Coxsackievirus infections with group A and B are usually asymptomatic. Symptomatic infections-usually with group B-include aseptic meningitis, polio-like illness, hand foot and mouth disease, rashes, respiratory disease, pleuritis, pericarditis, and myocarditis. No treatment or vaccination is available (Cohen, 2015a). Coxsackievirus may be transmitted by maternal secretions to the fetus at delivery in up to half of mothers who seroconverted during pregnancy (Modlin, 1988). Transplacental passage has also been reported (Ornoy, 2006).
Congenital malformation rates may be slightly increased in fetuses of pregnant women who had serological evidence of coxsackievirus (Brown, 1972). Viremia can cause fetal hepatitis, skin lesions, myocarditis, and encephalomyelitis, all of which may be fatal. Some have reported higher rates of cardiac anomalies and of low-birthweight, preterm, and small-for-gestational-age newborns (Chen, 2010; Koro'lkova, 1989). Maternal-fetal infection has been associated with massive perivillous ibrin deposition and fetal death (Yu, 2015). Finally, a rare association between maternal coxsackievirus infection and insulin-dependent diabetes in ofspring has been described (Viskari, 2012).
Polio viruses cause highly contagious infections that are subclinical or mild. he virus is trophic for the CNS, and it can cause paralytic poliomyelitis (Cohen, 2015a). Siegel (1955) demonstrated that pregnant women not only were more susceptible to polio but also had a higher death rate. Perinatal transmission has been observed, especially when maternal infection developed in the third trimester (Bates, 1955). Inactivated subcutaneous polio vaccine is recommended for susceptible pregnant women who must travel to endemic areas or are placed in other high-risk situations. Live oral polio vaccine has been used for mass vaccination during pregnancy without harmful fetal efects (Harjulehto, 1989).
This B 19 virus causes erythema inectiosum, orith disease. It is a small, single-stranded DNA virus that replicates in rapidly proliferating cells such as erythroblast precursors (Brown, 2015). his can lead to anemia, which is its primary fetal efect. Only individuals with the erythrocyte globoside membrane P antigen are susceptible. In women with severe hemolytic anemia-for example, sickle-cell disease-parvovirus infection may cause an aplastic crisis.
The main mode of parvovirus transmission is respiratory or hand-to-mouth contact, and the infection is common in spring months. The maternal infection rate is highest in women with school-aged children and in day-care workers, but not in schoolteachers. An infected person develops viremia 4 to 14 days after exposure, and an otherwise immunocompetent individual is no longer infectious at the onset of the rash. By adulthood, only 40 percent of women are susceptible. The annual seroconversion rate is 1 to 2 percent but is >10 percent during epidemic periods (Brown, 2015). The secondary attack rate approaches 50 percent.