Murine models susceptibility to distinct Trypanosoma cruzi I genotypes infection

CIELO M. LEÓN, MARLENY MONTILLA, RICARDO VANEGAS, MARIA CASTILLO, EDGAR PARRA, JUAN DAVID RAMÍREZ

Resultado de la investigación: Contribución a RevistaArtículo

7 Citas (Scopus)

Resumen

Copyright © Cambridge University Press 2016Chagas 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.
Idioma originalEnglish (US)
Páginas (desde-hasta)1-8
Número de páginas8
PublicaciónParasitology
DOI
EstadoPublished - nov 10 2016

Huella dactilar

Trypanosoma cruzi
Parasitemia
parasitemia
animal models
Genotype
National Institutes of Health
genotype
National Institutes of Health (U.S.)
Infection
infection
biological resistance
cardiomyopathy
Zoonoses
zoonoses
Cardiomyopathies
natural history
histopathology
genetic background
Chiroptera
geographical distribution

Citar esto

LEÓN, CIELO. M., MONTILLA, MARLENY., VANEGAS, RICARDO., CASTILLO, MARIA., PARRA, EDGAR., & RAMÍREZ, JUAN. DAVID. (2016). Murine models susceptibility to distinct Trypanosoma cruzi I genotypes infection. Parasitology, 1-8. https://doi.org/10.1017/S0031182016001980
LEÓN, CIELO M. ; MONTILLA, MARLENY ; VANEGAS, RICARDO ; CASTILLO, MARIA ; PARRA, EDGAR ; RAMÍREZ, JUAN DAVID. / Murine models susceptibility to distinct Trypanosoma cruzi I genotypes infection. En: Parasitology. 2016 ; pp. 1-8.
@article{b3eec794530a490ebbb4f666b94a7062,
title = "Murine models susceptibility to distinct Trypanosoma cruzi I genotypes infection",
abstract = "Copyright {\circledC} Cambridge University Press 2016Chagas 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.",
author = "LE{\'O}N, {CIELO M.} and MARLENY MONTILLA and RICARDO VANEGAS and MARIA CASTILLO and EDGAR PARRA and RAM{\'I}REZ, {JUAN DAVID}",
year = "2016",
month = "11",
day = "10",
doi = "10.1017/S0031182016001980",
language = "English (US)",
pages = "1--8",
journal = "Parasitology",
issn = "0031-1820",
publisher = "Cambridge University Press",

}

Murine models susceptibility to distinct Trypanosoma cruzi I genotypes infection. / LEÓN, CIELO M.; MONTILLA, MARLENY; VANEGAS, RICARDO; CASTILLO, MARIA; PARRA, EDGAR; RAMÍREZ, JUAN DAVID.

En: Parasitology, 10.11.2016, p. 1-8.

Resultado de la investigación: Contribución a RevistaArtículo

TY - JOUR

T1 - Murine models susceptibility to distinct Trypanosoma cruzi I genotypes infection

AU - LEÓN, CIELO M.

AU - MONTILLA, MARLENY

AU - VANEGAS, RICARDO

AU - CASTILLO, MARIA

AU - PARRA, EDGAR

AU - RAMÍREZ, JUAN DAVID

PY - 2016/11/10

Y1 - 2016/11/10

N2 - Copyright © Cambridge University Press 2016Chagas 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.

AB - Copyright © Cambridge University Press 2016Chagas 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.

U2 - 10.1017/S0031182016001980

DO - 10.1017/S0031182016001980

M3 - Article

SP - 1

EP - 8

JO - Parasitology

JF - Parasitology

SN - 0031-1820

ER -