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Infections remain a major cause of maternal and fetal morbidity and mortality worldwide. The unique maternal–fetal vascular interface in some cases serves to protect the fetus from infectious agents, but in other instances it provides a conduit for transmission. Maternal serological status, acquisition mode, gestational age at the time of infection, and immunological status of mother and fetus all influence disease outcome.

The TORCH acronym reflects the infections toxoplasmosis, others, rubella, and cytomegalovirus and herpesvirus infections. These can cross the placenta to cause fetal infection and substantial neonatal sequelae. Of members in the “others” category, parvovirus B19 infection is discussed here. Herpesvirus and syphilis infections are described in Chapter 68.


Maternal Immunological Changes

Despite significant advances, many of the maternal immunological adaptations to pregnancy remain unclear. Successful pregnancy results from a complex interplay between the innate and adaptive immune systems to establish fetal tolerance (Chap. 5, p. 93) (Liu, 2017). Within the innate system, decidual natural killer (dNK) cells interact with and aid invasion of fetal extravillous trophoblasts via human leukocyte antigen (HLA)-G (Fig. 21-8, p. 404). Also, cytokines produced during viral infection activate dNK cells to induce protective cytotoxicity (Tilburgs, 2015).

Within the adaptive immune system, a CD4+ subset of T helper cells called regulatory T cells (Tregs) express forkhead box P3 (FOXP3). This is an immune-suppressive transcription factor that plays a critical role in inducing maternal immune tolerance to the fetus (Kahn, 2010). However, this same mechanism compromises maternal defense against bacterial pathogens. Noncoding microRNAs, whose roles are incompletely defined, regulate activation and proliferation of both innate and adaptive immune cells (Robertson, 2017).

In describing infections, horizontal transmission is the spread of an infectious agent from one individual to another. Vertical transmission is passage of an infectious agent from the mother to her fetus through the placenta, during labor or delivery, or by breastfeeding. Thus, preterm rupture of membranes or prolonged labor may enhance the risk of some neonatal infections (American College of Obstetricians and Gynecologists, 2020b). Table 67-1 shows specific infections by mode and acquisition timing. A final term, the secondary attack rate, is the probability that infection develops in a susceptible individual following known contact with an infectious person.

TABLE 67-1Specific Causes of Some Fetal and Neonatal Infections

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