Congenital Infections (Cytomegalovirus - HHV-5)

Maternal primary CMV infection during pregnancy, especially in the first trimester, initiates fetal infection.

Reactivation of latent CMV in the mother can also lead to vertical transmission.

Exposure to CMV-infected bodily fluids such as saliva or urine from young children triggers maternal infection.

Transplacental passage of CMV from mother to fetus is the key event causing congenital infection.

Symptoms of congenital CMV typically manifest at birth or within the first few weeks of life.

Fetal infection occurs weeks to months before delivery, with a variable incubation period depending on timing of maternal infection.

Some infants remain asymptomatic at birth but develop sequelae such as sensorineural hearing loss months to years later.

Latency between maternal infection and fetal symptoms ranges from several weeks to months.

Lack of specific symptoms at birth leads to missed or delayed diagnosis in many infants.

Overlap of clinical features with other congenital infections or genetic disorders causes diagnostic confusion.

Limited use of CMV PCR testing or viral culture in newborn screening delays confirmation.

Asymptomatic infants with later-onset hearing loss are often diagnosed only after developmental delays appear.

Low clinical suspicion in mothers without known CMV exposure contributes to underdiagnosis.

Intrauterine growth restriction and low birth weight are common in affected neonates.

Jaundice and hepatosplenomegaly reflect systemic infection.

Sensorineural hearing loss is a frequent presenting symptom and may be progressive.

Seizures and lethargy indicate CNS involvement.

Petechiae and purpura result from thrombocytopenia.

Newborns may present with jaundice, petechiae, and hepatosplenomegaly shortly after birth.

Progressive microcephaly and developmental delay become apparent in the first months of life.

Hearing loss and chorioretinitis may be noted during infancy or early childhood.

Some infants have a history of intrauterine growth restriction and prematurity.

Neurologic symptoms such as seizures and hypotonia may develop as the disease progresses.

Maternal history of febrile illness or mononucleosis-like syndrome during pregnancy may be present.

Previous pregnancies complicated by fetal loss or congenital anomalies suggest possible CMV infection.

Lack of maternal immunity to CMV prior to pregnancy increases risk of fetal infection.

History of immunosuppressive conditions or therapies in the mother may predispose to reactivation.

No specific past medical history is required in the infant for congenital CMV diagnosis.

No classic heritable pattern is associated with congenital CMV infection.

Family history of sensorineural hearing loss may prompt evaluation for congenital infections including CMV.

No known familial syndromes directly linked to CMV infection exist.

Recurrent congenital infections in siblings are rare but may occur with maternal seroconversion during multiple pregnancies.

Genetic predisposition to severe CMV disease has not been clearly established.

Petechiae and purpura due to thrombocytopenia are common in congenital CMV infection.

Hepatosplenomegaly is frequently observed reflecting systemic viral involvement.

Microcephaly with or without intracranial calcifications is a hallmark of CNS involvement.

Jaundice and conjugated hyperbilirubinemia may be present from neonatal hepatitis.

Chorioretinitis can be detected on fundoscopic exam indicating ocular involvement.

Supportive care including management of hearing loss with hearing aids or cochlear implants.

Regular developmental and neurological assessments to monitor for sequelae.

Early intervention programs for developmental delays.