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Court, Denise Syndercombe (1984) African trypanosomiasis : its effect on platelet morphology, function and survival. Doctoral thesis, City of London Polytechnic.
Thrombocytopenia, occurring sometimes in conjunction with disseminated intravascular coagulation, has been reported sporadically in both human and animal trypanosomiases.
The extent of the thrombocytopenia and its relationship to the anaemia and parasitaemia has been investigated in experimental infections of Trypanosoma brucei brucei and Trypanosoma congolense in rabbits, and of Trypanosoma vivax in calves. Studies of platelet size, structure, function and survival have been undertaken in an attempt to ellucidate the mechanism for the thrombocytopenia.
A significant decrease in platelet number is associated with the early parasitaemia of the infection. A parasite-mediated mechanism, either immune or toxic, leads to in vivo platelet clumping, marked platelet ultrastructural changes and functional inhibition of the circulating platelets. The potential ischaemic action of the resultant microthrombi and the haemostatic problems of poorly functioning platelets may contribute significantly to the pathology of the disease.
Platelet destruction, precipitated by the parasite, occurs in the spleen resulting in a reduced platelet lifespan. Experiments in asplenic animals show that other organs can take over the splenic role in this respect.
Thrombocytopenic stimulation of platelet production from the increased megakaryocytic mass in the bone marrow only partially compensates for the platelet loss which continues late in the infection by a mechanism unrelated to parasite number. Evidence is provided suggesting that the expanded mononuclear phagocytic ability of the reticular endothelial system actively or passively continues the platelet destruction at this time. Support for two different mechanisms of platelet destruction, active at different stages of the disease, is also provided by experiments involving different strains of trypanosome and limited immunity experiments.
The pattern of platelet destruction is similar to that suggested for red cells of an early haemolytic anaemia with a non-haemolytic anaemia active in the later stages.
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