- Clinical science
African trypanosomiasis (sleeping sickness) is an infectious disease caused by the protozoan parasite Trypanosoma brucei and is transmitted by the bite of the tsetse fly. The disease is endemic to sub-Saharan Africa; all cases that occur in the US are the result of travel to endemic regions. There are two forms of the disease with distinct geographical distributions and rates of clinical progression. West African sleeping sickness is caused by T. b. gambiense and progresses slowly, while East African sleeping sickness is caused by T. b. rhodesiense and progresses rapidly. Patients with either subtype of the disease initially present with a painful nodule or chancre at the site of the bite, followed by a hemolymphatic phase with fever and lymphadenopathy (stage I). Eventually, patients develop CNS symptoms (stage II), which are characterized by behavioral changes and a reversal of the sleep-wake cycle. If the disease is left untreated, patients will succumb to coma and die. The disease is diagnosed if the trypomastigote is found in chancre fluid, lymph node aspirates, or blood smears. The drugs of choice for stage I T. b. gambiense infection are pentamidine and fexinidazole, while suramin is the drug of choice for stage I T. b. rhodesiense. An eflornithine-nifurtimox combination and fexinidazole monotherapy are the therapy of choice for stage II T. b. gambiense infection, while melarsoprol is the drug of choice for stage II T. b. rhodesiense. No vaccine or chemoprophylaxis for African trypanosomiasis is available.
- Distribution: sub-Saharan Africa
- Incidence: < 15,000 estimated cases in 2014
Epidemiological data refers to the US, unless otherwise specified.
|West African sleeping sickness (Gambian trypanosomiasis)||East African sleeping sickness (Rhodesian trypanosomiasis)|
|Pathogen||Trypanosoma brucei gambiense||Trypanosoma brucei rhodesiense|
|Glossina palpalis||Glossina morsitans|
|Regional distribution||Central and West Africa||Eastern and southeastern Africa|
|Incidence in the US||Extremely rare||1–2 cases per year|
Chronic, slowly progressive disease
Acute disease with poor demarcation between stages
Life cycle in the tsetse fly
- Ingestion of the trypomastigote form of T. brucei by the tsetse fly during a blood meal
- Transformation of the trypanosomal form of T. brucei into procyclic trypomastigotes within the gut of the tsetse fly
- Procyclic trypomastigotes leave the gut and transform into epimastigotes.
- Migration of epimastigotes to the salivary glands, where they transform into metacyclic trypomastigotes
- Injection of metacyclic trypomastigotes from the salivary gland to the bite site during the next blood meal
Life cycle in the human body
- Multiplication of the metacyclic trypomastigotes at the inoculation site causes a primary indurated lesion
- Entry into the bloodstream and transformation of metacyclic trypomastigotes into trypomastigotes
- Stage I (hemolymphatic phase): multiplication of trypomastigotes in blood (parasitemia) and lymphoid tissue
- Stage II (neurologic phase): Trypomastigotes cross the blood-brain barrier and enter the CNS → Immune-mediated damage causes progressive meningoencephalitis and diffuse demyelination.
Stage I (hemolymphatic phase)
Trypanosomal chancre (local primary lesion)
- A red, painful, indurated, nodular swelling; 2–5 cm in size that develops at the bite site within 2 weeks of the bite
- Resolves spontaneously within 1–2 weeks
- Intermittent fever: caused by antigenic variation , malaise, headache, weight loss, arthralgia
- Painless lymph node enlargement
- Erythematous, annular (targetoid), or maculopapular rash that may or may not be pruritic
- Symptoms of anemia
Stage II (neurologic phase)
- Behavioral changes: confusion, apathy, psychosis
- Daytime somnolence, which may be associated with night-time insomnia
- Kerandel sign: delayed hyperesthesia
- General findings
- Local primary lesion: direct visualization of trypomastigotes in chancre fluid
- Stage I: direct visualization of trypomastigotes in thin and thick peripheral blood smears or lymph node aspirates
- Stage II: lumbar puncture and CSF examination
A history of travel to an endemic region is an important diagnostic clue for trypanosomiasis.
CSF examination must be performed for all patients with suspected or confirmed African trypanosomiasis to rule out stage II disease because the drug of choice depends on the stage of the disease.
- Early in-patient treatment is very important.
- The drug of choice for trypanosomiasis is dependent on the stage of the disease and the subspecies of T. brucei (see the table below).
- Follow-up: CSF examination should be repeated every six months for two years.
Trypanosomal therapy 
|West African sleeping sickness||East African sleeping sickness|
|Stage I (bloodborne disease)|| |
|Stage II (CNS invasion)|
African trypanosomiasis is generally lethal without therapy.
To remember that in East African sleeping sickness bloodborne disease is treated with suramin and melarsoprol is used to treat invasion of the brain (CNS), think: BLOODy SURe, this MELody is stuck in my BRAIN.
Instructions for people traveling to or working in endemic regions
- Use preventive measures in the daytime
- Wear long-sleeved protective clothing with neutral colors
- Use insect repellants
Public health measures in endemic regions
- Vector control methods such as insecticide spraying and fly traps
- Population screening programs and early treatment of infections to decrease the number of human hosts