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American Journal of Pathology, Vol 144, 1403-1411, Copyright © 1994 by American Society for Investigative Pathology

REGULAR ARTICLES

Myocardial changes in acute Trypanosoma cruzi infection. Ultrastructural evidence of immune damage and the role of microangiopathy

ZA Andrade, SG Andrade, R Correa, M Sadigursky and VJ Ferrans
Goncalo Moniz Research Center (FIOCRUZ), Bahia, Brazil.

Histological and ultrastructural studies of the hearts of dogs sacrificed 18 to 26 days after intraperitoneal inoculation with 4 x 10(5) blood forms of the 12 SF strain of Trypanosoma cruzi/kg of body weight disclosed myocarditis characterized by parasitic invasion of some myocytes, damage and necrosis of nonparasitized myocytes, and interstitial infiltration by mononuclear cells. Nonparasitized myocytes showed alterations ranging from mild edema to severe myocytolysis. These changes often were accompanied by contacts of myocytes with lymphocytes (both granular and agranular) and macrophages. These contacts were characterized by focal loss of the myocyte basement membrane and close approximation of the plasma membranes of the two cells. Contacts between lymphocytes and capillary endothelial cells were also frequent. Platelet aggregates and fibrin microthrombi were observed in some capillaries. Our findings suggest that immune effector cells play a major role in the pathogenesis of the myocyte damage and the microangiopathy in acute Chagas' disease.


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J. A. Marin-Neto, E. Cunha-Neto, B. C. Maciel, and M. V. Simoes
Pathogenesis of Chronic Chagas Heart Disease
Circulation, March 6, 2007; 115(9): 1109 - 1123.
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Copyright © 1994 by the American Society for Investigative Pathology.