Polioviruses have infrequently been recovered from placental or fetal tissue, suggesting that in utero infection early in pregnancy is uncommon (3,8). Neonatal poliomyelitis most often occurred via acquisition from an infected mother; maternal illness between 1 week prior to delivery and 4 weeks after delivery posed the highest risk of neonatal disease (7). A minority of affected newborns had onset of illness at birth or within the first 5 days of life, suggesting intrauterine infection (3,59). Infection in the remainder was likely via contact with maternal blood or secretions during or after delivery. Exposure to nonmaternal contacts was also occasionally implicated (8).
The clearest evidence for in utero infection by nonpolio EVs comes from cases of spontaneous abortion or stillbirth with demonstration of EV infection in fetal tissues (9,10,16,17,60). Most abortions have been reported between the third and fifth months of pregnancy, although spontaneous abortion in the first trimester has also been described (9,10,60). Stillbirths have been reported between the fifth and ninth months of gestation (11,12,16,17). It should be noted that some stillbirths have occurred following EV infection of the placenta in the absence of evidence of direct fetal infection (14).
Further evidence of in utero infection is provided by the small number of reported cases of neonatal EV disease with onset in the first few hours after birth. In utero infection has been substantiated in these cases by viral culture of amniotic fluid and umbilical cord blood, antigen detection in myocardia hours after birth, culture of neonatal organs a few hours after delivery, and detection of serum-neutralizing immunoglobulin (Ig) M antibody on the first day of life (17,46,61-64). Identification of EVs in placentas, often in association with placentitis, villitis, villous necrosis, vasculitis, thrombosis, or other placental pathology, suggests that some fetal infections occur via a transplacental route (10,12,14,65). Shedding of EVs from the stool and cervixes of pregnant women, demonstration of susceptibility of amnion cells to EV infection in vitro, and growth of EVs from amniotic fluid in vivo point to the potential for ascending infection also (11,12,36,61,66-69). Based on the occurrence of viremia or symptoms in the first 1-2 days of life, it has been estimated that approx 22% of fatal neonatal coxsackie B virus infections and 11% of neonatal echovirus infections were acquired in utero (15,34,36,40).
Most EV-infected neonates are thought to be infected either intrapartum by exposure to maternal blood or genital secretions or after delivery by exposure to oropharyn-geal secretions or stool of mothers or other contacts (6,34,37). EVs have been grown from cervical swabs obtained from symptomatic pregnant women and from mothers of infected, ill neonates (62,66-68). Shedding of virus from maternal throat and rectum during pregnancy has also been documented, with or without symptoms (69). These observations lend support to the potential for viral transmission from mother during or after delivery. High rates of viral illness in the peripartum period among siblings and fathers of EV-infected newborns also suggest potential viral transmission from these family members (33).
Many episodes of both sporadic transmission and epidemic spread of EVs in hospital nurseries have been reported (34,36,39,62,64,70-75). Full-term and premature infants have been affected, and asymptomatic and symptomatic infections have resulted. Several outbreaks could be traced to vertically infected neonates, with spread by hospital staff. In other epidemics, adults likely introduced EVs into nurseries (34).
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