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CHAGAS' disease (South American trypanosomiasis) is caused by infection with Trypanosoma cruzi. The flagellate parasite enters the host when the exereta of the infected Triatoma vector come in contact with broken human skin or intact mucosa. The acute phase of the disease, characterized by a febrile illness with myocarditis and rarely meningoencephalitis, may subside completely without sequelae or progress to chronic myocarditis or gastrointestinal lesions or both; e.g., megaesophagus and megacolon. The course of the disease is unpredictable both in the experimentally infected animal and in the human host.1-3 Until recently most writers believed that the changes in the myocardium were sufficient to explain all the clinical cardiac findings in acute and chronic Chagas' disease. The early descriptions by Vianna4 and Torres5-7 set a pattern that served

The Pathologic Lesions of the Cardiac Autonomic Nervous System in Chronic Chagas' Myocarditis