Dr. Murai Éva - Gubányi András szerk.: Parasitologia Hungarica 31. (Budapest, 1998)

samples after the nested PCR as shown in Table 1. Sixteen out of 33 urine specimens were positive for the TgondiiBl gene. Seventeen urine samples were found to be negative and we were not able to isolate the T. gondii Bl gene specific sequence, DISCUSSION According to the work by Fuentes et al. (1996) we carried out a study trying to detect part of the T. gondii Bl gene from urine samples (non-invasively) collected from asymptomatic newborns born to women with serological evidence of acute toxoplas­mosis treated by spiramycin. Serological examination of the sera of these infants showed passively transmitted maternal CF titres without serological evidence of subclinical Toxoplasma infection (not detectable anti-P30 IgM and IgA antibodies). These serological findings are not surprising, since antibody synthesis may not begin until some months after birth or is often delayed in infants with congenital toxoplas­mosis or the assay may be insensitive (Desmonts et al. 1985; Lynfield and Eaton 1995). There are several publications reporting successful detection of the T. gondii Bl gene by PCR in urine samples of Toxoplasma infected and symptomatic patients congeni­tally infected infants (Desmonts et al. 1985; Fuentes et al. 1996), AIDS patients (Cingolani et al. 1996; Lamoril et al. 1996; Nicoll et al. 1996). However, the period of time for which the parasite or its genome is present in the urine is still unknown (Fuentes et al. 1996). We used the Bl gene because a number of publications verify that it is highly specific for T. gondii and is well conserved among all of the strains tested to date (Burg et al. 1989; Grover et al. 1990, Cingolani et al. 1996, Foudrinier et al. 1996, Fuentes et al. 1996; Lamoril et al. 1996). Thirty-three urine samples of infants born asymptomatic to mothers suspected of having acute toxoplasmosis were tested. The fetus acquires no congenital infection if the placenta is not infected; therefore, the Toxoplasma Bl gene should be undetectable in the urine of the infant by PCR. Transmission occurs in the majority of cases but results in few cases of congenital toxoplasmosis and more often subclinical, asymptomatic infections if transmission is delayed or if Toxoplasma infection is acquired during the final weeks prior to delivery by the mother therefore, the Toxoplasma Bl gene should be detected in the urine of the infant by PCR. Thus, clinical experiences suggest the initiation of the appropriate therapy (spiramycin) for the children at risk, because the earlier the treatment begins the less commonly will delayed-onset disease and late sequelae (neurologic and ophthalmologic diseases) appear in the children (Grover et al. 1990; Lynfield and Eaton 1995; Fuentes et al. 1996; Pinon et al. 1996). Subclinical infection in the child develops more often than clinical congenital toxoplasmosis when a maternal Toxoplasma infection acquired later in gestation is transmitted to the fetus. The extremely high likelihood (60%) of transmission is due to changes in the placenta (Lynfield and Eaton 1995). The follow-up of children born to mothers suspected of having acute toxoplasmosis is essential to recognise and prevent long-term complica­tions of congenital toxoplasmosis. It is carried out monthly up to 6 months of age and then every 6 months up to 2 years of age and includes serological examination, ophthalmoscopy, ultrasound, and X-ray examination of the skull. We suppose that the examined 16 newborns with PCR-detectable Toxoplasma Bl gene acquired Toxoplasma in the 3rd trimester of pregnancy. However, the Toxoplasma genome detectable in their urine shows their probable contact with the parasite. In our

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