Werner H, Janitschke K, Masihi M, Adusu E
Zentralbl Bakteriol Orig A. 1977 May;238(1):128-42.
Investigations on whether theprotective effects of maternal defence mechanisms against T. gondii could prevent a placental transmission of the parasite to the foetus were carried out on pregnant rabbits and mice. With rabbits which were infected 6 to 1 month before the conception and showed a high infection immunity, there was never a transmission to the foetus and likewise at no time after reinfection of such maternal animals during the pregnancy. In mice which were latent infected with 11 different Toxoplasma strains, placental transmission succeeded with only 6 strains intrauterine infection of the foetuses were confirmed in 1 to 3%. After active immunisation of rabbits with non-multiplying antigen before the conception and later primary infection during the pregnancy, intrauterine transmission to the foetus could be detected in 55%. After passive immunisation with hyperimmune serum, infected foetuses could be ascertained in 79% of rabbits and 24% of mice. Possible intrauterine transmission to foetus protected by maternal defence mechanisms is likely to be dependent on various factors. 1. On the host species, 2. the state of immunity (infection immunity), 3. on Toxoplasma strain. An infection immunity with the presence of living parasites in maternal organism is probably dependent on Toxoplasma strain in mice and offers in rabbits an apparently certain protection against congenital infection. On the contrary, serologically detectable humoral antibodies after active or passive immunisation do not prevent a transplacental transmission. On the basis of experimental findings it has been concluded that at least the immunoglobulins of type IgG, IgA and IgM in lower titer ranges offer no protection against congenital transmission after reinfection during pregnancy. Also, the protective effect can not be based on the structure of respective placenta. The roles of cellular immune defence and other possible factors in this connection are discussed.
针对母体防御机制对弓形虫的保护作用能否防止寄生虫经胎盘传播给胎儿这一问题，在怀孕的兔子和小鼠身上展开了研究。对于在受孕前6至1个月感染且具有高度感染免疫力的兔子，寄生虫从未传播给胎儿，同样，在孕期再次感染此类母体动物后，也从未发生过传播。在潜伏感染11种不同弓形虫菌株的小鼠中，仅6种菌株成功发生胎盘传播，胎儿宫内感染率为1%至3%。在受孕前用非增殖抗原对兔子进行主动免疫，随后在孕期进行初次感染，胎儿宫内传播率可达55%。用超免疫血清进行被动免疫后，79%的兔子和24%的小鼠体内可检测到受感染的胎儿。母体防御机制保护下的胎儿可能发生的宫内传播，可能取决于多种因素。1. 宿主物种；2. 免疫状态（感染免疫力）；3. 弓形虫菌株。母体体内存在活寄生虫时的感染免疫力，在小鼠中可能取决于弓形虫菌株，而在兔子中则能提供明显可靠的先天性感染防护。相反，主动或被动免疫后血清学可检测到的体液抗体并不能防止经胎盘传播。根据实验结果得出结论，至少低滴度范围的IgG、IgA和IgM型免疫球蛋白在孕期再次感染后无法提供先天性传播防护。此外，保护作用也不能基于各自胎盘的结构。本文讨论了细胞免疫防御及其他相关可能因素的作用。
