Background: Acinetobacter baumannii has emerged as an increasingly important and successful opportunistic human pathogen due to its ability to withstand harsh environmental conditions, its characteristic virulence factors and quick adaptability to stress. Methods: We developed a clinically relevant murine model of A. baumannii traumatic wound infection to determine the effect of local wound environment on A. baumannii virulence. Mice underwent rectus muscle crush injury combined with ischemia created by epigastric vessel ligation, followed by A. baumannii inoculation. Reiterative experiments were performed using 1) a mutant deficient in the production of the siderophore acinetobactin, or 2) iron supplementation of the wound milieu. Mice were euthanized 7 days later and rectus muscle analyzed for signs of clinical infection, HIF1[alpha] accumulation, bacterial abundance and colony morphotype. To determine the effect of wound milieu on bacterial virulence, the Galleria mellonella infection model was utilized. Results: The combination of rectus muscle injury with ischemia and A. baumannii inoculation resulted in 100% incidence of clinical wound infection that was significantly higher compared to other groups (n=15/group, p
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