The problem
An antibiotic can kill most bacteria in a culture while a small fraction survives. After the drug is removed, those survivors can regrow into a population that the same drug can still kill under the same conditions. This is antibiotic persistence. Which cell states let these bacteria survive, and which of those states matter during an infection?[1] [2]
A bacterial population exposed to a killing antibiotic can lose most of its cells quickly yet retain a slower-killed minority. What physiological states produce that minority, and how are they generated during infection?
The minimum inhibitory concentration, or MIC, measures the concentration that prevents visible growth under specified conditions. Resistance raises this threshold. Tolerance concerns survival time without an increased MIC; persistence concerns unequal killing within a population. A survival curve with a slow tail is a starting observation. Regrowing survivors and exposing their descendants again helps distinguish this phenotype from selection of resistant bacteria.
One Salmonella study followed fluorescently marked bacteria after macrophages engulfed them. Uptake rapidly generated nonreplicating persisters, linked to acidic and nutrient-poor conditions inside the cell. Some remained metabolically active and later resumed growth. This supplies a particular route to survival, rather than making inactivity the definition of every persister.[1] [2] [3]
Scope
Phenotypic persistence during antibiotic treatment, especially how heterogeneous bacterial states and host conditions generate survival.
What remains open
Why it matters
Preventing growth and killing every surviving cell are different outcomes. A test that asks whether bacteria can grow in a drug may miss a small group that survives without growing. That distinction matters when researchers investigate why an infection returns, without assuming that persistence explains every treatment failure.[1] [2]
The same growth-inhibition result can hide very different killing behavior. Connecting the survival curve to cell physiology and the host niche helps researchers distinguish a resistant strain, a tolerant population and a persistent minority. It also identifies what an experiment would need to change and measure to test a survival mechanism. This is a basis for studying recurrent infection, not a treatment recommendation or an established way to eliminate persisters.[1] [2] [3]
Definitions
2 terms
antibiotic persistence
Unequal survival in a bacterial population exposed to a killing antibiotic: a subset is killed much more slowly than the majority without an increased growth-resistance threshold. The label describes a phenotype, not one universal cell state.[1]
minimum inhibitory concentration
The lowest antibiotic concentration that prevents visible growth under specified assay conditions, usually abbreviated MIC. It measures growth inhibition; survival time during exposure is a different measurement.[1]
Sources
- Definitions and guidelines for research on antibiotic persistence
Notes on Definitions and guidelines for research on antibiotic persistence
Consensus definitions distinguish growth resistance, population tolerance and heterogeneous persistence. Surviving cells and regrown descendants must be tested; dormancy is not the definition.
- Bacterial heterogeneity and antibiotic persistence: bacterial mechanisms utilized in the host environment
Notes on Bacterial heterogeneity and antibiotic persistence: bacterial mechanisms utilized in the host environment
Reviews host stressors and niche-dependent persistence; mechanisms established in culture need testing in hosts.
- Internalization of Salmonella by Macrophages Induces Formation of Nonreplicating Persisters
Notes on Internalization of Salmonella by Macrophages Induces Formation of Nonreplicating Persisters
Fluorescent single-cell experiments link macrophage uptake to nonreplicating Salmonella persisters and later regrowth; a restricted host-cell model rather than a universal persister mechanism.