The etiologic agent of the human American trypanosomiasis was discovered by Chagas (1909a) initially in triatomine bugs, Panstrongylus megistus, collected in Lassance, State of Minas Gerais, Brazil. Its infectivity to some laboratory animals was soon confirmed, a peculiar small trypanosome appearing in the blood of these animals, which Chagas (1909a) named Trypanosoma cruzi in honor of Oswaldo Cruz. The first natural infection of a mammal with T. cruzi was recorded in a cat also by Chagas (1909b), who subsequently found the parasite in the blood of a child, and associated to it the illness found in that child, as well as in other persons living in houses infested with triatomine bugs in Lassance. At that time, Chagas (1909b) also carried out studies on this parasite in human beings, experimental mammal hosts, triatomines and axenic cultures. Believing that T. cruzi presented schizogonic stages in the lungs of vertebrate hosts, Chagas (1909b) temporarily placed it in a new genus, Schizotrypanum, but subsequently corrected such mistake (Chagas 1913). Chagas (1912, 1924) also found T. cruzi in wild animals, armadillos (incriminating P. geniculatus as its vector) and squirrel monkeys. The evolution of T. cruzi in Triatoma infestans and the possibility of this species and T. sordida actuating as vectors were also reported by Chagas (1912). Hartmann (1910) and Vianna (1911) discovered the intracellular multiplication of T. cruzi, but the latter correctly interpreted it as occurring by binary fission. Vianna (1911) carried out an extensive histopathological study in post-mortem patients and experimental animals, evidencing the parasite multiplication in several tissues, mainly myocardium and skeletal muscles. Brumpt (1912) studied the development of T. cruzi in P. megistus ,
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