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Antimicrobial resistance genes, including multidrug efflux pumps, evolved long before the ubiquitous use of antimicrobials in medicine and infection control. Multidrug efflux pumps often transport metabolites, signals and host-derived molecules in addition to antibiotics or biocides. Understanding their ancestral physiological roles could inform the development of strategies to subvert their activity. In this study, we investigated the response of  Acinetobacter baumannii  to polyamines, a widespread, abundant class of amino acid-derived metabolites, which led us to identify long-chain polyamines as natural substrates of the disinfectant efflux pump AmvA. Loss of  amvA  dramatically reduced tolerance to long-chain polyamines, and these molecules induce expression of  amvA  through binding to its cognate regulator AmvR. A second clinically-important efflux pump, AdeABC, also contributed to polyamine tolerance. Our results suggest that the disinfectant resistance capability that allows  A. baumannii  to survive in hospitals may have evolutionary origins in the transport of polyamine metabolites.

The Acinetobacter baumannii disinfectant resistance protein, AmvA, is a spermidine and spermine efflux pump