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Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: mmwrq@cdc.gov. Type 508 Accommodation and the title of the report in the subject line of e-mail. African TrypanosomiasisOn September 9, 1981, a 72-year-old male from Edinburg, Texas, developed fever and weakness 16 days after being bitten by tsetse flies during a hunting trip in northwest Tanzania. Several days after onset of fever, he noticed a raised, tender, erythematous nodule (6-8 cm in diameter) on the posterior aspect of his right arm. He was hospitalized in Africa and treated for 5 days with a cephalosporin for presumed cellulitis. After little improvement, he returned to Texas on September 20. On arrival, the patient had a temperature of 38.9 C (102 F), a morbilliform rash of the trunk, and right-sided, anterior cervical lymphadenopathy. Laboratory tests revealed a hemoglobin of 10.7 g/100 ml, a white-cell count of 2,400/mm((3)), and a platelet count of 75,000/mm((3)); peripheral blood smears showed trypanosomes. Cerebrospinal fluid (CSF) contained 12 red cells and 18 mononuclear cells/mm((3)), with a normal protein (32 mg/dL); no trypanosomes or morula cells of Mott (thought to be degenerated plasma cells) were observed. Serum obtained on September 21 and tested at CDC reacted to trypanosome antigen by indirect immunofluorescence at a dilution of 1:4096. Treatment with suramin (1 g intravenously on days 1, 3, 7, 14, and 21) was initiated on September 22, and within 48 hours of the first dose, neck swelling decreased noticeably, and rash and fever disappeared. The thrombocytopenia, anemia, and leukopenia resolved over a 2-week period. A second lumbar puncture on October 1, 10 days after therapy was begun, showed five lymphocytes/mm((3)), a protein of 27 mg/dL, and no IgM. Several follow-up examinations during the past year showed no clinical evidence of recurrent illness, but the patient declined additional lumbar punctures. Reported by R Reves, H Dupont, W Sievert, University of Texas Health Sciences Center, Houston; Protozoal Diseases Br, Div of Parasitic Diseases, Center for Infectious Diseases, CDC. Editorial NoteEditorial Note: This is the sixth published report since 1967 of imported African trypanosomiasis (African sleeping sickness) in Americans (1). All six patients have shared several characteristics: exposure to infected tsetse flies while visiting game parks in eastern or southern Africa, development of acute, febrile illness consistent with Trypanosoma brucei rhodesiense infection 1-21 days after visiting Editorial Note: This is the sixth published report since 1967 of imported African trypanosomiasis (African sleeping sickness) in Americans (1). All six patients have shared several characteristics: exposure to infected tsetse flies while visiting game parks in eastern or southern Africa, development of acute, febrile illness consistent with Trypanosoma brucei rhodesiense infection 1-21 days after visiting the game parks, detectable typanosomes on peripheral blood smears, and recovery after appropriate therapy. Only two of the five earlier cases showed clear evidence of central nervous system (CNS) involvement; both patients had elevated CSF protein, increased CSF cell count, and trypanosomes in the CSF. Suramin is recommended for treating the hemolymphatic stage of African trypanosomiasis, but because it does not cross the blood-brain barrier, it is ineffective against trypanosomes in the CNS. Melarsoprol, a relatively toxic drug, is used either alone or in combination with suramin when infection has progressed to involve the CNS (2). The patient described here illustrates the difficulty a physician may encounter in determining whether CNS invasion has occurred. Little diagnostic difficulty occurs when trypanosomes are observed in the CSF, and similarly, the presence of morula cells of Mott or an elevated CSF IgM is thought to strongly suggest CNS involvement (4). An elevated CSF cell count usually accompanies these other findings, but the significance of a mildly elevated cell count alone is difficult to assess. Physicians caring for the patient reported here elected to use suramin alone, and the decreased CSF cell count after 10 days of treatment was reassuring. Another patient, with an elevated CSF cell count (10/mm((3))) and normal IgM, presented a similar diagnostic dilemma in 1980; he was also treated successfully with suramin alone, and has shown no signs of CNS involvement during the past 2 years (3). Any individual with African trypanosomiasis should be monitored for evidence of CNS involvement during treatment and at regular intervals for 1-2 years thereafter (4). References
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