It has been well established that E. coli has a highly plastic genome capable of rapid alteration to facilitate survival in diverse environments. In addition, the role of host anatomy, physiology, and immune response may dramatically impact the susceptibility of individual strains of E. coli to colonize the host. Because of these factors, no specific genome structure or content has been identified that serves as a signature for the ability of E. coli to cause UTI.
We have completed the full genome sequence of multiple urinary and fecal E. coli isolates and are analyzing this data to better understand UPEC pathogenesis requirements. Using a blend of comparative genomics and molecular evolution, we are looking for functional genes and positively selected gene sequences that enable E. coli to cause disease in the urinary tract and exist within the gut.
This approach gives us a better perspective on sequence data. More extensive characterizations of strains from patients with differing disease syndromes will lead to a better understanding of the UPEC pathoadaptations which promote UTI occurrence.
Collaborators: Ann Stapleton, Jeff Gordon, Swaine Chen, Ashlee Earle, Gordan Dougan