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Thrombocytopenia in experimental trypanosomiasis.

C E Davis, R S Robbins, R D Weller

    The Journal of Clinical Investigation
    |May 1, 1974
    PubMed
    Summary

    Experimental trypanosomiasis causes severe thrombocytopenia (low platelet count) in rats. Trypanosomes directly induce platelet aggregation, suggesting a novel mechanism of microbial injury independent of immune responses.

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    Area of Science:

    • Parasitology
    • Hematology
    • Immunology

    Background:

    • Rhodesian trypanosomiasis can lead to thrombocytopenia and disseminated intravascular coagulation.
    • Understanding the mechanisms of coagulation disorders in trypanosomiasis is crucial for patient management.

    Purpose of the Study:

    • To investigate the effect of experimental trypanosomiasis on coagulation, specifically platelet counts.
    • To elucidate the mechanism by which Trypanosoma rhodesiense induces thrombocytopenia.

    Main Methods:

    • Induction of trypanosomiasis in rats using Trypanosoma rhodesiense.
    • Monitoring of platelet counts, hematocrit, fibrinogen, and fibrin split products in infected rats.
    • In vitro studies of platelet aggregation using concentrated trypanosomes and disrupted trypanosome supernates with blood from rats, rabbits, and humans.
    • In vivo studies in complement-deficient rabbits and splenectomized rats.

    Main Results:

    • Infected rats developed severe thrombocytopenia (mean platelet count 18,000/mm³) without significant changes in hematocrit, fibrinogen, or fibrin split products.
    • In vitro, trypanosomes and their disrupted products induced rapid platelet aggregation, independent of ADP, kinins, or complement.
    • Thrombocytopenia occurred in vivo in complement-deficient and splenectomized animals.
    • The platelet-aggregating substance from trypanosomes is heat-labile and active despite complement inhibition.

    Conclusions:

    • Trypanosoma rhodesiense directly induces severe thrombocytopenia through a mechanism involving platelet aggregation.
    • This platelet aggregation is mediated by a heat-labile trypanosomal product, likely a protein enzyme or toxin.
    • The observed thrombocytopenia is independent of immune complexes, complement, ADP, and kinins, representing a novel pathway of microbial platelet injury.

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