Sleeping sickness (African trypanosomiasis) is caused by Trypanosoma brucei, of which there are two morphologically indistinguishable subspecies: T. brucei rhodesiense and T. brucei gambiense.
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.
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