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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 &gt;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.

Preconceptual Priming Overrides Susceptibility to Escherichia coli Systemic Infection during Pregnancy