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The following heteroxenous and cyst-forming coccidian genera, Besnoitia, Cystoisospora, Frenkelia, Hammondia, Neospora, Sarcocystis and Toxoplasma have been compared biologically, and a key to determine their tissue cysts is provided.

We tested 124 isolates of Toxoplasma gondii, as determined morphologically and by their ability to elicit antibodies in the dye test with the RH strain of Toxoplasma in mice. They were compared for their capacity to immunize CF-1 mice against isolate T-1, and T-1 immune mice for their capacity to resist each of the 123 other isolates. Of the 125 isolates, 52 had been isolated in the continental USA, 33 in Central America, 15 in Europe, 9 in Hawaii, five in Japan, two in Taiwan, five in Australia, one in Indonesia, one in Tunisia, and one was of unknown origin. Complete cross-immunity was found. This suggests that only one immunotype of Toxoplasma is prevalent in the United States, and perhaps all over the earth. Vaccines are likely to immunize against most or all Toxoplasma isolates.

We enumerate identical and divergent findings concerning the obligate heteroxenous Hammondia hammondi and the facultatively homoxenous or heteroxenous Toxoplasma gondii. Differences exist in life-cycles, transmission, and host range, especially transmissibility to birds and mammals other than rodents, in ultrastructural morphology, immunity and serology in cats and to lesser degree in rodents, in DNA sequences and in isoenzymes. Because the recognition of obligate heteroxeny is essential to study these organisms and to recognize them as taxa, it is advantageous to give heteroxeny a generic rather than a specific value. Characterization of organisms with the life-cycle patterns of Hammondia, Sarcocystis, Frenkelia, and Toxoplasma is best achieved by means of the genera presently used.

We review herein studies concerning the genomic polymorphism of Toxoplasma gondii including 3 clones (1 linked with mouse pathogenicity), 5 zymodemes, and 13 schizodemes. Because mutations occur with some frequency and several allelic configurations are present in isolates grown in the same environment, we conclude that many of the mutations may not be affected by selection pressure. However, the gametocyte-forming ability is under selection pressure from the hose and depends on the development of bradyzoites in tissue cysts. After prolonged multiplication exclusively in the tachyzoite stage in mice and, possibly, in patients the gametocyte-forming ability may be lost. To avoid this genomic change, isolates should be passed in the laboratory, permitting bradyzoite and tissue-cyst formation. Mouse pathogenicity is selected for during mouse passage. We find no major genomic instability justifying species or subspecies distinctions.

Several published biologic times for the stage conversion of Toxoplasma gondii from tachyzoite to bradyzoite in mice are critically examined. There are several reports of 3 days and many of longer times. Possible errors, related to delay from dissemination of the infection, are pointed out. The time to the appearance of the 36-kDa surface antigen, sometimes used for the diagnosis of bradyzoites, should be compared with the biologic attribute of bradyzoites, inducing the short prepatent period in cats. It is recalled that the development of acid pepsin resistance is not exclusively correlated with the biologic definition of bradyzoites. Reactivation of toxoplasmosis in mice does not necessarily follow the administration of a corticosteroid. The daily dose, the type of corticosteroid, its solubility, whether alcohol or ester, the route of administration, the host, and, probably, other factors are important in giving rise to sufficient immunosuppression for reactivation to occur. The plea is made to examine biologic measurements in the context of parasitologic and host factors.