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7:781-787. was possible to demonstrate a neosynthesis of specific anti-MIC2 and anti-SAG1 immunoglobulin G, mainly of the IgG2 subtype, in 13 out of 20 infants with congenital toxoplasmosis. IgM antibodies in 97% of infected infants reacted with at least one of the recombinant antigens, confirming the diagnosis of congenital infection as soon as 2 months after birth ( 0.0001). The use of recombinant antigens is effective in distinguishing acquired during pregnancy can be transmitted to the fetus and may cause miscarriage, neonatal malformations, or reduced eyesight (15, 37, 43). Toxoplasmosis in gestation represents a challenge for the clinician due to its subclinical course in the majority of pregnant women and to the unpredictable long-term outcome of congenital infection. Transplacental transmission occurs in 10 to 80% of maternal infections, depending on gestational age of the fetus (10, 11). The clinical severity for the fetus decreases and the transmission rate increases as gestational PSI-7409 age at the time of maternal infection progresses (10, 21). At birth, up to 90% of congenitally infected infants PSI-7409 are asymptomatic but are at risk of developing retinochoroiditis during the first year of life or in early adulthood. Evidence from cohort studies shows that 15% to 80% of children with prenatal toxoplasmosis develop ocular disease (19, 25-27). Treatment should be started soon after birth, which requires rapid diagnosis (11, 19, 32, 42). Detection of fetal infection before birth can be established using PCR assays or isolating parasites by mouse inoculation from amniotic liquid samples. However, diagnosis of congenital toxoplasmosis during pregnancy by PCR and/or mouse inoculation usually identifies no more than 60 to 70% of the infected fetuses (13, 24, 38, 39, 41). Thus, exploring the antibody response to in the newborn child seems an obvious approach to improve the neonatal diagnosis of congenital toxoplasmosis. Detection of antigen (6, 7, 12, 37). Only the persistence or increase of IgG antibodies within the first 12 months of life can confirm congenital infection in the absence of clinical signs. To overcome this extended time lag between diagnosis and initiation of therapy, several additional tests based on comparison of the mother’s immunological profile to that of her child have been developed (8, 17, 30, 34-36, 38). The aim of this study was to improve the early serologic diagnosis of toxoplasmosis in children at risk of congenital infection by using recombinant antigens. Using sera from infants born to mothers with primary toxoplasmosis acquired during pregnancy, we found that recombinant antigens containing regions of the gene products in enzyme immunoassays improve early diagnosis of congenital toxoplasmosis in newborns. MATERIALS AND METHODS Patients. One hundred four infants born to mothers with primary toxoplasmosis in pregnancy and referred for postnatal follow-up at the Center for Perinatal Infection of Campania Region, Italy, were included in the study. Maternal diagnosis of PSI-7409 primary infection was based on seroconversion during gestation. All of the women were offered tests for the antenatal diagnosis of congenital toxoplasmosis. When informed consent was granted, amniotic fluid was drawn and then analyzed by PCR for the presence of IgM and/or Rabbit Polyclonal to Synaptotagmin (phospho-Thr202) IgA was detected in the infant serum or a lack of IgG decay was demonstrated in two consecutive samples taken more than 2 weeks apart during the diagnostic follow-up. The disease onset was considered severe, benign, or subclinical according to the criteria of Hohlfeld et al. (21). Treatment of cases of severe-onset disease consisted of 6 months of P/S combination (pyrimethamine, 2 mg/kg of body weight per day in the first 3 days, then 1 mg/kg alternating days; sulfadiazine, 100 mg/day) and folinic PSI-7409 acid supplementation (5 mg/day, alternating days) followed by 6 months of a regimen alternating 4 weeks of the P/S combination (same dosage as above) with 4 weeks of spiramycin (125 mg/day). Cases of benign or subclinical disease were treated for 12.