CONCLUSION

Both phenotypic and genotypic characterisation have radically changed our understanding of the diversity and epidemiology of T. cruzi. There is evidence that T. cruzi can undergo genetic recombination in natural populations, and now some preliminary indication that genetic exchange can also be obtained experimentally. Although clonal propagation may predominate in transmission cycles involving humans, genetic exchange in natural populations might yield T. cruzi strains with new combinations of biological properties, such as virulence and drug resistance, with potential for spread to human populations.

However, significant unanswered questions remain that are worthy of further research. What is the relationship between the two main genetic lineages of T. cruzi and what are their origins? Are primates indeed an early host of Z2 and what is the full range of its geographical distribution? Will further studies confirm the ancient link between T. cruzi and trypanosomes of Australasia, proposed by Stevens et al. (1999)? Were the antecedents of T. cruzi monoxenous parasites of primitive mammals such as Didelphis, which can have infective forms in anal glands, or parasites of insects? What are the vectors, if any, of T. cruzi clade trypanosomes in Australasia? What mechanisms are involved in genetic recombination in T. cruzi? Does infection with particular T. cruzi strains predict a poor prognosis for Chagas disease? To what extent does human genotype predispose to chronic Chagas disease, or protect against it?

Although human Chagas disease can eventually virtually be eliminated by control of domestic triatomine vector populations and prevention of blood transfusion transmission these research questions are nevertheless of interest and some of the answers may affect intervention strategies. It is certain that, with time and coordinated effort, all the necessary technologies are now available to answer these questions.