Host pathogenicity

When dealing with pathogenicity and virulence, only natural infection by the oral route is considered, where infection is acquired from oocysts or tissue cysts, and not artificial infection routes like intraperitoneal, subcutaneous, or intracerebellar inoculation, unless specifically mentioned. Pathogenicity is determined by the virulence of the strain and the susceptibility of the host species, usually the mice (Ferguson and Hutchison 1981; Suzuki et al. 1989).

Toxoplasma gondii usually infect the host without producing any clinical signs. After ingestion, bradyzoites, or sporozoites penetrate the intestinal wall, often multiplying in cells lining the lamina propria and epithelium. However, infection may spread to other tissues within a short time after ingestion; T. gondii was isolated from mesenteric lymph nodes of cats 4h after feeding on tissue cysts (Dubey and Frenkel, 1972). Infection is disseminated to distant organs through the blood and lymphatics.

An infected host may die from necrosis of the intestine and mesenteric lymph nodes before other organs are severely damaged (Dubey and Frenkel 1973), or focal necrosis may develop in many organs. The clinical picture is determined by damage to different organs, especially organs such as the eye, the heart, and the adrenals. Necrosis is caused by the intracellular growth of tachyzoites. Toxoplasma gondii does not produce a toxin.

Usually by about the third week after infection, the tachyzoites begin to disappear from the visceral tissues (in mice), and tissue cysts are found in increasing numbers in neural and muscular tissues.

Tachyzoites may persist longer in the spinal cord and brain because immunity is less effective in neural organs than in visceral tissues.

The intracellular tachyzoite, and later the bradyzoite, are found within the parasitophorous vacuole within the host cell endocytic system. The host cell is unable to fuse the lysosomes and the parasitophorous vacuole, which explains the ability of the parasite to

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survive intracellularly (Joiner et al. 1990). Toxoplasma gondii resist the phagosomes by creating a membranous network between the parasite and the host cell (Sibley and Krahenbuhl 1988). How T. gondii survives intracellularly is not completely known. Immunity to T. gondii is mainly cell mediated and this subject was recently reviewed by Gazzinelli et al. (1993). The fate of tissue cysts is not fully known. It has been proposed that tissue cysts may at times rupture during life of the host. The released bradyzoites may be destroyed by the host's immune response (Frenkel 1990), which may cause focal necrosis and inflammation, but hypersensitivity may also play a role in such reactions. The rupture of tissue cysts is rarely observed histologically (Ferguson et al. 1989).

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