Congenital toxoplasmosis
Fetal infection with toxoplasmosis occurs exclusively via the transplacental route. The disease leaves extremely adverse consequences, manifested by persistent organic defects of the nervous tissue, as well as irreversible loss of hearing and vision.
The clinical presentation consists of severe combined lesions of the visual system and the central nervous system. Typical manifestations include:
- Meningoencephalitis and progressive hydrocephalus.
- Chorioretinitis and optic atrophy.
- A systemic sign is generalized lymphadenopathy (polylimphadenopathy).
Serological tests are used to confirm the diagnosis. A key marker on computed tomography (CT) of the brain is the detection of diffuse calcifications. They have a specific localization: the basal ganglia, thalamus, and cerebellar structures are predominantly affected. Specific therapy consists of a combination of sulfonamides with pyrimethamine.
Congenital rubella
As with toxoplasmosis, the rubella pathogen penetrates the fetus through the placenta. If infection occurs in early gestation, the child develops a classic symptom complex — Gregg's triad. It includes congenital heart defects, eye pathology (specifically cataracts and chorioretinitis), and deafness.
In addition, the infection is characterized by pronounced intrauterine growth restriction (IUGR). Meningoencephalitis and severe impairment of nerve fiber myelination processes develop in the nervous system.
Diagnostic workup is based on serological tests and PCR diagnostics using blood and cerebrospinal fluid samples. The prognosis for the disease is unequivocally unfavorable, and specific etiological treatment has not yet been developed—care is exclusively supportive.
Cytomegalovirus infection (CMV)
Cytomegalovirus is transmitted to the fetus transplacentally, and the disease is characterized by enormous clinical polymorphism. The prognosis for CMV depends directly on the severity of the symptom complex. The chances of recovery (or retaining only minimal defects) and the risk of severe disability are distributed approximately as 50:50.
Clinical presentation of CMV infection includes:
- Neurological deficit: microcephaly, meningoencephalitis, sensorineural hearing loss.
- Eye involvement: chorioretinitis.
- Systemic manifestations: hepatosplenomegaly, hemolytic anemia, hyperbilirubinemia, pneumonia, and severe hemorrhagic syndrome.
- Intrauterine growth restriction.
To establish a clinical diagnosis, the physician must identify 2–3 characteristic syndromes, after which the diagnosis is confirmed serologically. CT reveals a specific triad: periventricular leukomalacia, cortical atrophy, and necrotic changes in the basal nuclei. Treatment is comprehensive and includes antiviral drugs (ganciclovir, foscarnet), interferon alfa-2b preparations, and specific immunoglobulins.
Congenital herpes infection
Unlike other pathogens of the TORCH complex, herpes is dominated by the intrapartum (contact) route of transmission — meaning the child is infected during passage through the birth canal. Transplacental and ascending routes of infection are much less common.
The infection occurs in two main forms:
- Localized: isolated involvement of the eyes, skin, or CNS. In this case, the prognosis is conditionally favorable, with recovery occurring in about 60% of cases.
- Generalized (disseminated): severe combined involvement of the nervous system, parenchymal organs, and skin. Mortality in this form exceeds 60%.
The main laboratory method for confirming herpes is PCR. Instrumentally, the pathology can be suspected by specific EEG patterns, and neuroimaging structurally reveals polycystic encephalomalacia. The foundation of therapy is the use of the antiviral drug acyclovir in mandatory combination with specific immunoglobulins.
Gregg's triad in rubella: "HAE" — Heart (defects), Eyes (cataracts), Ears (deafness).
Class and exam questions
How does the route of infection in herpes differ from other congenital infections?
Unlike toxoplasmosis, rubella, and cytomegalovirus, which are transmitted via the placenta, herpetic infection is most often transmitted intrapartum — upon contact of the fetus with infected birth canals.
What CT changes are characteristic of congenital toxoplasmosis?
Tomograms reveal diffuse calcifications. Their typical localization is the basal ganglia, thalamus, and cerebellum.
How is congenital rubella treated?
Specific etiological therapy for congenital rubella has not yet been developed. The disease has an unfavorable prognosis.
What is the primary drug in the treatment of herpetic congenital infection?
The mainstay of treatment for congenital herpes is acyclovir. It is prescribed in combination with specific immunoglobulins.
What else to study on this topic
- Pathogenesis of intracerebral calcification formation
- Specific EEG patterns in herpetic encephalitis
- Differential diagnosis of periventricular leukomalacia
- Mechanisms of impaired myelination processes in rubella
- Dosages and regimens of interferons in neonatology
Master the entire topic in the Pediatrics course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Congenital Infections (CI)" and 3,738 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 71 video lessons on the subject
Other topics in «Chapter 2. Neonatology»
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.