Antenatal viral infections can be transmitted transplacentally, as well as perinatally from infected blood or vaginal secretions. More mother-to-child transmission may occur postnatally, for example, from breastfeeding.
Rubella may be asymptomatic in up to 50% of cases but may present with prodromal symptoms, such as low-grade pyrexia, conjunctivitis, sore throat, malaise and tender lymphadenopathy.1
The risk to the fetus of primary rubella is significant, particularly in the first trimester. Fetal rubella syndrome includes intrauterine growth restriction, intracranial calcification, deafness, cataracts and cardiac defects. Rubella infection at 16-20 weeks'
gestation is associated with a minimal risk of deafness; after this time there is no documented risk.1 There is routine antenatal testing for rubella antibody. Antenatal screening does not determine whether rubella has occurred in the current pregnancy.
2. Parvovirus B19
Parvovirus B19 is a DNA virus that causes erythema infectiosum. It may present with fever, a 'slapped cheek' appearance and a reticulate rash over the trunk or limbs.1
Parvovirus B19 may cause a mild illness in a pregnant woman but infection via transplacental spread in the first 20 weeks of pregnancy can lead to intrauterine death, fetal anaemia and hydrops fetalis.1
Up to one-third of women are seronegative for parvovirus B19 and susceptible to infection.2 If a pregnant woman presents with a rash and/or arthropathy or there has been exposure to a parvovirus B19-related infection or to a rash illness of unknown cause, testing for immunity may be appropriate.1
More than 90% of the antenatal population are seropositive for varicella IgG antibody.1 Chickenpox may complicate three in every 1,000 pregnancies.3
There is little evidence to suggest that pregnancies complicated by chickenpox in the first trimester are more likely to result in an increased risk of miscarriage.3 Chickenpox infection during the first two trimesters of pregnancy can lead to intrauterine infection in up to a quarter of cases but only a small proportion will develop congenital varicella syndrome.
The risk of congenital varicella syndrome is estimated to be 0.4% when maternal infection occurs before 12 weeks of pregnancy and nearly 2% between 12-20 weeks of pregnancy.1 Fetal varicella syndrome is associated with skin scarring in a dermatomal distribution, cataracts, chorioretinitis, limb hypoplasia, low birthweight and neurological abnormalities such as microcephaly.3
If a mother acquires the infection in the perinatal period, there is a risk of severe neonatal varicella, as maternal antibodies have not developed to confer passive immunity to the fetus.1
If the woman has a history of chickenpox or shingles or two doses of a varicella containing vaccine, and is not immunosuppressed, protection can be assumed and reassurance given if there has been a history of exposure.1 If there is no history of chickenpox or shingles and the woman is not fully vaccinated, susceptibility to infection should be urgently determined. Varicella zoster immunoglobulin should be offered to susceptible women within 10 days of the exposure.3
Cytomegalovirus (CMV) is an endemic DNA herpes virus and is the most common congenital infection.4 CMV is transmitted through contact with body fluids; this includes transplacental transmission as well as transmission through breast milk. Seroprevalence in developed countries is around 50%.
Primary infection in immunocompetent adults is usually asymptomatic.4 Some pregnant women may be asymptomatic and congenital CMV may be suspected on the basis of abnormal fetal ultrasound findings.5
Existing maternal CMV seropositivity significantly reduces the risk of intrauterine transmission. The risk of infection is greatest in the third trimester, especially from a primary infection, while the congenital effects of CMV are greatest in the first trimester.5 The Health Protection Agency estimates the overall birth prevalence of congenital CMV infection in the UK is around three in 1,000. For women with a primary infection during pregnancy, the risk of vertical transmission is approximately 30-40%.4
Congenital CMV infection may cause intrauterine growth restriction, intracranial calcifications, microcephaly, hydrocephalus, hepatosplenomegaly and sensorineural hearing loss, as well as an increased risk of mortality.
Up to 95% of neonates who have been infected are asymptomatic at birth.4 Up to 15% of this group may develop sensorineural hearing loss or developmental delay in later life.5 Congenital hearing loss is the most common sequela of recurrent CMV infection.5
Herpes simplex virus type 1 or 2 can cause genital herpes and may be acquired by the neonate at or near the time of delivery.6 Transmission is usually due to contact with infected maternal secretions but transplacental passage is possible.
Mother-to-child transmission may be affected by whether the maternal infection is primary or recurrent and the duration of rupture of membranes.6 Neonatal herpes is associated with a high morbidity and mortality and is fortunately rare.
There is an increased risk of infection with primary genital herpes occurring in the third trimester or within six weeks of the expected date of delivery, therefore these pregnant women should be offered caesarean section. Intrapartum aciclovir may be considered.7
Herpes may cause encephalitis, which may present up to four weeks postnatally; this causes neurological morbidity and 6% mortality. Mortality may increase up to 30% with disseminated multi-organ disease.7
In the UK, there is universal antenatal screening for HIV infection. If a woman declines antenatal screening, screening should be offered again at 28 weeks.8 Mother-to-child transmission of HIV may be reduced from 25-30% to less than 1% through antiretroviral therapy, avoidance of breastfeeding in the developed world and management of delivery.9
Antiretroviral therapy may be initiated between 20-28 weeks and discontinued at delivery for those pregnant women who do not require HIV treatment themselves.8
Elective caesarean section is recommended for women taking highly active antiretroviral therapy with a low viral load. A planned vaginal delivery may be considered in those women with undetectable viral loads.
Invasive procedures during delivery should be avoided.9 In the neonatal period, all babies should receive antiretroviral therapy within four hours of birth.8
- Dr Kochhar is a GP principal in St Leonards, East Sussex
1. HPA Rash Guidance Working Group. Guidance on Viral Rash in Pregnancy; 2011, HPA.
2. Ismail KM, Kilby MD. TOG 2003; 5: 4-9.
3. RCOG. Guideline 13: Chickenpox in pregnancy. 2007.
4. Bhide A, Papageorghiou AT. BJOG 2008; 115: 805-7.
5. Duff P. Perinatology 2010; 1: 1-6.
6. Gupta R, Warren T, Wald A. Lancet 2007; 370: 2127-37.
7. RCOG. Guideline 30: Management of Genital Herpes in Pregnancy. 2007.
8. RCOG. Guideline 39: Management of HIV in Pregnancy. 2010.
9. Gray GE, McIntyre JA. BMJ 2007; 334: 950-3.