PREVENTION AND TREATMENT OF CONGENITAL INFECTIONS

L. Schrod Würzburg

Universität Würzburg, Würzburg

Recent developments in the fields of epidemiology, diagnostic methods, and immunology have expanded our knowledge of congenital infections. Most fetal infections are of viral origin with an incidence of about 2-3 percent of all live births. Nowadays, congenital CMV is the leading cause of sensorineural hearing loss in children. The majority of congenital infections occur after primary maternal infection. However, CMV infection resulting from a recurrence of maternal infection is quite common. Preventive strategies against viral congenital infections consist of vaccination programs (e.g. HBV), but there is still no efficient maternal therapy in case of acute viral infection during pregnancy. Studies are underway to test a genetically engineered vaccine against a CMV glycoprotein, which is clearly immunogenic, because the live attenuated CMV vaccine (Towne) did not provide sufficient protection. Except for Aziclovir in HSV infection, there are no evidence based data to demonstrate the efficacy of any antiviral therapy in the affected infant after birth. The excretion of CMV resumes shortly after cessation of a 6 weeks course of Ganciclovir. In acute disease apparent at birth, symptoms of different congenital infections are often unspecific. Therefore, diagnostic strategies and pitfalls have to be discussed also in view to prenatal rarely transmitted microorganisms. As in Rubella, CMV, toxoplasmosis, or syphilis, congenital infections can result in asymptomatic infection in the neonatal period but a persistent postnatal infection with sequelea later in life. Diagnosis requires serologic screening programs with regard to cultural and socioeconomic factors. The prevalence of congenital toxoplasmosis is 0.08 per 1,000 live births in the USA, but 3 per 1,000 births in Paris or Vienna. The prenatal incubation period of toxoplasmosis, the delay of as long as 16 weeks between placental infection and subsequent infection of the fetus, offers the chance to control placental infection by maternal treatment with spiramycin. However, spiramycin does not reach the brain in contrast to pyrimethamine and sulfadiazine, which have to be used in cases of demonstrated fetal or neonatal infection. In some parts of the world, the incidence of congenital syphilis is increasing again. Reasons are mismanagements of prenatal care and infections late in pregnancy. It is well documented that treponema can be detected in fetal tissues in cases of early infection at gestational ages of 9 to 12 weeks. However, severe disease and fetal loss due to syphylis occurs only after 15 to 18 weeks of gestation, when the fetus has acquired the immunologic ability to recognize treponema antigens and is able to react with a specific inflammatory response. Prevention includes routine screening also in late pregnancy with rigorous therapy following the official recommendations. Moreover, asymptomatic newborns whose disease can emerge in the weeks after delivery with multisystem infection including hepatitis, nephrotic syndrome, and central nervous system involvement, and all neonates born to mothers who were treated within 30 days of delivery, who are considered to have been treated inadequately, should receive a full course of therapy.