A new study challenges a long-standing assumption about how bacteria survive antibiotic treatment. Researchers have found that, in some cases, rapidly growing bacterial cells may be more likely to enter a drug-tolerant “persister” state than slow-growing ones.
Persister cells are a small subset of bacteria that can survive high doses of antibiotics without being genetically resistant. These cells are thought to contribute to chronic and recurring infections, as they can “wake up” after treatment and repopulate.
Traditionally, scientists have associated persister formation with slow growth and stressful conditions, such as those found in stationary phase. However, the new study shows that this is not always the case.
Using detailed experiments tracking bacterial populations over time, the researchers found that in the pathogen Pseudomonas aeruginosa, peaks in persister formation can occur during periods of rapid growth, including early stages of the growth cycle.
In contrast, the commonly studied bacterium Escherichia coli largely followed the expected pattern, with persisters forming mainly in stationary phase. This highlights important differences between species and suggests that widely used model organisms may not fully capture the dynamics of clinically relevant pathogens.
Lead author Saran Davies says:
“Our results show that persistence is not simply a response to slow growth. Instead, it appears to be linked to the internal state of cells — such as their metabolic activity and division history.”
The study found that higher metabolic activity and increased variability between cells were associated with earlier peaks in persister formation. These findings suggest that persistence may emerge from complex, dynamic processes within growing populations rather than a single uniform mechanism.
This work has important implications for treating infections. If persister cells can arise during rapid growth, antibiotic strategies that target actively dividing bacteria may not be sufficient on their own.
More broadly, the findings contribute to an ongoing debate about whether persistence is an adaptive survival strategy or a by-product of cellular processes. By revealing how persister formation varies across growth conditions and species, the study provides a new framework for understanding — and ultimately combating — antibiotic tolerance.
To read more about this research, published in JOURNAL, visit: https://royalsocietypublishing.org/rspb/article/293/2069/20253285/481406
