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Six month old calves kept on pasture were experimentally infected three times with O. ostertagi and 15 days later each infection was abbreviated with oxfendazole. After the immunisation period the animals were allowed to graze naturally contaminated pasture. The results obtained clearly show that immunised animals produced significantly fewer eggs than the non-immunised controls. The protection obtained was associated with increased daily liveweight gains.
The studies were undertaken to investigate the development of some cell-mediated immune responses in experimental toxocarosis in mice and to assess the influence of these responses on the course of infection. Mice were infected orally with 350 eggs of Toxocara canis and reinfected with the same dose of parasites after 8 weeks. Groups of infected animals were killed each week of the experiments to obtain spleens, livers and brains for further studies. Lymphocytes from removed spleens were analysed by flow-cytometry for CD4 and CD8 expression and cultured in vitro to measure their responses to Concanavalin A and excretory-secretory (ES) antigen of T. canis in a lymphocyte transformation test. Pieces of livers were used to prepare paraffin sections to be stained later with haematoxylin and eosin, whereas whole brains of the infected animals were examined for the presence of parasite larvae. The results of the studies showed depression of T-cell responses to ConA in early stages of infection and significant increase in the blastogenic responses to the ES antigen from week 4 following infection. The depression of T-cell responses was accompanied by lowered CD4+/CD8+ ratio resulting from increased percentages of CD8+ T cells. Histopathological examination of liver sections revealed trapping of larvae in T. canis reinfected mice. The intensity of infection as measured by larval recoveries from the brains of mice increased gradually up to the 8th week of infection, but did not show significant changes after reinfection, testifying to the development of long-lasting protective immunity during primary infection.
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