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.
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