CONGENITAL CYTOMEGALOVIRUS INFECTION: DESCRIPTION OF THE VIRUS

3 Feb
2010

CMV is the largest and most complex member of the Herpesviridae family of DNA viruses. The genome is composed of a linear double-stranded DNA, approximately 240 kilobases in size (150xl0 daltons), and is capable of isomer-ization. The genome has been completely sequenced and shown to contain non-overlapping open-reading frames for more than 200 potentially immunologic proteins. The genome is surrounded by an icosahedral capsid composed of 162 capsomeres. The capsid is surrounded by a poorly defined amorphous tegment which is itself surrounded by lipid envelope, giv­ing the complete and mature viral particle a diameter of about 200 n. The virus lacks the enzyme thymidine kinase, which renders it resistant to those antiviral agents that depend on this enzyme for their action.

The virus is named for the intranuclear and intracytoplasmic inclusions seen with symptomatic disease, cytomegalic inclusion disease. CMV is highly species specific, and humans are the only known reservoir for disease among humans. kamagra jelly uk

EPIDEMIOLOGY

Congenital CMV infection occurs in approximately 0.2%-2.5% of all live births; infection is more prevalent in underdeveloped countries and among lower socioeconomic groups in developed countries, where crowding is more common. Both primary and recurrent infections in the mother during pregnancy may result in congenital CMV infection. On average, 1-4% of susceptible women acquire primary CMV infection during their pregnancy. Approximately 10% of sero-positive pregnant women have reactivation of CMV infection during their pregnancy. The transmission rate after primary infection is about 40%, whereas the transmission rate after recurrent infection is about l-3%.

PATHOGENESIS AND PATHOLOGY

Congenital CMV infection results from transplacental transmission of the virus during maternal viremia. Maternal viremia is more likely to occur with primary than with recurrent infection. After transplacental transmission, the virus spreads through the fetus by a hematogenous route. Infection at an earlier gestational age often correlates with a less favorable outcome.

Infants born to mothers with primary CMV infection during pregnancy are more likely to have symptoms at birth. The presence of maternal antibody to CMV before conception provides substantial protection against intrauterine trans­mission of the virus and severe fetal infections. The protection, however, is incomplete, and congenital CMV infection may follow recurrent maternal infection. More recent studies suggest symptomatic congenital CMV infection after a recurrent maternal infection occurs more frequently than previously documented.

Figure 1. A newborn infant with symptomatic

Figure 1. A newborn infant with symptomatic congenital CMV infection presenting with petechiae, jaundice, and hepatosplenomegaly.

Although CMV affects most cell types, it has a special affinity for epithelial cells, ependymal cells lining the ventricles, the organ of Corti, and the neurons of the eighth cranial nerve. The characteristic pathologic features include cytomegaly, intranuclear inclusions (“owl’s eye” appearance), intracytoplasmic inclusions, and multinucleated giant cells.

CLINICAL MANIFESTATIONS

About 90% of congenitally infected infants are asymptomatic at birth. Jaundice (62%), petechi-ae (58%), and hepatosplenomegaly (50%) are the most frequently noted classical triad (Figure 1). Other clinical manifestations include oligohydramnios, polyhydramnios, prematurity, intrauterine growth retardation, nonimmune hydrops, fetal ascites, hypotonia, poor feeding, lethargy, thermal instability, cerebral ventriculomegaly, microcephaly, intracranial calcifications usually periventricular in distribution, “blueberry muffin” spots, and chorioretinitis. Sensorineural hearing loss develops in 30% of symptomatic infants at birth. Infants with symptomatic CMV infection may be at increased risk for congenital malformations such as inguinal hernia in males, high-arched palate, defective enamelization of the deciduous teeth, hydrocephalus, clasp thumb deformity, and clubfoot. Some affected infants may develop hepatitis, pneumonia, osteitis, and intracranial hemorrhage. canada pharmacy mall

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