Three different technologies are currently being used to unravel the epidemiology of African and South American trypanosomiasis: these are the use of isoenzymes as gentic markers, direct analysis of DNA and the production of highly specific monoclonal antibodies. For African sleeping sickness, isoenzyme analysis has enabled reservoir hosts of the disease to be identified and the origin of epidemics to be traced. Together with nuclear and kinetoplast DNA analysis, it has contributed to our understanding of speciation among Trypanosoma brucei group trypanosomes. In particular, no definitive markers for man-infectivity have been demonstrated, although a limited subset of T. b. gambiense , the parasite causing sleeping sickness in West Africa, can be identified by a combination of its low virulence to redents, characteristic isoenzyme markers and variant surface antigen repertoire. For South American trypanosomiasis, isoenzyme analysis has revealed three principal, radically dissimilar, strain groups of Trypanosoma cruzi and heterogeneity within these groups. All three groups are infective to man but they have different geographical distributions, are associated with different transmission cycles and might be linked to different forms of chronic disease. Heterozygous isoenzyme patterns suggest that T. cruzi is diploid. Genetic exchange has not been found but this may be obscured by the domestic epidemiology. Monoclonal antibodies have demonstrated that T. cruzi vary in the quantitative expression of an immunodominant cell-surface glycoprotein.