One of two diseases cause by Trypanosome parasites
Tsetse fly (bite during the day)
- Trypanosoma brucei gambiense (west coast of Africa)
- Trypanosome brucei rhodesiense (east coast of Africa)
Clinical features and pathogenesis
- T.gambiense- causes slow wasting illness with long latency
- T.rhodesiense- causes more rapidly progressive illness
- Trypanosomes injected in saliva of tsese fly when bites
- Localised inflammatory reaction
- Tender subcutateous (chancre) develops at site (2-3 days after bite)
Stage 1 (haemolyphatic)
- Multiplication of trypanosomes in the lymphatics and bloodstream leads to parasitaemia 5-12 days after bite
- Trypanosomes evade the immune response by antigenic variation (meaning they switch to be no longer recognized by existing antibodies the body has made)
- Results in peaks of parasitaemia and production of auto-antibodies
- The disease progresses into immunosuppression with hypergammaglobulinaemia
- Infiltration of endocrine organs occurs
- Alteration hormonal balance and circadian rhythm.
Features of Stage 1
- Hepatosplenomegaly and Lymphadenopthy secondary to immune activation
- Joint pains
- Post cervical lymphadenopathy (Winterbottom’s sign)
Stage 2 (meningoencephalytic)
Weeks after initial infection, parasites enter the CNS via the choroid plexus and infiltrate the white matter drawing in inflammatory cells and stimulating macrophages.
If untreated, patients progress to coma, severe organ failure.
Death usually occurs within few months of onset stage 2
Trypomastigotes isolated in blood film (thick and thin)/bone marrow/ lymph node aspirate/CSF.
Serology may be helpful
More effective if started before neurological involvement.
Pre-CNS involvement: (don’t penetrate BBB) suramin / pentamidine
Post-CNR involvement: melarsoprol/nitrofurazone
Prevention of insect bites
Insect repellant, long sleeves and bed nets