Toxoplasmose congênita humana: caracterização de cepas de Toxoplasma gondii em linhagens isogênicas de camundongos

• Ano de defesa: 2014
• Autor(a) principal: Breno Veloso Pinheiro
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Parasitologia
• Link de acesso: http://hdl.handle.net/1843/BUOS-9KXJF4

The pathogenesis of toxoplasmosis depends on the genetic structure of the parasite strain and the host, as well as the dose and route of infection, among other factors. There is a lack of pathological studies using inbred strains of mice after inoculation with strains of Toxoplasma gondii belonging to atypical genotypes commonly found in Brazil. Previously, 26 strains were isolated from human cases of congenital toxoplasmosis in the state of Minas Gerais, among which three were selected for this study: TgCTBR5, TgCTBR9 and TgCTBR16. BALB/c and C57BL/6 inbred mice were inoculated perorally with 10 tissue cysts of each of the three strains and were evaluated for survival, morbidity and histopathology. While all mice inoculated with the TgCTBR5 strain survived, none of them resisted to infection with the TgCTBR9. The TgCTBr16 strain showed 80% survival, regardless of the mice lineage. Mice inoculated with TgCTBr5 strain had significantly body weight loss and irreversible tissue damage, demonstrating that even non-lethal, avirulent strains can be pathogenic for mice. C57BL/6 mice were more susceptible than BALB/c in the analysis of morbidity and histopathology. However, the former were more resistant than the latter for the formation of tissue cysts in the brains 30 days after infection. Histopathologic examination showed the liver and lungs as the most affected organs, as previously described by others, and associated with lethality during second week of infection. TgCTBr9 strain caused more damage to mice tissue than the others parasites. Serology of survivors after 30 days confirmed 100% infection in both lineages of mice inoculated with TgCTBR5 strain. In contrast, TgCTBR16 strain showed low infectivity, especially by peroral infection. Genotyping of TgCTBR16 strain revealed the atypical genotype BrIII (similar to TgCTBr5), already described by others. Our results strongly suggest that the pathogenesis of toxoplasmosis depends mainly on intrinsic factors of the T. gondii strains.