Host parasite relationships in Trypanosoma (duttonella) vivax with special reference to the influence of antigenic variation

A mouse model system was used to study various aspects of host and parasite relationships in Trypanosoma vivax infections. These included the phenomenon of antigenic variation, the variable parasite antigens responsible for this phenomenon, parasite-host adaption, host immune responses and the role of genes in the major histocompatibility complex in the control of infection. While the mouse model system has allowed investigation of these aspects of host parasite relationships, it is clear that the system is much more limited than those generally used in T. brucei spp and T. congolense infections. This is indicated by the discovery that not all VATs of T. vivax were equally infective for mice, though in some cases infectivity could be improved by bovine serum supplementation and/or immunosuppression of the mouse host. In the case of rats, infection was even restricted to a smaller number of the VATs studied. It was, however, possible to biochemically characterize the variable surface antigen carried by T. vivax and show its similarity to those carried by T. brucei and T. congolense. The H-2 complex was found not to influence acquired resistance of inbred strains. Cyclic transmissions of T. vivax infections to goats combined with chemotherapy were carried out in an attempt to induce protection to subsequent infection as has been shown in T. brucei and T. congolense infections. Such protection could, however, not be obtained, The failure of the metacyclic VATs to induce immunity, was perhaps due to rapid decrease in antibody titres to bloodstream VATs found after treatment and prior to rechallenge. The usefulness of the mouse model system in elucidating the mechanisms responsible for the non-H-2 linked differences in susceptibility to T. vivax infections should be further explored and its relevance to mechanisms of trypanotolerance in domestic ruminants defined.