure was 80/50 mm Hg. She had central cyanosis, was sweating profusely, and had cold peripheries. Heart sounds showed triple rhythm and she had fi ne basal crepitations in her lungs. Her abdomen was soft and non-tender; there was no sign of hepatosplenomagaly or ascites. She was promptly resuscitated with intravenous fl uids, but required intubation and mechanical ventilation in the intensive care unit. Broad-spectrum antibiotics including benzylpenicillin and ceftriaxone were given. Hypotension and tachycardia persisted despite maximum inotropic support. She subsequently developed acute renal failure and severe hepatic dysfunction; peritoneal dialysis and liver failure regimen were started. A 12-lead ECG showed ST segment depressions in leads I, aVL, and V2 to V6. Troponin T concentration was high. Initial echocardiography showed dilatation of all cardiac chambers and a hypokinetic left ventricle with left ventricular ejection fraction 42%; the latter declined to 36% on day 3. C-reactive protein was high (>1000 mg/L). White blood cell count was 10·8×109/L (76% neutrophils; 20% lymphocytes; 4% eosinophils). Blood and peritoneal fl uid cultures were repeatedly negative. No antibodies to the following were detectable: dengue virus, coxackievirus, infl uenza A and B viruses, parainfl uenza virus, adenovirus, RSV, hanta virus, herpes virus, HIV. Tests for leptospirosis were also negative. She had a generalised tonic-clonic convulsion on day 7; EEG showed generalised slow waves. The seizures were managed, but she died on day 15. At autopsy, purulent ascitic fl uid and organised pus on serosal surfaces were found. The caecum had multiple transverse ulcers and a perforation in the lateral wall. The heart was dilated, and the myocardium was fl abby and weighed 0·2 kg. There was a thin layer of pericardial eff usion. Staining of the myocardium for gram-negative bacteria and eosinophils was negative. However, fl orid colitis with Entamoeba histolytica in abundance was detected in the caecum, which also showed many fl ask-shaped ulcers, some of which had penetrated up to the serosa. The ulcer base and the adjacent caecal wall showed multiple amoebae with ingested red blood cells. Amoebae were also noted to be invading the muscular propria and the subserosal surface (fi gure A). However, molecular identifi cation was not done because of limited available resources. There were several foci of myocardial necrosis, some of which were organised with little infl ammation, suggestive of toxic myocarditis (fi gure B). A viral aetiology was initially considered because it is the most common cause of myocarditis. The possibility of an amoebic cause was not entertained antemortem, but the autopsy fi ndings confi rmed toxic cardiomyopathy. The absence of eosinophils and gramnegative bacteria in the myocardium supports the possible amoebic aetiology secondary/concurrent to bowel pathology. Pre-existing heart failure was unlikely because the patient was in good health just before the illness. E histolytica is primarily a bowel pathogen that causes colitis and liver abscesses. Rarely it causes mening oencephalitis and pericarditis. There are about 50 million cases of amoebiasis in the world and nearly 100 000 people die annually from complications. The case fatality rate remains high at 29% in some parts of Asia; the case fatality rate in Sri Lanka is 0·6/100 000 per year. Although E histolytica has been implicated in cases of dilated cardiomyopathy in animals, it has not been reported in human beings. Our case shows an uncommon consequence of a relatively common disease.