Figure 1. Adaptation of metabolism and basic physiology allows E. coli to replicate in diverse host microenvironments.

Extraintestinal pathogenic E. coli that cause urinary tract infection, bacteremia, sepsis, and meningitis, have adapted to grow as a harmless commensal in the nutrient-replete, carbon-rich human intestine but rapidly transition to pathogenic lifestyle in the nutritionally poor, nitrogen-rich urinary tract. In order to establish a commensal association within the human intestine, adaptive factors such as metabolic flexibility allow E. coli to successfully compete for carbon and energy sources with a large and diverse bacterial population. E. coli acquires nutrients from the intestinal mucus, including N-acetylglucosamine, sialic acid, glucosamine, gluconate, arabinose, fucose and simple sugars released upon breakdown of complex polysaccharides by anaerobic gut residents. When UPEC transition to the urinary tract, the bacteria encounter a drastic reduction in the abundance of nutrients and bacterial competition. Consequently, to replicate in a new host microenvironment, UPEC utilization of metabolic pathways required for growth in the dilute mixture of amino acids and peptides in the bladder signals the bacterium to elaborate virulence properties to successfully cause invasive disease and survive the onslaught of bactericidal host defenses. These adaptations are a unique and essential characteristic of ExPEC that enable a successful transition between disparate microenvironments within the same individual.