Drew Schwartz Lab

Our goal is to deliver personalized gut microbiome-based risk assessment and antibiotic stewardship for pediatric sepsis.

Bacterial infections are a leading cause of infant death worldwide. Preterm infants in neonatal intensive care units (NICU) are particularly susceptible due to their underdeveloped skin and gut barriers and other immature organs. Up to 40% of preterm infants are affected by bacterial infections, leading to frequent use of antibiotics for suspected or confirmed infections. When infants show signs of sepsis, their blood is cultured to check for bacteria and antibiotics are started immediately. While awaiting culture results, infants receive antibiotics targeted at common bloodstream infections. However, this approach has several negative consequences:

Many bacteria are increasingly resistant to the chosen antibiotics.
Unnecessary antibiotic use, especially when cultures show no bacterial growth, is linked to a higher likelihood of death.
Antibiotics disrupt the normal development of the infant gut microbiome and immune system, increasing the abundance of antibiotic-resistant bacteria and the risk of further episodes of sepsis.

Figure depicting three scenarios of infant gut microbiomes treated with antibiotics for the presence (or absence) of a pathogen, resulting in an immune response outcome. — Our central hypothesis is that antibiotic treatment disrupts the gut microbiome and immune development leading to infant sepsis.

Our lab aims to understand the microbiome-host interface before sepsis to improve diagnostics and treatments. We use microbial sequencing and culturing, immune profiling, and computational modeling of clinical cohorts and gnotobiotic mouse models to develop algorithms that predict sepsis risk and optimal antibiotic therapies. We hope to translate our findings to clinical populations to reduce morbidity and mortality from serious bacterial infections in pediatric patients.