The eagle effect and antibiotic-induced persistence: two sides of the same coin?
Abstract
The Eagle effect describes a phenomenon in which bacteria or fungi exposed to concentrations of antibiotic higher than an optimal bactericidal concentration (OBC) have paradoxically improved levels of survival than at the OBC due to a decreased net rate of cell death. Despite extensive observational reports of this effect in different microorganisms, its underlying mode of action is not well understood. Although aspects of the Eagle effect resemble persistence, there is strong evidence that these phenomena are substantially different phenotypic responses to antibiotic treatment. We present an overview of the microorganism and antimicrobial combinations in which the Eagle effect has been observed. Proposed underlying mechanism(s) are assessed, and the Eagle effect and microbial persistence are compared and contrasted. The clinical relevance of the Eagle effect is reviewed, incorporating evidence from experimental in vitro and in vivo studies, as well as clinical reports.
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Cell wall remodeling contributes to echinocandin tolerance, with changes in β-glucan synthesis or increased production of compensatory components like chitin strengthening the cell wall and reducing drug efficacy.
“Cell wall remodeling contributes to echinocandin tolerance, with changes in β-glucan synthesis or increased production of compensatory components, like chitin, strengthening the cell wall and reducing drug efficacy [118,119].”
From Insight into the Mechanisms and Clinical Relevance of Antifungal Heteroresistance (2025) · cites this paper as [119]
The paradoxical effect, also known as the Eagle effect, often observed with echinocandins may be confused with antifungal persistence because the drugs show reduced activity in vitro at higher concentrations.
“Notably, the paradoxical effect, also known as the “Eagle effect”, often observed in echinocandins may confused with antifungal persistence, as the drugs show reduced activity in vitro at higher concentrations [40,41].”
From Antifungal persistence: Clinical relevance and mechanisms (2025) · cites this paper as [41]
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References 133 · Cited by 101
- Authors
- Prasetyoputri, A., Jarrad, A. M., Cooper, M. A., & Blaskovich, M. A. T.
- Affiliations
- The University of Queensland (AU)
- Helmholtz Centre for Infection Research (DE)
- Corresponding author
- Blaskovich, Mark A.T.
- Venue
- Trends in Microbiology
- Publisher
- Elsevier BV
- Published
- 2019-04
- Volume
- 27
- Issue
- 4
- Pages
- 339-354
- ISSN
- 0966-842X (ISSN-L)
- OpenAlex
- W2901881548
- Cited by
- 101
- References
- 133
- Citations by year
- 2026: 18 · 2025: 23 · 2024: 14 · 2023: 12 · 2022: 13 · 2021: 11 · 2020: 7 · 2019: 3
- FWCI
- 0.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Microbiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Australia Awards Scholarship
- Ludwig Leichhardt Memorial Fellowship of the Alexander von Humboldt Foundation
- NHMRC Principal Research Fellowship (APP1059354, APP631632, APP1026922, APP1063214)
- Wellcome Trust Strategic Award (104797/Z/14/Z)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Health Sciences › Medicine › Pharmacology › Antibiotics Pharmacokinetics and Efficacy
- Keywords
- microbial persistence, subinhibitory antibiotic concentrations, bacterial survival, fungal survival, antibiotic mechanism of action
- MeSH terms
- Animals, Anti-Infective Agents, Bacteria, Dose-Response Relationship, Drug, Drug Combinations, Drug Tolerance, Fungi, Humans, Microbial Sensitivity Tests, Gene Expression Regulation, Bacterial, Drug Resistance, Bacterial
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