The Resistance of the Encysted Form of Toxoplasma gondii

Abstract

Studies on the transmission of Toxoplasma gondii have, in general, concerned the proliferative form of the parasite. These have resulted mainly in failures of attempts to obtain transmission by arthropod vectors, and in demonstrations of the fragility of free toxoplasmas (see Jacobs, 1956, for review). On the other hand, there are data indicating that the encysted form of the parasite is more hardy. Jacobs (1953, 1956) contrasted the results of feeding tissues from chronically infected mice or rats to other mice with results of similar feedings of tissues from acutely ill animals. Since the former was much more successful than the latter, he hypothesized that the form of the parasite, found in chronic infections, was better able to withstand the digestive process. Van Thiel and van der Waaij (1956) presented additional experimental work pointing to the same conclusion. The latter authors, in reviewing literature on feeding proliferative forms, conclude that the occasional positive results obtained are explainable by passage of the parasite through the buccal or pharyngeal mucosa, thus avoiding digestion. In the case of Eichenwald's (1948) success in producing infections in newborn mice through the milk of acutely infected mothers, the proliferative forms may have survived in the stomach because of the low content of digestive enzymes in the newborn. However, milk of acutely infected mothers has not always produced infection as Cowen and Wolf (1950) reported. With 3 other strains of the parasite, we also have not found infection transmitted via the milk (to be published). Frenkel (1949) and Rodhain and Gerebetzoff (1951) have described the wall of Toxoplasma as argyrophilic, tough, and elastic. There has been some conjecture as to its origin. Originally it was presumed by many authors to represent the residual membrane of the infected cell, after the nucleus was pushed out by the developing mass of parasites. If the wall were of host origin, the structure would properly be called a pseudocyst. If the parasite contributed to the production of its enclosing membrane, as Frenkel and Friedlander (1951) hypothesized, the structure should properly be called a cyst. Lainson (1958) has presented morphological evidence indicating that cysts do not originate from masses of proliferating intracellular forms, but develop separately from small structures which increase in size and in number of contained parasites. It may be possible to test his observations experimentally and to explain the mechanism of growth of cysts. In the light of his report, it seems reasonable to adopt the word cyst rather than pseudocyst for the definitely walled structures found in animals chronically infected with Toxoplasma. This does not rule out the presence of dormant intracellular masses of parasites that