mGem: Antibiotic tolerance across the growth-rate continuum in chronic human infections
- 1Center for Microbial Dynamics and Infection, School of Biological Sciences, Georgia Institute of Technology
Abstract
Antibiotic failure is frequently attributed to genetic resistance, yet many chronic infections persist despite clinical isolates remaining susceptible to antibiotics. Antibiotic tolerance offers an alternative explanation, but is commonly interpreted through persisters, dormancy, and growth arrest. We argue this theory is incomplete. In vitro studies consistently demonstrate that growth rate strongly influences antibiotic susceptibility, while bacteria in chronic human infections occupy a broad continuum of growth states. However, experimental models of tolerance largely examine rapidly growing or growth-arrested bacteria and rarely encompass the substantially slower growth rates found in chronic infection. We propose that tolerance can emerge from stochastic growth-rate heterogeneity within clonal populations without requiring transition into dormancy. Thus, understanding tolerance requires defining how antibiotic survival changes across the growth-rate continuum. Further studies directly examining antibiotic tolerance at slow growth rates representative of chronic infection are needed to understand tolerance during human infection.
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BibTeX
@article{roberts2026mgem,
title = {{mGem: Antibiotic tolerance across the growth-rate continuum in chronic human infections}},
author = {Bethan Roberts and Sam P. Brown and Stephen P. Diggle and Marvin Whiteley},
journal = {mBio},
year = {2026},
month = oct,
doi = {10.1128/mbio.01926-26},
url = {https://journals.asm.org/doi/10.1128/mbio.01926-26},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - mGem: Antibiotic tolerance across the growth-rate continuum in chronic human infections
AU - Bethan Roberts
AU - Sam P. Brown
AU - Stephen P. Diggle
AU - Marvin Whiteley
PY - 2026
DA - 2026/10/23
JO - mBio
DO - 10.1128/mbio.01926-26
UR - https://journals.asm.org/doi/10.1128/mbio.01926-26
AB - Antibiotic failure is frequently attributed to genetic resistance, yet many chronic infections persist despite clinical isolates remaining susceptible to antibiotics. Antibiotic tolerance offers an alternative explanation, but is commonly interpreted through persisters, dormancy, and growth arrest. We argue this theory is incomplete. In vitro studies consistently demonstrate that growth rate strongly influences antibiotic susceptibility, while bacteria in chronic human infections occupy a broad continuum of growth states. However, experimental models of tolerance largely examine rapidly growing or growth-arrested bacteria and rarely encompass the substantially slower growth rates found in chronic infection. We propose that tolerance can emerge from stochastic growth-rate heterogeneity within clonal populations without requiring transition into dormancy. Thus, understanding tolerance requires defining how antibiotic survival changes across the growth-rate continuum. Further studies directly examining antibiotic tolerance at slow growth rates representative of chronic infection are needed to understand tolerance during human infection.
SN - 2150-7511
ER -