Host bacterial associations have a profound impact on health and disease. The human gastrointestinal (GI) tract is inhabited by trillions of commensal bacteria that aid in the digestion of food and vitamin production and play crucial roles in human physiology. Disruption of these relationships and the structure of the bacterial communities that inhabit the gut can contribute to dysbiosis, leading to disease. This fundamental relationship between the host and microbiota relies on chemical signaling and nutrient availability and exchange. GI pathogens compete with the endogenous microbiota for a colonization niche (1, 2). The ability to monitor nutrients and combine this information with the host physiological state is important for the pathogen to precisely program the expression of its virulence repertoire. A major nutrient source is carbon, and although the impact of carbon nutrition on the colonization of the gut by the microbiota has been extensively studied, the extent to which carbon sources affect the regulation of virulence factors by invading pathogens has not been fully defined. The GI pathogen enterohemorrhagic E. coli (EHEC) gages sugar sources as an important cue to regulate expression of its virulence genes. EHEC senses whether it is in a gluconeogenic versus a glycolytic environment, as well as fluctuations of fucose levels to fine tune regulation of its virulence repertoire.