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78 results for “Cost of resistance”
Data from: Costs of antibiotic resistance genes depend on host strain and environment and can influence community composition
<p>Antibiotic resistance genes (ARGs) benefit host bacteria in environments containing corresponding antibiotics, but it is less clear how they are maintained in environments where antibiotic selection is weak or sporadic. In particular, few studies have measured the effect of ARGs on host fitness in the absence of direct selection or determined if any costs are fixed or depend on the host strain, perhaps marking some ARG-host combinations as reservoirs that can maintain ARGs in the absence of antibiotic selection. We quantified the fitness effects of six ARGs in 11 diverse <em>Escherichia spp</em>. strains. Three ARGs (blaTEM-116, cat, and dfrA5, encoding resistance to β-lactams, chloramphenicol, and trimethoprim, respectively) imposed an overall cost but all ARGs had an effect in at least one host strain, reflecting a significant strain interaction effect. A simulation predicts these interactions cause the success of ARGs to depend on available host strains, and, to a lesser extent, for successful host strains to depend on the ARGs present in a community. These results indicate the importance of considering ARG effects over different host strains, especially the potential of reservoir strains that allow resistance to persist in the absence of direct selection, in efforts to understand resistance dynamics.</p>
Diet can alter the cost of resistance to a natural parasite in Caenorhabditis elegans
<p>Resistance to parasites confers a fitness advantage, yet hosts show substantial variation in resistance in natural populations. Evolutionary theory indicates that resistant and susceptible genotypes can coexist if resistance is costly, but there is mixed evidence that resistant individuals have lower fitness in the absence of parasites. One explanation for this discrepancy is that the cost of resistance varies with environmental context. We tested this hypothesis using Caenorhabditis elegans and its natural microsporidian parasite, Nematocida ironsii. We used multiple metrics to compare the fitness of two near-isogenic host genotypes differing at regions associated with resistance to N. ironsii. To quantify the effect of the environment on the cost associated with these known resistance regions, we measured fitness on three microbial diets. We found that the cost of resistance varied with both diet and the measure of fitness. We detected no cost to resistance, irrespective of diet, when fitness was measured as fecundity. However, we detected a cost when fitness was measured in terms of population growth, and the magnitude of this cost varied with diet. These results provide a proof-of-concept that, by mediating the cost of resistance, environmental context may govern the rate and nature of resistance evolution in heterogeneous environments.</p>
Multispecies coinfections and presence of antibiotics shape resistance and fitness costs in a pathogenic bacterium
<p>Increasing antimicrobial resistance (AMR) poses a challenge for treatment of bacterial diseases. In real life, bacterial infections are typically <span>embedded within complex multispecies communities and influenced by the environment, which can shape </span>costs and benefits of AMR. However, knowledge of such interactions and their implications for AMR <em>in vivo</em> is limited. <span>To address this knowledge gap, we investigated fitness-related traits of a pathogenic bacterium (</span><em>Flavobacterium</em> <em>columnare</em><span>)</span> <span>in its fish host, capturing the effects of bacterial antibiotic resistance, multispecies coinfections</span> <span>(metazoan fluke </span><span><em>Diplostomum</em> <em>pseudospathaceum</em></span><span>), and antibiotic exposure. </span>We quantified real-time replication and virulence of sensitive and resistant bacteria and demonstrate that both bacteria can benefit from coinfection in terms of persistence and replication, depending on the coinfecting partner and antibiotic presence. We also show that antibiotics can benefit resistant bacteria by increasing bacterial replication under coinfection with flukes. These results emphasize the importance of diverse, inter-kingdom coinfection interactions and antibiotic exposure in shaping costs and benefits of AMR, supporting their role as significant contributors to the spread and long-term persistence of resistance.</p>
Multispecies coinfections and presence of antibiotics shape resistance and fitness costs in a pathogenic bacterium
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Diet can alter the cost of resistance to a natural parasite in Caenorhabditis elegans
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Data from: Disease resistance is more costly at younger ages: An explanation for the maintenance of juvenile susceptibility
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Data from: Costs of antibiotic resistance genes depend on host strain and environment and can influence community composition
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Data from: Evolutionary trade-offs of insecticide resistance – the fitness costs associated with target-site mutations in the nAChR of Drosophila melanogaster
<p>The evolution of resistance to drugs and pesticides poses a major threat to human health and food security. Neonicotinoids are highly effective insecticides used to control agricultural pests. They target the insect nicotinic acetylcholine receptor and mutations of the receptor that confer resistance have been slow to develop, with only one field-evolved mutation being reported to date. This is an arginine to threonine substitution at position 81 of the nAChR_β1 subunit in neonicotinoid resistant aphids. To validate the role of R81T in neonicotinoid resistance and to test whether it may confer any significant fitness costs to insects, CRISPR/Cas9 was used to introduce an analogous mutation in the genome of <i>Drosophila melanogaster</i>. Flies carrying R81T showed an increased tolerance (resistance) to neonicotinoid insecticides, accompanied by a significant reduction in fitness. In comparison, flies carrying a deletion of the whole nAChR_α<em>6</em> subunit, the target-site of spinosyns, showed an increased tolerance to this class of insecticides but presented almost no fitness deficits.</p>
Data from: Context-dependent costs and benefits of tuberculosis resistance traits in a wild mammalian host
Disease acts as a powerful driver of evolution in natural host populations, yet individuals in a population often vary in their susceptibility to infection. Energetic trade-offs between immune and reproductive investment lead to the evolution of distinct life-history strategies, driven by the relative fitness costs and benefits of resisting infection. However, examples quantifying the cost of resistance outside of the laboratory are rare. Here, we observe two distinct forms of resistance to bovine tuberculosis (bTB), an important zoonotic pathogen, in a free-ranging African buffalo (Syncerus caffer) population. We characterize these phenotypes as 'infection resistance', in which hosts delay or prevent infection, and 'proliferation resistance', in which the host limits the spread of lesions caused by the pathogen after infection has occurred. We found weak evidence that infection resistance to bTB may be heritable in this buffalo population (h2=0.10) and comes at the cost of reduced body condition and marginally reduced survival once infected, but also associates with an overall higher reproductive rate. Infection resistant animals thus appear to follow a 'fast' pace of life syndrome, in that they reproduce more quickly but die upon infection. In contrast, proliferation resistance had no apparent costs and was associated with measures of positive host health- such as having a higher body condition and reproductive rate. This study quantifies striking phenotypic variation in pathogen resistance and provides evidence for a link between life history variation and a disease resistance trait in a wild mammalian host population.
Data from: Exogenous glucocorticoids amplify the costs of infection by reducing resistance and tolerance, but effects are mitigated by co-infection
Individual variation in parasite defenses, such as resistance and tolerance, can underlie heterogeneity in fitness and could influence disease transmission dynamics. Glucocorticoid hormone concentrations often change in response to fluctuating environmental conditions and mediate changes in immune function, resource allocation, and tissue repair. Thus, changes in glucocorticoid hormone concentrations might mediate individual variation in investment in resistance versus tolerance. In this study, we experimentally increased glucocorticoid concentrations in red-winged blackbirds (Agelaius phoeniceus) that were naturally infected with haemosporidian parasites and assessed changes in resistance and tolerance of infection. Glucocorticoid treatment increased burdens of Plasmodium, the parasite causing avian malaria, but only in the absence of co-infection with another Haemosporidian, Haemoproteus. Thus, glucocorticoids might reduce resistance to infection, but co-infection can mitigate the negative consequences of increased hormone concentrations. Glucocorticoid treatment also decreased tolerance of infection. We found no evidence that the inflammatory immune response or rate of red blood cell production underlie the effects of glucocorticoids on resistance and tolerance. Our findings suggest that exogenous glucocorticoids can increase the costs of haemosporidian infections by both increasing parasite numbers and reducing an individual's ability to cope with infection. These effects could scale up to impact populations of both host and parasite.
Fitness costs associated with a GABA receptor mutation conferring dieldrin resistance in Aedes albopictus
<p><span>Understanding the dynamics of insecticide resistance genes in mosquito populations is pivotal for a sustainable use of insecticides. Dieldrin resistance in <em>Aedes</em> <em>albopictus</em> is conferred by the alanine to serine substitution (A302S or <em>Rdl<sup>R</sup></em> allele) in the γ-aminobutyric acid (GABA) receptor encoded by the <em>Rdl</em> gene. On Reunion Island, dieldrin resistance was initially reported in natural <em>Ae</em>. <em>albopictus</em> populations sampled in 2008 despite the ban of dieldrin since 1994. To monitor insecticide resistance in <em>Ae</em>. <em>albopictus</em> on the island and to identify its drivers, we measured (i) the frequency of resistance alleles in 19 distinct natural populations collected between 2016 and 2017, (ii) fitness costs associated with dieldrin resistance in laboratory-controlled experiments, and (iii) the resistance conferred by </span><span><em>Rdl<sup>R</sup></em></span><span> to fipronil, an insecticide widely used on the island and reported to cross-react with </span><span><em>Rdl<sup>R</sup></em></span><span>. The results show a persistence of </span><span><em>Rdl<sup>R</sup></em></span><span> in <em>Ae</em>. <em>albopictus</em> natural populations at low frequencies. Among the measured life history traits, mortality in pre-imaginal stages, adults' survival as well as the proportion of egg-laying females were significantly affected in resistant mosquitoes. Finally, bioassays revealed resistance of </span><span><em>Rdl<sup>R</sup></em></span><span> mosquitoes to fipronil, suggesting that the use of fipronil <em>in</em> <em>natura</em> could select for the </span><span><em>Rdl<sup>R</sup></em></span><span> allele. This study shows that dieldrin resistance is persistent in natural mosquito populations likely as a result of combined effects between fitness costs associated with </span><span><em>Rdl<sup>R</sup></em></span><span> and selection exerted by cross-reacting environmental insecticides such as fipronil.</span></p>
Resistance to bacteriophage incurs a cost to virulence in drug resistant Acinetobacter baumannii
<p>Introduction<em>: Acinetobacter baumannii</em> is a critical priority pathogen (World Health Organisation) because of the rise in nosocomial<em> </em>infections and its ability to evolve resistance to last resort antibiotics, which makes <em>A. baumannii</em> a priority target for phage therapy. Two strains of a novel, lytic bacteriophage (LemonAid and Tonic) able to infect carbapenem-resistant <em>A. baumannii</em> (strain NCTC 13420), were isolated from environmental water samples collected through a citizen science program.</p> <p>Methods: <em>In vitro </em>and <em>in vivo</em> assays, genomics and microscopy techniques were used to characterise the phages, determine mechanisms of phage resistance and the efficacy of the phages against <em>A. baumannii</em>.</p> <p>Results: <em>A. baumannii </em>developed resistance to both viruses, LemonAid and Tonic. Resistance came at a cost to virulence, with the resistant variants causing significantly reduced mortality in a <em>Galleria mellonella </em>larval <em>in vivo</em> model. A replicated 8bp insertion increased in frequency (~40% higher frequency than in the wildtype) within phage-resistant <em>A. baumannii </em>mutants, putatively resulting in early truncation of a protein of unknown function. Evidence from comparative genomics and an adsorption assay suggests this protein acts as a novel phage receptor site in <em>A. baumannii</em>. We find no evidence linking resistance to changes in capsule structure, a known virulence factor. LemonAid efficiently suppressed growth of <em>A. baumanni</em> <em>in vitro</em> across a wide range of titres. However, <em>in vivo</em>, while survival of <em>A. baumannii</em> infected larvae significantly increased with both remedial and prophylactic treatment with LemonAid (10<sup>7 </sup>PFU/mL), the effect was weak and not sufficient to save larvae from morbidity and mortality.</p> <p>Conclusion: While LemonAid and Tonic did not prove effective as a treatment in a <em>Galleria </em>larvae model, there is potential to harness their ability to attenuate virulence in drug-resistant <em>A. baumannii</em>.</p>
Fig. 1 in Fitness cost in field Anopheles labranchiae populations associated with resistance to the insecticide deltamethrin
Fig. 1. Geographic origin of Tunisian populations of Anopheles labranchiae.
Molecular constraints on tolerance-resistance trade-offs: Is there a cost?
<p>Plants possess myriad defenses against their herbivores, including constitutive and inducible chemical compounds and regrowth strategies known as tolerance. Recent studies have shown that plant tolerance and resistance are positively associated given they are co-localized in the same molecular pathway, the oxidative pentose phosphate pathway. However, given that both defensive strategies utilize carbon skeletons from a shared resource pool in the oxidative pentose phosphate pathway there are likely costs in maintaining both resistance-tolerance strategies. Here we investigate fitness costs in maintaining both strategies by utilizing a double knockout of cyp79B2 and cyp79B3, key enzymes in the biosynthetic process of indole glucosinolates, which convert tryptophan to indole-3-acetaldoxime (IAOx) and is further used to produce indole glucosinolates. These mutant plants are devoid of any indole glucosinolates thus reducing plant resistance. Results show that knocking out indole glucosinolate production and thus one of the resistance pathways leads to an approximate 46% increase in fitness compensation shifting the undercompensating wild-type Columbia-0 to an overcompensating genotype following damage. We discuss the potential mechanistic basis for the observed patterns.</p>
Resistance to bacteriophage incurs a cost to virulence in drug resistant Acinetobacter baumannii
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Data from: Costs of resistance and correlational selection in the multiple-herbivore community of Solanum carolinense
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Fitness costs associated with a GABA receptor mutation conferring dieldrin resistance in Aedes albopictus
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Sexual selection reveals a cost of pathogen resistance undetected in life history assays
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Data from: Exogenous glucocorticoids amplify the costs of infection by reducing resistance and tolerance, but effects are mitigated by co-infection
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Cytochrome P450 metabolic resistance (CYP6P9a) to pyrethroids imposes a fitness cost in the major African malaria vector Anopheles funestus
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