Large tandem chromosome duplications facilitate niche adaptation during persistent infection with drug-resistant Staphylococcus aureus

Bacterial antibiotic resistance is an increasingly serious global problem. It is well known that resistance gene acquisition or small changes in specific bacterial genes called point mutations can lead to antibiotic resistance. In this study we reveal yet another means by which the hospital superbug Staphylococcus aureus is evading our best antibiotic treatments. We have discovered that during human infection the bacterium makes multiple copies of additional segements of its DNA, increasing the number of genes in specific sections of its chromosome. We show that such gene expansion helps S. aureus to beat the last-line antibiotic vancomycin and evade human immune responses. This study reveals yet another tool in the arsenal of S. aureus that helps explain why it is such a formidable pathogen and often so difficult to treat.