The significance of human serum sensitivity in the context of T.B. rhodesiense sleeping sickness epidemiology and control.

Earlier this century the postulate that Trypanosoma brucei brucei and T.b. rhodesiense had a common identity and that human infectability was linked with resistance to normal human serum (NHS) in vitro, were both finally refuted in the classical Tinde experiment. Interest in serum sensitivity was reawakened with the advent of the BIIT in 1970 and the studies that followed demonstrated the presence of both human-serum-resistant (HSR) and sensitive (HSS) variant antigen types, within the surface antigen repertoire of a single T.b. rhodesiense organism. This confirmed the bimodal human-infectivity potential of some, if not of all, 'brucei' trypanosomes. Changes from sensitive ('S') to resistant ('R') forms in a T.b. brucei clone have been shown to occur in chickens and have also been reported in a 'clean' bushbuck infected with a T.b. rhodesiense clone. The subsequent expression of 'S' forms by T.b. rhodesiense, when isolated from man into clean rats, has also been demonstrated. Sera from some game animals in Zambia have been shown to be highly trypanolytic. Trypanozoon organisms are almost constantly in contact with mammalian blood elements, in the vertebrate and invertebrate hosts, and more recent studies have demonstrated changes in the serum sensitivity/resistance of Trypanozoon, during metacyclic development in Glossina. In view of this, it is felt that the effects of physiological host factors, on these parasites, may well prove to be a scientifically lucrative field for further research. The bimodal potentiality for human infectivity is clearly a character of fundamental epidemiological and epizootiological importance in the transmission dynamics of this parasite complex.