Emergence of persister cells in Staphylococcus aureus: calculated or fortuitous move?

A stable but reversible phenotype switch from normal to persister state is advantageous to the intracellular pathogens to cause recurrent infections and to evade the host immune system. Staphylococcus aureus is a versatile opportunistic pathogen known to cause chronic infections with significant mortality. One of the notable features is the ability to switch to a per-sisters cell, which is found in planktonic and biofilm states. This phenotypic switch is always an open question to explore the hidden fundamental science that coheres with a calculated or fortuitous move. Toxin-antitoxin modules, nutrient stress, and an erroneous translation-enabled state of dormancy entail this persistent behaviour in S. aureus. It is paramount to get a clear picture of why the cell chooses to enter a persistent condition, as it would decide the course of treatment. Analyzing the exit from a persistent state to an active state and the subsequent repercussion of this transition is essential to determine its role in chronic infections. This review attempts to provide a constructed argument discussing the most widely accepted mechanisms and identifying the various attributes of persistence.

Automated summary

A stable but reversible phenotype switch from normal to persister state is advantageous to the intracellular pathogens to cause recurrent infections and to evade the host immune system. Staphylococcus aureus is a versatile opportunistic pathogen known to cause chronic infections with significant mortality. One of the notable features is the ability to switch to a per-sisters cell, which is found in planktonic and biofilm states. This review attempts to provide a constructed argument discussing the most widely accepted mechanisms and identifying the various attributes of persistence.