GBS colonizes the gastrointestinal (GI) tract and the vaginal tract of ~30% of individuals. During pregnancy, GBS can be transmitted vertically from a colonized mother to the newborn in utero or during childbirth, which frequently causes early-onset neonatal invasive disease (EOD) such as sepsis and pneumonia in the first week of life. Thus, maternal vaginal carriage is an important risk factor for newborn disease.

Our studies seek to characterize the bacterial and host factors as well as microbiome interactions that promote GBS vaginal persistence and accession to the uterus. We use a murine model of vaginal colonization, human cell lines as well as human isolates to study mechanistic interactions and immune responses.

GBS is the leading cause of neonatal meningitis, which can result in mortality rates of up to 9% and long-lasting neurological sequelae in survivors. GBS meningitis typically presents after 1 week of life and is classified as late-onset disease (LOD), which accounts for approximately 60% of GBS meningitis cases reported. GBS LOD is thought to occur following colonization of the neonatal GI tract, which can result from ingestion of infected amniotic fluid in utero, vaginal fluid during childbirth, or infected breast milk postnatally.

We use a neonatal murine model of GBS LOD to study GI colonization, dissemination to the brain and the inflammatory response that promotes meningitis. We seek to identify bacterial factors that promote penetration of gut and brain barriers as well as how host factors, such as mucins, and immune cells, such as neutrophils, contribute to pathogenesis

Diabetes mellitus affected 589 million adults worldwide in 2024 with a predicted global incidence to reach 853 million by 2050. Of these individuals, approximately one quarter will develop a diabetic foot ulcer (DFU) often resulting in non-healing wounds and chronic infection. DFUs frequently harbor complex polymicrobial communities dominated by bacterial species including GBS which is increasing isolated from diabetic wounds.

We developed a diabetic mouse model of GBS wound infection and are using a human cell line as well as human diabetic wound isolates to study host defense, and polymicrobial interactions in this niche.

We are interested in the ways that polymicrobial interactions can impact microbial physiology at the host interface. The interactions between bacteria and fungi have been understudied. Candida albicans (Ca) and GBS frequently colonize the vaginal tract, and we have recently demonstrated that Ca-GBS polymicrobial biofilms can protect GBS from antibiotic treatment and anchor GBS to the vaginal epithelial surface.

We have developed a new murine model to characterize the association between Ca and GBS in the vagina and seek to understand how these interkingdom interactions contribute to vaginal colonization and well as GBS persistence on other niches like the neonatal GI and diabetic wound.