Acinetobacter baumannii is a critical public health threat due to its rapid spread in healthcare facilities and its high rates of multidrug resistance. The human gut has been identified as a potential reservoir for A. baumannii colonization and spread in hospitals. Colonization by Acinetobacter spp. is associated with diet, antibiotics, illness, and hospitalization. Asymptomatic colonization by A. baumannii is associated with increased risk of invasive infections, emphasizing the importance of colonization in A. baumannii virulence. Therefore, disruption of gut colonization has the potential to prevent A. baumannii infections. A major limitation to this approach is the lack of understanding of how A. baumannii colonizes and replicates in the gut. Therefore, we developed a mouse model to identify strategies A. baumannii has evolved to colonize the gut. We discovered that ornithine catabolism is crucial for A. baumannii gut colonization. We found that A. baumannii and related species appear to have ornithine catabolism by a partial duplication of an arginine catabolic operon and that ornithine catabolism is regulated by the presence of arginine and ornithine. Our central hypothesis is that A. baumannii ornithine catabolism and regulation are critical for gut colonization. Our aims are to define the molecular determinants of ornithine catabolism and their role in gut colonization, to elucidate the regulatory mechanisms of arginine and ornithine catabolism aross Acinetobacter spp., and to dissect the role of microbiota, host, and diet in A. baumannii ornithine catabolism and gut colonization. Together, these approaches will identify genetic factors required for A. baumannii nutrient utilization in the gut. The findings of these studies will establish a framework for disrupting A. baumannii gut colonization and preventing infections.