Congenital toxoplasmosis is usually occurs when the infection is acquired by an immunologically normal pregnant woman. Though fetal manifestations are severest early in gestation, the rate of transmission is least in early in gestation and highest later in gestation.
If the fetus escapes abortion, a wide variety of manifestations involving different systems may be encountered.
Neonatal manifestations include low birth weight, hepatosplenomegaly, jaundice, anemia, meningoencephalitis, thrombocytopenic purpura and fever.
Congenital defects include hydrocephalus or microcephaly
Late sequelae include chorioretinitis and mental retardation.
The protozoon may be demonstrated in the CSF or tissues.
Additional tests include specific IgM indirect fluorescent antibody, paired maternal and cord sera for complement fixation and hemagglutination inhibition tests.
A combination of pyrimethamine and sulfadiazine plus folinic acid should be administered for 1 year. Steroids are indicated in the presence of infalmmatory lesions such as chorioretinitis involving macula, CSF protein above 2 g/dl at birth or a generalized infection.
The pregnant women must avoid contact with oocytes excreted by cats and eat only well-cooked meat.
Serelogical screening and ultrasound monitoring of pregnant women contributes to prevention of congenital toxoplasmosis
Treatment of maternal toxoplasmosis with spiramycin (not pyrimethamine and sulfadiazines which are known teratogenics) is yet another vital preventive measure.