ABSTRACT
Extraintestinal pathogenic Escherichia coli (ExPEC) act as commensals within the mammalian gut, but can induce pathology upon dissemination to other host environments such as the urinary tract and bloodstream. It is thought that ExPEC genomes are shaped in large part by evolutionary forces encountered within the gut where the bacteria spend much of their time, provoking the question of how their extraintestinal virulence traits arose. The principle of coincidental evolution, in which a gene that evolved in one niche happens to be advantageous in another, has been used to argue that ExPEC virulence factors originated in response to selective pressures within the gut ecosystem. As a test of this hypothesis, the fitness of ExPEC mutants lacking canonical virulence factors was assessed within the intact murine gut in the absence of any antibiotic treatment. We found that most of the tested factors—including CNF1, Usp, colibactin, flagella, and the plasmid pUTI89—were dispensable for gut colonization. Deletion of genes encoding the adhesin PapG or the toxin HlyA caused transient defects, but did not affect longer-term persistence. In contrast, a mutant missing the type 1 pilus-associated adhesin FimH displayed reduced persistence within the gut. However, this phenotype was variable, being dependent on the presence of specific competing strains and partially attributable to aberrant flagellin expression by the fimH mutant. These data indicate that FimH and other key ExPEC-associated factors are not strictly required for gut colonization, suggesting that selective pressures within the gut do not drive the development of all extraintestinal virulence traits.
