Neonatal infection, especially in its early stages, may be dificult to diagnose because these newborns often fail to express classic clinical signs. If the fetus was infected in utero, there may be depression and acidosis at birth for no apparent reason. The neonate may suck poorly, vomit, or show abdominal distention. Respiratory insuiciency can develop, which may present similarly to idiopathic respiratory distress syndrome. he neonate may be lethargic or jittery. he response to sepsis may be hypothermia rather than hyperthermia, and the total leukocyte and neutrophil counts may be depressed.
Several viruses cause severe maternal infections, and some can also cause devastating fetal infections. Of these, cytomegalovirus (CMV) is a ubiquitous DNA herpes virus that eventually infects most humans. CMV is also the most common perinatal infection in the developed world. Speciically, some evidence of fetal infection is found in 0.2 to 2.2 percent of all neonates (American College of Obstetricians and Gynecologists, 2017). The virus is secreted into all body luids, and person-to-person contact with viral-laden saliva, semen, urine, blood, and nasopharyngeal and cervical secretions can transmit infection. The fetus may become infected by transplacental viremia, or the neonate is infected at delivery or during breastfeeding. vloreover, acquisition continues to accrue. Day-care centers, for example, are a frequent source. Revello and coworkers (2008) reported that amniocentesis in women whose blood is positive for CMV DNA does not result in iatrogenic fetal transmission.
Up to 85 percent of women from lower socioeconomic backgrounds are seropositive by the time of pregnancy, whereas only half of women in higher income groups are immune. Following primary CMV infection, and in a manner similar to other herpesvirus infections, the virus becomes latent with periodic reactivation characterized by viral shedding. This occurs despite high serum levels of anti-CMV IgG antibody. These antibodies do not prevent maternal recurrence, reactivation, or reinfection, nor do they totally mitigate fetal or neonatal infection.
Women who are seronegative before pregnancy, but who develop primary CMV infection during pregnancy, are at greatest risk to have an infected fetus. It is estimated that 25 percent of congenital CMV infections in the United States are from primary maternal infection (Wang, 2011). Most CMV infections are clinically silent, but they can be detected by seroconversion, and this may be as high as 1 to 7 percent annually (Hyde, 2010). Conversely, diagnosis of CMV nonprimary infection is a challenge (Picone, 2017).
Pregnancy does not increase the risk or severity of maternal CMV infection. Most infections are asymptomatic, but 10 to 15 percent of infected adults have a mononucleosis-like syndrome characterized by fever, pharyngitis, lymphadenopathy, and polyarthritis. Immunocompromised women may develop myocarditis, pneumonitis, hepatitis, retinitis, gastroenteritis, or meningoencephalitis. Nigro and associates (2003) reported that most women in a cohort with primary infection had elevated serum aminotransferases or lymphocytosis. Reactivation disease usually is asymptomatic, although viral shedding is common.