Human African trypanosomiasis (HAT) is more commonly known as African sleeping sickness. It is a vector-borne disease caused by two subspecies of Trypanosoma brucei: T.b. gambiense and T.b. rhodesiense. Both of these parasites are transmitted to humans by the bite of tsetse flies (Glossina spp.), which have acquired the parasites from infected animals. However, they differ in epidemiology and disease progression. 

T.b. gambiense is found in 24 countries in west and central Africa and accounts for approximately 92% of HAT cases globally. T.b. gambiense causes a slowly progressive form of HAT. A person can be infected for months or even years without major signs or symptoms. When symptoms emerge, the disease is often advanced with central nervous system involvement. 

T.b. rhodesiense is endemic in 13 countries in east and south Africa. Domestic cattle and several big-game animals are reservoirs for T.b. rhodesiense. It is often the cause of HAT in short-term travelers to endemic regions. The incubation period ranges from weeks to months. T.b. rhodesiense causes an acute and quickly progressive form of the disease. During the first stage of rhodesiense HAT, the parasite multiplies in the blood and lymphatic system, causing fever, hemolysis, anemia, thrombocytopenia, hepatosplenomegaly, and renal disease. 

In the second stage of disease, the parasite crosses the blood-brain barrier and infects the central nervous system. followed by death within weeks to months Approximately 90% of cases are fatal without treatment. 

Parasite burden is high in rhodesiense HAT. Relapse is possible if treatment fails to eliminate all parasites. WHO recommends follow-up at 3, 6, and 12 months after treatment.

Diagnosis involves 3 steps:

  • Screening for potential infection using clinical examination and serological tests (only available for T. b.gambiense) 
  • Confirmation by microscopic observation of the parasite in body fluids
  • Disease staging via clinical examination and analysis of cerebrospinal fluid

Laboratory diagnosis relies on microscopic examination of chancre fluid, lymph node aspirates, blood, or bone marrow. Cerebrospinal fluid should be examined in patients with late stage disease. A wet preparation should be examined for motile trypanosomes. Blood smears should be examined after staining with Giemsa. 

Concentration techniques can be used to enhance the odds of detecting trypanosomes. Blood samples can be centrifuged to obtain buffy coats.  Other fluids can be centrifuged to obtain a sediment for examination. 

Serologic tests are useful for the diagnosis of T.b. gambiense. However, with T. b. rhodesiense, seroconversion occurs after the onset of clinical symptoms and is of limited use. No nucleic acid-based tests have been validated for the diagnosis of African trypanosomiasis. 

References

Franco JR, Simarro PP, Diarra A, Jannin JG. Epidemiology of human African trypanosomiasis. Clin Epidemiol 2014;6:257–75.

Wendt EM, Tobolowsky FA, Priotto G, Franco JR, Chancey R. Notes from the Field: Rhodesiense Human African Trypanosomiasis (Sleeping Sickness) in a Traveler Returning from Zimbabwe — United States, August 2024. MMWR Morb Mortal Wkly Rep 2025;74:158–159.


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