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146 results for “Acinetobacter baumannii”
Genomic Epidemiology Dataset for Important Nosocomial Pathogenic Bacteria Acinetobacter baumannii
<p>The<strong> </strong>infections caused by various bacterial pathogens both in clinical and community settings represent a significant threat to public healthcare worldwide. The growing resistance to antimicrobial drugs acquired by bacterial species causing healthcare-associated infections has already become a life-threatening danger noticed by the World Health Organization. Several groups or lineages of bacterial isolates usually called 'the clones of high risk' often drive the spread of resistance within particular species. </p><p>Thus, it is vitally important to reveal and track the spread of such clones and the mechanisms by which they acquire antibiotic resistance and enhance their survival skills. Currently, the analysis of whole genome sequences for bacterial isolates of interest is increasingly used for these purposes, including epidemiological surveillance and developing of spread prevention measures. However, the availability and uniformity of the data derived from the genomic sequences often represents a bottleneck for such investigations. </p><p>In this dataset, we present the results of a comprehensive genomic epidemiology analysis of 17,546 genomes of a dangerous bacterial pathogen <i>Acinetobacter baumannii</i>. Important typing information including multilocus sequence typing (MLST)-based sequence types (STs), intrinsic<i> blaOXA-51-like</i> gene variants, capsular (KL) and oligosaccharide (OCL) types, CRISPR-Cas systems, and cgMLST profiles are presented, as well as the assignment of particular isolates to nine known international clones of high risk. The presence of antimicrobial resistance genes within the genomes is also reported. </p><p>These data will be useful for researchers in the field of <i>A. baumannii</i> genomic epidemiology, resistance analysis and prevention measure development.</p>
Macrophage phagocytosis assay of Acinetobacter baumannii AB074, passaged 15 days in antibiotics or transferrin.
<p>Macrophage phagocytosis assay of Acinetobacter baumannii AB074, passaged 15 days in antibiotics or transferrin. Experiment #1, replica #1-2, from March 7th, 2017 and Experiment #2, replica #1-2 from March 16th, 2017</p> <p>MICs for AB074: transferrin = 4 mcg/ml; ciprofloxacin = 1 mcg/ml; meropenem = 0,5 mcg/ml</p> <p>6 groups of treatment:</p> <p>1. No drug</p> <p>2. Transferrin only, last passage dose = 16 mcg/ml </p> <p>3. Ciprofloxacin only, last passage dose = 5 mcg/ml </p> <p>4. Ciprofloxacin + transferrin, last passage dose = 0,5 mcg/ml of cipro + 16 mcg/ml of transferrin</p> <p>5. Meropenem only, last passage dose = 2,5 mcg/ml </p> <p>6. Meropenem + transferrin, last passage dose = 2,5 mcg/ml + 16 mcg/ml of transferrin</p> <p>The file name structure: group_picture#_strain_timeOfPassage_ experiment#_replica#</p>
Alterations of antimicrobial resistance genes in the clinical multi-drug resistance Acinetobacter baumannii isolates in Vietnam
<p><strong>FIGURE 1 </strong>List of antibiotic resistance gene expression.</p> <p><strong>TABLE 1 </strong>Primers used in this study.</p> <p><strong>TABLE 2 </strong>Clinical characteristics of 30 patients with <em>A. baumannii </em>isolates.</p> <p><strong>TABLE 3 </strong>Antimicrobial resistance values of <em>A. baumannii</em> isolated during 2017 to 2019 year in the Military Hospital 103.</p> <p><strong>TABLE 4 </strong>Relationship between genotype and phenotype antimicrobial resistance of isolates in this study.</p> <p><strong>TABLE 5 </strong>List of altered antibiotic resistance genes expression in isolates of <em>A. baumannii</em> (up or down two-fold changes of related genes compare with <em>16S rRNA</em> gene).</p> <p><strong>TABLE 6 </strong>The multiple antimicrobial resistance gene profile of 30 <em>A. baumannii</em> isolates.</p> <p> </p>
Insights into Acinetobacter baumannii AMA205's Unprecedented Antibiotic Resistance
<p><span>The rise of antibiotic-resistant bacteria in clinical settings has become a significant global concern. Among these bacteria, <em>Acinetobacter baumannii</em> stands out due to its remarkable ability to acquire resistance genes and persist in hospital environments, leading to some of the most challenging infections. Horizontal gene transfer (HGT) plays a crucial role in the evolution of this pathogen. The <em>A. baumannii</em> AMA205 strain, belonging to sequence type ST79, was isolated from a COVID-19 patient in Argentina in 2021. This strain’s antimicrobial resistance profile is notable as it harbors multiple resistance genes, some of which had not been previously described in this species. The AmpC family β-lactamase <em>bla</em><sub>CMY-6</sub>, commonly found in Enterobacterales, had never been detected in <em>A. baumannii </em>before. Furthermore, this is the first ST79 strain known to carry the carbapenemase <em>bla</em><sub>NDM-1 </sub>gene. Other acquired resistance genes include the carbapenemase <em>bla</em><sub>OXA-23</sub>, further complicating treatment. Susceptibility testing revealed high resistance to most antibiotic families, including cefiderocol, with significant contributions from <em>bla</em><sub>CMY-6 </sub>and <em>bla</em><sub>NDM-1 </sub>genes to the cephalosporin and carbapenem resistance profiles. The <em>A. baumannii</em> AMA205 genome also contains genetic traits coding for 111 potential virulence factors, such as the iron-uptake system and biofilm-associated proteins. This study underscores <em>A. baumannii's </em>ability to acquire multiple resistance genes and highlights the need for alternative therapies and effective antimicrobial stewardship to control the spread of these highly resistant strains.</span></p>
Resazurin-based time-kill assay in Acinetobacter baumannii AB074. Fluorescence measurement data for excitation 544 nm, emission 590 nm, gain 1000.
<p>There were 21 groups: 3 groups of transferrin alone in 3 different concentrations (1/3, 1, and 3 times of its MIC); 4 groups of antibiotics alone (ciprofloxacin and meropenem in 1/3 and 1 MIC concentration each), 6 combo groups for ciprofloxacin and 6 combo groups for meropenem, 1 group of positive control with bacteria but without any drug and 1 group of negative control without bacteria, with RPMI only. 20 µL of 0.1% aqueous resazurin solution was added to each well and the plate was incubated at 37°C without shaking for 24 hours. After incubation fluorescence was measured (excitation 544 nm, emission 590 nm) at 0h, 1h, 2h, 4h, 6h, 8h, and 24 hrs using the FLUOstar Omega plate reader (BMG LABTECH GmbH, Germany). Plate layouts may vary.</p> <p>For more information contact author.</p>
Capsular Polysaccharide Restrains Type VI Secretion in Acinetobacter baumannii
<p><span>Imaging dataset: All scripts, models, and classifiers relevant to the image analyses descripted in the study by Flaugnatti et al., 2024 have been deposited.</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>
Research data for: Replicative Acinetobacter baumannii strains interfere with phagosomal maturation by modulating the vacuolar pH
<p>Bacterial pneumonia is a common infection of the lower respiratory tract that can afflict patients of all ages. Multidrug-resistant strains of <em>Acinetobacter</em> <em>baumannii</em> are increasingly responsible for causing nosocomial pneumonias, thus posing an urgent threat. Alveolar macrophages play a critical role in overcoming respiratory infections caused by this pathogen. Recently, we and others have shown that new clinical isolates of <em>A. baumannii</em>, but not the common lab strain ATCC 19606 (19606), can persist and replicate in macrophages within spacious vacuoles that we called Acinetobacter Containing Vacuoles (ACV). In this work, we demonstrate that the modern <em>A. baumannii</em> clinical isolate 398, but not the lab strain 19606, can infect alveolar macrophages and produce ACVs in vivo in a murine pneumonia model. Both strains initially interact with the alveolar macrophage endocytic pathway, as indicated by EEA1 and LAMP1 markers; however, the fate of these strains diverges at a later stage. While 19606 is eliminated in an autophagy pathway, 398 replicates in ACVs and are not degraded. We show that 398 reverts the natural acidification of the phagosome by secreting large amounts of ammonia, a by-product of amino acid catabolism. We propose that this ability to survive within macrophages may be critical for the persistence of clinical <em>A. baumannii </em>isolates in the lung during a respiratory infection.</p>
Study to Evaluate the Efficacy and Safety of Intravenous Sulbactam-ETX2514 in the Treatment of Patients With Infections Caused by Acinetobacter Baumannii-calcoaceticus Complex
ClinicalTrials.gov study NCT03894046. IPD Sharing: Not stated. Countries: 17. Publications: 1.
Resistance to bacteriophage incurs a cost to virulence in drug resistant Acinetobacter baumannii
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Research data for: Replicative Acinetobacter baumannii strains interfere with phagosomal maturation by modulating the vacuolar pH
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Data from: Pangenome and immuno-proteomics analysis of Acinetobacter baumannii strains revealed the core peptide vaccine targets
Background: Acinetobacter baumannii has emerged as a significant nosocomial pathogen during the last few years, exhibiting resistance to almost all major classes of antibiotics. Alternative treatment options such as vaccines tend to be most promising and cost effective approaches against this resistant pathogen. In the current study, we have explored the pan-genome of A. baumannii followed by immune-proteomics and reverse vaccinology approaches to identify potential core vaccine targets. Results: The pan-genome of all available A. baumannii strains (30 complete genomes) is estimated to contain 7,606 gene families and the core genome consists of 2,445 gene families (~32 % of the pan-genome). Phylogenetic tree, comparative genomic and proteomic analysis revealed both intra- and inter genomic similarities and evolutionary relationships. Among the conserved core genome, thirteen proteins, including P pilus assembly protein, pili assembly chaperone, AdeK, PonA, OmpA, general secretion pathway protein D, FhuE receptor, Type VI secretion system OmpA/MotB, TonB dependent siderophore receptor, general secretion pathway protein D, outer membrane protein, peptidoglycan associated lipoprotein and peptidyl-prolyl cis-trans isomerase are identified as highly antigenic. Epitope mapping of the target proteins revealed the presence of antigenic surface exposed 9-mer T-cell epitopes. Protein-protein interaction and functional annotation have shown their involvement in significant biological and molecular processes. The pipeline is validated by predicting already known immunogenic targets against Gram negative pathogen Helicobacter pylori as a positive control. Conclusion: The study, based upon combinatorial approach of pan-genomics, core genomics, proteomics and reverse vaccinology led us to find out potential vaccine candidates against A. baumannii. The comprehensive analysis of all the completely sequenced genomes revealed thirteen putative antigens which could elicit substantial immune response. The integration of computational vaccinology strategies would facilitate in tackling the rapid dissemination of resistant A.baumannii strains. The scarcity of effective antibiotics and the global expansion of sequencing data making this approach desirable in the development of effective vaccines against A. baumannii and other bacterial pathogens.
Phenotype evaluation rawdata of Acinetobacter baumannii harboring chromosomal parallel mutations or an evolved plasmid
<p>OXA-23 is the predominant carbapenemase in carbapenem-resistant <em>Acinetobacter baumannnii</em>. The co-evolutionary dynamics of <em>A. baumannii</em> and OXA-23-encoding plasmids are poorly understood. Here, we transformed <em>A. baumannnii</em> ATCC 17978 with pAZJ221, a <em>bla</em><sub>OXA-23</sub>-containing plasmid from a clinical <em>A. baumannnii</em> isolate A221, and subjected the transformant to experimental evolution in the presence of a sub-inhibitory concentration of imipenem for nearly 400 generations. We used population sequencing to track genetic changes at six time-points and evaluated phenotypic changes. Increased fitness of evolving populations, temporary duplication of <em>bla</em><sub>OXA-23</sub> in pAZJ221, interfering allele dynamics, and chromosomal locus-level parallelism were observed. To characterize genotype-to-phenotype associations, we focused on six mutations in parallel targets predicted to affect small RNAs and a cyclic dimeric (3'→5') GMP-metabolizing protein. Six isogenic mutants with or without pAZJ221 were engineered to test for the causal effects of these mutations on fitness costs and plasmid kinetics, the evolved plasmid containing two copies of <em>bla</em><sub>OXA-23</sub> was transferred to ancestral ATCC 17978. Five of the six mutations contributed to improved fitness in the presence of pAZJ221 under imipenem pressure, and all but one of them impaired plasmid conjugation ability. The duplication of <em>bla</em><sub>OXA-23</sub> contributed to host fitness under carbapenem pressure but imposed a burden on the host in antibiotic-free media relative to the unevolved pAZJ221. Overall, our study provides a framework for the co-evolution of <em>A. baumannii</em> and a clinical blaOXA-23-containing plasmid, involving early <em>bla</em><sub>OXA-23</sub> duplication followed by chromosomal adaptations.</p>
Turbidity and Colony Count of Acinetobacter baumannii suspensions after meropenem-based antibiotic combination exposure
<p class="MsoNormal"><strong><span>Background</span></strong><span>: Carbapenems are the treatment of choice for multidrug-resistant (MDR) <em>A. baumannii</em> infection but are inadequate for carbapenem-resistant <em>A.baumannii </em>(CRAB) infections. Combination therapy came into the spotlight in the last decade. This study compares the colony count reduction after exposure to meropenem-based antibiotics in clinically achieved concentration with the time-kill test.</span></p> <p class="MsoNormal"><strong><span>Results</span></strong><span>: A bactericidal effect was achieved in isolates that were intermediate to ampicillin sulbactam at the administration of meropenem and ampicillin-sulbactam with a 2 MIC + 2 MIC. The combination of meropenem and ampicillin-sulbactam showed a bacteriostatic effect in isolates resistant to both antibiotics. The bactericidal effect was not achieved when meropenem and amikacin were administered to isolates that were intermediate or resistant to meropenem and amikacin.</span></p> <p class="MsoNormal"><strong><span>Conclusion</span></strong><span>: There is a significant difference in the colony count reduction between groups of <em>A. baumannii</em> isolates after exposure to antibiotic combinations.</span></p>
Screening of anti-Acinetobacter baumannii plant-based compounds, based on potential inhibition of OmpA and OmpW functions
<p><span>Considering the adverse effect of antimicrobial resistance (AMR) crisis on human life, there is an immediate need for finding new alternatives for treatment of emerging infectious diseases. Therapeutic options, including last-line or combined antibiotic therapies for <i>Acinetobacter baumannii</i>, as an emergent multi-drug resistant (MDR) human pathogen responsible for severe nosocomial and several other infections, are apparently ineffective. The outer membrane protein A (OmpA) and outer membrane protein W (OmpW) are two porins known as virulence factors with different cellular functions. Identification of natural compounds with potentials to block these putative virulence factors can possibly attenuate the growth of the bacteria and control the relating diseases. The current work aimed to screen the therapeutic potential of a library of 371 phytochemicals, as multi-blockers of OmpA and OmpW in <em>A. baumannii</em>. Although the anti-virulence activities of these biomolecules are reported previously, no evaluation on <i>A. baumannii </i>has been performed so far. Moreover, there is no safety screening and early alerts of these compounds. In this study, hits were initially selected based on their physicochemical, absorption, distribution, metabolism, excretion, and toxicity (ADMET) drug-like properties. Afterwards, the selected ligands were subjected to standard docking calculations against predicted three-dimensional structure of OmpA and OmpW in <i>A. baumannii</i>. We identified five phytochemicals (Amorphigenin (PUBCHEM CID 92207), Bisdemethoxy-curcumin (PUBCHEM CID 5315472), Dalbinol (PUBCHEM CID 44257412), Epicatechin gallate (PUBCHEM CID 72276) and Nordihydroguaiaretic acid (PUBCHEM CID 4534)) bearing appreciable binding affinity towards the selected binding pocket of OmpA and OmpW. </span></p>
Figure 14: Theoretical Prediction of Imipenem Resistance in Acinetobacter Baumannii(2020-2030)
<p><strong>Figure 14: Theoretical Prediction of Imipenem Resistance in Acinetobacter Baumannii(2020-2030)</strong></p>
Fig13: Antibiotic sensitivity and resistance pattern of Acinetobacter Baumannii
<p><strong>Fig13: Antibiotic sensitivity and resistance pattern of Acinetobacter Baumannii</strong></p>
Colistin Versus Colistin Plus Fosfomycin for Infections Caused by MDR Acinetobacter Baumannii
ClinicalTrials.gov study NCT01297894. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Impact of Plasma Levels of Colistin in Patients With Carbapenem Resistant Acinetobacter Baumannii Infection
ClinicalTrials.gov study NCT02482961. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Phenotype evaluation rawdata of Acinetobacter baumannii harboring chromosomal parallel mutations or an evolved plasmid
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