Cytomegalovirus (CMV) is the most common congenital infection, occurring in 0.2–2.2% of neonates. The majority of these infections are asymptomatic; approximately 5% of infected neonates are symptomatic at birth. Congenital CMV is the leading cause of congenital hearing loss. Transmission can occur via transplacental passage of the virus, contact of the fetus with infectious secretions at the time of birth, infected breast milk or blood transfusion.

There is regional variation in the prevalence of primary (0.7–4%) and recurrent (13.5%) infection among pregnant women. CMV is transmitted by contact with infected blood, saliva or urine, or by sexual contact. The mean incubation period is 40 days, with a range of 28–60 days. Primary CMV infection in adults is usually asymptomatic, although a mononucleosis-like syndrome with fever, malaise, myalgias, chills, lymphocytosis, and abnormal liver function tests can occur. Recurrent infection can occur following reactivation of latent virus.

Vertical transmission can occur at any point in pregnancy; the greatest risk is with maternal infection during the third trimester. Maternal CMV infection during the first trimester results in more serious fetal sequelae, should vertical transmission occur. The risk of transmission to the fetus is 30–40% with primary maternal CMV infection; 10% of infants infected in utero following primary infection will have signs and symptoms of CMV infection at birth and develop sequelae.

Clinical findings at birth can include jaundice, petechiae, thrombocytopenia, hepatosplenomegaly, intrauterine growth restriction, and nonimmune hydrops. Approximately 30% of infants with symptomatic infection following primary maternal infection die and 80% of surviving infants have severe neurologic sequelae. Vertical transmission after recurrent infection is much lower: 0.15–2%. Infants infected during maternal recurrent infection usually are asymptomatic at birth. Congenital hearing loss is the most common severe sequela of vertical transmission following maternal recurrent infection, and multiple sequelae are unlikely.

Routine serologic screening of women or neonates for CMV is not recommended. The presence of immunoglobulin M (IgM) CMV antibody indicates primary maternal infection. However, both false-positive and false-negative results are possible. Establishing that seroconversion has occurred is the most accurate method for demonstrating maternal primary infection. Detection of the CMV virus by polymerase chain reaction (PCR) from amniotic fluid is the most sensitive test for detecting fetal infection.

There is currently no vaccine for CMV prevention, nor a routinely recommended treatment for maternal or neonatal infection or interventions to prevent vertical transmission.

Parvovirus B19 is the cause of erythema infectiosum, also known as fifth disease. In healthy adults, parvovirus B19 infection is often asymptomatic. Symptoms are generally mild, with a rash on the trunk and peripheral arthropathy, but can rarely include transient aplastic crisis. Transmission occurs through respiratory secretions and hand to mouth contact. Otherwise healthy patients with erythema infectiosum are contagious 5–10 days after exposure, during the week before the onset of the rash, and are not infectious after this. Immunocompromised patients remain contagious from before the onset of symptoms through the period of the rash. Exposure to an infected household member results in approximately 50% risk of acquiring the infection. Over half of pregnant women in the USA are immune to parvovirus B19.

Transplacental transmission occurs in up to 33%. Spontaneous abortion or fetal death occurs in less than 10% of infected pregnancies. Most maternal infections that have resulted in fetal deaths occur between 10 and 20 weeks’ gestation, and the spontaneous abortions usually occurred 4–6 weeks after infection. Teratogenicity has not been proven. Parvovirus B19 can infect fetal erythroid precursors and cause anemia, leading to nonimmune hydrops and fetal death. Hydrops is unlikely to develop beyond 8 weeks after maternal infection. Fetal ultrasound examination can easily demonstrate hydrops and the hydropic fetus can be treated by intrauterine transfusions, if severe anemia is demonstrated. Spontaneous resolution may occur, however. There appear to be no long-term sequelae to in utero parvovirus B19 infection.

In view of the high prevalence of parvovirus B19 and the relatively low risk of serious harm to the fetus, pregnant women should not be routinely excluded from workplaces where parvovirus B19 is present. Infection control should consist of handwashing, standard precautions and droplet precautions.

Varicella zoster virus causes chickenpox and herpes zoster. VZV is transmitted by respiratory droplets or close contact. The attack rate in nonimmune people is 60–90% after exposure. The incubation period after infection is 10–20 days. The period of infectivity begins 48 hours before the rash appears and continues until the vesicles crust over. Primary infection, chickenpox, is characterized by fever, malaise, and a pruritic rash that develops vesicles. After the primary infection, VZV remains dormant in the sensory ganglia and if reactivated causes herpes zoster. Most people in the United States are immune to varicella, and therefore infection is uncommon in pregnancy, occurring in approximately 0.6 per 1000 pregnant women. While chickenpox is usually a benign and self-limited illness in children, severe complications such as pneumonia and encephalitis are more common in adults. Varicella pneumonia is more serious in pregnant women than in nonpregnant adults, and can be life-threatening. Pregnant women with varicella should be monitored closely for any signs of pneumonia.

Fetal infection after maternal varicella during the first 20 weeks of pregnancy occasionally results in varicella embryopathy, which can include limb atrophy, scarring of the skin of the extremities and central nervous system and ocular lesions. Congenital varicella syndrome occurs in approximately 2% of exposed fetuses when maternal infection occurs before 20 weeks’ gestation.

The neonate is at risk for life-threatening neonatal varicella if the mother develops varicella within 5 days before to 2 days after delivery.

Over 95% of women with a positive history of varicella have serologic immunity; therefore it is unnecessary to perform serologic testing in women with a prior history of varicella. Also, 70–90% of women in the USA with a negative or uncertain history of varicella are immune. A pregnant woman who is exposed to varicella should be tested for immunity if she has no history of prior infection with varicella or vaccination.

Postexposure prophylaxis within 96 hours of exposure with VZV immune globulin (VZIG or VariZIG) is recommended for nonimmune pregnant women with varicella exposure and for infants born to mothers with peripartum varicella. Acyclovir therapy should be considered for pregnant women with chickenpox.

The varicella vaccine contains live-attenuated VZV and should not be given to pregnant women. Women who do not have varicella immunity should receive the first dose of the VZV vaccine post partum prior to hospital discharge.

Rubella during pregnancy and congenital rubella are extremely rare in the United States; most cases occur in women born outside the country. All women should be screened for serologic evidence of immunity to rubella at the first prenatal visit. Seropositive women need no further testing.