INTRODUCTION: Q fever, caused by Coxiella burnetti, is a zoonotic infection which naturally infects animals. Humans can contract it by inhalation of contaminated feces, ingestion of contaminated milk, and very rarely by ingestion of contaminated organs. Q fever can have varying clinical presentations including flu-like illness, pneumonia, or endocarditis, but hepatitis is the most common amongst young, healthy patients. We present a striking case of cholestatic jaundice secondary to Q fever. CASE DESCRIPTION/METHODS: A 43 year old male presented with a two week history of severe myalgias, headache, jaundice, fever, and abdominal pain which began after returning to the US from his 7th military tour in Afghanistan. He denied exposure to contaminated water or ticks but had eaten local cuisine including goat liver. He was febrile to 102.5 F, had scleral icterus, conjunctival suffusion, was jaundice, and had hepatosplenomegaly. Pertinent labs: platelets 59,500, total bilirubin 12.4 mg/dL, direct bilirubin 8 mg/dL, AST 41 units/L, ALT 56 units/L, and alkaline phosphatase 138 units/L. Pipercillicin/tazobactam and doxycycline were started empirically. There was no biliary obstruction on MRCP. Testing for CMV, EBV, HIV, syphilis, malaria, Rocky Mountain Spotted Fever, tularemia, ehrlichiosis, chikungunya, leptospirosis, histoplasmosis, tuberculosis, Q fever, and dengue were obtained. Ten days into his hospital stay the Coxiella burnetii DNA PCR returned positive. Despite optimum therapy on doxycyline, he did not defervesce for 14 days, 24 hours after hydroxychloroquine was added. At follow up, he remained afebrile and his total bilirubin had normalized to 0.9 mg/dL (peak of 13.7 mg/dL). DISCUSSION: This is a rare presentation of a rare disease given the degree of hyperbilirubinemia as Q fever typically causes a hepatocellular pattern of injury. It is unusual for Q fever to cause a bilirubin greater than 5 mg/dL. Also, febrile duration despite appropriate pharmacologic therapy has been found to be prolonged in patients with hyperbilirubinemia as opposed to those without, as was the case with our patient. Thrombocytopenia has also been described as a rare feature of Coxiella burnettii infection. Given this clinical picture, it is important to consider Q fever for a direct hyperbilirubinemia, prolonged fever, and thrombocytopenia in patients with a potential exposure history. It is also essential to consider oral transmission of Coxiella burnetti as a potential rare mode of transmission.