Asymptomatic colonization is often critical for persistence of antimicrobial-resistant pathogens, such as Acinetobacter baumannii, and can increase the risk of clinical infections. However, the ecological factors shaping A. baumannii gut colonization remain unclear. We show that A. baumannii and other pathogenic Acinetobacter evolved to utilize the amino acid ornithine, a non-preferred carbon source, to compete with resident microbiota and persist in the gut in mice. A. baumannii encodes ornithine succinyltransferase (AstO) necessary for catabolizing ornithine, especially in conditions of increased microbial diversity. Supplemental dietary ornithine promotes long-term fecal shedding of A. baumannii. By contrast, supplementation of preferred carbon sources-monosodium glutamate or histidine-abolishes the requirement for ornithine catabolism. Additionally, A. baumannii gut carriage is higher in formula-fed human infants, who generally consume higher levels of protein, revealing dietary impacts on Acinetobacter colonization. Together, these results reveal that ornithine catabolism facilitates A. baumannii colonization, providing a reservoir for pathogen spread.
Ren et al. (Fri,) studied this question.