Although viruses remain the most common cause of hepatitis, other causes like rickettsial hepatitis are also well known. However, this aetiology has not been well recognized and it has been rarely reported in the Indian literature. Here, we are discussing a case of acute hepatitis, its clinical presentation, diagnosis and treatment, which was later found to be caused by Indian tick typhus (a spotted fever group rickettsia), which was diagnosed on the basis of serology and its clinical response to doxycycline. Further literature review has been done, to discuss various clinical presentations and prevalence of rickettsial infection in this part of the world.
CASe RepoRTA 42-year-old male patient who was from district Una, Himachal Pradesh, India, presented with a 5 days history of intermittent fever and right upper quadrant abdominal pain, which were preceded at the onset by loose stools and vomiting of 1 day duration. Fever was high-grade, intermittent and it was associated with chills, myalgia, headache, generalized weakness and which responded well to antipyretics. His past history showed that he was a known case of Gilbert's syndrome since 1995, who had multiple episodes of self resolving jaundice in past 15 years. Examination showed icterus and anaemia. Abdominal examination revealed tender hepatomegaly with a liver span of 17 cm and mild splenomegaly. On investigating, haemogram revealed haemoglobin of 11.5 gm% (normal 12-15 gm%) and a total leucocyte count of 18500 µl -1 (Reference range = 4000 -11000 µl -1 ), with predominance of polymorphonuclear leucocytes and an erythrocyte sedimentation rate (ESR) of 40 mm/first hour. Liver function tests (LFT) showed unconjugated hyperbilirubinaemia (total 5.6 mg%, conjugated 0.93 mg %) (Reference range 0-1.2 mg %), aspartate aminotransferase (AST) -288 IU/L (Normal = 10-21 IU/L), alanine aminotransferase (ALT) -322 IU/L (Normal=2-15 IU/L) and serum alkaline phosphatase -27 KAU (N<13 KAU). Serum amylase and lipase values were normal. Cultures done from blood and urine were sterile. His peripheral blood film as well as Qdx test for malarial parasite showed negative results. Widal test showed negative results. His viral markers (Hepatitis A-E, CMV and HSV) and hemolytic work-up were negative. Ultrasound of abdomen showed features suggestive of acute hepatitis and cholecystitis. He empirically received antibiotics ciprofloxacin, metronidazole and cloxacillin initially and piperacillin plus tazobactam later, because of the little response in severity of fever. However, his Weil-Felix turned out to be positive, with OX 2 titre of 1:320 and subsequently, he was given doxycycline. Fever resolved within next 36 hours. The transaminases showed a decreasing trend, with normalization of LFT by next 4 weeks. Weil-Felix test was again repeated in convalescent sera, which showed a fourfold decrease in the titre (1:80).