[6] Recognition of bacterial persister cells dates back to 1944 when Joseph Warwick Bigger, an Irish physician working in England, was experimenting with the recently discovered penicillin.
Persister cells have entered a non-growing, or extremely slow-growing physiological state which makes them tolerant (insensitive or refractory) to the action of antimicrobials.
[2][5] The bacteria species Listeria monocytogenes, the main causal agent of listeriosis, has been shown to demonstrate persistence during infection in hepatocyte and trophoblast cells.
The usual active lifestyle can change and the bacteria can remain in intracellular vacuoles entering into a slow non-growing state of persistence thus promoting their survival from antibiotics.
Resistance is caused by newly acquired genetic traits (by mutation or horizontal gene transfer) that are heritable and confer the ability to grow at elevated concentrations of antibiotics.
[2][7][10] The molecular mechanisms that underlie persister cell formation, and antimicrobial tolerance are largely unknown.
[18] Owing to their transient nature and relatively low abundance, it is hard to isolate persister cells in sufficient numbers for experimental characterization, and only a few relevant genes have been identified to date.
[20] Persister cells in E. coli can transport intracellular accumulations antibiotic using an energy requiring efflux pump called TolC.
[22] In response to antifungals, fungal persister cells activate stress-response pathways, and two stress-protective molecules – glycogen, and trehalose accumulate in large amounts.