Dr. Murai Éva - Gubányi András szerk.: Parasitologia Hungarica 29-30. (Budapest, 1997)

in the fetus or the newborn was described by Wolf et al. as early as in 1939. It is now universally acknowledged that congenital toxoplasma infection can lead to significant morbidity (Eaton et al. 1996, Pinon et al. 1996). The frequency of transplacental ly acquired congenital infection can be determined from the percentage of susceptible women reaching the child-bearing age without anti-toxoplasma antibody and the incidence rates observed during the productive period. The transmission of infection to the fetus has been limited almost exclusively to those women who acquired primary, acute toxoplasma infection during their gestation. In the parasitaemic phase of this primary maternal infection, the placenta will be infected and after an undefined lag period fetal infection may occur. Toxoplasma gondii can infect virtually all fetal cells and tissues, and its dissemination is widespread. Nevertheless, the damage caused by the proliferation of tachyzoites in the form of microinfarcts and subependymal necrosis will be the most severe in the central nervous system. The transplacentally acquired fetal infection is generalized but it is followed by passive immunization with maternal IgG. Infection persists for a long time because of fetal immaturity and the slow development of active immunity. Progressive infection persists longest in the central nervous system, in the form of microinfarcts and periventricular necrosis. Hydrocephalus starts with aqueductal obstruction and accumulation of fluid in the lateral and third ventricles. Proliferation of tachyzoites disseminates toxoplasma in the ventricular system. This is followed by the development of periventricular necrosis. The antigen trapped in the ventricles seeps out and impacts on the blood vessels containing maternal anti-toxoplasma IgG. This is associated with peripheral arteritis, and thrombosis of the arteries. As the periventricular infarction necrosis progresses, the ventricles become larger. Although asymptomatic infection is the most common (60%), a wide range of signs and symptoms may accompany congenital toxoplasmosis. The incidence and severity of fetal infection are related to the stage of gestation at which a pregnant woman acquires toxoplasma infection. The incidence is approx. 15% for infection acquired during the first trimester, 25% in the second trimester, and 60%» during the third trimester (Desmonts and Couvreur 1986). Even a 90% infection rate may occur in the last weeks before delivery (Stray-Pedersen 1992). The severity of fetal damage shows, however, an opposite tendency: a decrease from the first trimester to the third trimester (Couvreur et al. 1984). Thus, the most severely damaged newborn are those born to mothers who acquired the infection during the first trimester. Almost all infected newborn of mothers who acquired the infection during the third trimester are, however, bom without obvious signs of infection. Prospective studies have revealed that a substantial proportion of asymptomatic infants subsequently develop serious untoward sequelae, including especially retinochoroiditis and retarded development. A minority of congenitally infected neonates will have severe manifestations presenting at birth or during infancy. These manifestations include one or more components of the "classic triad" of congenital toxoplasmosis: retinochoroiditis, hydrocephalus, and intracranial calcifications. Involvement of the central nervous system, occasionally with widespread tissue destruction, and also of the eyes, are the most important manifestations of symptomatic congenital toxoplasmosis, but there may also be extensive involvement of other organs. There is an opportunity for successful medical intervention. In 152 sick babies with toxoplasmosis, a breakdown of symptomatology can be achieved (Eichenwald 1960). Generalized infection was seen in 44% of these patients and it was accompanied by splenomegaly (90%), jaundice (80%), fever (77%), anaemia (77%), hepatomegaly (77%), lymphadenopathy (68%), pneumonia (40%), and rash (25%), with occasional eosinophilia