The study investigates how antibiotic-associated pathogens, *Salmonella typhimurium* and *Clostridium difficile*, exploit the disruption of the intestinal microbiota to facilitate their expansion in the gut. The researchers found that these pathogens utilize mucosal carbohydrates, particularly sialic acid and fucose, which are liberated by the resident microbiota when the microbiota is disturbed by antibiotics. *S. typhimurium* accesses these carbohydrates in a microbiota-dependent manner, and genetic ablation of the catabolic pathways for sialic acid and fucose reduces its competitiveness in vivo. Similarly, *C. difficile* expansion is enhanced by elevated levels of sialic acid in the gut, which are induced by the presence of the model gut symbiont *Bacteroides thetaiotaomicron (Bt)*. In gnotobiotic mice colonized with a sialidase-deficient mutant of *Bt*, free sialic acid levels were reduced, leading to impaired expansion of both *S. typhimurium* and *C. difficile*. Exogenous administration of free sialic acid reversed this impairment. Additionally, antibiotic treatment in conventional mice increased free sialic acid levels, and mutants of both pathogens that cannot catabolize sialic acid showed impaired expansion. These findings suggest that the disruption of the microbiota and the resulting alteration in mucosal carbohydrate availability are exploited by these pathogens to promote their growth and disease-causing potential.The study investigates how antibiotic-associated pathogens, *Salmonella typhimurium* and *Clostridium difficile*, exploit the disruption of the intestinal microbiota to facilitate their expansion in the gut. The researchers found that these pathogens utilize mucosal carbohydrates, particularly sialic acid and fucose, which are liberated by the resident microbiota when the microbiota is disturbed by antibiotics. *S. typhimurium* accesses these carbohydrates in a microbiota-dependent manner, and genetic ablation of the catabolic pathways for sialic acid and fucose reduces its competitiveness in vivo. Similarly, *C. difficile* expansion is enhanced by elevated levels of sialic acid in the gut, which are induced by the presence of the model gut symbiont *Bacteroides thetaiotaomicron (Bt)*. In gnotobiotic mice colonized with a sialidase-deficient mutant of *Bt*, free sialic acid levels were reduced, leading to impaired expansion of both *S. typhimurium* and *C. difficile*. Exogenous administration of free sialic acid reversed this impairment. Additionally, antibiotic treatment in conventional mice increased free sialic acid levels, and mutants of both pathogens that cannot catabolize sialic acid showed impaired expansion. These findings suggest that the disruption of the microbiota and the resulting alteration in mucosal carbohydrate availability are exploited by these pathogens to promote their growth and disease-causing potential.