− | The signs of toxoplasmosis in sheep manifest following the exposure of a naive pregnant ewe to infectious oocysts. The sporozoites ingested excyst in the digestive tract and penetrate the intestinal epithelium, before reaching the mesenteric lymph nodes around day 4 post-infection. Here, they cause lymphomegaly and focal necrosis before contributing to a parisitaemia from day 5. Pyrexia is associated with the development of parasitaemia. | + | The signs of toxoplasmosis in sheep manifest following the exposure of a naive pregnant ewe to oocysts. The sporozoites ingested excyst in the digestive tract and penetrate the intestinal epithelium, before reaching the mesenteric lymph nodes around day 4 post-infection. Here, they cause lymphomegaly and focal necrosis before contributing to a parisitaemia from day 5. Pyrexia is associated with the development of parasitaemia. |
− | Following dissemination of ''T. gondii'' in the blood, many tissues become infected. Parasitaemia ends when the maternal immune response becomes effective, and protozoa start to encyst as bradizoites. In pregnant animals, the uterus is an immunoprivileged site, and the outcome of foetal infection is influenced by the stage of gestation. In early pregnancy, the foetus is unable to mount any immune response, and so cannot inhibit parasite multiplication. The foetus rapidly dies and is resorbed. In mid-gestation, infection can again be fatal. This causes a mummified foetus which is often twinned with a lamb that dies later in gestation, or is born weakly. Because the foetal immune system is well developed in late pregnancy, infection at this stage will be resisted, and the lamb will be born infected but alive. Infection of the placentome has a different pathogenesis. Multiplication of ''Toxoplasma gondii'' in the placenta causes multiple foci of necrosis, which continue to expand throughout gestation. If this renders placental function non-viable, abortion may occur in late gestation. | + | Following dissemination of ''T. gondii'' in the blood, many tissues become infected. Parasitaemia ends when the maternal immune response becomes effective, and protozoa start to encyst as bradizoites. In pregnant animals, the uterus is an immunoprivileged site, and the outcome of foetal infection is influenced by the stage of gestation. In early pregnancy, the foetus is unable to mount any immune response, and so cannot inhibit parasite multiplication. The foetus rapidly dies and is resorbed. In a flock, this is visable clinically as large numbers of barren ewes. In mid-gestation (70-120 days), infection can again be fatal. This causes a mummified foetus which is often twinned with a lamb that is stillborn or weak. Abortion due to infection at 70-120 days gestation tends to occur in very late pregnancy. Because the foetal immune system is well developed in late pregnancy, infection at this stage will be resisted, and the lamb will be born infected but alive. |