Tissue-Dwelling Intracellular Parasites: Infection and Immune Responses in the Mammalian Host toToxoplasma, Sarcocystis and Trichinella

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Abstract
The cycles, pathogenicity and immune processes observed in 3 intracellular infections, with the protozoa Toxoplasma gondii, several Sarcocystis species, and the nematode Trichinella spirahs are described. All three organisms have cycles that have co-existed with their hosts for an evolutionarily long period. Natural hosts of the protozoa generally are able to develop immunity after primary infection in a timely manner. However infection is often fatal in certain unusual hosts not naturally exposed to Toxoplasma and Sarcocystis. It is suggested that whereas hosts may have selected strains of intermediate pathogenicity, the two protozoa may have selected for hosts that can develop timely immune responses and survive with chronic persistent infection. Stability of cycle is maintained by co-evolution in the definitive host through which the cycle must pass almost regularly. Toxoplasmosis and sarcosporidiosis join malaria and African trypanosomiasis as infections that co-evolved with their hosts, selecting for immunocompetency and intermediate to low pathogenicity (Allison, 1982). The plea is made to consider the probable evolutionary experience of experimental hosts when studying their specific immune mechanisms and before possibly generalizing from such studies, because the immune response is dependent on evolutionary experience. In respect to infection with Trichinella spiralis one might consider carnivores to have been selected and pure herbivores unselected. However, infection occurs in a wide variety of hosts, with carnivorous, scavenging and accidental transmission, some of which are of recent modification by man. Because infection is of low prevalence, and involves a wide variety of hosts, and pathogenicity is more related to the degree of hypersensitivity, than to frequency of transmission and worm load, no uniform effects of selection are apparent. Trichinella infected athymic mice have a high worm load with little pathogenic effect. Immunologic processes, while restricting the number of worms, are much more important in making the host sick. In all three intracellular infections both protective immunity and delayed type hypersensitivity are operative. In balance, these immune responses are protective in Toxoplasma and Sarcocystis infection, but are pathogenic in trichinellosis, often causing the death of the infected host.

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