Peer-reviewed veterinary case report
Different Trypanosoma cruzi strains cause unique heart damage
By Duz, Ana Luiza Cassin et al.·Published in Memorias do Instituto Oswaldo Cruz·2014·Laborató·View original on PubMed →
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Original publication title: The TcI and TcII Trypanosoma cruzi experimental infections induce distinct immune responses and cardiac fibrosis in dogs.
- Species:
- dog
Plain-English summary
A group of dogs was infected with different strains of the Trypanosoma cruzi parasite, which can cause Chagas disease, to see how their immune systems responded. Some dogs infected with the Colombian strain showed signs of liver issues and increased inflammatory cells in the heart, while those with the Y strain experienced low white blood cell counts and significant heart inflammation and scarring. The study found that the immune response varied between the strains, affecting the severity of heart problems. Understanding these differences can help in managing and treating dogs with Chagas disease.
People also search for: dog Chagas disease symptoms · Trypanosoma cruzi treatment for dogs · dog heart inflammation causes
Abstract
Trypanosoma cruzi infection may be caused by different strains with distinct discrete typing units (DTUs) that can result in variable clinical forms of chronic Chagas disease. The present study evaluates the immune response and cardiac lesions in dogs experimentally infected with different T. cruzi strains with distinct DTUs, namely, the Colombian (Col) and Y strains of TcI and TcII DTU, respectively. During infection with the Col strain, increased levels of alanine aminotransferase, erythrocytes, haematocrit and haemoglobin were observed. In addition, CD8+ T-lymphocytes isolated from the peripheral blood produced higher levels of interleukin (IL)-4. The latter suggests that during the acute phase, infection with the Col strain may remain unnoticed by circulating mononuclear cells. In the chronic phase, a significant increase in the number of inflammatory cells was detected in the right atrium. Conversely, infection with the Y strain led to leucopoenia, thrombopoenia, inversion of the ratio of CD4+/CD8+ T-lymphocytes and alterations in monocyte number. The Y strain stimulated the production of interferon-γ by CD4+ and CD8+ T-lymphocytes and IL-4 by CD8+ T-cells. In the chronic phase, significant heart inflammation and fibrosis were observed, demonstrating that strains of different DTUs interact differently with the host.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/25591108/