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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Published inParasitology Vol. 144; no. 4; pp. 512 - 519
Main Authors LEÓN, CIELO M., MONTILLA, MARLENY, VANEGAS, RICARDO, CASTILLO, MARIA, PARRA, EDGAR, RAMÍREZ, JUAN DAVID
Format Journal Article
LanguageEnglish
Published Cambridge, UK Cambridge University Press 01.04.2017
Subjects
Animals
Anthropogenic factors
Chagas Disease - parasitology
Disease Susceptibility
Genetic diversity
Genotype
Genotypes
Geographical distribution
Histopathology
Immune response
Mice
Parasites
Trypanosoma cruzi
Trypanosoma cruzi - genetics
Vector-borne diseases
Inbred line
mice
Trypanosoma cruzi
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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.
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ISSN:0031-1820
1469-8161
DOI:10.1017/S0031182016001980