Taenia solium: Development of an Experimental Model of Porcine Neurocysticercosis.

Human neurocysticercosis (NC) is caused by the establishment of Taenia solium larvae in the central nervous system. NC is a severe disease still affecting the population in developing countries of Latin America, Asia, and Africa. While great improvements have been made on NC diagnosis, treatment, an...

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Bibliographic Details
Published in:PLOS Neglected Tropical Diseases
Main Authors: Agnès Fleury, Armando Trejo, Humberto Cisneros, Roberto García-Navarrete, Nelly Villalobos, Marisela Hernández, Juana Villeda Hernández, Beatriz Hernández, Gabriela Rosas, Raul J Bobes, Aline S de Aluja, Edda Sciutto, Gladis Fragoso
Format: Article in Journal/Newspaper
Language:English
Published: Public Library of Science (PLoS) 2015
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Online Access:https://doi.org/10.1371/journal.pntd.0003980
https://doaj.org/article/706c5e578a0d4fbbb22911712b3e643b
Description
Summary:Human neurocysticercosis (NC) is caused by the establishment of Taenia solium larvae in the central nervous system. NC is a severe disease still affecting the population in developing countries of Latin America, Asia, and Africa. While great improvements have been made on NC diagnosis, treatment, and prevention, the management of patients affected by extraparenchymal parasites remains a challenge. The development of a T. solium NC experimental model in pigs that will allow the evaluation of new therapeutic alternatives is herein presented. Activated oncospheres (either 500 or 1000) were surgically implanted in the cerebral subarachnoid space of piglets. The clinical status and the level of serum antibodies in the animals were evaluated for a 4-month period after implantation. The animals were sacrificed, cysticerci were counted during necropsy, and both the macroscopic and microscopic characteristics of cysts were described. Based on the number of established cysticerci, infection efficiency ranged from 3.6% (1000 oncospheres) to 5.4% (500 oncospheres). Most parasites were caseous or calcified (38/63, 60.3%) and were surrounded by an exacerbated inflammatory response with lymphocyte infiltration and increased inflammatory markers. The infection elicited specific antibodies but no neurological signs. This novel experimental model of NC provides a useful tool to evaluate new cysticidal and anti-inflammatory approaches and it should improve the management of severe NC patients, refractory to the current treatments.