We report the case of a 26-year-old male who presented to us with the complaint of fever for 7 days which was insidious in onset, low grade without chills, and rigors. He also noted diarrhea for 5 days which was watery, 4-5 times per day associated with diffuse abdominal discomfort but not associated with the passage of blood or mucous. He then noticed jaundice and passage of dark urine for 3 days without any decrease in the frequency or volume of urine. There was no prior history of blood in urine or cola colored urine or burning micturition. There was no history of jaundice, pruritus, clay stools, melaena, hematemesis, abdominal distension, or altered sensorium. He reported only an occasional intake of ethanol. The patient denied intake of indigenous medications or intoxication. The patient did not report any past major surgeries, blood transfusions, or IV drug abuse prior to onset of the disease. He did not report any history of diabetes, hypertension, tuberculosis, thyroid disease, trauma, exposure to industrial toxins or radiation, blood or blood component therapy, bleeding disorders, promiscuity, or similar complaints in the family or neighbourhood. At the time of admission, he was conscious, was oriented, and was febrile. His blood pressure was 110/70 mm of Hg in the right arm, pulse-108/min. He was icteric and did not have pallor, clubbing, cyanosis, pedal edema, or lymphadenopathy. He did not have any skin rash or stigmata of chronic liver disease such as spider angioma, palmar erythema, and parotid enlargement. His initial lab data revealed a hemoglobin of 12 g/dL, total leucocyte counts 11330/dL, and INR (international normalized ratio) of 2.69. His serum bilirubin was 4.5 mg/dL with predominant direct fraction of 3 mg/dL and indirect fraction of 1.5 mg/dL. Liver enzymes showed aspartate transaminase (AST) 452 IU/L, alanine transaminase (ALT) 2750 IU/L, alkaline phosphatase 254, and gamma glutamyl transferase (GGT) 169. Serum albumin was reduced at 2.2 g/dL with globulins 2.7 g/dL. His blood urea was 132 mg/dL with serum creatinine levels of 9.37 mg/dL with normal serum electrolytes suggestive of acute kidney injury. His IgM anti-HEV was positive and serology for hepatitis A, hepatitis B, hepatitis C, HIV, dengue, and Leptospira was negative. His peripheral blood smear and rapid malaria test was negative. Due to his deranged renal functions, he was started on slow low efficiency dialysis (SLED) sessions and gradually his urine output improved over the next few days. He was managed conservatively with IV antibiotics, IV fluids, nutritional therapy, and other supportive measures. After two sessions of SLED, he progressed to a polyuric phase, so dialysis was stopped and patient was managed conservatively. On day 6 of presentation, he developed fever again with left sided pleuritic pain and sudden onset of shortness of breath. He was found to be restless and dyspneic and on auscultation he had an S 3 gallop rhythm. Due to increasing respiratory distress, he was intubated and required mechanical ventilation for 3 days. Arterial blood gas analysis revealed type 1 respiratory failure with hypoxemia, and ECG showed sinus tachycardia and dynamic ST-T changes. Chest X-ray was suggestive of pulmonary congestion. Urgent 2D echocardiography revealed global hypokinesia, with normal LV and RV size, but ejection fraction was reduced to 25-30% with preserved right ventricular function. Troponin I was positive at 0.5 ng/mL and creatinine kinase-MB fraction levels were increased at 68 IU/L, 28% of total CK. This was suggestive of myocarditis. He was followed up by daily echocardiograms (see Figure 1). Over a period of 2 days, he gradually improved and was weaned off mechanical ventilation. His ejection fraction improved to 45% by day 3 and 60% with normal ventricular function by day 6. We performed a cardiac magnetic resonance imaging study on day 10 of myocarditis, but by then there was only marginal hypokinesia of the lateral left ventricular wall (see Figures 2 and 3). He was discharged on day 11 of hospital stay.