Chapter 112 - Congenital toxoplasmosis

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Abstract

Congenital toxoplasmosis results from the transplacental transmission of the parasite Toxoplasma gondii after a maternal infection acquired in pregnancy. Prevalence of congenital infection ranges from 0.1 to 0.3 per 1000 live births. The maternal–fetal transmission rate increases with gestational age at maternal seroconversion, from less than 15% at 13 weeks of gestation to over 70% at 36 weeks. Conversely, the later the maternal infection, the lower the risk of symptomatic congenital infection (infections acquired during the third trimester are most often asymptomatic at birth). Prenatal diagnosis is currently performed by PCR analysis in amniotic fluid. Antenatal management and treatment vary considerably among countries. In some European countries, maternal infections are detected through serological screening allowing a prompt treatment with spiramycin, which is expected to reduce the risk of vertical transmission. If PCR analysis in amniotic fluid is positive or if maternal infection was acquired in the third trimester of pregnancy, a combination with pyrimethamine and sulphonamide is given until delivery. Benefits of antenatal treatments remain controversial. Infected newborns are prescribed pyrimethamine and sulphonamide for 12 months. Despite antenatal and postnatal treatment, chorioretinitis can occur at any age (prevalence > 20% at 10 years of age): long-term ophthalmological follow-up remains necessary.

Section snippets

Epidemiology of toxoplasma infection

Congenital Toxoplasma infection results from the transplacental transmission of Toxoplasma gondii after maternal primary infection during pregnancy. The three stages of this intracellular parasite are: the oocyst which is present in cat feces and remains infectious in the soil for over 1 year; the tachyzoite which replicates rapidly and destroys infected cells before being transformed into the bradyzoite under the pressure of the host immune system; and the tissue cyst that contains bradyzoites

Congenital infection

Acute maternal infection may lead to the hematogenous propagation of T. gondii through the placenta. Overall risk of transmission is 30% and increases with the date of maternal infection, from less than 15% at 13 weeks of gestation to almost 71% at 36 weeks (Fig. 112.1). Prevalence of congenital infection ranges from 0.1 to 0.3 per 1000 live births.

Potential damage to the nervous system of the fetus includes multifocal and diffuse parenchymal necrosis that can transform into calcification, and

Antenatal diagnosis

As Toxoplasma infection is often asymptomatic, prenatal screening with repeated serological testing for nonimmune pregnant women is performed in several countries or regions to prospectively identify maternal seroconversions. The biological diagnosis of fetal infection is performed on amniotic fluid sampled after 18 weeks of gestation and at least 4 weeks after the date of maternal infection. Polymerase chain reaction assays for the detection of T. gondii DNA are 100% specific. Current

Postnatal diagnosis and management

Clinical examination is most frequently normal or can reveal nonspecific signs of evolving (hepatomegaly, splenomegaly, icterus, thrombocytopenic purpura, anemia) or not fetopathy (hydro- or microcephalus, seizures). Indirect ophthalmoscopy should ideally be used to disclose retinochoroiditis. Imaging of the brain relies on ultrasound or computed tomography to detect nodular or curvilinear calcifications, or hydrocephalus (Fig. 112.3). Magnetic resonance has not been well-studied in this

Conclusion

Despite the lack of evidence regarding the effectiveness of treatment for congenital Toxoplasma infection, early diagnosis and treatment have improved its long-term prognosis. Long-term follow-up of infected children remains necessary because of the risk of late ocular lesions.

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