Spatiotemporal Diffusion, Colonization, and Antibody Responses in Susceptible C57BL/6J Mice Orally Infected with Toxoplasma gondii Cysts

<i>Toxoplasma gondii</i> is an obligate intracellular protozoan that infects humans and other mammals. The C57BL/6J mouse strain is regarded as an ideal model organism for studying <i>T. gondii</i> due to its susceptibility to <i>T. gondii</i> infection and its other advantages over other laboratory animals. However, systematic studies on the response dynamics of the susceptible C57BL/6J mice after oral infection with <i>T. gondii</i> cysts are lacking. To address this research gap, we investigated the spatiotemporal dynamics of infection, colonization, and antibody fluctuations in susceptible C57BL/6J mice orally infected with Type II <i>T. gondii</i> ME49 strain cysts. Mice were orally challenged with <i>T. gondii</i> cysts to examine the infection dynamics. Daily monitoring was conducted for 60 days post-infection (dpi) to assess animals' clinical signs and survival rates. The parasite burden in various organs was quantified using qPCR targeting the <i>T. gondii</i> B1 gene. The serum antibody responses were evaluated using ELISA. The cyst burden in the mouse brain was assessed via histology and immunofluorescence. <i>T. gondii</i> infection induced clinical symptoms in the mice, including fever and weight loss. <i>T. gondii</i> rapidly invaded the mice's small intestine, spleen, lungs, liver, and heart via the bloodstream within 1-5 dpi. <i>T. gondii</i> had breached the blood-brain barrier and colonized the brain by 7 dpi. The levels of <i>Toxoplasma</i>-specific IgG antibodies increased and stabilized for two months (until the experiment ended). Systemic parasite dissemination occurred rapidly, infiltrating most tissues and organs, leading to pronounced enteritis and multi-organ damage due to inflammation. The tachyzoites differentiated into bradyzoites when <i>T. gondii</i> infection progressed from the acute to the chronic phase in mice, forming tissue cysts in organs, including the muscles and brain. As a result, the predilection site of <i>T. gondii</i> in mice is the brain, which is where the cysts persisted for the host's lifetime and continuously induced meningitis. These findings provide valuable insights into the spatiotemporal diffusion, colonization, predilection sites, temporal antibody dynamics, pathogen detection methodologies, and histopathological changes in C57BL/6J mice following oral infection with <i>T. gondii</i> cysts. These insights are important for elucidating <i>T. gondii</i>'s pathogenesis and host-<i>T. gondii</i> interaction.