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ABSTRACT Pseudomonas aeruginosa is a multidrug-resistant opportunistic human pathogen that can survive in many natural and anthropogenic environments. It is a leading cause of morbidity in individuals with cystic fibrosis and is one of the most prevalent pathogens associated with nosocomial infections in the United States. It has been shown that this organism can survive and persist in low-nutrient environments, such as sink drains. How adaptation to these types of environments influences the phenotypic traits of this organism has not been well studied. Here, we implemented an experimental evolution system in which six strains of P. aeruginosa were subjected to low-nutrient conditions over the course of 12 weeks and assessed phenotypic and genotypic changes that occurred as a result of adaptation to such environments. We observed that adaptation to low-nutrient environments resulted in decreased generation time, reduced cell size, reduced biofilm formation, increased pyocyanin production, and decreased motility for some of the strains. Furthermore, some of the evolved isolates were significantly more virulent/competitive against a phagocytic predator. This study is significant as it allows us to predict how this organism will evolve in hospital and domestic environments and can help us improve treatment options for patients. IMPORTANCE Human commensal and pathogenic organisms undergo dynamic cycles across human and non-human environments. Despite the crucial implications for human health, the understanding of bacterial adaptations to these diverse environments and their subsequent impact on human-bacterial interactions remains underexplored. This study shows how Pseudomonas aeruginosa , an opportunistic human pathogen, adapts phenotypically in response to a shift from high nutrients (like those found in the human body) to low nutrients (like those found in many other environments, like sink drains). This work also shows that, in some cases, resistance to predatory forces can evolve in the absence of a predator. This work is important as it contributes to the growing body of knowledge concerning how external, non-host-related abiotic conditions influence host–pathogen interactions.
Cecil et al. (Fri,) studied this question.