A pilgrim's progress: severe Rickettsia conorii infection complicated by gangrene.

A 47-year-old Australian man of Vietnamese origin presented to hospital 3 days after returning from a 2-week pilgrimage to Nepal and India in January 2012 with a 10-day history of fever and myalgia. He had developed high-grade fever with chills and rigors associated with myalgia 7 days after arriving in Nepal. Two days later, he developed nausea and vomiting. He had been vaccinated for hepatitis B and cholera before travel. He was not taking prophylactic antibiotics. He travelled with a group of 10 others who remained well. He recalled receiving a few mosquito bites, and noted rodent infestation and stray dogs in some of the temples he visited. A doctor in the group treated him empirically with oseltamivir after his initial symptoms began. A rash developed 2 days before his admission and 9 days after the onset of symptoms. The main fi ndings of an examination on admission were a high fever (40°C), a macular erythematous rash over his trunk and extremities sparing his palms and soles, and facial fl ushing. There were no eschars. Laboratory investigations on admission showed a platelet count of 44 109/L (reference interval [RI], 150–450 109/L), white cell count of 14 109/L (RI, 4–11 109/L; 88% neutrophils), and haemoglobin concentration of 124 g/L (RI, 135–175 g/L). Biochemical tests and liver function tests showed the following levels (with RIs in parentheses): sodium, 124 mmol/L (137–145 mmol/L); urea, 6.1 mmol/L (2.7–8.0 mmol/L); creatinine, 74 μmol/L (50–120 μmol/L); albumin, 21 g/L (34–48 g/L); lactate dehydrogenase, 478 U/L (110–230 U/L); bilirubin, 31 μmol/L (2–24 μmol/L); γ-glutamyl transferase, 242 U/L (< 60 U/L); alkaline phosphatase, 243 U/L (30–110 U/L); alanine aminotransferase, 136 U/L (< 55 U/L); and aspartate aminotransferase, 159 U/L (< 45 U/L). The international normalised ratio was 1.2 (0.9– 1.2). Laboratory features of disseminated intravascular coagulation such as elevated D-dimer and low fi brinogen concentrations were not present. There was no evidence of glucose-6-phosphate dehydrogenase (G6PD) defi ciency. Differential diagnoses included leptospirosis, enteric fever, dengue fever, chikungunya, malaria, rickettsiosis and infl uenza. Results of initial investigations were suggestive of dengue fever (IgM-positive, IgG-negative, although a test for dengue virus NS-1 antigen was negative). Blood cultures and serological tests for leptospirosis and rickettsia at admission were negative. Because of the broad differential diagnosis, and despite the initial positive serological test for dengue virus, the patient was treated empirically with ceftriaxone and doxycycline and nursed in a side room with infection control droplet precautions. Over the next 48 hours, the patient developed increasing thigh pain, conjunctival injection, and his rash evolved into a petechial/haemorrhagic rash, particularly over the legs. He developed bilateral leg oedema. His fi ngertips and toes became dusky and swollen with poor capillary refi ll (Box 1). His oxygen requirement increased and he was transferred to the intensive care unit. Compartment syndrome was ruled out. A skin biopsy showed epidermal necrosis, fi brin thrombi and associated vascular necrosis with variable infl ammatory A pilgrim’s progress: severe Rickettsia conorii infection complicated by gangrene