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(See also Herpesviruses: Cytomegalovirus (CMV) Infection.)
Cytomegalovirus (CMV) infection may be acquired prenatally or perinatally and is the most common congenital viral infection. Signs at birth, if present, are intrauterine growth restriction, prematurity, microcephaly, jaundice, petechiae, hepatosplenomegaly, periventricular calcifications, chorioretinitis, and pneumonitis. If acquired later in infancy, signs may include pneumonia, hepatosplenomegaly, hepatitis, thrombocytopenia, and atypical lymphocytosis. Diagnosis of neonatal infection is best made by virus isolation. Treatment is supportive. Parenteral ganciclovir can prevent hearing deterioration, but its use remains controversial.
CMV is frequently isolated from neonates. Although most infants shedding this virus are asymptomatic, others have life-threatening illness and devastating long-term sequelae.
It is not known when a woman with primary CMV can safely conceive. Because risk to the fetus is difficult to assess, women who develop primary CMV during pregnancy should be counseled, but few experts recommend routine serologic testing for CMV before or during pregnancy in healthy women.
Etiology
Congenital CMV infection, which occurs in 0.2 to 2.2% of live births worldwide, may result from transplacental acquisition of either a primary or recurrent maternal infection. Clinically apparent disease in the neonate is much more likely to occur after a primary maternal exposure, particularly in the first half of pregnancy. In some higher socioeconomic groups in the US, 50% of young women lack antibody to CMV, making them susceptible to primary infection.
Perinatal CMV infection is acquired by exposure to infected cervical secretions, breast milk, or blood products. Maternal antibody is thought to be protective, and most exposed term infants are asymptomatic or not infected. In contrast, preterm infants (who lack antibody to CMV) can develop serious infection or can die, particularly when transfused with CMV-positive blood. Efforts should be made to transfuse these infants with only CMV-negative blood or components or to use blood that has been filtered to remove leukocytes (leukoreduced).
Symptoms and Signs
Many women who become infected with CMV during pregnancy are asymptomatic, but some develop a mononucleosis-like illness.
About 10% of infants with congenital CMV infection are symptomatic at birth. Manifestations include the following:
Infants who acquire CMV after birth, especially if they are premature, may develop a sepsis-like syndrome, pneumonia, hepatosplenomegaly, hepatitis, thrombocytopenia, and atypical lymphocytosis, as well as sensorineural hearing loss.
Diagnosis
Symptomatic congenital CMV infection must be distinguished from other congenital infections, including toxoplasmosis, rubella, and syphilis.
In neonates, viral culture of a urine, saliva, or tissue sample is the primary diagnostic tool; maternal diagnosis can also be made by serologic testing (see Herpesviruses: Diagnosis). Culture specimens should be refrigerated until inoculation of fibroblast cells. Congenital CMV is diagnosed if the virus is isolated from urine or other body fluids obtained within the first 3 wk of life. After 3 wk, positive cultures may indicate perinatal or congenital infection. Infants may shed CMV for several years after either type of infection. A positive PCR result using neonatal urine, saliva, blood, or tissue is helpful in making a diagnosis, but a negative PCR result does not rule out an infection. PCR can also establish maternal infection.
A CBC and differential and liver function tests may be helpful but are not specific. Cranial ultrasonography or CT and an ophthalmologic evaluation should also be done. Periventricular calcifications are commonly found on CT. Hearing tests should be routinely done at birth in all infected neonates, but close monitoring is required because hearing loss may be progressive.
Prognosis
Symptomatic neonates have a mortality rate of up to 30%, and 70 to 90% of survivors have some neurologic impairment, including
Among asymptomatic neonates, 10% eventually develop neurologic sequelae.
Treatment
No specific therapy is available. Ganciclovir decreases viral shedding in neonates with congenital CMV and may prevent hearing deterioration at 6 mo. When therapy stops, the virus is again shed; therefore, its role in treatment remains controversial.
Prevention
Nonimmune pregnant women should attempt to limit exposure to the virus. For instance, because CMV infection is common among children attending day care centers, pregnant women should always wash their hands thoroughly after exposure to urine and oral or respiratory secretions from children.
Transfusion-associated perinatal CMV disease can be avoided by giving preterm neonates blood products from CMV-seronegative donors or leukoreduced products.
A vaccine to prevent congenital CMV is being developed. Using CMV hyper immune globulin in pregnant women with primary CMV infection to prevent or treat congenital infection is also under investigation.
Last full review/revision October 2009 by Mary T. Caserta, MD
Content last modified October 2009
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