Staphylococcus aureus and Staphylococcus epidermis were experimentally evolved to have increased resistance to the antimicrobial skin lipid D-sphingosine.

Staphylococci are opportunistic pathogens, frequently causing skin, soft tissue and implanted medical device infection. Their ability to colonise human skin and epithelial surfaces is strongly linked to their capability to cause infections, with the majority of infections caused by a staphylococci from the patients own microflora. Understanding factors that promote skin colonisation may therefore provide opportunities to prevent infection. Many of the lipids produced by skin are antimicrobial to staphylococci. Here, we evolved two species of staphylococci, Staphylococcus aureus and Staphylococcus epidermis, to have increased resistance to the strongly antimicrobial lipid D-sphingosine. Whole-genome sequencing of these evolved isolates revealed mechanisms of resistance against these antimicrobial lipids, including a putative lipid efflux pump.