Gestational malaria, a severe clinical manifestation of Plasmodium falciparum infection observed in pregnant women, is a major cause of severe maternal illness and neonatal mortality worldwide. I have developed a novel mouse model for transgestational malaria infection utilizing outbred Swiss Webster mice. When infected with Plasmodium chabaudi in early gestation, several inbred mouse strains abort their pregnancies at midgestation. However, outbred Swiss Webster mice infected with P. chabaudi in early gestation carry their pregnancies to term and produce live offspring. Maternal malaria infection is associated with reduced fetal viability and fetal weight at term, as well as reduced postnatal survival. This novel model allows for the exploration of the impact of maternal malaria infection on postnatal outcomes and the immunological balance between parasite clearance and pregnancy success. The composition of the gut microbiota alters this balance. We find that the composition of the gut microbiota transcends the outbred genetics of Swiss Webster mice as a determinant of infection severity. The administration of fecal microbiota transplants consisting of resistance- or susceptibility-conferring gut microbes results in the establishment of distinct microbial communities in recipient mice. Mice receiving resistance-conferring gut microbes develop lower parasite burdens and reduced morbidity compared to mice receiving susceptibility-conferring gut microbes. In addition, fetal viability and weight at gestational term, as well as postnatal survival, are improved in infected dams possessing resistance-conferring gut microbes. To explore the immunological and placental environment at peak infection in Swiss Webster mice displaying gut microbiota-mediated susceptibility or resistance to malaria infection, mice were sacrificed at 10 days post-infection. Uterine weight was significantly reduced in infected susceptible dams compared to uninfected controls, but maternal infection severity did not significantly alter embryo viability. Although peripheral cytokine titers were not influenced by maternal infection severity, the transcriptional response of susceptible conceptuses differed subtly from the response observed in resistant conceptuses. Specifically, Il10 was elevated in conceptuses collected from infected susceptible mice compared to infected resistant mice, perhaps indicating that susceptible mice had a more severe proinflammatory response prior to sacrifice, necessitating a greater compensatory response to reduce damaging inflammation at the maternal-fetal interface.