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338 results for “antibiotic resistance”
Data from: Constitutive presence of antibiotic resistance genes within the bacterial community of a large subalpine lake
The fate of antibiotic resistance genes (ARGs) in environmental microbial communities is of primary concern as prodromal of a potential transfer to pathogenic bacteria. Although of diverse origin, the persistence of ARGs in aquatic environments is highly influenced by anthropic activities, allowing potential control actions in well-studied environments. However, knowledge of abundance and space–time distribution of ARGs in ecosystems is still scarce. Using quantitative real-time PCR, we investigated the presence and the abundance of twelve ARGs (against tetracyclines, β-lactams, aminoglycosides, quinolones and sulphonamides) at different sampling sites, depths and seasons, in Lake Maggiore, a large subalpine lake, and in the area of its watershed. We then evaluated the correlation between each ARG and a number of ecological parameters in the water column in the deepest part of the lake. Our results suggest the constitutive presence of at least four ARGs within the bacterial community with a high proportion of bacteria potentially resistant to tetracyclines and sulphonamides. The presence of these ARGs was independent of the total bacterial density and temperature. The dynamics of tet(A) and sulII genes were, however, positively correlated with dissolved oxygen and negatively to chlorophyll a, suggesting that the resistant microbes inhabit specific niches. These observations indicate that the lake is a reservoir of antibiotic resistances, highlighting the need of a deeper understanding of the sources of ARGs and the factors allowing their persistence in waters.
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: Heterogeneity in efflux pump expression predisposes antibiotic-resistant cells to mutation
<p>Antibiotic resistance is often the result of mutations that block drug activity; however, bacteria also evade antibiotics by transiently expressing genes such as multidrug efflux pumps. A crucial question is whether transient resistance can promote permanent genetic changes. Previous studies have established that antibiotic treatment can select tolerant cells that then mutate to achieve permanent resistance. Whether these mutations result from antibiotic stress or preexist within the population is unclear. To address this question, we focused on the multidrug pump AcrAB-TolC. Using time-lapse microscopy, we found that cells with higher acrAB expression have lower expression of the DNA mismatch repair gene mutS, lower growth rates, and higher mutation frequencies. Thus, transient antibiotic resistance from elevated acrAB expression can promote spontaneous mutations within single cells.</p>
Data from: Persistence and resistance as complementary bacterial adaptations to antibiotics
Bacterial persistence represents a simple of phenotypic heterogeneity, whereby a proportion of cells in an isogenic bacterial population can survive exposure to lethal stresses such as antibiotics. In contrast, genetically based antibiotic resistance allows for continued growth in the presence of antibiotics. It is unclear, however, whether resistance and persistence are complementary or alternative evolutionary adaptations to antibiotics. Here, we investigate the co-evolution of resistance and persistence across the genus Pseudomonas using comparative methods that correct for phylogenetic nonindependence. We find that strains of Pseudomonas vary extensively in both their intrinsic resistance to antibiotics (ciprofloxacin and rifampicin) and persistence following exposure to these antibiotics. Crucially, we find that persistence correlates positively to antibiotic resistance across strains. However, we find that different genes control resistance and persistence implying that they are independent traits. Specifically, we find that the number of type II toxin–antitoxin systems (TAs) in the genome of a strain is correlated to persistence, but not resistance. Our study shows that persistence and antibiotic resistance are complementary, but independent, evolutionary adaptations to stress and it highlights the key role played by TAs in the evolution of persistence.
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.
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 related to the manuscript "Sequence-specific aggregation of magnetic nanoparticles and single-stranded DNA amplification products for detection of antibiotic resistance gene sul1."
<p>Absorbance and AC susceptometry raw and processed excel files used.</p>
Insertion sequences and other mobile elements associated with antibiotic resistance genes in Enterococcus isolates from an inpatient with prolonged bacteremia.
<p>Insertion sequences (ISs) and other transposable elements are associated with the mobilization of antibiotic resistance determinants and the modulation of pathogenic characteristics. In this work, we aimed to investigate the association between ISs and antibiotic resistance genes, and their role in dissemination and modification of the antibiotic resistant phenotype. To that end, we leveraged fully resolved <em>Enterococcus faecium</em> and <em>Enterococcus faecalis</em> genomes of isolates collected over five days from an inpatient with prolonged bacteremia. Isolates from both species harbored similar IS family content but showed significant species-dependent differences in copy number and arrangements of ISs throughout their replicons. Here, we describe two inter-specific IS-mediated recombination events and IS-mediated excision events in plasmids of <em>E. faecium</em> isolates. We also characterize a novel arrangement of the ISs in a Tn1546-like transposon in <em>E. faecalis</em> isolates likely implicated in a vancomycin genotype-phenotype discrepancy. Furthermore, an extended analysis revealed a novel association between daptomycin resistance mutations in <em>liaSR</em> genes and a putative composite transposon in<em> E. faecium</em>, offering a new paradigm for the study of daptomycin resistance and novel insights into the dissemination of daptomycin resistance. In conclusion, our study highlights the role ISs and other transposable elements play in the rapid adaptation and response to clinically relevant stresses such as aggressive antibiotic treatment in enterococci.</p>
Sequencing data for "Rapid heuristic inference of antibiotic resistance and susceptibility by genomic neighbor typing"
<p>This repository contains sequencing data from the following paper:</p> <p>Karel Břinda, Alanna Callendrello, Kevin C. Ma, Derek R MacFadden, Themoula Charalampous, Robyn S Lee, Lauren Cowley, Crista B Wadsworth, Yonatan H Grad, Gregory Kucherov, Justin O’Grady, Michael Baym, and William P Hanage. Rapid heuristic inference of antibiotic resistance and susceptibility by genomic neighbor typing<strong>.</strong> 2019.</p>
Insights into antibiotic resistance promoted by quinolone exposure
<p>These data were collected as part of a study looking into the effect of exposing <em>E. coli</em> MG1655 to sub-MIC concentrations of quinolones and other antibiotics. See abstract below:</p> <p>Quinolone-induced antibiotic resistance (QIAR) refers to the phenomenon by which bacteria exposed to sub-lethal levels of quinolones acquire resistance to non-quinolone antibiotics. We have explored this in Escherichia coli MG1655 using a variety of compounds and bacteria carrying a quinolone-resistance mutation in gyrase, mutations affecting the SOS response and mutations in error-prone polymerases. The nature of the antibiotic-resistance</p> <p>mutations was determined by whole-genome sequencing. Exposure to low levels of most quinolones tested led to mutations conferring resistance to chloramphenicol, ampicillin, kanamycin and tetracycline. The mutations included point mutations and deletions, and could mostly be correlated with the resistance phenotype. QIAR depended upon DNA gyrase, and involved the SOS response but was not dependent on error-prone polymerases. Only moxifloxacin, among the quinolones tested, did not display a significant QIAR effect. We speculate that the lack of QIAR with moxifloxacin may be attributable to it acting via a different mechanism. In addition to the concerns about antimicrobial resistance (AMR) to quinolones and other compounds, QIAR presents an additional challenge in relation to the usage of quinolone antibacterials.</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.
Data from: Reversion of antibiotic resistance in Mycobacterium tuberculosis by spiroisoxazoline SMARt-420
Antibiotic resistance is one of the biggest threats to human health globally. Alarmingly, multidrug-resistant and extensively drug-resistant Mycobacterium tuberculosis have now spread worldwide. Some key antituberculosis antibiotics are prodrugs, for which resistance mechanisms are mainly driven by mutations in the bacterial enzymatic pathway required for their bioactivation. We have developed drug-like molecules that activate a cryptic alternative bioactivation pathway of ethionamide in M. tuberculosis, circumventing the classic activation pathway in which resistance mutations have now been observed. The first-of-its-kind molecule, named SMARt-420 (Small Molecule Aborting Resistance), not only fully reverses ethionamide-acquired resistance and clears ethionamide-resistant infection in mice, it also increases the basal sensitivity of bacteria to ethionamide.
Treatment Outcome With Antibiotic Use and Its Resistance Pattern Among Patient With Neonatal Sepsis
ClinicalTrials.gov study NCT05742477. IPD Sharing: NO. Countries: 0. Publications: 4.
Comparison of Three Interventions for Antibiotic-Resistant Bacteria (ARB) Decolonization From the Gastrointestinal Tract
ClinicalTrials.gov study NCT07094984. IPD Sharing: YES. Countries: 1. Publications: 0.
Detection of Microorganisms and Antibiotic Resistance Genes Using the Curetis Unyvero LRT55 Application
ClinicalTrials.gov study NCT01922024. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Antibiotic-resistant Bacterial Infection of Hepatic Patients
ClinicalTrials.gov study NCT03855709. IPD Sharing: NO. Countries: 0. Publications: 6.
Trial of Antibiotic Treatment for Skin Abscess in Patients at Risk for Methicillin-Resistant Staphylococcus Aureus (MRSA) Infection
ClinicalTrials.gov study NCT00829686. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Nasopharyngeal Bacterial Carriage and Antibiotic Resistance in Children With Sickle Cell Disease in Ile-De-France
ClinicalTrials.gov study NCT05197205. IPD Sharing: Not stated. Countries: 0. Publications: 4.
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