Novel Rat Model for Neurocysticercosis Using Taenia solium

Manuela R. Verastegui, Alan Mejia, Taryn Clark, Cesar M. Gavidia, Javier Mamani, Fredy Ccopa, Noelia Angulo, Nancy Chile, Rogger Carmen, Roxana Medina, Hector H. García, Silvia Rodriguez, Ynes Ortega, Robert H. Gilman

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38 Citas (Scopus)

Resumen

© 2015 American Society for Investigative Pathology. Neurocysticercosis is caused by Taenia solium infecting the central nervous system and is the leading cause of acquired epilepsy and convulsive conditions worldwide. Research into the pathophysiology of the disease and appropriate treatment is hindered by lack of cost-effective and physiologically similar animal models. We generated a novel rat neurocysticercosis model using intracranial infection with activated T. solium oncospheres. Holtzman rats were infected in two separate groups: the first group was inoculated extraparenchymally and the second intraparenchymally, with different doses of activated oncospheres. The groups were evaluated at three different ages. Histologic examination of the tissue surrounding T. solium cysticerci was performed. Results indicate that generally infected rats developed cysticerci in the brain tissue after 4 months, and the cysticerci were observed in the parenchymal, ventricle, or submeningeal brain tissue. The route of infection did not have a statistically significant effect on the proportion of rats that developed cysticerci, and there was no dependence on infection dose. However, rat age was crucial to the success of the infection. Epilepsy was observed in 9% of rats with neurocysticercosis. In histologic examination, a layer of collagen tissue, inflammatory infiltrate cells, perivascular infiltrate, angiogenesis, spongy change, and mass effect were observed in the tissue surrounding the cysts. This study presents a suitable animal model for the study of human neurocysticercosis.
Idioma originalInglés estadounidense
Páginas (desde-hasta)2259-2268
Número de páginas10
PublicaciónAmerican Journal of Pathology
DOI
EstadoPublicada - 1 ago. 2015

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