Cooperation, competition and antibiotic resistance in bacterial colonies

Bacteria commonly live in dense and genetically diverse communities associated with surfaces. In these communities, competition for resources and space is intense, and yet we understand little of how this affects the spread of antibiotic-resistant strains. Here, we study interactions between antibio...

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Bibliographic Details
Published in:The ISME Journal 2018-06, Vol.12 (6), p.1582-1593
Main Authors: Frost, Isabel, Smith, William P J, Mitri, Sara, Millan, Alvaro San, Davit, Yohan, Osborne, James M, Pitt-Francis, Joe M, MacLean, R Craig, Foster, Kevin R
Format: Article
Language:English
Subjects:
Anti-Bacterial Agents - pharmacology
Antibiotic resistance
Antibiotics
Bacteria
beta-Lactamases - metabolism
Biodegradation
Biological Physics
Carbenicillin
Carbenicillin - chemistry
Colonies
Communities
Competition
Computer Simulation
Drug resistance
Drug Resistance, Microbial
Ecology, environment
Elongation
Life Sciences
Opportunist infection
Physics
Plasmids - metabolism
Pseudomonas aeruginosa
Pseudomonas aeruginosa - drug effects
Pseudomonas aeruginosa - physiology
Strains (organisms)
Streptomycin
Streptomycin - pharmacology
Symbiosis
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Summary:Bacteria commonly live in dense and genetically diverse communities associated with surfaces. In these communities, competition for resources and space is intense, and yet we understand little of how this affects the spread of antibiotic-resistant strains. Here, we study interactions between antibiotic-resistant and susceptible strains using in vitro competition experiments in the opportunistic pathogen Pseudomonas aeruginosa and in silico simulations. Selection for intracellular resistance to streptomycin is very strong in colonies, such that resistance is favoured at very low antibiotic doses. In contrast, selection for extracellular resistance to carbenicillin is weak in colonies, and high doses of antibiotic are required to select for resistance. Manipulating the density and spatial structure of colonies reveals that this difference is partly explained by the fact that the local degradation of carbenicillin by β-lactamase-secreting cells protects neighbouring sensitive cells from carbenicillin. In addition, we discover a second unexpected effect: the inducible elongation of cells in response to carbenicillin allows sensitive cells to better compete for the rapidly growing colony edge. These combined effects mean that antibiotic treatment can select against antibiotic-resistant strains, raising the possibility of treatment regimes that suppress sensitive strains while limiting the rise of antibiotic resistance. We argue that the detailed study of bacterial interactions will be fundamental to understanding and overcoming antibiotic resistance.
ISSN:1751-7362
1751-7370
DOI:10.1038/s41396-018-0090-4