Chagas disease is caused by infection with the protozoan parasite Trypanosoma cruzi; the major manifestations are Chagas cardiomyopathy and gastrointestinal disease. Issues related to the pathologic findings and the pathogenesis of infection will be reviewed here. The diagnosis and management of Chagas disease is discussed in detail separately. (See "Clinical manifestations and diagnosis of Chagas heart disease" and "Chagas disease: Natural history and diagnosis" and "Gastrointestinal Chagas disease" and "Epidemiology and control of Chagas disease".)
The natural history of infection consists of acute and chronic phases. (See "Chagas disease: Natural history and diagnosis".)
In general, the acute phase consists of parasitemia in the absence of clinical manifestations and typically lasts 8 to 12 weeks. The chronic phase typically begins with a long period of latency (indeterminate form) characterized by lack of objective evidence of organ damage . About 20 to 30 percent of these individuals progress over a period of years to decades to clinically evident chronic disease; heart disease develops more commonly than gastrointestinal disease. The clinical aspects of these phases are outlined separately.
Acute phase — Organ damage during the acute phase occurs as a result of high grade parasitemia and direct tissue parasitism. Affected sites typically include the heart, gastrointestinal tract, and central nervous system. Lymphadenopathy, hepatomegaly, and splenomegaly are markers of widespread immunologic reaction, which probably exacerbates tissue damage. Histopathology during the acute phase demonstrates intense parasitism in virtually every organic system, with prominent inflammatory changes in the vicinity of ruptured infected cells [2-7].
All four cardiac chambers may become dilated, and pericardial effusion is common. Myocarditis is intense and diffuse with myocyte necrosis, interstitial edema, vascular dilation, and mononuclear and polymorphonuclear infiltration (picture 1). Involvement may extend to the endocardium, resulting in thrombus formation. Involvement also includes the conduction system as well as the intramural and extracardiac neuronal ganglia.