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.