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CMV infection can be diagnosed by isolation of the virus from the urine or saliva within the first three weeks of life. This can be accomplished by traditional virus culture methods which may take one to two weeks to obtain a result or rapid culture methods (“shell vial assay”) using centrifugation to enhance infectivity and monoclonal antibody to detect early antigens in infected tissue culture cells which may yield results in 24 hours. Rapid diagnosis of CMV can also be accomplished by detection of CMV DNA by DNA amplification techniques via the polymerase chain reaction (PCR) or DNA hybridization techniques. Culture, however, maintains a slight advantage over PCR in terms of specificity.

The presence of CMV-specific IgM in cord blood or in the infant’s blood within the first three weeks of life suggests the diagnosis of congenital CMV infection. However, CMV-specific IgM can only be detected in about 70% of congenitally infected newborn infants. On the other hand, a negative CMV-specific IgG titer in cord blood excludes the diagnosis of congenital CMV infection whereas its presence may merely imply passive transfer from the mother or may indicate a congenital infection. cheap cialis canadian pharmacy

Prenatal detection of fetal infection can be established by isolation of the virus from the amniotic fluid obtained by amniocentesis. A negative culture does not exclude fetal infection especially if the amniocentesis is carried out too early with respect to the maternal infection. Diagnosis of a primary maternal CMV infection can be established by the demonstration of an IgG seroconversion during pregnancy, especially if accomplished by the detection of CMV-specific IgM antibodies in the maternal blood. Fetal abnormalities detected by prenatal ultrasonography generally indicate more severe fetal disease.

In symptomatic infants, anemia, thrombocytopenia, hyperbilirubinemia, atypical lymphocytosis, elevated serum transaminases, and elevated cerebrospinal fluid protein may be found. Skull radiographs, CT scan, and MRI may demonstrate periventicular calcifications and venticulomegaly. Radiographs of the long bones many show longitudinal radiolucent streaks (“celery stalk” appearance).


Congenital CMV infection should be distinguished from other congenital infections such as toxoplasmosis, rubella, herpes simplex, and syphilis. Such distinction can be done both clinically and serologically. Toxoplasmosis is more likely to be associated with chorioretinitis, microphthalmia, hydrocephalus, and scattered cerebral calcifications. Petechial and purpuric eruptions, which are common in symptomatic congenital CMV infections, are rare in congenital toxoplasmosis; the latter often presents with a maculopapular rash. The presence of congenital heart disease and cataracts points to congenital rubella infection. Vesicular skin lesions or scarring present at birth suggest congenital herpes simplex infection. Rhinitis and radiological evidence of osteochondritis and epiphysitis favor the diagnosis of congenital syphilis. Other differential diagnoses include bacterial sepsis, erythroblastosis fetalis, and metabolic disorders such as galactosemia and tyrosinemia.


Infants with symptomatic congenital CMV infection have a mortality rate of 10-15%. Approximately 50-90% of symptomatic survivors have long-term sequelae such as sensorineural hearing loss, mental retardation, developmental delay, cerebral palsy, epilepsy, ocular abnormality, and microcephaly. The former occurs in up to 50% of affected infants. The worst prognosis occurs in infants born to mothers with primary CMV infection during pregnancy, infants with CMV-specific IgM in the cord blood, and infants symptomatic at birth, particularly those with microcephaly, intracranial calcifications, chorioretinitis, or raised cerebrospinal fluid protein. Some of the late complications such as hearing loss and central nervous system damage presumably result from ongoing viral replication.

Approximately 7-15% of asymptomatic infants have sensorineural hearing loss. Whether these infants are at increased risk of mental retardation is controversial. Hanshaw et al compared 44 children with asymptomatic congenital CMV infection with both matched and random controls and found school failure and deafness to be associated with asymptomatic congenital CMV infection. On the other hand, Kashden et al. compared 204 children who had asymptomatic congenital CMV infection with 177 uninfected siblings and found that there was no statistically significant difference between the two groups on intellectual measure. levitra tablets