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Trypanosoma cruzi: mixture of two populations can modify virulence and tissue tropism in rat
Deila J Franco1, Annamaria R Vago, Egler Chiari
1Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte 31270-901, Brazil.
Abstract:
In rats, CL-Brener clone caused high mortality, severe acute myocarditis, and myositis that subsided completely in surviving animals. Accordingly, no parasite kDNA could be amplified in several organs after 4 months. The monoclonal JG strain caused null mortality, acute predominantly focal myocarditis, discrete and focal myositis, and a chronic phase with sparse inflammatory foci. Double infection with both Trypanosoma cruzi populations turned mortality very low or null. At the end of the acute phase, the heart exhibited only JG strain kDNA (LSSP-PCR), while skeletal muscles and rectum exhibited only CL-Brener kDNA. Molecular and histopathological findings were accordant. In double infection chronic phase, JG strain remains in heart and appeared in organs previously parasitized by CL-Brener clone. Understanding the virulence and histotropism shifts now described could be important to clarify the variable clinical course and epidemiological peculiarities of Chagas' disease.
Insights
Different Trypanosoma cruzi strains exhibit distinct virulence and tissue tropism in rats. Understanding these differences is key to explaining the varied clinical presentations of Chagas' disease.
Area of Science:
- Infectious Diseases
- Parasitology
- Immunology
Background:
- Chagas' disease, caused by Trypanosoma cruzi, presents with variable clinical outcomes.
- The parasite exhibits diverse strains with potentially different pathogenic profiles.
- Understanding strain-specific virulence and tissue tropism is crucial for disease management.
Purpose of the Study:
- To compare the pathogenicity and tissue distribution of the CL-Brener and JG strains of Trypanosoma cruzi in a rat model.
- To investigate the effects of a dual infection with both strains on disease progression and parasite localization.
- To correlate molecular findings with histopathological observations.
Main Methods:
- Infection of rats with either the CL-Brener clone or the JG strain of Trypanosoma cruzi.
- Experimental induction of dual infections with both strains.
- Monitoring mortality, histopathological analysis of myocarditis and myositis.
- Detection of parasite kinetoplast DNA (kDNA) in various organs using LSSP-PCR.
Main Results:
- CL-Brener clone induced high mortality and severe acute myocarditis/myositis, with no detectable parasite DNA after 4 months in survivors.
- The JG strain caused low mortality, milder focal myocarditis/myositis, and a chronic phase with sparse inflammation.
- Dual infections resulted in low mortality; parasite DNA distribution varied between strains and tissues during acute and chronic phases.
- Molecular and histopathological findings were consistent, with JG strain persisting in the heart and CL-Brener strain in muscles/rectum during acute phase.
Conclusions:
- Trypanosoma cruzi strains CL-Brener and JG exhibit distinct virulence and tissue tropism patterns in rats.
- Dual infections modulate the course of Chagas' disease, influencing parasite localization.
- These findings highlight the importance of strain variability in understanding Chagas' disease pathogenesis and epidemiology.
