Cases reported "Trypanosomiasis, African"

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1/14. Evidence for the occurrence of trypanosoma brucei rhodesiense sleeping sickness outside the traditional focus in south-eastern uganda.

    The occurrence of trypanosoma brucei rhodesiense west of the River Nile, in Masindi district in the mid-western part of uganda, is confirmed. Masindi borders the traditional belt of T. b. gambiense infection in the north-west, Gulu in the north and the Democratic Republic of congo in the west. Of the 702 persons tested for sleeping sickness in Masindi, 113 (16%) were positive by the card agglutination test for trypanosomiasis (CATT). Trypanosomes were observed in samples of cerebrospinal fluid (CSF) from two (0.3%) of the subjects: a 7-year-old girl, who had been ill for 2 weeks and yet was in good general condition, with three white blood cells (WBC)/microliter CSF; and a 47-year-old woman who had been ill for 8 months, looked sickly, had seven WBC/microliter CSF, but was still able to dig in her gardens. rats and mice inoculated with blood from the two parasitologically confirmed cases became parasitaemic on day 3 post-inoculation, indicating that the parasites were T. b. rhodesiense. Isoenzyme analysis revealed that the parasites isolated from one of these confirmed cases belonged to a zymodeme (449) which has not been previously observed among isolates from south-eastern or north-western uganda. Although the isolate shared PGM2 and ICD3 patterns with T. b. gambiense and T. b. rhodesiense, respectively, it did not have the SOD3:5 pattern characteristic of T. b. gambiense. The spread of T. b. rhodesiense beyond its traditional focus and the development of areas where this subspecies and T. b. gambiense are co-endemic will complicate the control of sleeping sickness in uganda; although the CATT is very useful for the mass screening of populations for T. b. gambiense area, it is not applicable in the detection of T. b. rhodesiense.
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2/14. African sleeping sickness in tourists returning from tanzania: the first 2 Italian cases from a small outbreak among European travelers.

    A recent cluster of cases of African trypanosomiasis in humans (HAT) has been reported in tourists (most of whom were European) returning from tanzania; we describe the first 2 patients (both of whom were Italian travelers) with HAT, who have been treated successfully. Because neither vaccine nor drug prophylaxis is currently recommended and/or available for persons traveling to areas of endemicity, physicians should be alerted about this uncommon but potentially life-threatening disease.
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3/14. Winterbottom's sign and hypertrophic cardiomyopathy.

    We present the case of a patient who presented with hypertrophic cardiomyopathy, generalized lymphadenopathy and serological evidence of African sleeping sickness (Trypanosoma gambiense). He made a full recovery after intravenous administration of eflornithine, a drug that is no longer distributed for antiparasitic indications for pharmacoeconomic reasons.
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4/14. East African sleeping sickness in Chennai.

    A traveler to East africa developed fever, an eschar on his forearm and thrombocytopenia shortly after returning home to Chennai, india. trypanosoma brucei rhodesiense infection was diagnosed on examination of his peripheral smear. He made a full recovery after receiving a course of suramin.
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5/14. Sleeping sickness in brothers in london.

    Brothers 9 and 14 years of age presented in london with fever and skin lesions after a safari in East africa. malaria films were negative, but trypanosomes were seen in blood films and chancre fluid. Sleeping sickness should be considered in children returning from East africa.
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6/14. orchitis as an unusual manifestation of human African trypanosomiasis.

    African trypanosomiasis is a re-emerging disease. We report the case of an African patient whose predominant symptom was infertility due to a granulomatous orchitis. The patient was afebrile and had not been in africa for years. Lymphadenopathy and splenomegaly led us eventually to the diagnosis of sleeping sickness. After treatment with suramin his spermiogram returned to normal. Sleeping sickness evolves through clinically different stages and leads to death if left untreated. The disease may, however, present clinically extremely variable and may thus be difficult to diagnose.
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7/14. 24 hour polysomnographic evaluation in a patient with sleeping sickness.

    A 24 h polysomnographic recording was performed in a patient with sleeping sickness presenting an atypical neurological syndrome. Trypanosoma gambiense was found in a lymph gland puncture and the CSF, and a serologic immunofluorescence test was positive. The scoring technique of the polygraphic traces had to be adapted because of the presence of a permanent EEG delta wave activity during the NREM sleep stages, and the method used by Schwartz and Escande (1970) was applied. REM sleep and wakefulness presented normal polygraphic characteristics. The patient had 8 sleep episodes throughout the recording period, occurring during the daytime and at night, forming the classical diurnal sleepiness and nocturnal restlessness of sleeping sickness. All but one episode represented 1-3 complete REM-NREM sleep cycles. On all occasions, REM latency was short and 2 SOREM episodes were observed. The nychthemeral organization of the stages of vigilance differed from one state to another. wakefulness and REM sleep had a circadian rhythmicity, while NREM sleep, total sleep time and deep sleep (corresponding to stages 3 and 4) had an ultradian periodicity. The concordance between the higher pressure for wakefulness and lower pressure for sleep around 20.00 h defined the time of occurrence of a 'forbidden zone' for sleep.
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8/14. Treatment of arsenical refractory Rhodesian sleeping sickness in kenya.

    Case histories of three Rhodesian sleeping sickness patients who relapsed after Mel-B therapy are presented. Repeated Mel-B therapy was clinically effective but not curative, and all three patients subsequently relapsed again and required further treatment.
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9/14. Treatment of human late stage gambiense trypanosomiasis with alpha-difluoromethylornithine (eflornithine): efficacy and tolerance in 14 cases in cote d'ivoire.

    alpha-Difluoromethylornithine (DFMO; eflornithine), an inhibitor of polyamine biosynthesis, was used to treat 14 patients with late stage gambiense sleeping sickness, 12 cases having been previously treated with and considered refractory to melarsoprol. alpha-Difluoromethylornithine was administered intravenously at a dose of 400 mg/kg/day for 14 days followed by oral treatment, 300 mg/kg/day, for 21-28 days. In all patients treatment was associated with rapid disappearance of trypanosomes from body fluids (in several cases within 24 hr) and decreased cerebrospinal fluid white blood cell counts. In all but one patient, who died of a pulmonary infection during treatment, alpha-difluoromethylornithine produced a dramatic reversal of clinical signs and symptoms of the disease. Determination of drug concentrations in serum and cerebrospinal fluid of 5 patients demonstrated that alpha-difluoromethylornithine diffuses into the central nervous system with cerebrospinal fluid levels representing up to 51% of corresponding serum concentrations. diarrhea, abdominal pain, and anemia were the most frequent side effects associated with therapy, but were reversible and did not necessitate discontinuation of treatment. Four patients have been followed for more than 2 years post-treatment without evidence of relapse.
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10/14. African sleeping sickness in the united states. Successful treatment with eflornithine.

    The traditional treatment of African sleeping sickness (trypanosomiasis) with central nervous system involvement is an organic arsenical compound, melarsoprol, which is associated with severe and even life-threatening side effects. A polyamine biosynthesis inhibitor, eflornithine (chemical name, DL-alpha-difluoromethylornithine, supplied as monohydrochloride monohydrate), was used to treat a 3 1/2-year-old child with newly diagnosed severe trypanosomiasis that had been acquired more than two years previously in Zaire or the congo. Treatment consisted of 300 to 400 mg/kg/d of eflornithine by continuous intravenous infusion for 25 days followed by 300 mg/kg/d of eflornithine by mouth divided in four equal doses daily for 17 days. The child's recovery was dramatic, with eradication of blood and cerebrospinal fluid parasites in the first week. cerebrospinal fluid pleocytosis resolved completely. Her generalized adenopathy and fever gradually resolved. Severe ataxia, inability to walk or to change posture on her own, marked language regression, and lethargy all improved during and after her therapy. The drug was well tolerated; the only noted adverse effect was transient thrombocytopenia during the fourth week of therapy. eflornithine was a safe and effective agent for treatment of trypanosomiasis with central nervous system involvement in this child.
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