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
anomalous, cephalic, singleton pregnancies, exposed to labor, and delivered at 37,0 to 41,6 weeks were included. Women with hypertensive disorders, pregestational/gestational diabetes, or whose race/ ethnicity was unknown or classified as "other" were excluded. Maternal race/ethnicity as recorded on the birth certificate was used to categorize women and infants as follows: non-Hispanic White (White), non-Hispanic Black (Black), Hispanic, or non-Hispanic Asian (Asian). Multivariable Poisson regression models with robust error variance were used to evaluate the association between maternal race/ethnicity and composite adverse neonatal outcome (CANO), infant mortality, and composite adverse maternal outcome (CAMO). RESULTS: Of 9,205,873 women who met inclusion criteria, 55.5% were White, 13.7% Black, 24.3% Hispanic, and 6.5% Asian. Compared with neonates of White women, the risk of CANO was higher for neonates of Black women, and lower for neonates of Hispanic and Asian women. Infant mortality was also highest for infants born to Black women, and lower for infants born to Hispanic and Asian women (Table 1). The risk of CAMO was similar for Black women, lower for Hispanic women, and higher for Asian women compared with White women. A sensitivity analysis of CAMO without maternal transfusion noted a higher risk for all racial/ethnic groups when compared with White women (Table 2). CONCLUSION: Among low-risk pregnancies at 37 to 41 weeks, racial/ ethnic disparities in adverse outcomes persist. While infants of Black women appear to be at highest risk for morbidity and mortality, Asian mothers have the highest risk of maternal morbidity.
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