| Feature . | Class I . | Class II . |
|---|---|---|
| Growth state of bacterial population | Most cells replicating | Most cells not replicating |
| Persistence phenotype | Small minority; different cells tolerate different antibiotics | Large majority; same cells tolerate many antibiotics |
| Inducers of persistence | Unknown; stochastic | Acidification, ROS, RNS, hypoxia, deprivation of C, N, P, or Fe; sublethal exposure to antibiotics |
| Speculative mechanisms | Epigenetic, transcriptional, translational, or posttranslational expression or suppression of any process for which genetic change can produce heritable resistance | Decreased uptake, increased export, or increased catabolism of drug; metabolic stress leading to oxidative stress and adaptation; increase in proteostasis pathways; preferential transcription and translation; alternate respiratory pathways and electron acceptors |
| Therapeutic implications | Combine different drugs that each reach the sites of infection | Include new kinds of drugs active on nonreplicating cells that reach the sites of infection |
| Feature . | Class I . | Class II . |
|---|---|---|
| Growth state of bacterial population | Most cells replicating | Most cells not replicating |
| Persistence phenotype | Small minority; different cells tolerate different antibiotics | Large majority; same cells tolerate many antibiotics |
| Inducers of persistence | Unknown; stochastic | Acidification, ROS, RNS, hypoxia, deprivation of C, N, P, or Fe; sublethal exposure to antibiotics |
| Speculative mechanisms | Epigenetic, transcriptional, translational, or posttranslational expression or suppression of any process for which genetic change can produce heritable resistance | Decreased uptake, increased export, or increased catabolism of drug; metabolic stress leading to oxidative stress and adaptation; increase in proteostasis pathways; preferential transcription and translation; alternate respiratory pathways and electron acceptors |
| Therapeutic implications | Combine different drugs that each reach the sites of infection | Include new kinds of drugs active on nonreplicating cells that reach the sites of infection |
Based on Nathan (2012) and modified from Nathan and Barry (2015).