Infective endocarditis by Abiotrophia defectiva presenting as acute coronary syndromeAbiotrophia defectiva accounts for <1% of infective endocarditis (IE), 1 with <10 documented case reports from India. Interestingly, all these were insidious in onset with chronic duration and adequate time to plan for corrective surgery. [1][2][3][4] We report probably the first case of IE presenting with features of acute coronary syndrome by Abiotrophia defectiva from India.A 65-year-old man on mechanical ventilation was referred from a local hospital with complaints of worsening dyspnoea and chest pain for 4 days. His blood examination was within normal limits. His random blood sugar was 428 mg/dl, and fasting sugar 419 mg/dl. HbA1c was 11.3%, urine sugar was strongly positive and ketones were present. On admission his renal function test was normal. Troponin I levels (2598 ng/L) were elevated and an echocardiogram showed severe aortic regurgitation with vegetations on the aortic valve and a normal chamber. Three sets of blood cultures were processed in BacT/ ALERT microbial detection system. Gram-stain from flagged positive blood culture bottles showed Gram-positive bacilli. Chocolate and blood agar grew α-haemolytic colonies after 48 hours of incubation. There was no growth on MacConkey agar. Colony smear showed short slender irregularly stained pleomorphic Gram-positive bacilli with many showing clubbed ends (Fig. 1). It was catalase-negative, urease-negative and non-motile both at 37 ºC and room temperature. Acid-fast and modified acid-fast staining showed non-acid-fast bacilli. Albert staining did not show metachromatic granules. As VITEK identification gave inconclusive result, the isolate was sent for confirmation by MALDI-TOF and was identified as Abiotrophia defectiva (high confidence level 99.9).On the day of admission, the patient was started on ceftriaxone 2 g i.v. and other supportive measures. By day 4 of hospital admission, his renal parameters worsened (urea 95 mg/dl, creatinine 3 mg/dl, decreased urine output), developed pulmonary oedema and died due to cardiac arrest.