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MORPHOLOGICAL ASPECTS OF THE MYOCARDITIS AND MYOSITIS IN CALOMYS CALLOSUS EXPERIMENTALLY INFECTED WITH TRYPANOSOMA CRUZI: FIBROGENESIS AND SPONTANEOUS REGRESSION OF FIBROSIS.
Calomys callosus
Myocarditis
Myositis
Fibrogenesis
Fibroclasia
Ultrastructure
Collagen
Fibrose Endomiocárdica/patologia
Músculo Esquelético/ultraestrutura
Miosite/patologia
Animais
Cricetinae
Modelos Animais de Doenças
Reservatórios de Doenças
Miocárdio/ultraestrutura
Miosite/parasitologia
Roedores/parasitologia
Afiliación
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
Instituto de Medicina Tropical de São Paulo. Departamento de Parasitologia. São Paulo, SP, Brasil
Instituto de Medicina Tropical de São Paulo. Departamento de Parasitologia. São Paulo, SP, Brasil
Pathology Branch National Heart Blood. Lung Institute. Bethesda, MD, United States of America
Instituto de Medicina Tropical de São Paulo. Departamento de Parasitologia. São Paulo, SP, Brasil
Instituto de Medicina Tropical de São Paulo. Departamento de Parasitologia. São Paulo, SP, Brasil
Pathology Branch National Heart Blood. Lung Institute. Bethesda, MD, United States of America
Resumen en ingles
Calomys callosus a wild rodent, is a natural host of Trypanosoma cruzi. Twelve C. callosus were infected with 10(5) trypomastigotes of the F strain (a myotropic strain) of T. cruzi. Parasitemia decreased on the 21st day becoming negative around the 40th day of infection. All animals survived but had positive parasitological tests, until the end of the experiment. The infected animals developed severe inflammation in the myocardium and skeletal muscle. This process was pronounced from the 26th to the 30th day and gradually subsided from the 50th day becoming absent or residual on the 64th day after infection. Collagen was identified by the picro Sirius red method. Fibrogenesis developed early, but regression of fibrosis occurred between the 50th and 64th day. Ultrastructural study disclosed a predominance of macrophages and fibroblasts in the inflammatory infiltrates, with small numbers of lymphocytes. Macrophages had active phagocytosis and showed points of contact with altered muscle cells. Different degrees of matrix expansion were present, with granular and fibrillar deposits and collagen bundles. These alterations subsided by the 64th days. Macrophages seem to be the main immune effector cell in the C. callosus model of infection with T. cruzi. The mechanisms involved in the rapid fibrogenesis and its regression deserve further investigation.
Palabras clave en ingles
Trypanosoma cruziCalomys callosus
Myocarditis
Myositis
Fibrogenesis
Fibroclasia
Ultrastructure
Collagen
DeCS
Cardiomiopatia Chagásica/patologiaFibrose Endomiocárdica/patologia
Músculo Esquelético/ultraestrutura
Miosite/patologia
Animais
Cricetinae
Modelos Animais de Doenças
Reservatórios de Doenças
Miocárdio/ultraestrutura
Miosite/parasitologia
Roedores/parasitologia
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