Evolutionary pathways to antibiotic resistance are dependent upon environmental structure and bacterial lifestyle
Abstract
Bacterial populations vary in their stress tolerance and population structure depending upon whether growth occurs in well-mixed or structured environments. We hypothesized that evolution in biofilms would generate greater genetic diversity than well-mixed environments and lead to different pathways of antibiotic resistance. We used experimental evolution and whole genome sequencing to test how the biofilm lifestyle influenced the rate, genetic mechanisms, and pleiotropic effects of resistance to ciprofloxacin in Acinetobacter baumannii populations. Both evolutionary dynamics and the identities of mutations differed between lifestyle. Planktonic populations experienced selective sweeps of mutations including the primary topoisomerase drug targets, whereas biofilm-adapted populations acquired mutations in regulators of efflux pumps. An overall trade-off between fitness and resistance level emerged, wherein biofilm-adapted clones were less resistant than planktonic but more fit in the absence of drug. However, biofilm populations developed collateral sensitivity to cephalosporins, demonstrating the clinical relevance of lifestyle on the evolution of resistance.
Data availability
Sequencing data were deposited to NCBI as Bioproject 485123.R code for filtering and data processing can be found here:https://github.com/sirmicrobe/U01_allele_freq_code.
Article and author information
Author details
Funding
National Institutes of Health (U01AI124302-01)
- Vaughn S Cooper
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2019, Santos-Lopez et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Further reading
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The way that bacteria grow – either floating in liquid or attached to a surface – affects their ability to evolve antimicrobial resistance and our ability to treat infections.
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