Beginning as a silvatic enzoosis involving Trypanosoma cruzi and a range of
small mammals and marsupials, human Chagas disease probably emerged as a sparse focal
disease at different points in the Americas well before the Christian period. Subsequently
spread through internal population migrations, the disease would have become more
widespread where the insect vectors became associated with rural settlements. It appears to
have spread most widely during the post-Colombian period, especially from the mid 19th to
mid 20th centuries when the human infection appears to have peaked in incidence and
prevalence. In historical terms, there are sparse indications of probable acute cases, chronic
cardiopathy, and megacolon, but such conditions are difficult to diagnose accurately. In
contrast, megaoesophagus seems a more specific marker of chronic Chagas disease, with a
number of reports of its occurrence in various parts of Brazil, especially since the 18th
century. The main impact of chronic Chagas disease corresponds primarily to the
occurrence of chronic chagasic cardiopathy, and recognition and characterization of this has
been the main stimulus for large-scale control interventions in the endemic countries since
the 1950s.