Oocyst-Induced Murine Toxoplasmosis: Life Cycle, Pathogenicity, and Stage Conversion in Mice Fed Toxoplasma gondii Oocysts

Abstract

The development of sporozoites to tachyzoites and bradyzoites was studied in mice after feeding 1-7.5 x 10(7) Toxoplasma gondii oocysts. Within 2 hr after inoculation (HAI), sporozoites had excysted and penetrated the small intestinal epithelium. At 2 HAI, most sporozoites were in surface epithelial cells and in the lamina propria of the ileum, and by 8 HAI, T. gondii was also seen in mesenteric lymph nodes. At 12 HAI, sporozoites had divided into 2 tachyzoites in the lamina propria of the small intestine. By 48 HAI, there was a profuse growth of tachyzoites in the intestine and mesenteric lymph nodes of mice fed 7.5 x 10(7) oocysts. Parasites had disseminated via the blood and lymph to other organs by 4 days after inoculation (DAI). Toxoplasma gondii was first isolated from peripheral blood at 4 HAI. Tissue cysts were visible histologically in the brain at 8 DAI. By using immunohistochemical staining with anti-bradyzoite-specific (BAG-5 antigen) serum, BAG-5-positive organisms were first seen at 5 DAI in the intestine and at 8 DAI in the brain. Using the bioassay in cats, bradyzoites were first detected in mouse tissues between 6 and 7 DAI, and they were found in intestines before they were found in the brain. Cats fed murine tissues containing bradyzoites shed oocysts in their feces with a short (< 10 days) prepatent period, whereas cats fed tissues containing tachyzoites did not shed oocysts within 3 wk. Using a pepsin-digestion procedure and mouse bioassay, bradyzoites were first detected in brain tissue at 7 DAI and in many organs of mice at 51 and 151 DAI. Individual bradyzoites, small and large tissue cysts, and tachyzoites were seen in the brains of mice at 87 and 236 DAI.

Parasite Manipulation of the Invariant Chain and the Peptide Editor H2-DM Affects Major Histocompatibility Complex Class II Antigen Presentation during Toxoplasma gondii Infection

“…Encystation can occur as early as 6 to 9 days postinfection (p.i.) (4), timing concomitant with the development of a potent parasite-specific adaptive immune response. Although toxoplasmosis is generally asymptomatic in healthy individuals, congenital toxoplasmosis can lead to serious birth defects, such as hydrocephaly, mental retardation, blindness, and chorioretinitis (5).…”

Long-Term Relationships: the Complicated Interplay between the Host and the Developmental Stages of Toxoplasma gondii during Acute and Chronic Infections

“…Within intermediate hosts infected with oocysts, excysted sporozoites are detectable in epithelial cells of the small intestines within 2 h postinoculation (22). By 12 h postinoculation, sporozoites have differentiated into tachyzoites in the intestinal epithelium, and by 48 h rapid replication occurs (23). Consumption of encysted bradyzoites in infected tissue is another leading cause of infection (Fig.…”

Expansion of host range as a driving force in the evolution of Toxoplasma

“…Until recently, highly sensitive methods have not existed to allow this question to be addressed with the necessary sensitivity, but previous methods have failed to detect infection of epithelial cells of mice infected with oocysts (Dubey et al 1997).…”