Modulatory effects of T-cell immunosuppression on pigeon protozoal encephalitis induced by Sarcocystis calchasi

Abstract

Sarcocystis calchasi is the causative agent of Pigeon Protozoal Encephalitis, a neurological disease in pigeons. The biphasic disease is characterized by neurological signs in the chronic phase. Parasite stages are generally not associated with inflammatory brain lesions and the parasite has been suggested to modulate the host’s immune system. To test this hypothesis, pigeons experimentally infected with S. calchasi were T-cell immunosuppressed beginning from 14 days post infection (dpi) until the end of the experiment (59/60 dpi) and compared with immunocompetent animals. When scored histologically (sum encephalitis score consisting of lympho-histiocytic perivascular cuffs, lymphocytic encephalitis and gliosis), encephalitis was markedly less pronounced in immunosuppressed pigeons than in immunocompetent animals (6.8 ± 4.4 s.d. versus 11.2 ± 3.0 s.d.). Thus, the alleviation of the disease by immunosuppression supports the hypothesis of an immune-mediated mechanism rather than direct damage by the pathogen. Results from a second infection trial, where the effect of immunosuppression only during early (12–20 dpi) or late phase (30 dpi – end of experiment) was compared, did not show significant differences between both groups and suggest that immunomodulation is triggered during the early stage of parasite development by sporozoites and/or more likely merozoites.