Sleeping sickness B56.-

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 30.09.2022

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African trypanosomiasis; Trypanosomiasis African

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Atkins, 1734; Winterbottom, 1803; Bruce, 1894; Dutton, 1902; Stephens and Fantham, 1910

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Sleeping sickness (African trypanomiasis) is an infectious disease caused by protozoa of the genus Trypanosoma, which are transmitted to humans by tse tse flies.

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V.a. Trypanosoma brucei rhodesiense (East and South Africa) and Trypanosoma brucei gambiense (Central and West Africa). The main reservoir is humans. Secondary hosts are versch. Mammals (dog, pig, also wild animals).

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300,000-500,000 new cases/year worldwide (according to WHO estimates). Prevalence in endemic areas (esp. Angola, Congo, Sudan): 20-50%.

Endemic areas: sub-Saharan Africa, West and Central Africa (T. b. gambiense), East Africa (T. b. rhodesiense).

Sleeping sickness is rarely imported by tourists. Most cases are T.rhodesiense cases from East African national parks (e.g., Queen Elisabeth National Park in Uganda).

Clinical features
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The incubation period for infection with T. rhodesiense is 3-21 days and varies with infection with T. gambiense (weeks-years). The clinic proceeds in 2 phases:

  • Stage I (febril-glandular): Moderately painful or painless, 0.5-5.0 cm large furunculoid, inflammatory primary effect for about 1 week (tryponasome chancre). Possible development of central necrosis. The primary effect recedes within 2-3 weeks with post-inflammatory hyper- or depigmentation. Furthermore, irregular fever spikes develop over months, regional or generalized lymphadenopathies, edema, muscle weakness, apathy, pleural effusions, ascites, myocarditis. In the dangerous T. rhodesiense infection, in the stage of generalisation, there is also the development of trunk-accentuated maculo-papular exanthema.
  • Stage II (meningeal): 6-12 months after infection. Apathy, character changes, convulsions, insomnia, meningoencephalitis, finally coma and death.

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Microscopic pathogen detection Stage I: from blood (thick drop, concentration method) or in lymph node punctate in the case of T. gambiense infection.

Stage II: cerebrospinal fluid. If the diagnosis of African trypanosomiasis has been made, a cerebrospinal fluid (CSF) puncture should always be performed to exclude CNS involvement (in the absence of pathogen detection but with inflammatory changes in the CSF, therapy should be given according to stage II).

Detection of antibodies in the blood (ELISA, IFT, PHA). For T. gambiense: card agglutination test (CATT).

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Toxic encephalopathy with melarsoprol therapy in 2-10% of those treated (often fatal).

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Due to the high toxicity of the drugs, therapy should always be inpatient, moreover symptomatic according to clinic in collaboration with neurologists.

Stage I: Suramin (e.g. Germanin): Initial injection of a test dose of 2 mg/kg bw (max. 100 mg) Suramin slowly applied i.v. (to exclude rare idiosyncrasy). Then infuse 1 g TD (children 20 mg/kg bw) slowly on days 1, 3, 7, 14 and 21.

Alternative: Pentamidine diisethionate (e.g. pentacarinate): 4 mg/kg bw/day i.m. or 2-3 mg/kg bw/day i.v. for min. 5, max. 10 days. Recommended especially in case of infection with T. gambiense.

Stage II: Melarsoprol (arsenic preparation; often Herxheimer reaction and toxic encephalopathies!) 3 times 0.6-1.2 mg/kg bw/day for 3 days, repeated after 10-21 days. Pretreatment with suramin is recommended.

Alternative: (only effective in case of infection with T. gambiense): Eflornithine 4 times 50-75 mg/kg bw/day i.v. for 6 weeks.

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Avoidance of tsetse-infested endemic areas (e.g., river courses or savannas). Vector control (destruction of insects), avoidance of tsetse fly bites by wearing appropriate clothing (tsetse flies prefer dark colors) and the use of insect repellents (e.g. Icaridin, Zanzarin) or insecticides. Special care should be taken to avoid tsetse flies in the car (tsetse flies usually bite during the day).

No chemoprophylaxis (to be rejected because of the potential toxicity of the drugs, development of resistance, and possible suppression of clinical symptoms in less sensitive trypanosome strains)!

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The APOL1 gene encodes the protein apolipoprotein L1 (APOL1), which circulates mainly bound to HDL particles. This circulating fraction of APOL1 confers resistance to trypanosomiasis by rapidly lysing infecting trypanosomes of the species Trypanosoma brucei, trypanosome parasites endemic to Africa. APOL1 is thus an innate immune effector that protects humans from infection by some trypanosome parasites.

The seminal discovery that genetic variations in the APOL1 gene are associated with non-diabetic kidney disease in people of African descent has led to investigation of the biological mechanisms underlying this association (O'Toole JF et al 2017). The high allele frequency of these variants is thought to be due to the resistance they confer to the disease-causing trypanosome species involved in human African sleeping sickness. People of African descent have an increased risk of developing kidney disease, largely due to two variants in the apolipoprotein L1 (APOL1) gene that are unique to people of West African descent. These variants are thought to be genetically dominant because they provide protection against African sleeping sickness (Tzur S et al. 2010

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Last updated on: 30.09.2022