[The effect of cyclosporine A on the development of Toxoplasma gondii in the muscles and brain. Ultrastructural study].

Presented are histological and electron microscopic findings of alterations in the muscles and brains of mice infected with T. gondii and suppressed with CyA during infection. Cya in the acute phase of infection promoted parasitemia. In the chronic stage it modified the formation of clustered cysts. Following repeated infection active tachyzoites appeared in the repleted macrophage populations of the interstitium. Polymyositis with manifested muscle fiber atrophy and allergic toxoplasmic encephalitis in the acute phase of infection is caused by: 1. active penetration of tachyzoites into non-phagocytizing muscle and nerve cells, 2. toxins (necrotizing enzymes) released by the destroyed reticuloendothelial cells due to rapid multiplication of tachyzoites and pseudocysts, 3. immunologic processes affecting factors regulating the multiplication rate and subsequent transformation of tachyzoites into cystozoites, and vice versa. The altered tissue tropism during toxoplasmic infection, i.e. suppression of the granulating tissue and fibrosis, results in a necrotizing process induced by tachyzoites or in the rupture of cysts. (Fig. 8, Ref. 18.)