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Main Cardiac Histopathologic Alterations in the Acute Phase of Trypanosoma cruzi Infection in a Murine Model
Mariana C de Alba Alvarado1, Elia Torres Gutiérrez1, Margarita Cabrera Bravo1
1Departamento de Microbiología y Parasitología, Facultad de Medicina, Universidad Nacional Autónoma de México, Coyoacán, Mexico City 04510, Mexico.
Insights
Acute Chagas disease shows mild symptoms but causes cardiac damage. This study in mice reveals early fibrosis and inflammation, highlighting the need for timely interventions to prevent severe heart complications.
Area of Science:
- Pathology
- Infectious Diseases
- Cardiology
Background:
- Chagas disease presents nonspecific acute symptoms, delaying diagnosis.
- Severe cardiac complications and mortality occur in the chronic phase.
- Understanding acute phase cardiac pathology is crucial for early intervention.
Purpose of the Study:
- To analyze cardiac histopathology during the acute phase of Chagas disease in a mouse model.
- To assess parasitism, fibrosis, and cellular infiltrate in cardiac tissue.
- To determine the role of these factors in acute cardiac lesion pathogenesis.
Main Methods:
- Utilized a CD1 mouse model infected with Trypanosoma cruzi.
- Monitored parasitemia and parasite load (amastigote nests).
- Evaluated cardiac tissue for inflammation, fibrosis, perivasculitis, and myocytolysis.
Main Results:
- Acute phase lasted approximately 62 days post-infection.
- Parasitemia peaked at 33 dpi; amastigote nests were present from 15-62 dpi.
- Early infiltration of macrophages/neutrophils, followed by increased lymphocytes (40-62 dpi).
- Interstitial fibrosis increased significantly (40-60 dpi), with 50% mortality.
- Perivasculitis, thrombi, and myocytolysis observed by 62 dpi.
Conclusions:
- Histopathological changes, including fibrosis and inflammation, occur during the acute phase of Chagas disease.
- These alterations contribute to cardiac tissue damage and fibrosis development.
- Findings enhance understanding of acute Chagas disease pathology, aiding preclinical drug development.
Abstract:
Symptoms in the acute phase of Chagas disease are usually mild and nonspecific. However, after several years, severe complications like dilated heart failure and even death may arise in the chronic phase. Due to the lack of specific symptoms in the acute phase, the aim of this work was to describe and analyze the cardiac histopathology during this phase in a CD1 mouse model by assessing parasitism, fibrotic damage, and the presence and composition of a cellular infiltrate, to determine its involvement in the pathogenesis of lesions in the cardiac tissue. Our results indicate that the acute phase lasts about 62 days post-infection (dpi). A significant increase in parasitemia was observed since 15 dpi, reaching a maximum at 33 dpi (4.1 × 106). The presence of amastigote nests was observed at 15-62 dpi, with a maximum count of 27 nests at 35 dpi. An infiltrate consisting primarily of macrophages and neutrophils was found in the cardiac tissue within the first 30 days, but the abundance of lymphocytes showed an 8 ≥ fold increase at 40-62 dpi. Unifocal interstitial fibrosis was identified after 9 dpi, which subsequently showed a 16 ≥ fold increase at 40-60 dpi, along with a 50% mortality rate in the model under study. The increased area of fibrotic lesions revealed progression in the extent of fibrosis, mainly at 50-62 dpi. The presence of perivasculitis and thrombus circulation disorders was seen in the last days (62 dpi); finally, cases of myocytolysis were observed at 50 and 62 dpi. These histopathological alterations, combined with collagen deposition, seem to lead to the development of interstitial fibrosis and damage to the cardiac tissue during the acute phase of infection. This study provides a more complete understanding of the patterns of histopathological abnormalities involved in the acute phase, which could help the development of new therapies to aid the preclinical tests of drugs for their application in Chagas disease.
