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In the fifteen minutes it takes to read this short commentary, more than 400 babies will have been born too early, another 300 expecting mothers will develop preeclampsia, and 75 unborn third trimester fetuses will have died in utero (stillbirth). Given the lack of meaningful progress in understanding the physiological changes that occur to allow a healthy, full term pregnancy, it is perhaps not surprising that effective therapies against these great obstetrical syndromes that include prematurity, preeclampsia, and stillbirth remain elusive. Meanwhile, pregnancy complications remain the leading cause of infant and childhood mortality under age five. Does it have to be this way? What more can we collectively, as a biomedical community, or individually, as clinicians who care for women and newborn babies at high risk for pregnancy complications, do to protect individuals in these extremely vulnerable developmental windows? The problem of pregnancy complications and neonatal mortality is extraordinarily complex, with multiple unique, but complementary perspectives from scientific, epidemiological and public health viewpoints. Herein, we discuss the epidemiology of pregnancy complications, focusing on how the outcome of prior pregnancy impacts the risk of complication in the next pregnancy — and how the fundamental immunological principle of memory may promote this adaptive response.

Maternal sepsis is a leading cause of morbidity and mortality during pregnancy. Escherichia coli is a primary cause of bacteremia in women and occurs more frequently during pregnancy. Several key outstanding questions remain regarding how to identify women at highest infection risk and how to boost immunity against E. coli infection during pregnancy. Here, we show that pregnancy-induced susceptibility to E. coli systemic infection extends to rodents as a model of human infection. Mice infected during pregnancy contain >100-fold-more recoverable bacteria in target tissues than nonpregnant controls. Infection leads to near complete fetal wastage that parallels placental plus congenital fetal invasion. Susceptibility in maternal tissues positively correlates with the number of concepti, suggesting important contributions by expanded placental-fetal target tissue. Remarkably, these pregnancy-induced susceptibility phenotypes are also efficiently overturned in mice with resolved sublethal infection prior to pregnancy. Preconceptual infection primes the accumulation of E. coli-specific IgG and IgM antibodies, and adoptive transfer of serum containing these antibodies to naive recipient mice protects against fetal wastage. Together, these results suggest that the lack of E. coli immunity may help discriminate individuals at risk during pregnancy, and that overriding susceptibility to E. coli prenatal infection by preconceptual priming is a potential strategy for boosting immunity in this physiological window of vulnerability. IMPORTANCE Pregnancy makes women especially vulnerable to infection. The most common cause of bloodstream infection during pregnancy is by a bacterium called Escherichia coli. This bacterium is a very common cause of bloodstream infection, not just during pregnancy but in all individuals, from newborn babies to the elderly, probably because it is always present in our intestine and can intermittently invade through this mucosal barrier. We first show that pregnancy in animals also makes them more susceptible to E. coli bloodstream infection. This is important because many of the dominant factors likely to control differences in human infection susceptibility can be property controlled for only in animals. Despite this vulnerability induced by pregnancy, we also show that animals with resolved E. coli infection are protected against reinfection during pregnancy, including having resistance to most infection-induced pregnancy complications. Protection against reinfection is mediated by antibodies that can be measured in the blood. This information may help to explain why most women do not develop E. coli infection during pregnancy, enabling new approaches for identifying those at especially high risk of infection and strategies for preventing infection during pregnancy.

INTRODUCTION: To describe changes in rate of no prenatal care (PNC) in US between the years 2012–2016, and identify patient demographic and maternal medical risk factors for receiving no PNC. METHODS: Case-control study of US live births between 20–42 weeks gestation using vital statistics birth records. We analyzed maternal sociodemographic factors and medical characteristics as risk factors. Logistic regression estimated the influence of factors on outcome of no PNC, as indicated on the US birth certificate. No prenatal care was defined by having 0 visits prior to delivery. RESULTS: The frequency of births to mothers with no PNC increased each year during the study period, from 1.36% to 1.58%, P<.001. The rate of no PNC was highest among mothers with low maternal education level, Medicaid insurance and maternal hepatitis C (rates 2–5% and adjusted odds >2.2). Maternal black race, unmarried, and tobacco use were also significant risk factors (adjusted odds ratio >1.4). CONCLUSION: The rate of no PNC in the US has risen in recent years, 2012–2016. Women with factors that are associated with increased risk for adverse pregnancy outcome are those most likely to have no PNC. Public health initiatives should focus educational efforts on the importance of prenatal care to minimize risk of adverse pregnancy outcomes. Programs aimed to increase access to prenatal care in at-risk pregnancies should be developed to address the increase in no PNC in the US.

Transplantation is increasingly used in individuals with irreversible organ damage. An important consideration is preventing rejection of genetically foreign donor allograft tissues which requires life-long immune-suppressive therapies. Allograft rejection is primarily mediated by T cells, and post-transplant therapies primarily target these immune cell subsets. 1 The widely used calcineurin inhibitor, tacrolimus, is currently prescribed to >90% of solid organ transplant recipients. 2,3 Tacrolimus primarily inhibits T-cell activation, but does not discriminate between graft-specific cells that mediate donor tissue rejection from cells with other specificities that sustain host defense against microbial infection. Accordingly, transplant recipients are at increased infection risk, especially infection by intracellular pathogens such as Listeria monocytogenes (Lm) normally controlled by Tcell-mediated immunity. [4][5][6][7][8] Vaccination is an effective approach for boosting antimicrobial immunity against specific pathogens in defined developmental contexts. However, transplant recipients, especially in the first months following transplant, consistently show diminished responsiveness to both inactivated and live attenuated vaccines. [9][10][11] Another consideration is the risk of infection from live attenuated vaccines, compared with inactivated vaccines, in transplant recipients on

Objective To evaluate fetomaternal bleeding following routine cesarean delivery compared with cesarean delivery involving transplacental transection. Study Design A prospective cohort study evaluating cesarean delivery in which the placenta was transected (cases) versus controls (placenta not transected) from January 2016 to April 2018. A maternal Kleihauer–Betke's (KB) test and newborn hematocrit were performed shortly after delivery. Results The rate of a positive KB test was not significantly different between cases (n = 31) and controls (n = 61) (19 vs. 14%; odds ratio [OR]: 1.44; 95% confidence interval [CI]: 0.46–4.49; p = 0.74). Median neonatal hematocrits were not different. However, the rate of newborn hematocrits <40% at delivery was higher in cases compared with controls (23 vs. 3%; OR: 8.90; 95% CI: 1.72–45.90; p = 0.005). Conclusion A cesarean requiring transplacental transection to accomplish delivery does not significantly increase the rate of fetomaternal bleeding but is associated with a higher likelihood of newborn hematocrit <40% at delivery.

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