Mechanisms of myocardial damage in Trypanosoma cruzi infection.
A study of pathological lesions caused by Trypanosoma cruzi in human and experimental hosts indicated that the main mechanisms of myocardial damage in Chagas' disease are the following. (1) During acute infection inflammatory lesions are related to parasite-induced destruction of myocardial cells, with probable participation of immune-complex reactions. When parasitism decreases, inflammation subsides and may disappear completely. (2) After recovery from acute infection the hosts remain infected but asymptomatic for a prolonged period of time. Focal fibrotic areas may be present in the myocardium, conducting tissue and autonomic nervous system, representing sequelae from the acute phase. Such sequelae may have or may acquire functional significance in some special circumstances. (3) Some patients with latent T. cruzi infection may progress to show a diffuse, active and fibrosing myocarditis without an apparent change in parasitological and immunological status from the asymptomatic phase. The microscopic changes in the heart are compatible with the presence of a delayed-type hypersensitivity process. An abolition of the suppressive factors of delayed hypersensitivity which are present during latent infection may be involved.
D000818:Animals; D000941:Antigens / Q000276:immunology; D002598:Chagas Cardiomyopathy / Q000276:immunology / Q000473:pathology; D014355:Chagas Disease / Q000473:pathology*; D004195:Disease Models, Animal; D004285:Dogs; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000276:immunology; D009206:Myocardium / Q000473:pathology*; D014349:Trypanosoma cruzi / Q000254:growth & development / Q000276:immunology / Q000472:pathogenicity
D000941:Antigens