Trypanosomiasis is a chronic disease caused by flagellar protozoa of the genus Trypanosoma, occurring in the form of African (Gambian and Rhodesian) trypanosomiasis, as well as Chaga disease a. Etiology. The causative agent of Gambian trypanosomiasis is Trypanosoma brucei, a variant of gambiense. The causative agent of Rhodesian trypanosomiasis is Trypanosoma brucei, a variant of rhodesiense. The causative agent of Chaga a disease is Trypanosoma cruzi.


    • The carrier of Gambian trypanosomiasis is the tsetse fly Glossina palpalis, which lives in thickets of rivers and lakes. The natural reservoir of the pathogen is a sick person. The disease is more often recorded in Central Africa, especially in places located along the banks of reservoirs.
    • The carrier of Rhodesian trypanosomiasis is the tsetse fly Glossina morsitans, which lives in the savannas of East Africa. Natural reservoir – all kinds of small antelopes. Infection often occurs when grazing livestock or hunting. Transmission routes are from person to person and from person to pets. The disease is common in Zambia and Tanzania.
    • Carriers of Chaga a disease are bugs of the genus Triatoma and related forms of the Reduviidae family. The disease develops when wounds are contaminated with infected carrier feces or when infected blood is transfused. The disease is registered in South America, especially in Brazil, Argentina, Chile.

Clinical picture

    • African trypanosomiasis
    • The incubation period is 2-3 weeks. In some patients, after 2-3 days, an ulcerative papule (chancre) appears at the site of the vector bite. In the initial stage, there are no clinical manifestations, but the pathogen rapidly multiplies at the site of penetration and disseminates through the lymphatic system into the bloodstream. Some patients observe regional lymphadenopathy (especially the occipital lymph nodes). In the stage of parasitemia, the circulation of the pathogen in the bloodstream reaches its peak after 2-3 weeks and causes the development of a characteristic symptom complex: erythematous spots and local edema, pain of various localization, convulsions, tremors and paresthesias, swollen lymph nodes, spleen and liver, exhaustion and evening rises in temperature. –

body tours; in the later stages, disturbances of consciousness appear. Possible mental disorders. CNS lesions develop over several years after the onset of the disease: drowsiness, tremor of the extremities, transient paralysis, speech disorders, loss of CNS control over sphincters

    • Rhodesian trypanosomiasis is more severe, with damage to the brain and myocardium, which develops already 3-6 weeks after the onset of the disease. Characterized by coma, convulsions, acute heart failure, severe exhaustion, leading to the death of the patient within 6-9 months.
    • Chaga disease a (South American trypanosomiasis)
    • Acute form (observed mainly in small babies). In the early stages, fever, lymphadenopathy, liver enlargement, facial edema are characteristic. Sometimes meningoencephalitis with convulsive syndrome is recorded, leading to mental and physical defects or death. Acute myocarditis often develops with a possible fatal outcome.
    • The chronic form is mild, sometimes asymptomatic, but may be accompanied by myocardiopathy, megaesophagus, and fatal megacolon. In Brazil and Argentina, severe forms are more often observed, in Chile – light ones.

Research methods

    • Isolation of the pathogen. Materials for research: CSF, blood, biopsy material of lymph nodes. Centrifugation facilitates the detection of the pathogen in the blood and CSF. When the central nervous system is affected, the blood and lymph nodes of the pathogen do not contain. In the initial stage of the disease, the pathogen is found at the site of the bite and in the cervical lymph nodes.
    • With negative results of microscopy, the test material is administered to white mice or rats (s / c or / and). For 2-3 days, the pathogen is detected in the blood
    • Serological studies reveal AT class IgM in diagnostic titers in all patients
    • When studying the histological products of sectional material, similar lesions of the central nervous system are found in African trypanosomiasis and syphilis.


    • Eflornithine 400 mg/kg/day IV in 4 doses for 14 days – in the early and late stages of Gambian trypanosomiasis
    • Suramin first at a trial dose of 100 mg IV, the next day and then on days 3, 7, 14, 21 – 1 g IV (total 5 g) (children after a trial dose of 100 mg – 20 mg / day). kg) – with Rhodesian trypanosomiasis
    • Melarsop-rol – 3 courses for 3 days, during which 3.6 mg / kg / day is administered intravenously. The second course is prescribed 1 week after the first, the third – no later than 3 weeks after the second (for babies, the initial dose is 0.36 mg / day with a gradual increase to 3.6 mg / day / in 1 time per day). 1-5 days, course of treatment -9~10 doses) – at all stages of Gambian and Rhodesian trypanosomiasis, especially indicated for the Rhodesian form with CNS damage
    • pentamidine
    • Pentadion.

Current and forecast. The course is traditionally chronic progressive. May persist for months or years with subsequent CNS damage. Prevention

    • Prevention of African trypanosomiasis
    • In endemic areas, it is recommended to wear clothing that covers the arms and legs.
    • Pentamidine 4 mg/kg iv provides protection against Gambian trypanosomiasis (may mask infection and lead to kidney failure)
    • Prevention of Chaga a disease
    • Avoid visiting dilapidated houses and outbuildings
    • Use of protective nets and insecticides
    • Spraying with 5% solution of y-benzenehexachloride.


    • Sleeping sickness
    • Sleeping sickness
    • chronic sleeping sickness


  • B56 African trypanosomiasis
  • B56.0 Gambian trypanosomiasis
  • B56.1 Rhodesian trypanosomiasis
  • B57 Chagas disease

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