Antibiotic Persisters
Antibiotic Persisters - Related Videos
02:57
Assessing Intracellular Bacterial Persistence and Antibiotic Resistance in a Mouse Model
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2026
Source: Zhang, C., et al., Development and Assessment of Intracellular Infection Models for Staphylococcus aureus. J. Vis. Exp. (2025)The video demonstrates the isolation of kidneys containing Staphylococcus aureus-infected macrophages, followed by tissue homogenization to release intracellular bacteria. It quantifies bacterial persistence within macrophages in control and antibiotic-treated groups by counting colony-forming units.
05:02
Microfluidic Time-Lapse Microscopy to Study Antibiotic Persistence in Bacteria
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2025
Source: Oms, T., et al. Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli. J. Vis. Exp. (2023)This video presents a protocol for monitoring individual bacterial cells expressing a fluorescently labeled DNA-binding protein within a microfluidic system. It illustrates how antibiotics inhibit most cells, while a subpopulation of persister cells survives the treatment and regrows following antibiotic removal.
04:54
In Vitro Persister Assay: A Method to Evaluate the Effect of Osmolytes on Bacterial Persistence
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2025
In this video, we demonstrate a method to evaluate the effect of osmolytes on the formation of bacterial persisters. The bacterial cells are first exposed to osmolytes to induce osmotic stress, triggering persister formation, then treated with antibiotics to enumerate the persisters.
12:29
Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli
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Cited by 3 •
2023
Antibiotic persistence describes the ability of small subpopulations within a sensitive isogenic population to transiently tolerate high doses of bactericidal antibiotics. The present protocol combines approaches to characterize the antibiotic persistence phenotype at the molecular and cellular levels after exposing Escherichia coli to lethal doses of ofloxacin.
13:39
Antibiotic Susceptibility Testing: Epsilometer Tests to Determine MIC Values of Two Antibiotics and Evaluate Antibiotic Synergy
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2023
Source: Anna Bläckberg1, Rolf Lood1 1 Department of Clinical Sciences Lund, Division of Infection Medicine, Biomedical Center, Lund University, 221 00 Lund Sweden Knowledge of the interactions between antibiotics and bacteria is important in understanding how microbes evolve antibiotic resistance. In 1928, Alexander Fleming discovered penicillin, an antibiotic that exerts its antibacterial function by interfering with cell wall regeneration (1). Other antibiotics with diverse mechanisms of...
FAQs
Reduced growth can make antibiotic action less effective because many drug targets and essential cellular processes become less active in the persister state. This creates a temporary survival condition rather than a permanent change in drug susceptibility. Once exposure ends, renewed activity allows surviving cells to resume growth, making the state especially important for recurrence.
The distinction is whether survival reflects a reversible physiological state or a heritable genetic change. Persisters tolerate treatment while in a low-growth state, then can produce a susceptible population after treatment stops. Heritable resistance, by contrast, is not the defining explanation for their survival. This distinction affects how researchers interpret treatment failure and relapse.
Studies focus on how persister formation is associated with bacterial stress responses and shifts toward low growth or dormancy. They also examine what happens when treatment ends, including the return to active growth. Linking these transitions helps explain why a small surviving fraction can regenerate bacteria that remain susceptible to antibiotics.
A supported approach is to examine bacterial survival during antibiotic exposure, then assess whether surviving cells resume growth after treatment is removed. Researchers can pair this analysis with investigation of formation, stress responses, and interactions with host defenses. Together, these observations distinguish temporary persistence from mechanisms associated with treatment failure and relapse.
Their importance extends beyond drug exposure because survival occurs within infections where bacterial cells encounter host defenses. Studying those interactions can clarify whether persister formation, stress responses, and host responses influence clearance. This context helps connect bacterial physiology with recurrent or difficult-to-clear infections, rather than treating persistence as an isolated laboratory phenomenon.
Combination strategies can pair antibiotics with therapies aimed at dormant cells or at their return to active growth. The rationale is to address both phases: survival during treatment and regrowth afterward. Such approaches are intended to reduce the reservoir that can repopulate an infection, offering a way to target treatment failure and relapse.