Acinetobactin-Mediated Inhibition of Commensal Bacteria by Acinetobacter baumannii.

Acinetobacter baumannii is an important hospital-associated pathogen that causes antibiotic resistant infections and reoccurring hospital outbreaks. A. baumannii's ability to asymptomatically colonize patients is a risk factor for infection and exacerbates its spread. However, there is little information describing the mechanisms it employs to colonize patients. A. baumannii often colonizes the upper respiratory tract and skin. Antibiotic use is a risk factor for colonization and infection suggesting that A. baumannii likely competes with commensal bacteria to establish a niche. To begin to investigate this possibility, we cocultured A. baumannii and commensal bacteria of the upper respiratory tract and skin. In conditions that mimic iron starvation experienced in the host, we observed that A. baumannii inhibits Staphylococcus epidermidis, Staphylococcus hominis, Staphylococcus haemolyticus and Corynebacterium striatum. Then using an ordered transposon library screen we identified the A. baumannii siderophore acinetobactin as the causative agent of the inhibition phenotype. Using mass spectrometry, we show that acinetobactin is released from A. baumannii under our coculture conditions and that purified acinetobactin can inhibit C. striatum and S. hominis. Together our data suggest that acinetobactin may provide a competitive advantage for A. baumannii over some respiratory track and skin commensal bacteria and possibly support its ability to colonize patients. IMPORTANCE The ability of Acinetobacter baumannii to asymptomatically colonize patients is a risk factor for infection and exacerbates its clinical spread. However, there is minimal information describing how A. baumannii asymptomatically colonizes patients. Here we provide evidence that A. baumannii can inhibit the growth of many skin and upper respiratory commensal bacteria through iron competition and identify acinetobactin as the molecule supporting its nutritional advantage. Outcompeting endogenous commensals through iron competition may support the ability of A. baumannii to colonize and spread among patients.