African Trypanosomiasis (Sleeping Sickness)

AFRICAN TRYPANOSOMIASIS (SLEEPING SICKNESS)

Sleeping sickness (African trypanosomiasis) is caused by Trypanosoma brucei, of which there are two morphologically indistinguishable subspecies: T. brucei rhodesiense and T. brucei gambiense. After infection the parasite undergoes a period of local multiplication then enters the general circulation via the lymphatics. Recurrent fever, headache, lymphadenopathy and splenomegaly may occur. Later, signs of meningo-encephalitis appear, followed by somnolence (sleeping sickness), coma and death.

T. brucei, unlike T. cruzi, multiplies in the blood or cerebrospinal fluid. Trypanosomes ingested by a feeding fly must reach the salivary glands within a few days, where they reproduce actively as epimastigotes attached to the microvilli of the salivary gland where they transform into metacyclic trypomastigotes, which are found free in the lumen. Around 15–35 days after infection the fly becomes infective through its bite.

The pathology of the infection is due to inflammatory changes associated with an induced autoimmune demyelination of nerve cells. Interestingly, the immuno-suppressive action of components of the parasite’s membrane is probably responsible for frequent secondary infections such as pneumonia. Liberation of common surface antigens (the mechanism involved in immune evasion) in every trypanolytic crisis (episode of trypanosome lysis) leads to antibody and cellmediated hypersensitivity reactions. It is believed that some cytotoxic and pathological processes are the result of biochemical and immune mechanisms.