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78 results for “Cost of resistance”
Data from: Estimating costs of aphid resistance to parasitoids conferred by a protective strain of the bacterial endosymbiont Regiella insecticola
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Data from: Fitness costs of herbicide resistance across natural populations of the common morning glory, Ipomoea purpurea
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Data from: Soft selective sweeps in fungicide resistance evolution: recurrent mutations without fitness costs in grapevine downy mildew
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Data from: The fitness costs of antibiotic resistance mutations
Antibiotic resistance is increasing in pathogenic microbial populations and is thus a major threat to public health. The fate of a resistance mutation in pathogen populations is determined in part by its fitness. Mutations that suffer little or no fitness cost are more likely to persist in the absence of antibiotic treatment. In this review, we performed a meta-analysis to investigate the fitness costs associated with single mutational events that confer resistance. Generally, these mutations were costly, although several drug classes and species of bacteria on average did not show a cost. Further investigations into the rate and fitness values of compensatory mutations that alleviate the costs of resistance will help us to better understand both the emergence and management of antibiotic resistance in clinical settings.
Data from: Reverse evolution: selection against costly resistance in disease-free microcosm populations of Paramecium caudatum
Evolutionary costs of parasite resistance arise if genes conferring resistance reduce fitness in the absence of parasites. Thus, parasite-mediated selection may lead to increased resistance and a correlated decrease in fitness, whereas relaxed parasite-mediated selection may lead to reverse evolution of increased fitness and a correlated decrease in resistance. We tested this idea in experimental populations of the protozoan Paramecium caudatum and the parasitic bacterium Holospora undulata. After 8 years, resistance to infection and asexual reproduction were compared among paramecia from (i) infected populations, (ii) uninfected naive populations and (iii) previously infected, parasite-free (recovered) populations. Paramecia from infected populations were more resistant (+12%), but had lower reproduction (-15%) than naive paramecia, indicating an evolutionary trade-off between resistance and fitness. Recovered populations showed similar reproduction to naive populations; however, resistance of recently (<3 years) recovered populations was similar to paramecia from infected populations, while longer (>3 years) recovered populations were as susceptible as naive populations. This suggests a weak, convex trade-off between resistance and fitness, allowing recovery of fitness, without complete loss of resistance, favouring the maintenance of a generalist strategy of intermediate fitness and resistance. Our results indicate that (co)evolution with parasites can leave a genetic signature in disease-free populations.
Data from: Temperature-sensitive fitness cost of insecticide resistance in Chinese populations of the diamondback moth Plutella xylostella
Alleles conferring a higher adaptive value in one environment may have a detrimental impact on fitness in another environment. Alleles conferring resistance to pesticides and drugs provide textbook examples of this trade-off as, in addition to conferring resistance to these molecules, they frequently decrease fitness in pesticide/drug-free environments. We show here that resistance to chlorpyrifos, an organophosphate (OP), in Chinese populations of the diamondback moth, Plutella xylostella, is conferred by two mutations of ace1 – the gene encoding the acetylcholinesterase enzyme targeted by OPs – affecting the amino acid sequence of the corresponding protein. These mutations were always linked, consistent with the segregation of a single resistance allele, ace1R, carrying both mutations, in the populations studied. We monitored the frequency of ace1R (by genotyping more than 20 000 adults) and the level of resistance (through bioassays on more than 50 000 individuals) over several generations. We found that the ace1R resistance allele was costly in the absence of insecticide and that this cost was likely recessive. This fitness costs involved a decrease in fecundity: females from resistant strains laid 20% fewer eggs, on average, than females from susceptible strains. Finally, we found that the fitness costs associated with the ace1R allele were greater at high temperatures. At least two life history traits were involved: longevity and fecundity. The relative longevity of resistant individuals was affected only at high temperatures and the relative fecundity of resistant females – which was already affected at temperatures optimal for development – decreased further at high temperatures. The implications of these findings for resistance management are discussed.
Data from: Virus resistance is not costly in a marine alga evolving under multiple environmental stressors
Viruses are important evolutionary drivers of host ecology and evolution. The marine picoplankton Ostreococcus tauri has three known resistance types that arise in response to infection with the Phycodnavirus OtV5: susceptible cells (S) that lyse following viral entry and replication; resistant cells (R) that are refractory to viral entry; and resistant producers (RP) that do not all lyse but maintain some viruses within the population. To test for evolutionary costs of maintaining antiviral resistance, we examined whether O. tauri populations composed of each resistance type differed in their evolutionary responses to several environmental drivers (lower light, lower salt, lower phosphate and a changing environment) in the absence of viruses for approximately 200 generations. We did not detect a cost of resistance as measured by life-history traits (population growth rate, cell size and cell chlorophyll content) and competitive ability. Specifically, all R and RP populations remained resistant to OtV5 lysis for the entire 200-generation experiment, whereas lysis occurred in all S populations, suggesting that resistance is not costly to maintain even when direct selection for resistance was removed, or that there could be a genetic constraint preventing return to a susceptible resistance type. Following evolution, all S population densities dropped when inoculated with OtV5, but not to zero, indicating that lysis was incomplete, and that some cells may have gained a resistance mutation over the evolution experiment. These findings suggest that maintaining resistance in the absence of viruses was not costly.
Data from: Variation in costs of parasite resistance among natural host populations
Organisms that can resist parasitic infection often have lower fitness in the absence of parasites. These costs of resistance can mediate host evolution during parasite epidemics. For example, large epidemics will select for increased host resistance. In contrast, small epidemics (or no disease) can select for increased host susceptibility when costly resistance allows more susceptible hosts to outcompete their resistant counterparts. Despite their importance for evolution in host populations, costs of resistance (which are also known as resistance trade-offs) have mainly been examined in laboratory-based host-parasite systems. Very few examples come from field-collected hosts. Furthermore, little is known about how resistance trade-offs vary across natural populations. We addressed these gaps using the freshwater crustacean Daphnia dentifera and its natural yeast parasite, Metschnikowia bicuspidata. We found a cost of resistance in two of the five populations we studied – those with the most genetic variation in resistance and the smallest epidemics in the previous year. However, yeast epidemics in the current year did not alter slopes of these trade-offs before and after epidemics. In contrast, the no-cost populations showed little variation in resistance, possibly because large yeast epidemics eroded that variation in the previous year. Consequently, our results demonstrate variation in costs of resistance in wild host populations. This variation has important implications for host evolution during epidemics in nature.
Data from: The genetic basis of the fitness costs of antimicrobial resistance: a meta-analysis approach
The evolution of antibiotic resistance carries a fitness cost, expressed in terms of reduced competitive ability in the absence of antibiotics. This cost plays a key role in the dynamics of resistance by generating selection against resistance when bacteria encounter an antibiotic-free environment. Previous work has shown that the cost of resistance is highly variable, but the underlying causes remain poorly understood. Here, we use a meta-analysis of the published resistance literature to determine how the genetic basis of resistance influences its cost. We find that on average chromosomal resistance mutations carry a larger cost than acquiring resistance via a plasmid. This may explain why resistance often evolves by plasmid acquisition. Second, we find that the cost of plasmid acquisition increases with the breadth of its resistance range. This suggests a potentially important limit on the evolution of extensive multidrug resistance via plasmids. We also find that epistasis can significantly alter the cost of mutational resistance. Overall, our study shows that the cost of antimicrobial resistance can be partially explained by its genetic basis. It also highlights both the danger associated with plasmidborne resistance and the need to understand why resistance plasmids carry a relatively low cost.
Data from: Linking system-wide impacts of RNA polymerase mutations to the fitness cost of rifampin resistance in Pseudomonas aeruginosa
Fitness costs play a key role in the evolutionary dynamics of antibiotic resistance in bacteria by generating selection against resistance in the absence of antibiotics. Although the genetic basis of antibiotic resistance is well understood, the precise molecular mechanisms linking the genetic basis of resistance to its fitness cost remain poorly characterized. Here, we examine how the system-wide impacts of mutations in the RNA polymerase (RNAP) gene rpoB shape the fitness cost of rifampin resistance in Pseudomonas aeruginosa. Rifampin resistance mutations reduce transcriptional efficiency, and this explains 76% of the variation in fitness among rpoB mutants. The pleiotropic consequence of rpoB mutations is that mutants show altered relative transcript levels of essential genes. We find no evidence that global transcriptional responses have an impact on the fitness cost of rifampin resistance as revealed by transcriptome sequencing (RNA-Seq). Global changes in the transcriptional profiles of rpoB mutants compared to the transcriptional profile of the rifampin-sensitive ancestral strain are subtle, demonstrating that the transcriptional regulatory network of P. aeruginosa is robust to the decreased transcriptional efficiency associated with rpoB mutations. On a smaller scale, we find that rifampin resistance mutations increase the expression of RNAP due to decreased termination at an attenuator upstream from rpoB, and we argue that this helps to minimize the cost of rifampin resistance by buffering against reduced RNAP activity. In summary, our study shows that it is possible to dissect the molecular mechanisms underpinning variation in the cost of rifampin resistance and highlights the importance of genome-wide buffering of relative transcript levels in providing robustness against resistance mutations. IMPORTANCE Antibiotic resistance mutations carry fitness costs. Relative to the characteristics of their antibiotic-sensitive ancestors, resistant mutants show reduced growth rates and competitive abilities. Fitness cost plays an important role in the evolution of antibiotic resistance in the absence of antibiotics; however, the molecular mechanisms underlying these fitness costs is not well understood. We applied a systems-level approach to dissect the molecular underpinnings of the fitness costs associated with rifampin resistance in P. aeruginosa and showed that most of the variation in fitness cost can be explained by the direct effect of resistance mutations on the enzymatic activity of the mutated gene. Pleiotropic changes in transcriptional profiles are subtle at a genome-wide scale, suggesting that the gene regulatory network of P. aeruginosa is robust in the face of the direct effects of resistance mutations.
Data from: Lytic phages obscure the cost of antibiotic resistance in Escherichia coli
The long-term persistence of antibiotic-resistant bacteria depends on their fitness relative to other genotypes in the absence of drugs. Outside the laboratory, viruses that parasitize bacteria (phages) are ubiquitous, but costs of antibiotic resistance are typically studied in phage-free experimental conditions. We used a mathematical model and experiments with Escherichia coli to show that lytic phages strongly affect the incidence of antibiotic resistance in drug-free conditions. Under phage parasitism, the likelihood that antibiotic-resistant genetic backgrounds spread depends on their initial frequency, mutation rate and intrinsic growth rate relative to drug-susceptible genotypes, because these parameters determine relative rates of phage-resistance evolution on different genetic backgrounds. Moreover, the average cost of antibiotic resistance in terms of intrinsic growth in the antibiotic-free experimental environment was small relative to the benefits of an increased mutation rate in the presence of phages. This is consistent with our theoretical work indicating that, under phage selection, typical costs of antibiotic resistance can be outweighed by realistic increases in mutability if drug resistance and hypermutability are genetically linked, as is frequently observed in clinical isolates. This suggests the long-term distribution of antibiotic resistance depends on the relative rates at which different lineages adapt to other types of selection, which in the case of phage parasitism is probably extremely common, as well as costs of resistance inferred by classical in vitro methods.
The cost effectiveness of surgery for drug resistant temporal lobe epilepsy in the US
<p><strong>Objective:</strong> Surgery is an effective but costly treatment for many patients with drug resistant temporal lobe epilepsy (DR-TLE). We aim to evaluate whether, in the United States, 1) surgery is cost-effective compared to medical management for patients deemed surgical candidates, 2) surgical evaluation is cost-effective for DR-TLE patients in general.</p> <p><strong>Methods:</strong> We use a semi-Markov model to assess the cost-effectiveness of surgery and surgical evaluation over a lifetime horizon. We use 2<sup>nd</sup> order Monte Carlo simulations to conduct probabilistic sensitivity analyses to estimate variation in model output. We adopt both healthcare and societal perspectives, including direct healthcare costs (e.g. surgery, AEDs) and indirect costs (e.g. lost earnings by patients and care providers.) We compare incremental cost-effectiveness ratio (ICER) to societal willingness-to-pay (~$100,000 per Quality Adjusted Life Year) to determine whether surgery is cost-effective.</p> <p><strong>Results:</strong> Epilepsy surgery is cost effective compared to medical management in surgically eligible patients by virtue of being cost saving ($328K vs. 423K) and more effective (16.6 QALY vs. 13.6 QALY) than medical management in the long run. Surgical evaluation is cost-effective in DR-TLE patients even if the probability of being deemed a surgical candidate is only 5%. From a societal perspective, surgery becomes cost effective within 3 years and 89% of simulations favor surgery over the lifetime horizon.</p> <p><strong>Conclusion:</strong> For surgically eligible DR-TLE patients, surgery is cost-effective. For DR-TLE patients in general, referral for surgical evaluation (and possible subsequent surgery) is cost-effective. DR-TLE patients should be referred for surgical evaluation without hesitation on cost-effectiveness grounds.</p>
Individual and population level costs and health-related quality of life outcomes of third-generation cephalosporin resistant bloodstream infection in Malawi
<p>This file contains the original cleaned dataset used in the analysis</p>
Cost-Effectiveness Study Comparing Chlorhexidine Bathing With Active Surveillance Cultures to Prevent Methicillin-resistant Staphylococcus Aureus & Other Hospital Infections
ClinicalTrials.gov study NCT00779246. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Impact Of Bacterial Resistance On Healthcare Costs For Hospitalized Patients With Complicated Intra-Abdominal Infections
ClinicalTrials.gov study NCT00929643. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Data from: Costs of CRISPR-Cas mediated resistance in Streptococcus thermophilus
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Data from: Costs of resistance and infection by a generalist pathogen
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Data from: The cost of phage resistance in a plant pathogenic bacterium is context-dependent
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Data from: Fitness costs of key point mutations that underlie acaricide target-site resistance in the two-spotted spider mite Tetranychus urticae
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Data from: The effectiveness and costs of pathogen resistance strategies in a perennial plant
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Allen Brain Atlas
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DANDI Archive for NWB datasets
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International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.