RESUMO
Staphylococcus aureus is a pathogen that causes critical diseases, such as pneumonia, endocarditis, and bacteremia, upon gaining access to the bloodstream of the host. Because host innate immunity alone cannot fight against this rapidly expanding pathogen, the use of antibiotic agents is necessary to clear out S. aureus. However, sub-populations of S. aureus fail to respond to the antibiotics resulting in ineffective clearance of the bacteria. One mechanism by which S. aureus does not respond to the antibiotics is by developing resistance through alterations in its genetic makeup, and genetic studies have revealed a major portion of mechanisms that are responsible for the rise of these antibiotic-resistant strains. Another sub-population that fails to respond to the antibiotics is called persister cells. There is a mounting clinical evidence that these persister cells significantly contribute to the antibiotic failure and persistent infection, but a clear mechanistic picture of the formation of the S. aureus persister cells is unavailable. This review focuses on drawing out a mechanistic map of factors that contribute to the formation of S. aureus persister cells. Understanding the mechanism will provide future direction for the development of novel antibiotic strategies to more efficiently tackle infections caused by S. aureus.
