Murine models susceptibility to distinct Trypanosoma cruzi i genotypes infection

Chagas disease is a complex zoonosis that affects around 8 million people worldwide. This pathology is caused by Trypanosoma cruzi, a kinetoplastid parasite that shows tremendous genetic diversity evinced in six distinct Discrete Typing Units (TcI-TcVI) including a recent genotype named as TcBat and...

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Autores:
Tipo de recurso:
Fecha de publicación:
2017
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/22758
Acceso en línea:
https://doi.org/10.1017/S0031182016001980
https://repository.urosario.edu.co/handle/10336/22758
Palabra clave:
Immunoglobulin G antibody
T6 antigen
Animal experiment
Animal model
Article
Cardiomyopathy
Chagas disease
Controlled study
Female
Follow up
Genetic predisposition
Genetic variability
Genotype
Histopathology
Immune response
Immunofluorescence test
Inbred strain
Inoculation
Male
Mouse
Murine model
Nonhuman
Parasitemia
Phylogeny
Survival rate
Trypanosoma cruzi
Animal
Chagas disease
Disease predisposition
Genetics
Parasitology
Animals
Chagas Disease
Disease Susceptibility
Genotype
Mice
Trypanosoma cruzi
Inbred line
Mice
Trypanosoma cruzi
Rights
License
Abierto (Texto Completo)
Description
Summary:Chagas disease is a complex zoonosis that affects around 8 million people worldwide. This pathology is caused by Trypanosoma cruzi, a kinetoplastid parasite that shows tremendous genetic diversity evinced in six distinct Discrete Typing Units (TcI-TcVI) including a recent genotype named as TcBat and associated with anthropogenic bats. TcI presents a broad geographical distribution and has been associated with chronic cardiomyopathy. Recent phylogenetic studies suggest the existence of two genotypes (Domestic (TcIDom) and sylvatic TcI) within TcI. The understanding of the course of the infection in different mouse models by these two genotypes is not yet known. Therefore, we infected 126 animals (ICR-CD1, National Institute of Health (NIH) and Balb/c) with two TcIDom strains and one sylvatic strain for a follow-up period of 60 days. We quantified the parasitaemia, immune response and histopathology observing that the maximum day of parasitaemia was achieved at day 21 post-infection. Domestic strains showed higher parasitaemia than the sylvatic strain in the three mouse models; however in the survival curves Balb/c mice were less susceptible to infection compared with NIH and ICR-CD1. Our results suggest that the genetic background plays a fundamental role in the natural history of the infection and the sympatric TcI genotypes have relevant implications in disease pathogenesis. © 2016 Cambridge University Press.