Immunohistochemical studies in acute and chronic canine chagasic cardiomyopathy

Abstract

A major characteristic of Chagas' disease is a myocarditis constituted primarily of mononuclear cells, both during the acute and chronic phases of the disease. Using monoclonal antibodies and image analyses we have quantified canine CD8(+) T cells (caCD8(+) T cells), canine CD4(+) T cells (caCD4(+) T cells) and neutrophils in canine chagasic myocardiopathy induced by two strains isolated from the first human clinical case of Chagas' disease. We also evaluated the influence of tissue parasitism in the genesis of chronic myocarditis through immunohistochemistry. As in human myocarditis, there was a predominance of T lymphocytes in the inflammatory infiltrate in all animals studied. In the dogs inoculated with strain Berenice 78 (Be78) and necropsied during the acute phase of infection, we found 58% caCD8(+) and 42% caCD4(+) T cells. In chronically infected animals, 53% of T cells were represented by caCD8(+) and 47% were caCD4(+) T cells. Since normal canine lymphoid organs are constituted by 70-80% caCD4(+) T cells and 20-30% caCD8(+) T cells our results indicate a higher proliferation of caCD8(+) T cells in dogs inoculated with the Be78 strain. In chronic myocarditis induced by the Berenice 62 (Be62) strain, caCD8(+) cells constituted 33% of the T cells and 67% were caCD4(+) T cells, a proportion similar to that found in normal canine lymphoid organs. Since the Be78 strain induces greater loss of myocardiocytes than strain Be62, we believe that the caCD8(+) T cells, among other factors, can be important in the genesis of these lesions. Amastigote nests and immunohistochemically labelled Trypanosoma cruzi antigen were not found in dogs necropsied during the chronic phase. The absence of the parasite in the myocardium suggests the involvement of other mechanisms in the genesis of the inflammatory process.

Trypanosoma cruzi Circulating in the Southern Region of the State of Mexico (Zumpahuacan) Are Pathogenic: A Dog Model

“…Perimysial and endomysial lymphoplasmacytic infiltration in the heart of infected dogs was probably caused by evolution of adaptive immune responses and inflammatory processes that induce hyalinization and fibrosis. Others have reported the presence of myocardial necrosis14,15 and inflammatory infiltrate27,28 associated with fibrosis in dogs in indeterminate phases of T. cruzi infection and disease, thus providing support to our observations.…”

Papel do óxido nítrico no desenvolvimento de lesões cardíacas na fase aguda da infecção experimental pelo Trypanosoma cruzi

“…Na imagem polarizada o tecido conjuntivo fibroso apresentou-se birrefringente sendo marcado pelo observador, obtendo assim o percentual de fibrose por área analisada. A análise foi realizada em todos os campos do fragmento, totalizando 20 campos 8 .…”

“…Posteriormente, as lâminas foram incubadas com a proteína A conjugada com peroxidase (1:500) e reveladas com H 2 O 2-0,05% + DAB-diaminobenzidina, em tampão tris-HCl pH 7,4. Os cortes foram contracorados com hematoxilina e as lâminas foram então montadas para análise em microscópio de luz comum 8 .…”

Histological Characterization of Dilated Cardiomyopathy in the Juvenile Toy Manchester Terrier

“…Postmortem reports were available for 14 TMTs that were confirmed to be affected based on microscopic lesions identified by microscopic examination of submitted slides or paraffin-embedded tissues (TMT CM Nos. [1][2][3][4][5][6][7][8][9][10][11][12] or based on microscopic cardiac lesions described in the submitted postmortem reports (TMT CM Nos. 13 and 14).…”

“…Five dogs (TMT CM Nos. 1,5,8,9, and 14 with ratios of 1.07, 1.44, 1.07, 1.08, and 1.00, respectively) had increased HW/BW ratios (normal range is 0.58%-0.94% of total body weight), 48 and the remaining dog had a decreased ratio (TMT CM No. 12 with a ratio of 0.56).…”