Infections have historically been a major cause of maternal and fetal morbidity and mortality worldwide, and they remain so in the 21st century. The unique maternal-fetal vascular connection in some cases serves to protect the fetus from infectious agents, whereas in other instances it provides a conduit for their transmission to the fetus. Maternal serological status, gestational age at the time infection is acquired, the mode of acquisition, and the immunological status of both the mother and her fetus all influence disease outcome.
Maternal and Fetal Immunology
Pregnancy-Induced Immunological Changes
Even after intensive study, many of the maternal immunological adaptations to pregnancy are not well elucidated. It is known that pregnancy is associated with an increase in CD4-positive T cells secreting Th2-type cytokines—for example interleukins 4, 5, 10, and 13. Th1-type cytokine production—for example, interferon gamma and interleukin 2—appears to be somewhat suppressed, leading to a Th2 bias in pregnancy. This bias affects the ability to rapidly eliminate certain intracellular pathogens during pregnancy, although the clinical implications of this suppression are unknown (Jamieson, 2006a; Raghupathy, 2001; Svensson-Arvelund, 2014). Importantly, the Th2 humoral immune response remains intact.
Fetal and Newborn Immunology
The active immunological capacity of the fetus and neonate is compromised compared with that of older children and adults. That said, fetal cell-mediated and humoral immunity begin to develop by 9 to 15 weeks’ gestation (Warner, 2010). The primary fetal response to infection is immunoglobulin M (IgM). Passive immunity is provided by IgG transferred across the placenta. By 16 weeks, this transfer begins to increase rapidly, and by 26 weeks, fetal concentrations are equivalent to those of the mother. After birth, breast feeding is protective against some infections, although this protection begins to decline at 2 months of age. Current World Health Organization (2013) recommendations are to exclusively breast feed for the first 6 months of life with partial breast feeding until 2 years of age.
Vertical transmission refers to passage from the mother to her fetus of an infectious agent through the placenta, during labor or delivery, or by breast feeding. Thus, preterm rupture of membranes, prolonged labor, and obstetrical manipulations may increase the risk of neonatal infection. Those occurring less than 72 hours after delivery are usually caused by bacteria acquired in utero or during delivery, whereas infections after that time most likely were acquired afterward. Table 64-1 details specific infections by mode and timing of acquisition.
TABLE 64-1Specific Causes of Some Fetal and Neonatal Infections |Favorite Table|Download (.pdf) TABLE 64-1 Specific Causes of Some Fetal and Neonatal Infections
| Transplacental |
| Viruses: varicella-zoster, coxsackie, human parvovirus B19, rubella, cytomegalovirus, HIV |
| Bacteria: Listeria, syphilis, Borrelia |
| Protozoa: toxoplasmosis, malaria |
| Ascending infection |
| Bacteria: group B streptococcus, coliforms |
| Viruses: HSV |
| Maternal exposure |
| Bacteria: ...|
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