The ultrastructural features of the early development and tissue cyst formation of Toxoplasma gondii were examined in the brains of mice at various intervals from 7 days to 22 months post inoculation (PI). At 11 days PI toxoplasmas, with the ultrastructural features of the proliferative (endozoite) form, were identified undergoing multiplication within both inflammatory and neural cells. Early tissue cyst formation was also observed, predominantly within neurons. By 21 days PI the proliferative forms had disappeared and only developing tissue cysts containing densely packed cystozoites were present. The proportion of dividing cystozoites decreased with increasing size and age of the cysts. The wall of the tissue cyst developed as an adaptation of the lining of the parasitophorous vacuole. In the majority of older cysts, numerous tubular structures were present beneath the cyst wall. All the cysts observed were retained within intact host cells. The only morphological change with increasing age was that a proportion of the older cysts contained loosely packed cystozoites in an electron lucent ground substance. There was no evidence of any degenerative changes within the cystozoites.

The incidence and effect of tissue cyst rupture in the brains of mice chronically infected with Toxoplasma gondii was studied by immunocytochemistry and electron microscopy. Cyst rupture was extremely rare (2 of 750 tissue cysts) irrespective of the interval post-infection. The event was associated with a rapid cell-mediated immune response, giving rise to microglial or inflammatory nodules. Macrophages were observed to engulf and degrade the cystozoites and cyst debris. Initially, the nodules contained large amounts of immunologically reactive material, but this was degraded with the majority (94%) of lesions containing no recognizable parasites or Toxoplasma antigens. There was little evidence of parasite multiplication or new cyst formation associated with cyst rupture. This study shows that although intermittent cyst rupture occurs, in immunocompetent individuals the immune response limits the potential damage from the release of large numbers of infective organisms to small microglial/inflammatory nodules.

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Toxoplasma gondii undergoes schizogony and microgametogony in the epithelial cells of the cat ileum. On the basis of cytoplasmic structures, it is impossible to distinguish between the early stages of these processes but nuclear differentiation appears to have occurred. In the early schizont the chromatin is distributed in small patches throughout the nucleus but in the nucleus of the microgametocyte the chromatin is condensed into a few large areas. In the schizont, the first distinguishing cytoplasmic features are the appearance of the dome‐shaped membranes of the merozoite anlagen. In the schizogonic process, nuclear division precedes merozoite formation which occurs by multiple internal budding in a manner similar to endodyogeny. The appearance of flagella is the first cytoplasmic feature to distinguish the microgametocyte. Microgamete formation is similar to that reported for other coccidian species. The microgamete consists of a dense elongate nucleus anterior to which is a single mitochondrion. The anterior consists of a perforatorium and two flagella between which 4 microtubules run longitudinally.

The host parasite relationship in the brains of asymptomatic mice chronically infected with Toxoplasma gondii was examined at 3, 6 and 12 months post-infection (PI) using electron microscopy. The parasites were located in large numbers within tissue cysts which ranged in size from 10-50 microns in diameter. The cysts were predominantly found in the grey matter. The toxoplasms were enclosed by a cyst wall consisting of a membrane, with irregular invaginations, and an underlying layer of homogeneous osmiophilic material. A detailed examination of 50 cysts revealed that all the cysts were present within intact host cells irrespective of their size or the period PI. The majority of host cells could be positively identified as neurons by the presence of synapses. No extracellular cysts were observed. It is probable that the intracellular location of the cysts protects them from recognition and attack by the host immune system.