Cytomegalovirus (CMV) is one of the most common causes of intrauterine infection [89]. CMV can pass from mother to fetus through the placenta or during a vaginal delivery. Fetal CMV infection is mostly associated with maternal primary CMV infection during pregnancy. However, fetal CMV infection has been reported in recurrent infection as well, albeit with a much lower risk [90, 91]. Transmission of the virus from the mother to the fetus occurs more frequently in more advanced gestational age, but the risk for permanent sequelae is higher if transmission to the fetus occurred in the first trimester [92]. The estimated risk of transmission in cases of maternal primary CMV infection is 30–40 % [93]. Birth abnormalities, including microcephaly, ventriculomegaly, intracranial calcifications, jaundice, and deafness, are apparent in about 10 % of infants born with congenital CMV infection. The cranial ultrasound findings have been extensively described in the literature. Most of the symptomatic infants will suffer from sequelae such as sensorineural hearing loss and learning disabilities, and the most severe cases will have a high mortality rate [89, 90]. The asymptomatic cases (about 90 % of children born with congenital CMV) may develop progressive sensorineural hearing loss at a frequency of 13–15 %. In cases of recurrent infection, only 0.2–1 % of infants will be infected [93]. Of these, less than 1 % will show symptoms at birth, and 10 % of the asymptomatic newborns may experience hearing loss later in life.

Approximately 50 % of pregnant women are believed to be immune to B19. In cases of maternal infection during pregnancy, vertical transmission has been reported as 25–33 % [94, 95]. Parvovirus does not seem to increase the risk for birth defects. However, fetal infection has been associated with fetal hydrops and death, mostly with infection before 20 weeks. The estimated risk for fetal death, if maternal infection occurs before 20 weeks gestation, is 1–9 %. If maternal infection occurs after 20 weeks gestation, the risk of hydrops is estimated to be 1 % [96].

Due to widespread childhood vaccination, rubella infections rarely occur nowadays. Rubella in pregnancy may infect the fetus, producing congenital malformations, miscarriage or fetal death [97, 98]. The main defects associated with congenital rubella infection are cataracts, glaucoma, heart defects, deafness, pigmentary retinopathy, microcephaly, developmental delay, and radiolucent bone disease. Infants with congenital rubella syndrome usually present with more than one of these signs or symptoms. More than half of the patients will have three or more defects. Hearing impairment is the most frequently reported clinical manifestation, and is most likely to present as a single defect [97–99]. Almost all birth defects caused by rubella are associated with infections in the first 16 weeks. However, later infection has been associated with growth restriction and cases of deafness and pulmonary artery stenosis have been reported [99]. Congenital rubella survivors have an increased risk for type I diabetes, thyroid dysfunction, and progressive rubella panencephalitis [99, 100]. In cases of maternal rubella infection during the first trimester, the risk of malformation may be as high as 90 %.

The overall maternal-fetal transmission rate in cases of maternal toxoplasmosis in pregnancy was reported to be about 30 %. The risk of transmission to the fetus increases with gestational age from 6 % at 13 weeks to 72 % at 36 weeks. However, fetuses infected in early pregnancy were much more likely to show clinical signs of infection [101]. Symptoms of congenital toxoplasmosis present at birth can include a maculopapular rash, generalized lymphadenopathy, hepatomegaly, splenomegaly, jaundice, and/or thrombocytopenia. However, 70–90 % of infants with congenital infection are asymptomatic at birth and sequelae can develop months or even years later. Up to 85 % will develop chorioretinitis, 20–75 % will have some form of developmental delay and 10–30 % will have moderate hearing loss [102–104].

Treponema Pallidum can infect the fetus at 14 weeks gestation, and possibly earlier. The risk for fetal infection increases with gestational age. In cases of fetal infection 40–50 % of the fetuses will die in utero while 30–40 % will be born with signs of congenital syphilis [105]. Signs of congenital syphilis may include hydrops fetalis, an unexpectedly large placenta, intractable diaper rash, jaundice, hepatosplenomegaly and anemia. Hepatosplenomegaly has been reported in almost 90 % of all such babies, and jaundice in 33 % of these neonates. The jaundice may be caused by syphilitic hepatitis or by hemolytic components of the disease [106]. Generalized lymphadenopathy usually occurs in association with hepatosplenomegaly and has been described in 50 % of the patients. In one study of nine patients with congenital syphilis, eight had evidence of anemia, four had evidence of thrombocytopenia, and six had jaundice [107].

Varicella zoster virus infection (chickenpox) is a very common childhood infection which is usually mild in children, but can be more serious in newborn babies and adults. Pregnant women in the third trimester are at higher risk for more severe disease including varicella pneumonia [108]. Fetal infection has been associated with a syndrome of congenital anomalies. Features of the congenital varicella embryopathy include skin lesions and hypopigmentation, eye defects (cataracts, microphthalmia, chorioretinitis), neurologic abnormalities (microcephaly, mental retardation, cortical atrophy), limb and muscle hypoplasia, gastrointestinal reflux, urinary tract malformations, intrauterine growth restriction, developmental delay, and cardiovascular malformations [108]. Based on the case reports and larger studies it is now believed that the sensitive period for fetal effects is from 0 to 20 weeks of pregnancy, although there are case reports of clinical embryopathy after maternal infection at up to 28 weeks of gestation [109]. The risk for congenital varicella embryopathy in cases of maternal infection before 20 weeks gestation ranges from less than 1 % [109–111] to 3 % [112]. Maternal infection in the third trimester does not cause malformation; however, it can cause severe neonatal varicella and herpes zoster in the infant. There seems to be an increase in neonatal varicella severity when maternal rash appears 7 days before to 7 days after delivery, with most severe cases when rash appeared in the mother from 4 days before and up to 2 days after delivery [109].

High levels of ionizing radiation have been shown to interfere with fetal development. Exposure to high levels of ionizing radiation has been associated with fetal death, growth restriction, microcephaly, organ aplasia and hypoplasia, oral clefts, cataracts, CNS malformations, and mental retardation [113–116]. In very early pregnancy, especially in the preimplantation period of the pregnancy, the embryo is mainly sensitive to the lethal effect of radiation [117]. During early organogenesis the embryo is also sensitive to the growth-restricting and teratogenic effects of radiation [118], while during the early fetal period, the effects are mainly on fetal growth and CNS development [119]. Exposure to ionizing radiation is very common and is frequently associated with medical procedures [120]. While radiation exposure in pregnancy is a cause for much anxiety, in most cases, exposure to ionizing radiation in various diagnostic imaging tests is much below the 5 rad threshold, which is the commonly accepted safe level of exposure in pregnancy.

Exposure to electromagnetic fields is very common. Exposure to non-ionizing radiation can theoretically pose a risk of thermal damage, especially to the eyes (because they cannot dissipate heat efficiently). The nonthermal effects have not been clearly demonstrated. However, there is currently no indication that this type of radiation can produce malignancy or mutations [121].