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36 results for “evolution of antibiotic resistance”
Data supporting "Antibiotic dose and nutrient availability differentially drive the evolution of antibiotic resistance and persistence"
<p>Data supporting </p> <p><strong>Antibiotic dose and nutrient availability differentially drive the evolution of antibiotic resistance and persistence </strong></p> <p>E. M. Windels, L. Cool, E. Persy, J. Swinnen, P. Matthay, B. Van den Bergh, T. Wenseleers, J. Michiels</p> <p>Version April 16th, 2024</p>
GENOMIC INSIGHTS INTO THE GLOBAL EVOLUTION AND ANTIBIOTIC RESISTANCE OF THE MYCOBACTERIUM TUBERCULOSIS COMPLEX
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Processed data for Evidence of horizontal gene transfer and environmental selection impacting antibiotic resistance evolution in soil-dwelling Listeria
<p>Processed/source data for the manuscript Evidence of horizontal gene transfer and environmental selection impacting antibiotic resistance evolution in soil-dwelling <em>Listeria</em>.</p>
Data from: Phenotypic plasticity of antibiotic resistance, metabolism byproduct utilization and the evolution of mutually beneficial cooperation in Escherichia coli
<p><span>Although tag-based donation and recognition have well explained how the cooperative individuals are positively assorted if the cooperative individuals possess some signals and are also able to detect such signals, an additional mechanism is required to explain why some individuals pay the costs of evolving such a tag that may not be rewarded subsequently, and how such tag-based cooperative individuals will meet other similar individuals with a very low mutation rate. Here, we show that many and even all<em> Escherichia coli </em>bacteria cells in the increased antibiotic concentration will plastically evolve to be antibiotic resistant individuals who could protect antibiotic sensitive strain from the attack of antibiotics, and the antibiotic resistant strain could reversibly evolve to be antibiotic sensitive in non-antibiotic supplement medium but in a harsher environment with low glucose. A further experiment showed that antibiotic-sensitive <em>E. coli </em>strain could in turn help reduce the concentration of indole produced by the resistant strain. This metabolic product is harmful to the growth of the antibiotic-resistant strain but benefits the antibiotic-sensitive strain by helping turn on the multi-drug exporter to discharge the antibiotic. The utilization of metabolism byproduct indole produced by antibiotic-resistant cells benefits antibiotic-sensitive cells, while the indole-absorbing service of antibiotic sensitive cells unconsciously help in nullifying the indole side effect on antibiotic resistant strain, and a mutual benefit cooperation could therefore evolve.</span></p>
Data from: Phenotypic plasticity of antibiotic resistance, metabolism byproduct utilization and the evolution of mutually beneficial cooperation in Escherichia coli
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Data from: Historical contingency in the evolution of antibiotic resistance after decades of relaxed selection
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Antibiotic interactions shape short-term evolution of resistance in Enterococcus faecalis
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Data from: Cross-feeding constrains the evolution of antibiotic resistance in <em>Escherichia coli</em>
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Evolution of honey resistance in experimental populations of bacteria depends on the type of honey, and has no major side effects for antibiotic susceptibility
<p><span><span><span><span><span><span><span><span><span><span><span>With rising antibiotic resistance, alternative treatments for communicable diseases are increasingly relevant. One possible alternative for some types of infections is honey, used in wound care since before 2000 BCE and more recently in licensed, medical-grade products. However, it is unclear whether medical application of honey results in the evolution of bacterial honey resistance, and whether this has collateral effects on other bacterial traits such as antibiotic resistance. Here, we used single-step screening assays and serial transfer at increasing concentrations to isolate honey-resistant mutants of <i>Escherichia coli</i>. We only detected bacteria with consistently increased resistance to the honey they evolved in with two of the four tested honey products, and the observed increases were small (maximum two-fold increase in IC<sub>90</sub>). Genomic sequencing and experiments with single-gene knockouts showed a key mechanism by which bacteria increased their honey resistance was by mutating genes involved in detoxifying methylglyoxal, which contributes to the antibacterial activity of <i>Leptospermum</i> honeys. Crucially, we found no evidence that honey adaptation conferred cross-resistance or collateral sensitivity against nine antibiotics from six different classes. These results reveal constraints on bacterial adaptation to different types of honey, improving our ability to predict downstream consequences of wider honey application in medicine.</span></span></span></span></span></span></span></span></span></span></span></p>
Assemblies for 'Mixed strain pathogen populations accelerate the evolution of antibiotic resistance in patients'
<p>Antibiotic resistance poses a global health threat, but the within-host drivers of resistance remain poorly understood. Pathogen populations are often assumed to be clonal within hosts, and resistance is thought to emerge due to selection for de novo variants. Here we show that mixed strain populations are common in the opportunistic pathogen <i>P. aeruginosa</i>. Crucially, resistance evolves rapidly in patients colonized by multiple strains through selection for pre-existing resistant strains. In contrast, resistance evolves sporadically in patients colonized by single strains due to selection for novel resistance mutations. However, strong trade-offs between resistance and growth rate occur in mixed strain populations, suggesting that within-host diversity can also drive the loss of resistance in the absence of antibiotic treatment. In summary, we show that the within-host diversity of pathogen populations plays a key role in shaping the emergence of resistance in response to treatment.</p>
Data for: Host-specific plasmid evolution explains the variable spread of clinical antibiotic-resistance plasmids
<p><span>Antibiotic resistance encoded on plasmids is a pressing global health problem. Predicting which plasmids spread in the long term remains very challenging, even though some key parameters influencing plasmid stability have been identified, such as plasmid growth costs and horizontal transfer rates. Here, we show these parameters evolve in a strain-specific way among clinical plasmids and bacteria, and this occurs rapidly enough to alter the relative likelihoods of different bacterium-plasmid combinations spreading. We used experiments with <em>Escherichia</em> <em>coli</em> and antibiotic-resistance plasmids isolated from patients, paired with a mathematical model, to track long-term plasmid stability (beyond antibiotic exposure). Explaining variable stability across six bacterium-plasmid combinations required accounting for evolutionary changes in plasmid-stability traits, whereas initial variation of these parameters </span><span>was a relatively poor predictor of long-term outcomes</span><span>. Evolutionary trajectories were specific to particular bacterium-plasmid combinations, as evidenced by genome sequencing and genetic manipulation. This revealed epistatic (here, strain-dependent) effects of key genetic changes affecting horizontal plasmid transfer. Several genetic changes involved mobile elements and pathogenicity islands. Rapid strain-specific evolution can thus outweigh ancestral phenotypes as a predictor of plasmid stability. Accounting for strain-specific plasmid evolution in natural populations could improve our ability to anticipate and manage successful bacterium-plasmid combinations.</span></p>
Evolution of honey resistance in experimental populations of bacteria depends on the type of honey, and has no major side effects for antibiotic susceptibility
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Data for: Host-specific plasmid evolution explains the variable spread of clinical antibiotic-resistance plasmids
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Data from: Fight evolution with evolution: plasmid-dependent phages with a wide host range prevent the spread of antibiotic resistances
The emergence of pathogenic bacteria resistant to multiple antibiotics is a serious worldwide public health concern. Whenever antibiotics are applied, the genes encoding for antibiotic resistance are selected for within bacterial populations. This has led to the prevalence of conjugative plasmids that carry resistance genes and can transfer themselves between diverse bacterial groups. In this study, we investigated whether it is feasible to attempt to prevent the spread of antibiotic resistances with a lytic bacteriophage, which can replicate in a wide range of gram-negative bacteria harboring conjugative drug-resistance conferring plasmids. The counter-selection against the plasmid was shown to be effective, reducing the frequency of multi-resistant bacteria that formed via horizontal transfer by several orders of magnitude. This was true also in the presence of an antibiotic against which the plasmid provided resistance. Majority of the multi-resistant bacteria subjected to phage selection also lost their conjugation capability. Overall this study suggests that, while we are obligated to maintain the selection for the spread of the drug resistances, the 'fight evolution with evolution' approach could help us even out the outcome to our favor.
Data from: Bypass of genetic constraints during mutator evolution to antibiotic resistance
Genetic constraints can block many mutational pathways to optimal genotypes in real fitness landscapes, yet the extent to which this can limit evolution remains to be determined. Interestingly, mutator bacteria elevate only specific types of mutations, and therefore could be very sensitive to genetic constraints. Testing this possibility is not only clinically relevant, but can also inform about the general impact of genetic constraints in adaptation. Here, we evolved 576 populations of two mutator and one wild-type Escherichia coli to doubling concentrations of the antibiotic cefotaxime. All strains carried TEM-1, a β-lactamase enzyme well known by its low availability of mutational pathways. Crucially, one of the mutators does not elevate any of the relevant first-step mutations known to improve cefatoximase activity. Despite this, both mutators displayed a similar ability to evolve more than 1000-fold resistance. Initial adaptation proceeded in parallel through general multi-drug resistance mechanisms. High-level resistance, in contrast, was achieved through divergent paths; with the a priori inferior mutator exploiting alternative mutational pathways in PBP3, the target of the antibiotic. These results have implications for mutator management in clinical infections and, more generally, illustrate that limits to natural selection in real organisms are alleviated by the existence of multiple loci contributing to fitness.
Data from: Modified antibiotic adjuvant ratios can slow and steer the evolution of resistance: Co-amoxiclav as a case study
As antibiotic resistance spreads, developing sustainable methods to restore the efficacy of existing antibiotics is increasingly important. One widespread method is to combine antibiotics with synergistically acting adjuvants that inhibit resistance mechanisms, allowing drug killing. Here we use co-amoxiclav (a clinically important combination of the -lactam antibiotic amoxicillin and the -lactamase inhibitor clavulanate) to ask whether treatment efficacy and resistance evolution can be decoupled via component dosing modifications. A simple mathematical model predicts that different ratios of these two drug components can produce distinct evolutionary responses irrespective of initial efficacy. We test this hypothesis by selecting Escherichia coli with a plasmid encoded -lactamase (CTX-M-14), against different compositions of amoxicillin and clavulanate. Consistent with our theory, we found that while resistance evolved under all conditions, the component ratio influenced both the rate and mechanism of resistance evolution. Specifically, we found that the current clinical practice of high amoxicillin to clavulanate ratios resulted in the most rapid adaptation to antibiotics via gene dosing responses. Increased plasmid copy number allowed E. coli to increase -lactamase dosing and effectively titrate out low quantities of clavulanate, restoring amoxicillin resistance. In contrast, high clavulanate ratios were more robust - plasmid copy number did not increase, although porin or efflux resistance mechanisms were found, as in all drug ratios. Our results indicate that by changing the ratio of adjuvant to antibiotic we can slow and steer the path of resistance evolution. We therefore suggest using increased adjuvant dosing regimens to slow the rate of resistance evolution.
Data from: Exposure to phages has little impact on the evolution of bacterial antibiotic resistance on drug concentration gradients
The use of phages for treating bacterial pathogens has recently been advocated as an alternative to antibiotic therapy. Here we test a hypothesis that bacteria treated with phages may show more limited evolution of antibiotic resistance as the fitness costs of resistance to phages may add to those of antibiotic resistance, further reducing the growth performance of antibiotic-resistant bacteria. We did this by studying the evolution of phage-exposed and phage-free Pseudomonas fluorescens cultures on concentration gradients of single drugs, including cefotaxime, chloramphenicol, and kanamycin. During drug treatment, the level of bacterial antibiotic resistance increased through time, and was not affected by the phage treatment. Exposure to phages did not cause slower growth in antibiotic-resistant bacteria, although it did so in antibiotic-susceptible bacteria. We observed significant reversion of antibiotic resistance after drug use being terminated, and the rate of reversion was not affected by the phage treatment. The results suggest that the fitness costs caused by resistance to phages are unlikely to be an important constraint on the evolution of bacterial antibiotic resistance in heterogeneous drug environments. Further studies are needed for the interaction of fitness costs of antibiotic resistance with other factors.
Data from: Antibiotic resistance correlates with transmission in plasmid evolution
Conjugative (horizontally transmissible) plasmids are autonomous replicators, whose 'self-interests' do not necessarily overlap with those of their hosts. This situation causes plasmids and bacteria to sometimes experience differing selection pressures. Escherichia coli plasmid pB15 contains genes for resistance to several antibiotics, including tetracycline. When plasmid-bearing cells were experimentally evolved in the laboratory, changes in resistance level in the unselected tetracycline marker coincided with changes in plasmid rates of vertical versus horizontal transmission. Here we used minimum-inhibitory assays that measure resistance levels as quantitative traits to determine phenotypic correlations among plasmid characters and to estimate divergence among plasmid lineages. Results suggested that plasmid-level evolution led to formation of two phenotypically-dissimilar groups: virulent (highly infectious) and avirulent (weakly infectious) plasmids. In contrast, measures of carbon-source utilization, and fitness assays relative to a common competitor revealed that bacterial hosts generally converged in phenotypic performance, despite divergence among their associated plasmids. Preliminary sequence analyses suggested that divergence in plasmid conjugation was due to altered configurations of a shufflon region (a site-specific recombination system), where genetic rearrangements affect conjugative ability. Furthermore, we proposed that correlated resistance and transmission in pB15 derivatives were caused by a tetracycline-resistance transposon inserted into a transfer operon, allowing transcription from its promoter to simultaneously affect both plasmid resistance and transmission.
The Evolution of Antibiotic Resistance in Europe, 1998-2019
<p>These data present antibiotic resistance and antibiotic consumption trends in Europe over two decades. The data on the antimicrobial resistance rates are released by the European Surveillance System - TESSy, provided by Finland, Sweden, Belgium, Germany, Greece, Ireland, Italy, Luxembourg, Netherlands, Norway, Portugal, United Kingdom, Austria, Bulgaria, Czech Republic, Denmark, Estonia, Spain, Malta, Slovenia, France, Croatia, Hungary, Poland, Slovakia, Romania, Cyprus, Latvia, Lithuania and released by the European Centre for Disease Prevention and Control (ECDC). The AMR data cover the years 1998-2019.</p> <p> </p> <p>Fields in summary_AMC_byclass.csv:</p> <p>class: ATC code of antibiotic class</p> <p>Country: country</p> <p>Year: year</p> <p>Sector: Community or Hospital</p> <p>Antimicrobial.Type: mode of consumption</p> <p>DDD: defined daily dose per 1000 inhabitant</p> <p>combC: combination of factors for data manipulation purpose</p> <p>Antibiotic_class: same as class</p> <p> </p> <p>Fields in summary_AMR_filtered.csv:</p> <p>Year: year</p> <p>Country: country</p> <p>Pathogen: bacterial species</p> <p>Antibiotic: antibiotic resistance tested</p> <p>patientType: INPAT for inpatient</p> <p>N_S: number of sensitive strains</p> <p>test: combination of factors for data manipulation purpose</p> <p>N_tested: number of strains tested</p> <p>N: total number of strains</p> <p>p: fraction resistant or intermediate</p> <p>ci_span: width of the binomial 95% confidence interval</p> <p>p_min: 2.5% confidence interval</p> <p>p_max: 97.5% confidence interval</p> <p>Antibiotic_long: long name of the antibiotic</p> <p>Antibiotic_class: antibiotic class</p> <p>Pathogen_long: long name of the bacterial species</p> <p>combR: combination of factors for data manipulation purpose</p> <p>N_I_R: number of intermediate and resistant strains</p> <p> </p> <p> </p> <p> </p> <p> </p>
Data from: Temporal variation in antibiotic environments slows down resistance evolution in pathogenic Pseudomonas aeruginosa
Antibiotic resistance is a growing concern to public health. New treatment strategies may alleviate the situation by slowing down the evolution of resistance. Here, we evaluated sequential treatment protocols using two fully independent laboratory-controlled evolution experiments with the human pathogen Pseudomonas aeruginosa PA14 and two pairs of clinically relevant antibiotics (doripenem/ciprofloxacin and cefsulodin/gentamicin). Our results consistently show that the sequential application of two antibiotics decelerates resistance evolution relative to monotherapy. Sequential treatment enhanced population extinction although we applied antibiotics at sub-lethal dosage. In both experiments, we identified an order-effect of the antibiotics used in the sequential protocol, leading to significant variation in the long-term efficacy of the tested protocols. These variations appear to be caused by asymmetric evolutionary constraints, whereby adaptation to one drug slowed down adaptation to the other drug, but not vice versa. An understanding of such asymmetric constraints may help future development of evolutionary robust treatments against infectious disease.
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