K homeostasis is important for survival of Acinetobacter baumannii ATCC 19606 in the nosocomial environment.

Pathogenic bacteria have developed several mechanisms to thrive within the hostile environment of the human host, but it is often disregarded that their survival outside this niche is crucial for their successful transmission. Acinetobacter baumannii is very well adapted to both the human host and the hospital environment. The latter is facilitated by multifactorial mechanisms including its outstanding ability to survive on dry surfaces, its high metabolic diversity, and, of course, its remarkable osmotic resistance. As a first response to changing osmolarities, bacteria accumulate K in high amount to counterbalance the external ionic strength. Here, we addressed whether K uptake is involved in the challenges imposed by the harsh conditions outside its host and how K import influences the antibiotic resistance of A. baumannii. For this purpose, we used a strain lacking all major K importer ∆kup∆trk∆kdp. Survival of this mutant was strongly impaired under nutrient limitation in comparison to the wild type. Furthermore, we found that not only the resistance against copper but also against the disinfectant chlorhexidine was reduced in the triple mutant compared to the wild type. Finally, we revealed that the triple mutant is highly susceptible to a broad range of antibiotics and antimicrobial peptides. By studying mutants, in which the K transporter were deleted individually, we provide evidence that this effect is a consequence of the altered K uptake machinery. Conclusively, this study provides supporting information on the relevance of K homeostasis in the adaptation of A. baumannii to the nosocomial environment.