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PubMed1999

Lack of value of specific IgA detection in the postnatal diagnosis of congenital toxoplasmosis.

To improve the performance of the postnatal diagnosis of congenital toxoplasmosis, we assessed the detection of IgA antibodies to Toxoplasma gondii by ELISA, compared with that of IgM by ELISA, ISAGA, and IFAT and neosynthesized antibodies using Western blot. From 1993 to 1996, IgA antibodies were detected using the Toxo IgA test (SFRI, Société Française de Recherches et d'Investissements, Bordeaux, France), in 195 serum and cord blood samples from 63 infants born to mothers who seroconverted during pregnancy. Eighteen infants had proven congenital toxoplasmosis (confirmed by the presence of IgG after 12 months of life) and 45 had no congenital toxoplasmosis (negativity of IgG after 6-12 months of life). The sensitivity of IgA detection by ELISA on serum and cord blood samples was 38.9 and 54.5% respectively, which is low when compared with the sensitivity of IgM detection by ISAGA (66.7% on serum samples, 90.9% on cord blood), ELISA (61.1% on sera, 81.8% on cord blood) and Western blot (83.3% on sera, 72.7% on cord blood). IgA antibodies were never detected by ELISA earlier than IgM or neosynthesized Ig (antibodies synthesized by infants). Thus, the detection of IgA antibodies by Toxo IgA is not useful in improving the diagnosis of congenital toxoplasmosis.

Aging↗
PubMed1999

[Immunoblot applied to the diagnosis of congenital toxoplasmosis].

Western blot was evaluated for the neonatal diagnosis of congenital toxoplasmosis based on a comparison of antibody profiles between serum samples obtained from the mother at delivery and from the neonate. Passively transferred antibodies can be distinguished from antibodies produced by the neonate, thus allowing early postdelivery diagnosis of congenital toxoplasmosis before the results of other tests are available. This method was developed at the Parasitology-Mycology laboratory of the Pitié-Salpêtrière Teaching Hospital, Paris, France, then evaluated in a retrospective study of 52 mother-infant pairs. The diagnosis of congenital toxoplasmosis was ruled out in 34 cases, confirmed in ten cases, and doubtful in 8 cases. Sensitivity was higher than with conventional serological tests. Antibody profile differences were found between mothers and affected infants; these differences usually involved IgGs (8 of 9 cases). Importantly, in two cases Western blot would have provided the diagnosis of congenital toxoplasmosis two months before the secondary elevation in IgM titers in one case and three weeks before the result of mouse placenta inoculation in another case. In conclusion, Western blot deserves to be used to complement established methods (serology and direct demonstration of the parasite by gene amplification, cell cultures, and mouse inoculations) as a means of rapidly (within 24 hours of receipt of the specimen) providing clinicians with information relevant to treatment decisions.

Antibodies↗
PubMed1995

Neurologic and developmental outcome in treated congenital toxoplasmosis.

BACKGROUND: Earlier studies have shown that infants with untreated congenital toxoplasmosis and generalized or neurologic abnormalities at presentation almost uniformly develop mental retardation, seizures, and spasticity. Children with untreated subclinical disease at birth have developed seizures, significant cognitive and motor deficits, and diminution in cognitive function over time. OBJECTIVE: To determine neurologic, cognitive, and motor outcomes for children with congenital toxoplasmosis who were treated for approximately 1 year with pyrimethamine and sulfadiazine. DESIGN AND METHODS: Systematic, prospective, and longitudinal neurologic, cognitive, and motor evaluations were performed for 36 individuals with congenital toxoplasmosis. These infants were born between December 1981 and January 1991 and were treated with pyrimethamine and sulfadiazine for approximately 1 year beginning in the first months of life. Compliance with medications was documented. These individuals were evaluated in a standardized manner in a single center in the first months of life and at approximately 1, 3.5, 5, 7.5, and 10 years of age. Their cognitive function was compared with the cognitive function of a nearest-age, same-sex sibling when such siblings older than 3.5 years were available for study. RESULTS: Signs of active central nervous system infection (eg, cerebrospinal fluid [CSF] pleiocytosis, hypoglycorrhachia, elevated CSF protein, and, in some instances, seizures and motor abnormalities) resolved during therapy. Six of the 36 children had perinatal seizures. Four had their anticonvulsant therapy discontinued successfully within the first months of life, and two additional children developed new seizures at 3 and 5 years of age. Tone and motor abnormalities resolved by 1 year of age in 12 of 20 infants who exhibited abnormalities of tone and motor function at their initial neonatal evaluation. By February 1992, 29 of the 36 children had been evaluated when they were 1 year old, and 23 (79%) had a mean +/- standard deviation Mental Developmental Index (MDI) of 102 +/- 22 (range, 59 to 140). Six (21%) had a measure of their cognitive function that was less than 50. Results of sequential IQ tests, performed at 1.5 year intervals or greater, did not differ significantly over time (P > .05). Seven children with MDIs greater than 50 were compared with sibling controls; they had scores of 87 +/- 11 (range, 68 to 97) and their siblings had scores of 112 +/- 15 (range, 85 to 132) (P = .008). Seventeen of 18 children without hydrocephalus and six of eight children with obstructive hydrocephalus responsive to shunting had normal or near-normal neurologic and developmental outcomes. Children with hydrocephalus ex vacuo present at birth, with high CSF protein, and with lack of response to shunting have done less well. CONCLUSIONS: Neurologic and developmental outcomes were significantly better for most of these treated children than outcomes reported for untreated children or those treated for only 1 month (P < .001). Although the level of cognitive function for treated children was less than for their uninfected siblings (P < .008), there was no significant deterioration in neurologic and cognitive function of the treated children tested sequentially. These favorable treatment outcomes justify systematic identification and treatment of pregnant women with acute gestational Toxoplasma infection and young infants with congenital toxoplasmosis.

Child Development↗
PubMed1999

[Analysis of a case of severe congenital toxoplasmosis].

BACKGROUND: To describe a case of severe congenital toxoplasmosis because of inadequate surveillance of a seronegative pregnant woman and to evaluate the usefulness of different microbiological diagnostic methods after birth. METHODS: We applied serology, DNA amplification by one-tube semi-nested PCR, cell culture and mice inoculation analysis. RESULTS: Anti. T. gondii serology was useful for the diagnosis of congenital toxoplasmosis. PCR analysis of neonate cerebrospinal fluid and peripheral blood were positive, and yielded negative results after a few days of specific treatment. Cellular culture and mice inoculation yielded negative results. CONCLUSIONS: Our results suggest that serology and PCR are useful methods for the diagnosis of toxoplasmosis in newborns. Prenatal toxoplasmosis screening and suitable follow up of the seronegative pregnant women are necessary to prevent cases of severe infection in our area.

Acute Disease↗
PubMed2002

Preconception seroconversion and maternal seronegativity at delivery do not rule out the risk of congenital toxoplasmosis.

We describe two unusual cases of congenital toxoplasmosis, one occurring after preconception maternal infection with cervical adenopathies and the other occurring after maternal infection at the very end of pregnancy with maternal seronegativity at delivery. These documented cases of congenital toxoplasmosis demonstrate the value of extending the serologic monitoring period during pregnancy, according to the individual clinical context.

Adult↗
PubMed1995

Recurrent congenital toxoplasmosis in a woman with lupus erythematosus.

We describe the case of a patient with systemic lupus erythematosus, treated by corticosteroids, who presented during two successive pregnancies with serological reactivation of toxoplasmosis associated with fetal lesions. The first infected fetus died in utero with signs of hydrops. The second fetus was treated in utero with a combination of sulfadoxine and pyrimethamine, administered to the mother, and is now well. The increasing number of immunocompromised pregnant patients with immunity to Toxoplasma gondii may lead to a higher risk of reactivation of maternal toxoplasmosis and congenital infection.

Adult↗
PubMedDate not supplied

Precocious puberty: an endocrine manifestation in congenital toxoplasmosis.

We reviewed retrospectively seven children with congenital toxoplasmosis and precocious puberty. All seven showed very high levels of LH (25.2-155.0 IU/ml) and FSH (7.1-38.2) upon stimulation with GnRH. Three of them showed low GH response to an insulin tolerance test. All the children had severe mental retardation. We emphasize that children with congenital toxoplasmosis should have their hypothalamopituitary function evaluated even in subclinical situations that could be responsible for endocrinological disturbances such as precocious puberty.

Child↗