Latent toxoplasma-infection as a possible risk factor for CNS-disorders.
In histological and immunobiological studies of recognizable damage at the CNS level, mice with chronic or latent T. gondii infection were used as a model. It could be demonstrated that metabolic products of the encysted parasite may lead to toxicosis causing inflammatory granulomatous changes of perivascular areas. Progressive deposition of necrotic material may finally result in an occlusion and subsequent sclerosis of vessels. Immunologically, the presence of these metabolic products (exoantigens) could be demonstrated in the area of perivascular cuffing. In the damaged brains, only T. gondii cysts were found; other stages of the parasite were missing. The histopathological CNS changes observed in the mice were identical with those described in humans. Since toxoplasms preferentially settle in the CNS, infections of early childhood may indirectly result in degenerative disease causing an impairment of CNS function. This hypothesis is supported by other studies whose authors found that educationally subnormal children and adolescents exhibited a far greater proportion of antibodies to toxoplasms, i.e. were infected by the parasite, than normally developing children of identical ages.
D000818:Animals; D000941:Antigens / Q000032:analysis; D001921:Brain / Q000098:blood supply / Q000276:immunology / Q000469:parasitology / Q000473:pathology*; D051379:Mice; D009457:Neuroglia / Q000473:pathology; D051381:Rats; D014122:Toxoplasma / Q000276:immunology; D014124:Toxoplasmosis, Animal / Q000469:parasitology / Q000473:pathology*
D000941:Antigens