Persistence of Trypanosoma cruzi in Experimental Chagasic Cardiomyopathy

BAZAN C; MICUCCI L; FAURO R; TRIQUELL MF; LO PRESTI MS; BAEZ AL; STRAUSS M; CAMINO G; PAGLINI P; RIVAROLA H

Anti-Infective Agents

Bentham Science

Año: 2012 vol. 10 p. 136 - 141

2211-3533

The mechanisms by which patients infected with T. cruzi develop or not the disease are not completely understood. We investigated the importance of parasite persistence as a factor in generating cardiomyopathy. Fifty trypomastigote forms from the Tulahuen strain were used as inoculum for 160 Albino Swiss mice. Parasitemia, survival, histopathological and electrocardiographic studies were done on days 90, 180, 270 and 360 post infection (pi). Parasite presence in the tissues was determined by immunofluorescence. Maximum parasitemia was observed on day 21pi and became negative on day 42pi. By day 90pi, 50% of the infected mice presented electrocardiographic alterations and 67% by day 360pi; the non infected group of mice didn’t present elecrocardiographic alterations. Inflammatory infiltrates were observed throughout the infection, with a higher percentage in those mice with electrocardiographic alterations. The presence of the parasite was observed throughout the infection in skeletal muscle samples and on day 90pi in the myocardium. The highest mortality occurred on day 21pi, surviving 10% of the mice until the end of the experiments. These results demonstrate the presence of the parasite in the host tissues along the infection which could produce the injuries found in the myocardium and the electrocardiographic alterations. We investigated the importance of parasite persistence as a factor in generating cardiomyopathy. Fifty trypomastigote forms from the Tulahuen strain were used as inoculum for 160 Albino Swiss mice. Parasitemia, survival, histopathological and electrocardiographic studies were done on days 90, 180, 270 and 360 post infection (pi). Parasite presence in the tissues was determined by immunofluorescence. Maximum parasitemia was observed on day 21pi and became negative on day 42pi. By day 90pi, 50% of the infected mice presented electrocardiographic alterations and 67% by day 360pi; the non infected group of mice didn’t present elecrocardiographic alterations. Inflammatory infiltrates were observed throughout the infection, with a higher percentage in those mice with electrocardiographic alterations. The presence of the parasite was observed throughout the infection in skeletal muscle samples and on day 90pi in the myocardium. The highest mortality occurred on day 21pi, surviving 10% of the mice until the end of the experiments. These results demonstrate the presence of the parasite in the host tissues along the infection which could produce the injuries found in the myocardium and the electrocardiographic alterations. We investigated the importance of parasite persistence as a factor in generating cardiomyopathy. Fifty trypomastigote forms from the Tulahuen strain were used as inoculum for 160 Albino Swiss mice. Parasitemia, survival, histopathological and electrocardiographic studies were done on days 90, 180, 270 and 360 post infection (pi). Parasite presence in the tissues was determined by immunofluorescence. Maximum parasitemia was observed on day 21pi and became negative on day 42pi. By day 90pi, 50% of the infected mice presented electrocardiographic alterations and 67% by day 360pi; the non infected group of mice didn’t present elecrocardiographic alterations. Inflammatory infiltrates were observed throughout the infection, with a higher percentage in those mice with electrocardiographic alterations. The presence of the parasite was observed throughout the infection in skeletal muscle samples and on day 90pi in the myocardium. The highest mortality occurred on day 21pi, surviving 10% of the mice until the end of the experiments. These results demonstrate the presence of the parasite in the host tissues along the infection which could produce the injuries found in the myocardium and the electrocardiographic alterations. T. cruzi develop or not the disease are not completely understood. We investigated the importance of parasite persistence as a factor in generating cardiomyopathy. Fifty trypomastigote forms from the Tulahuen strain were used as inoculum for 160 Albino Swiss mice. Parasitemia, survival, histopathological and electrocardiographic studies were done on days 90, 180, 270 and 360 post infection (pi). Parasite presence in the tissues was determined by immunofluorescence. Maximum parasitemia was observed on day 21pi and became negative on day 42pi. By day 90pi, 50% of the infected mice presented electrocardiographic alterations and 67% by day 360pi; the non infected group of mice didn’t present elecrocardiographic alterations. Inflammatory infiltrates were observed throughout the infection, with a higher percentage in those mice with electrocardiographic alterations. The presence of the parasite was observed throughout the infection in skeletal muscle samples and on day 90pi in the myocardium. The highest mortality occurred on day 21pi, surviving 10% of the mice until the end of the experiments. These results demonstrate the presence of the parasite in the host tissues along the infection which could produce the injuries found in the myocardium and the electrocardiographic alterations.