Infecção de gerbils (Meriones unguiculatus) com Toxocara canis : migração de larvas e estudo morfológico com pesquisa imunohistoquímica de antígenos de larvas nas lesões

• Autor(a) principal: Flecher, Mayra Cunha
• Data de Publicação: 2010
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/5949
• topic: Toxocara canis; Toxocaraisis; Gerbils; Infecção de canídeo; Doenças Infecciosas e Parasitárias; 61

Introduction. In last years, the gerbils have been used as experimental model of toxocariasis, especially for studies of ocular lesions and central nervous system. Objectives. To study the migration of larvae and lesions with immunohistochemical study in gerbils infected or re-infected with Toxocara canis. Methods. Gerbils were infected with 1,500 embryonated eggs of T. canis and euthanized 4, 8, 12, 24, 48, 72 and 96 hours, 7, 15, 30 and 60 days after infection. Small and large intestine, liver and brain fragments were pressed between two slides for larvae counts, and lung, digested with acid pepsin solution for larvae counts in the sediment. Formalin fixed fragments of different organs were paraffin embedded for histology and immuniohistiochenmistry, using anti-Toxocara polyclonal serum obtained from rabbits infected with T. canis. Previously infected gerbils were re-infected 30 days after the first infection, with 1,500 or 1,000 eggs and sacrificed 4, 8, 48 and 72 hours, 7, 15, 30 and 60 days after reinfection and underwent the same procedures for larvae counts and histology and immunohistochemestry studies.. Results. Toxocara larvae migrate within the first 24 hours through the small intestine and cecum; from that time they began to be observed in large numbers in the liver, reaching higher number at 48 hours after infection. Then they began to migrate to the lungs and other organs, decreasing the number in the liver after a week of infection, and increased again after 15 days, and still observed until 60 days. In the lungs, the larvae were abundant after 72 hours, which induced large areas of hemorrhage, and were reduced progressively until 30 days after infection. After 96 hours, larvae start to be found in the brain, where the larval burden increased progressively until the end of the experiment. In re-infected animals was an increase in the proportion of larvae counted in the liver in relation to the first infection, and reduction in the brain, at the same times post infection. In animals that received one infection, the morphological changes in various organs, except in the nervous system, characterized by mild or moderate inflammation with large numbers of eosinophils and loose aggregates of macrophages and eosinophils. In the brain larvae were found intact, with scarce or absent inflammatory reaction. In re-infected animals, inflammatory lesions were more severe in all organs, with well organized epithelioid granulomas, with or without larva. Central nervous system lesions were severe, mainly injury in the white matter and Purkinge cells of cerebellum. Immunohistochemistry detected in all organs from all animals larval antigens in areas of diffuse inflammatory exudates, in granulomas and around intact larvae. Conclusion. The results showed that the Toxocara canis larval migration pattern in gerbils is similar to that described in mice and rats, with a neurotropic later stage, leading to concentration of larvae in the central nervous system. Lesions observed after reinfection showed evidence of a TH2 type adaptive immune response (eosinophils in the exsudate and epitheliod eosinophilic granulomas) that would be in relationship with retention of larvae in the liver, delaying their arrival to the brain. Although larvae were sometimes found inside epithelioid granulomas, there was not evidence that larvae were injured by inflammatory cells