The course of an infection with the BEV strain of
T. gondii was followed in splenectomized mice, and in cortisone-treated mice. It was observed that the pathogenesis of the disease was greatly altered in both groups of animals, geherally culminating in a fatal toxoplasmic ehcephalitis. Common findings were: symptoms of neurological disease, persistence of trophozoites in peritoneal exudate, suppression of immunity to reinfection, early appearance of cysts in the braih, development of many cysts in clusters, and evidehce of a strong inflammatory response in association with many of the cysts. These observations are interpreted as indicating that modification of the immune response to
Toxoplasma was achieved, and that as a consequence of this modification, parasite proliferation in tissues and hematogenous transport of trophozoites to the brain continued uncurtailed, leading to the increasingly severe neurological involvement and the terminal encephalitis.
The clusters of cysts are believed to be fortuitous gatherings, arising from the invasion of circumscribed areas of the brain by large numbers of blood-borne trophozoites, and the inflammation in response to the considerable cellular destruction wrought by the growing clusters of cysts.
The unsatisfactory status of the serology of toxoplasmosis, due to the lack of a purified and defined antigen, is described as a major handicap to the elucidation of the nature and significance of the immune response to
Toxoplasma.
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