Adhesion of Trypanosoma Evansi to Red Blood Cells (RBCs): Implications in the Pathogenesis of Anaemia and Evasion of Immune System

Abstract

Background: Trypanosoma evansi is the etiological agent of trypanosomosis, a disease of domestic (horses, cattle and goats) and wild (capybara, vampires) animals characterized by anaemia, degeneration, necrosis and inflammatory processes. This disease is of great concern because it produces growth retardation, loss of body weight, low production of animal proteins and diminished fertility and traction power. Because anaemia is considered the most characteristic symptom, the aim of this study was to assess the effects that T. evansi adhesion to erythrocytes has on their morphology, surface oligosaccharides profiles and trypanosome surface antigens. Methods: Blood and tissues samples from mice experimentally infected, were studied using scanning (SEM) and transmission (TEM) electron microscopes and lectin's histochemistry (sConA, sWGA, PNA, LFA, etc.). Furthermore immunoprecipitation of T. evansi radio iodinated surface antigens with specific anti-hosts and anti-trypanosome sera was performed and antigens analysed by electrophoresis and autoradiography. Results: T. evansi adhesion to erythrocytes as well as changes in the morphology of them, were frequent findings. SEM studies showed that adhesion of bloodstream trypomastigotes of T. evansi to mature erythrocytes and reticulocytes occurred through its flagellum, undulating membrane or cellular body and were mediated by filopodia. Minute pores and filamentous material were sometimes observed on erythrocytes membrane at the point of adhesion to the trypanosome. Oligosaccharides changes of RBCs glycocalix were characterized by a marked decrease in Man/Glc, terminal GalNAc and terminal Neu5Ac labelling accompanied by an increase in labelling of terminal GlcNAc. There were not labelling changes with the other lectins assayed. Preliminary immunoprecipitation studies of T. evansi radio iodinated surface antigens with anti-host sera, showed the presence of a of 45 kDa antigen from erythrocyte and host plasma on T. evansi plasma membranes. Furthermore, TEM studies demonstrated an increased abnormal erythrophagocytosis in adrenal gland, spleen and liver of experimentally infected mice. Conclusion: Adhesion of T. evansi to erythrocytes together with morphological and biochemical changes of these cells must be responsible for abnormally incremented erythrophagocytosis. On the other hand, detection of antigens from host on T. evansi membranes, suggests the operability of the antigen masking as an alternate immune response evasion mechanism to antigenic variation described in African trypanosomes.