Toxoplasma gondii exists in three forms: the tachyzoite, which is the asexual invasive form; the tissue cyst (containing bradyzoites), which persists in tissues of infected hosts during the chronic phase of the infection; and the oocyst (containing sporozoites), which is produced during the sexual cycle in the intestine of cats (the definitive host). The extraintestinal asexual cycle is present in all incidental hosts and in cats. After ingestion of tissue cysts or oocysts, either bradyzoites or sporozoites, respectively, are released into the intestinal lumen, where they invade surrounding cells, become tachyzoites, and disseminate throughout the body via the blood and lymphatics. The tachyzoite requires an intracellular habitat for survival and can infect all mammalian cell types. Tachyzoites are found in tissues during the acute stage of the infection or during reactivation of the chronic (latent) infection. Approximately 10 to 14 days after infection, tachyzoites disappear and cysts are formed in the tissues of the infected host. This phenomenon appears to be associated with development of immunity and acquisition of resistance to rechallenge with the parasite. Tissue cysts, which contain up to several thousand bradyzoi-tes, can be found in all organs and are most readily observed in myocardial, skeletal, and smooth muscle, and the central nervous system. Tissue cysts appear to persist for the life of the infected host. The enteroepithelial sexual cycle results in formation of oocysts in the intestine of the cat. Oocysts are shed in the feces of the cat and become infectious only after they are excreted and sporulation occurs. Transmission to intermediate hosts, including humans, occurs mainly by ingestion of undercooked or raw meat containing tissue cysts, ingestion of vegetables or other food products contaminated with oocysts, or by the transplacental route (Fig. 19.3.3).
Cell-mediated immunity plays a central role in resistance against T. gondii. In a model in which splenocytes from ts-4-immunized mice were adoptively transferred to naive mice, resistance to acute infection with a virulent strain of T. gondii was dependent on both CD4+ and CD8+ T cells (Suzuki and Remington, 1988; Gazzinelli et al., 1991). Although in this model, CD8+ T cells played the major role in protection against the parasite, experiments performed in other models indicate that CD4+ T cells are also central to the induction of protective immunity during acute T. gondii infection. Thus, depletion of CD4+ T cells prior to acute infection with the ME49 strain prevented acquisition of resistance to challenge with virulent T. gondii (Araujo, 1991). Moreover, reactivation of
Animal Models for Infectious Diseases
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