Chapter 18 Cytomegaloviral Infection
PATHOPHYSIOLOGY
Cytomegalovirus (CMV) is the leading cause of congenital viral infections in North America. A number of related strains of CMV exist. The virus is a member of the herpes family. CMV is probably transmitted through direct person-to-person contact with body fluids or tissues, including urine, blood, saliva, cervical secretions, semen, and breast milk. The period of incubation is unknown. The following are estimated incubation periods: after delivery, 3 to 12 weeks; after transfusion, 3 to 12 weeks; after transplantation, 4 weeks to 4 months. The urine often contains CMV months to years after infection. The virus can remain dormant in individuals and be reactivated. Currently, no immunizations exist to prevent infection with the virus.
Three types of CMV infection exist:
1. Congenital—acquired transplacentally in utero. The likelihood of congenital infection and the extent of the disease in the newborn depend on maternal immune status. Approximately 30% to 40% of infants born to women experiencing a primary (first) CMV illness during pregnancy will have clinical disease at birth. With recurrent maternal infection, (i.e., CMV infection that occurs repeatedly, leading to preconceptual immunity), the risk of transmission to the fetus is lower, ranging from 0.5% to 1.5%. Most of these infants appear normal at birth. The most severe form of congenital infection is referred to as cytomegalic inclusion disease.
2. Acute acquired—acquired anytime during or after birth through adulthood. Symptoms resemble those of mononucleosis (malaise, fever, pharyngitis, splenomegaly, petechial rash, respiratory symptoms). Infection is not without sequelae, especially in young children it can result from transfusions.
3. Generalized systemic disease—occurs in individuals who are immunosuppressed, especially if they have undergone organ transplantation. Symptoms include pneumonitis, hepatitis, and leukopenia, which can occasionally be fatal. Previous infection does not produce immunity and may result in reactivation of the virus.
INCIDENCE
1. Among live births, 0.4% to 2.5% of infants have congenital infection.
2. Premature infants are affected more often than full-term infants.
3. Of infected infants, 10% are symptomatic at birth; 90% suffer long-term sequelae (e.g., deafness, mental retardation, or ocular abnormalities).
4. Of severely infected infants, 4% to 30% die by 3 months of age; the remaining 60% to 75% will have some form of intellectual impairment or developmental delay.
5. Approximately one third of infected infants are normal in late childhood.
6. Prevalence of CMV infection is approximately 80% in children younger than 2 years of age who attend child care centers.
7. Seroprevalence of CMV approximates 50% in young adults of middle-upper socioeconomic status.
8. Incidence is higher in lower socioeconomic groups.
9. Of susceptible women, the seroconversion rate during pregnancy is 0.7% to 4.1%.
10. Both sexes are equally susceptible to infection and morbidity from CMV.
CLINICAL MANIFESTATIONS
In the newborn period, an infant infected with CMV is usually asymptomatic. Onset of symptoms from congenitally acquired infection can occur immediately after birth or as late as 12 weeks after birth.
There are no predictable indicators, but the following symptoms are common:
LABORATORY AND DIAGNOSTIC TESTS
1. Viral cultures of urine, pharyngeal secretions, and peripheral blood leukocytes. The most sensitive detection system is growth of the virus from urine in tissue culture, usually positive in 3 to 7 days.
2. A more rapid method of viral isolation is called the shell vial assay; after enhancing viral attachment to cells and staining, results are available in 24 hours.
3. Polymerase chain reaction and DNA hybridization or DNA amplification testing—to detect CMV in urine, amniotic fluid, fetal blood, and cerebrospinal fluid.
4. Microscopic examination of urinary sediment, body fluids, and tissues—to detect virus in large quantities (examining urine for intranuclear inclusions is not helpful; verification of congenital infection must be accomplished within first 3 weeks of life).
5. Toxoplasmosis, other infections, rubella, CMV infection, and herpes (TORCH) screen—used to assess presence of other viruses.
6. Serologic tests: Detection of immunoglobulin M (IgM) antibody should not be used to diagnose congenital CMV because it is less sensitive and more subject to false-positive results than culture or PCR. Only about 50% of congenitally infected infants produce IgM antibody.
7. Radiologic studies—skull radiographic studies or computed tomographic scans of head used to reveal intracranial calcifications, ventriculomegaly, cerebella hypoplasia, and, less commonly, myelination delay.
MEDICAL MANAGEMENT
The CMV virus differs from herpes and varicella viruses in that it lacks a specific enzyme. This feature renders it resistant to antiviral agents that depend on the enzyme for their action, such as acyclovir. Currently there are three antivirals licensed for treatment of CMV: ganciclovir, foscarnet, and cidofovir. There is limited experience using these agents in the setting of congenital and perinatal CMV infection; however, encouraging data from a controlled clinical trial indicate that ganciclovir therapy may be of value in limiting the neurodevelopmental injury caused by congenital infection, particularly sensorineural hearing loss. Clinical evaluation of vaccines against CMV is now underway. A vaccine using a construct of the glycoprotein B of the virus has been shown to be immunogenic and well tolerated by healthy adults and by children. CMV vaccines, once available, may ultimately be the best control strategy for this public health problem. The most important means of prevention are basic hygiene and handwashing for pregnant women, especially after contact with urine, diapers, oral secretions, and other body fluids. Caregivers should wear gloves, employ good handwashing techniques, and use universal precautions.
NURSING INTERVENTIONS
1. Monitor action and side effects of medications.
2. Monitor response to and side effects of blood transfusions.
3. Review and reinforce with parents importance of maintaining adequate caloric intake.
4. Weigh child upon admission and daily.
5. Monitor urine and serum electrolyte and glucose levels as needed.
6. Assess age and developmental level.
7. Provide age-appropriate stimulation.
8. Promote process of attachment between parents and infant.
9. Identify community resources that may be helpful in dealing with long-term sequelae.
Discharge Planning and Home Care
1. Instruct parents about methods to prevent spread of infection.
2. Instruct parents about long-term management of condition.
Presence of sequelae will necessitate further interventions beyond the scope of this section.
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Schleiss MR. Antiviral therapy of congenital cytomegalovirus infection. Semin Pediatric Infect Dis. 2005;16(1):50.
Yudin MH, Gonik B. Perinatal infections. Martin RJ, Fanaroff AA, Walsh MC. Fanaroff and Martin’s Neonatal-perinatal medicine: Diseases of the fetus and infant, ed 8, St. Louis: Mosby, 2006.
