Antiparasitic treatment suppresses production and avidity of Toxoplasma gondii-specific antibodies in a murine model of acute infection*.

Infection with Toxoplasma gondii during pregnancy may result in congenital transmission of the parasite. Infection is commonly diagnosed using serological tests for IgG, IgM and IgA antibodies. Avidity of IgG antibodies is used to exclude acute infection. Few studies have investigated the impact of antiparasitic treatment on the production of anti-T. gondii antibody and the avidity of IgG antibodies. We therefore investigated the production of IgG, IgM, and IgA antibodies and IgG avidity in a murine model of acute infection with 10 cysts of T. gondii. All antibody classes increased following infection. Treatment of mice with pyrimethamine/​sulfadiazine but not with spiramycin or azithromycin at dosages equivalent to those used in patients resulted in a significant decrease in the concentration of T. gondii-specific IgG and IgM antibodies postinfection. IgG and IgM antibody decreases were paralleled by a significant reduction in cyst numbers in brains of mice treated with pyrimethamine/sulfadiazine but not with other drugs. In contrast, treatment with atovaquone did significantly reduce the concentrations of IgM antibodies and resulted in reduced IgG avidity indices. T. gondii-specific DNA was not detected in blood between days 1 and 3. In conclusion, antiparasitic treatment with pyrimethamine/sulfadiazine and atovaquone appears to impact the generation of antibody responses against T. gondii. Future studies will have to determine the specific impact of antiparasitic treatment on antibody responses and the consequences for the management of patients infected with T. gondii.