Pathogenic mechanisms of Trypanosoma evansi infections

Insect-borne diseases exact a high public health burden and have a devastating impact on livestock and agriculture. To date, control has proved to be exceedingly difficult. One such disease that has plagued sub-Saharan Africa is caused by the protozoan African trypanosomes (Trypanosoma species) and transmitted by tsetse flies (Diptera: Glossinidae). This presentation describes Trypanosoma evansi (T. evansi) which causes the disease known as trypanosomosis (Surra) or trypanosomiasis in which several attempts have being made to unravel the clinical pathogenic mechanisms in T. evansi infections, yielding various reports which have implicated hemolysis associated to decrease in life span of erythrocytes and extensive erythrophagocytosis being among those that enjoy prominence. T. evansi generates Adenosine Triphosphate (ATP) from glucose catabolism which is required for the parasite motility and survival. Oxidation of the erythrocytes induces oxidative stress due to free radical generation. Lipid peroxidation of the erythrocytes causes membrane injury, osmotic fragility and destruction of the red blood cell (RBC) making anemia a hallmark of the pathology of T. evansi infections.