Comparative study of the biological properties of Trypanosoma cruzi I genotypes in a murine experimental model

Chagas disease is an endemic zoonosis in Latin America and caused by the parasite Trypanosoma cruzi. This kinetoplastid displays remarkable genetic variability, allowing its classification into six Discrete Typing Units (DTUs) from TcI to TcVI. T. cruzi I presents the broadest geographical distribut...

Full description

Autores:
Tipo de recurso:
Fecha de publicación:
2015
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/24295
Acceso en línea:
https://doi.org/10.1016/j.meegid.2014.11.012
https://repository.urosario.edu.co/handle/10336/24295
Palabra clave:
Immunoglobulin G
Animal model
Antibody titer
Antigenicity
Article
Body weight
Chagas disease
Comparative study
Controlled study
Epidemiological monitoring
Exon
Gene sequence
Genetic variability
Genotype
Histopathology
Immune response
Immunofluorescence test
Infection
Kinetoplastida
Molecular epidemiology
Mortality
Mouse
Nonhuman
Parasitemia
Protozoal genetics
Qualitative analysis
Quantitative analysis
Real time polymerase chain reaction
Trypanosoma cruzi
Animals
Chagas disease
Classification
Genetics
Genotype
Growth and development
Heart
Humans
Immunology
Male
Mice
Mice, Inbred ICR
Molecular Typing
Parasitemia
Parasitology
Pathology
Tropism
Trypanosoma cruzi
Murinae
Trypanosoma cruzi
Animals
Chagas Disease
Disease Models, Animal
Genotype
Heart
Humans
Male
Mice
Molecular Typing
Parasitemia
Tropism
Trypanosoma cruzi
Chagas disease
DTU
Epidemiological cycles
Molecular epidemiology
Trypanosoma cruzi I
Protozoan
Genome
Rights
License
Abierto (Texto Completo)
Description
Summary:Chagas disease is an endemic zoonosis in Latin America and caused by the parasite Trypanosoma cruzi. This kinetoplastid displays remarkable genetic variability, allowing its classification into six Discrete Typing Units (DTUs) from TcI to TcVI. T. cruzi I presents the broadest geographical distribution in the continent and has been associated to severe forms of cardiomyopathies. Recently, a particular genotype associated to human infections has been reported and named as TcIDOM (previously named TcIa-b). This genotype shows to be clonal and adapted to the domestic cycle but so far no studies have determined the biological properties of domestic (TcIDOM) and sylvatic TcI strains (previously named TcIc-e). Hence, the aim of this study was to untangle the biological features of these genotypes in murine models. We infected ICR-CD1 mice with five TcI strains (two domestic, two sylvatic and one natural mixture) and determined the course of infection during 91days (acute and chronic phase of the disease) in terms of parasitemia, tissue tropism, immune response (IgG titers) and tissue invasion by means of histopathology studies. Statistically significant differences were observed in terms of parasitemia curves and prepatent period between domestic (TcIDOM) and sylvatic strains. There were no differences in terms of IgG antibodies response across the mice infected with the five strains. Regarding the histopathology, our results indicate that domestic strains present higher parasitemias and low levels of histopathological damage. In contrast, sylvatic strains showed lower parasitemias and high levels of histopathological damage. These results highlight the sympatric and behavioral differences of domestic and sylvatic TcI strains; the clinical and epidemiological implications are herein discussed. © 2014 Elsevier B.V.