Host-microbe interactions are paramount for maintaining normal physiology of the human host, including the brain and behavior. Bacterial colonization of the gastrointestinal (GI) tract, formation of GI mucosal barrier function, and neural development all occur during a critical window of time in early life. Thus, exposure to trauma such as stress, infection or inflammation during neonatal life could detrimentally impact the developing microbiota, gut and brain (MGB) axis. Disrupted MGB axis signaling, including dysbiosis, mucosal barrier defects and/or changes in behavior, occur in multiple diseases, including inflammatory bowel disease (IBD), autism spectrum disorder, major depressive disorder, and obesity. Previous studies from our group have shown that infection of adult mice with a bacterial pathogen causes changes in the MGB axis, including intestinal dysbiosis and stress-induced behavioral deficits. However, the relationship between intestinal dysbiosis during the early stages of development and cognitive and behavioral deficits in adulthood have not been investigated. We hypothesized that infection in early life with a bacterial pathogen could lead to MBG axis deficits in adulthood. A mouse model (C57BL/6) of neonatal bacterial infection (P7) with enteropathogenic Escherichia coli (EPEC; strain e2348/69) was used to study effects of intestinal dysbiosis on behavior and intestinal physiology. We used the light/dark box test to assess anxiety-like behavior and the novel object recognition (NOR) task to study cognitive function in adult mice infected with EPEC as neonates, and sham-infected controls, with behavior analyzed using software (Noldus EthoVision XT). Intestinal physiology (short circuit current [Isc] and conductance [G]) was characterized by Ussing chambers, and the composition of the microbiota was determined by qPCR using well-characterized primer sets. Data is provided as the mean ± SE and p values calculated by Student T-test. Adult mice neonatally infected with EPEC showed impaired cognition (Exploration ratio [%]: 75.2±4.9 Sham vs. 62.3±2.6 EPEC; n=12-13, p<0.05), without evidence of anxiety-like behavior (Time spent in light box [s]: 295±27 Sham vs. 275±29 EPEC; n=13-15) compared to sham-infected controls. Intestinal physiology was altered, with increased secretory state (Isc [μA/cm2]; 38.4±5.3 Sham vs. 57.8±4.4 EPEC; n=4-6; p<0.05) and permeability (G [mS/cm2]; 3.2±0.3 Sham vs. 4.4±0.4 EPEC; n=4-6; p<0.05) as well as long-lasting intestinal dysbiosis (including decreased levels [% of Eubacteria] of Lactobacillus and increased levels of Enterobacteriaceae and Bacteroides; n=6-8, p<0.05). In conclusion, our data demonstrates that neonatal bacterial infection leads to alterations of the developing MGB axis that persist into adulthood.