Project description:We compared the transcriptional profiles of 12 E. coli O157:H7 isolates grown to stationary phase in LB broth. These isolates possess the same two enzyme PFGE profile and are related temporally or geographically to the above outbreak. These E. coli O157:H7 isolates included three clinical isolates, five isolates from separate bags of spinach, and single isolates from pasture soil, river water, cow feces, and a feral pig.
Project description:Escherichia coli bloodstream infections are common and associated with high mortality. A key feature of E. coli is the lipopolysaccharide (LPS) O-antigen, which contributes to immune evasion during invasive infection. We analyzed serial E. coli isolates from patients with relapsed bacteremia and identified frequent disruption of O-antigen synthesis due to mutations in wbbL, resulting in a rough LPS (R-LPS) phenotype. E. coli with rough LPS isolates were more serum sensitive and less pathogenic in mice. Despite this apparent attenuation, 11 of 66 (18%) E. coli sequence type 131 bloodstream isolates in our cohort lacked O-antigen and were associated with significantly worse clinical outcomes, including septic shock and mortality. Using a recurrent bacteremia model, we show that R-LPS isolates partially evade protective immunity generated against smooth-LPS E. coli, highlighting the importance of host immune context in invasive disease.
