According to many authorities, influenza exerts a very pernicious influence upon pregnancy. It would appear that the effects of influenza must vary with the severity of the epidemic, and more particularly with the frequency of pneumonic complications. As a rule, any septic condition offers a worse prognosis in pregnancy. Several instances have been reported of transmission of the offending bacteria to the foetus.
—J. Whitridge Williams (1903)
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 the CD4+ T cells that secrete Th2-type cytokines—for example interleukins (Fragiadakis, 2016). 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 (Kourtis, 2014; Svensson-Arvelund, 2014). Importantly, the Th2 humoral immune response remains intact. It also appears that human leukocyte antigen (HLA)-C expressed by extravillous trophoblasts elicits responses from decidual natural killer (dNK) and decidual CD8+ T cells (Crespo, 2017).
In describing infections, horizontal transmission is the spread of an infectious agent from one individual to another. Vertical transmission refers to passage from the mother to her fetus of an infectious agent through the placenta, during labor or delivery, or by breastfeeding. Thus, preterm rupture of membranes, prolonged labor, and obstetrical manipulations may enhance the risk of neonatal infection (Centers for Disease Control and Prevention, 2010). Table 64-1 details specific infections by mode and timing of acquisition. 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 64-1Specific Causes of Some Fetal and Neonatal Infections ||Download (.pdf) TABLE 64-1 Specific Causes of Some Fetal and Neonatal Infections
Viruses: varicella-zoster, coxsackie, human parvovirus B19, rubella, CMV, HIV, Zika
Bacteria: Listeria, syphilis, Borrelia
Protozoa: toxoplasmosis, malaria
Bacteria: gonorrhea, chlamydia, group B streptococcus, tuberculosis, mycoplasmas
Viruses: HSV, HPV, HIV, hepatitis B, hepatitis C, Zika