Holly Murphy,1 Aurélie Renvoisé,1 Prativa Pandey, Philippe Parola, and Didier Raoult
We report a case of Rickettsia honei infection in a human in Nepal. The patient had severe illness and many clinical features typical of Flinders Island spotted fever. Diagnosis was conﬁrmed by indirect immunoﬂuorescent assay with serum and molecular biologicaltechniques. Flinders Island spotted fever may be an endemic rickettsiosis in Nepal.
ick-borne rickettsioses are emerging zoonoses of marked endemicity caused by spotted fever group (SFG) rickettsia. Interest in rickettsioses is associated with increased description of new species and diseases, but this increase is unevenly distributed worldwide. Among patients with fever in Nepal, murinetyphus and scrub typhus are frequently described (1), but tick-borne rickettsioses remain underinvestigated. Rickettsia honei is an SFG species that was described as a new species in 1998 and as the cause of Flinders Island spotted fever (FISF) in Australia (2,3). One human case of FISF has been conﬁrmed in Thailand (4). We report a case of tick-borne rickettsiosis in Nepal caused by R. honei andhighlight the necessity for heightened interest in emerging rickettsioses in Asia.
The Patient A 67-year-old woman was admitted to the Canadian International Water and Energy Consultants Clinic Travel Medicine Center in Kathmandu, Nepal, in April 2009. She had a 5-day history of fever (40.3°C), headache, diarrhea, and severe arthralgias. Results of a physical examination were unremarkable.Laboratory tests showed a leukocyte count of 6,500 cells/mm3, an increase in immmature neutrophils and polymorphonuclear leukocytes, and thrombocytopenia. Treatment was initiated with intravenous ceftriaxone, 2 g every 24 h for 8 days, for suspected enteric fever. Within 48 hours, her condition worsened. The patient had photosensitivity, tinnitus, frontal headache, insomnia, confusion, cough, distress,hypotension, tachycardia, hypoxia (88% oxygenation with 2 L of O2), and fever (38.4°C). She was also disoriented regarding place and
Author afﬁliations: Canadian International Water and Energy Consultants Clinic Travel Medicine Center, Kathmandu, Nepal (H. Murphy, P. Pandey); and Université de la Méditerranée, Marseille, France (A. Renvoisé, P. Parola, D. Raoult) DOI:http://dx.doi.org/10.3201/eid1710.101943
time and had bilateral deafness, conjunctivitis, multiple lymphadenopathies, tender hepatosplenomegaly, bilateral rales, and a purpuric rash. The rash showed a predilection for the extremities, including palms and soles (Figure). There was no eschar. Pertinent laboratory values were the following: creatinine 2 mg/dL (baseline 0.8 mg/dL), aspartate aminotransferase 105 U/L,alkaline phosphatase 765 U/L, and minimum platelet count 40,000/mm3. Chest radiograph showed bilateral interstitial inﬁltrates. The patient was from New Zealand, had lived in Nepal for 30 years, and worked in wild dog protection. She reported removal of a tick 2 weeks before admission and contact with dogs, rats, ticks, ﬂeas, and mosquitoes. She had returned from a 1-month visit to Queenstown, NewZealand, 3 months earlier and had stayed for 2 days in Thailand. She spent 1 year in Canberra, Australian Capital Territory, Australia, 12 years earlier. She was treated with oral doxycycline (100 mg 2×/d for 14 days) and showed defervescence by day 16. She recovered slowly over 3 months but had persistent tinnitus and residual high-tone hearing loss bilaterally. Serum samples were sent to the Unité desRickettsies (Marseille, France) to identify the etiologic agent. Samples were tested by using a multiple-antigen immunoﬂuorescent test (5). Antigens included those from SFG Rickettsia spp., typhus group Rickettsia spp., and Orientia tsutsugamushi. Increased immunoglobulin (Ig) G and IgM titers were observed, mainly for SFG rickettsiae (Table). Kinetics of antibodies titers showed seroconversion...