Campy_AMR
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB42615 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5167520_1.fastq.gz | Fastqsanger.gz | |||
| ERR5167520_2.fastq.gz | Fastqsanger.gz | |||
| ERR5167511_1.fastq.gz | Fastqsanger.gz | |||
| ERR5167511_2.fastq.gz | Fastqsanger.gz | |||
| ERR5167512_1.fastq.gz | Fastqsanger.gz |
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Project description:<p>The study of antimicrobial resistance (AMR) in infectious diarrhea has generally been limited to cultivation, antimicrobial susceptibility testing and targeted PCR assays. When individual strains of significance are identified, whole genome shotgun (WGS) sequencing of important clones and clades is performed. Genes that encode resistance to antibiotics have been detected in environmental, insect, human and animal metagenomes and are known as "resistomes". While metagenomic datasets have been mined to characterize the healthy human gut resistome in the Human Microbiome Project and MetaHIT and in a Yanomani Amerindian cohort, directed metagenomic sequencing has not been used to examine the epidemiology of AMR. Especially in developing countries where sanitation is poor, diarrhea and enteric pathogens likely serve to disseminate antibiotic resistance elements of clinical significance. Unregulated use of antibiotics further exacerbates the problem by selection for acquisition of resistance. This is exemplified by recent reports of multiple antibiotic resistance in Shigella strains in India, in Escherichia coli in India and Pakistan, and in nontyphoidal Salmonella (NTS) in South-East Asia. We propose to use deep metagenomic sequencing and genome level assembly to study the epidemiology of AMR in stools of children suffering from diarrhea. Here the epidemiology component will be surveillance and analysis of the microbial composition (to the bacterial species/strain level where possible) and its constituent antimicrobial resistance genetic elements (such as plasmids, integrons, transposons and other mobile genetic elements, or MGEs) in samples from a cohort where diarrhea is prevalent and antibiotic exposure is endemic. The goal will be to assess whether consortia of specific mobile antimicrobial resistance elements associate with species/strains and whether their presence is enhanced or amplified in diarrheal microbiomes and in the presence of antibiotic exposure. This work could potentially identify clonal complexes of organisms and MGEs with enhanced resistance and the potential to transfer this resistance to other enteric pathogens.</p> <p>We have performed WGS, metagenomic assembly and gene/protein mapping to examine and characterize the types of AMR genes and transfer elements (transposons, integrons, bacteriophage, plasmids) and their distribution in bacterial species and strains assembled from DNA isolated from diarrheal and non-diarrheal stools. The samples were acquired from a cohort of pediatric patients and controls from Colombia, South America where antibiotic use is prevalent. As a control, the distribution and abundance of AMR genes can be compared to published studies where resistome gene lists from healthy cohort sequences were compiled. Our approach is more epidemiologic in nature, as we plan to identify and catalogue antimicrobial elements on MGEs capable of spread through a local population and further we will, where possible, link mobile antimicrobial resistance elements with specific strains within the population.</p>
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Project description:The increased prevalence of Salmonella spp. resistance in swine spurs the search for alternatives to antibiotics. Microcin J25 (MccJ25), a bacteriocin produced by Escherichia coli, is a potent inhibitor of several pathogenic bacteria including Salmonella enterica. In this study, we aimed to evaluate in vitro the impact of MccJ25 on the metabolic activity of the swine colonic microbiota. The PolyFermS in vitro continuous fermentation model was used with modified Macfarlane medium to simulate the porcine proximal colon. During 35 days of fermentation, a first-stage reactor containing immobilized swine fecal microbiota fed two second-stage control and test reactors operated in parallel and used to test the effectsof MccJ25 on the composition and the metabolic activity of the microbiota. Reuterin, a broad spectrum antimicrobial produced by Limosilactobacillus reuteri and the antibiotic rifampicin were tested for comparison. LC-MS analysis of the cell extracts was used to assess the bacteriocin/antibiotic degradation products and monitor changes in the swine colonic microbiota metabolome.
2021-11-13 | ST002014 | MetabolomicsWorkbench
Project description:Multidrug-resistant (MDR; resistance to >3 antimicrobial classes) Salmonella enterica serovar I 4,[5],12:i:- strains were linked to a 2015 foodborne outbreak from pork. Strain USDA15WA-1, associated with the outbreak, harbors an MDR module and the metal tolerance element Salmonella Genomic Island 4 (SGI-4). Characterization of SGI-4 revealed that conjugational transfer of SGI-4 resulted in the mobile genetic element (MGE) replicating as a plasmid or integrating into the chromosome. Tolerance to copper, arsenic, and antimony compounds was increased in Salmonella strains containing SGI-4 compared to strains lacking the MGE. Following Salmonella exposure to copper, RNA-seq transcriptional analysis demonstrated significant differential expression of diverse genes and pathways, including induction of numerous metal tolerance genes (copper, arsenic, silver, and mercury). Evaluation of swine administered elevated concentrations of zinc oxide (2,000 mg/kg) and copper sulfate (200 mg/kg) as an antimicrobial feed additive (Zn+Cu) in their diet for 4 weeks prior to and 3 weeks post-inoculation with serovar I 4,[5],12:i:- indicated that Salmonella shedding levels declined at a slower rate in pigs receiving in-feed Zn+Cu compared to control pigs (no Zn+Cu). The presence of metal tolerance genes in MDR Salmonella serovar I 4,[5],12:i:- may provide benefits for environmental survival or swine colonization in metal-containing settings.
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Project description:Swine streptococcosis has caused great economic loss in the swine industry, and the major pathogen responsible for this disease is Streptococcus Suis serotype 2 (SS2). Disease resistance breeding is a fundamental way of resolving this problem. With the development of GWAS and transcriptomic microarray technology, we now have powerful research tools to identify SS2 resistance genes. In this research, we generated an F2 generation of SS2 resistant C57BL/6 and SS2 susceptive A/J mice. With the F2 generation of these two mice strains and GWAS analysis, we identified 286 significant mouse genome SNPs sites associated with the SS2 resistance trait. Gene expression profiles for C57BL/6 and A/J were analyzed under SS2 infection pressure by microarray. In total, 251 differentially expressed genes were identified between these two mouse strains during SS2 infection. After combining the GWAS and gene expression profile data, we located two genes that were significantly associated with SS2 resistance, which were the UBA domain containing 1 gene (Ubac1) and Epsin 1 gene (Epn 1). GO classification and over-representation analysis revealed nine up-regulated related to immune function, which could potentially be involved in the C57BL/6 SS2 resistance trait. This is the first study to use both SNP chip and gene express profile chip for SS2 resistance gene identification in mouse, and these results will contribute to Swine SS2 resistance breeding.
2018-11-27 | GSE122963 | GEO
Project description:Whole genome sequencing of SYBARIS Aspergillus spp. known to be multi-drug resistant and difficult to treat. Aim of this experiment is to investigate the genetic basis of susceptibility to disease and elucidate molecular mechanisms of drug resistance in these strains.
2016-04-30 | E-SYBR-1 | biostudies-arrayexpress
Project description:Consumption of contaminated poultry products is one of the main sources of human campylobacteriosis, of which Campylobacter jejuni subsp. jejuni (C. jejuni) and C. coli are responsible for approximately 98% of the cases. The ceca of commercial turkeys are the main anatomical site where Campylobacter asymptomatically colonizes. We have previously colonized the ceca of commercial turkey poults with C. jejuni, and demonstrated acute changes in cytokine gene expression in cecal tissue and histologically scored intestinal lesions at 2 days post-inoculation (dpi). The host-response of turkeys to C. coli colonization is unknown. Cecal tonsils (CT) are an important part of the gastrointestinal-associated lymphoid tissue that function to sample material passing in and out of the ceca and generating immune responses against intestinal pathogens. The CT immune response towards Campylobacter is unknown. In this study, we generated a C. coli kanamycin-resistant construct (CcK) for enumeration from cecal contents after experimental challenge. In vitro analysis of CcK demonstrated no changes in motility when compared to the parent isolate, but in vitro growth rates were significantly different than the parent strain. Poults were inoculated by oral gavage with CcK (5x10^7 cfu) or sterile-media (mock-colonized), and euthanized at 1 and 3 dpi. At both time points, CcK was recovered from cecal contents, but not from the mock-colonized group. As a marker of acute inflammation, serum alpha-1 acid glycoprotein was significantly elevated at 3 dpi in CcK inoculated poults compared to mock-infected samples. Significant histological lesions were detected in cecal and CT tissues of CcK colonized poults at 1 and 3 dpi, respectively. RNAseq analysis identified 250 differentially expressed genes (DEG) in CT from CcK colonized poults at 3 dpi, of which 194 were upregulated and 56 were downregulated. From the DEG, 9 significantly enriched biological pathways were identified, including platelet aggregation, response to oxidative stress and negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathway. These data suggest that C. coli induced an acute inflammatory response in the intestinal tract of poults, and that platelet aggregation and oxidative stress in the CT may affect the turkey’s ability to resist Campylobacter colonization. Results from this study provide insight into host-response of the turkey CT to Campylobacter colonization. These findings will help to develop and test Campylobacter mitigation strategies to promote food safety in commercial turkeys.
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Project description:The pathogenic bacterium Campylobacter jejuni is the leading cause of bacterial foodborne gastroenteritis worldwide yet it does not grow in the aerobic environment. The paralogues RrpA and RrpB which are members of MarR family of DNA binding proteins have been shown to be important for the survival of C. jejuni under aerobic and redox stress. We report that RrpA is a positive regulator of mdaB, encoding a flavin-dependent quinone reductase. MdaB confers protection to the cell from redox stress mediated by structurally diverse quinones. RrpB negatively regulates the expression of nfrA (Cj1555c), a flavin reductase. NfrA reduces riboflavin at a much higher rate than flavin mononucleotide (FMN),suggesting exogenous free flavins are the natural substrate. Enzymatic activity of MdaB and NfrA towards their substrates revealed both reductases preferred NADPH as an electron donor. DNA-binding and post translational modification analyses showed that the mechanism of RrpA and RrpB DNA binding is likely a cysteine-based redox switch. Complete genome sequences analysis indicated that MdaB is predominant in Campylobacter spp. and the related Helicobacter spp., whilst NfrA is more often found in C. jejuni strains. Quinones and flavins are antimicrobial redox cycling agents secreted by a wide range of cell-types that can form damaging superoxide by one-electron reactions. We propose that MdaB and NfrA production allows a two-electron reduction mechanism to the less toxic quinol forms. These enzymes thus aid the survival and persistence of C. jejuni in the face of toxic compounds from competing microbes.
2021-11-03 | PXD028910 | Pride
Project description:The pathogenic bacterium Campylobacter jejuni is the leading cause of bacterial foodborne gastroenteritis worldwide yet it does not grow in the aerobic environment. The paralogues RrpA and RrpB which are members of MarR family of DNA binding proteins have been shown to be important for the survival of C. jejuni under aerobic and redox stress. We report that RrpA is a positive regulator of mdaB, encoding a flavin-dependent quinone reductase. MdaB confers protection to the cell from redox stress mediated by structurally diverse quinones. RrpB negatively regulates the expression of nfrA (Cj1555c), a flavin reductase. NfrA reduces riboflavin at a much higher rate than flavin mononucleotide (FMN),suggesting exogenous free flavins are the natural substrate. Enzymatic activity of MdaB and NfrA towards their substrates revealed both reductases preferred NADPH as an electron donor. DNA-binding and post translational modification analyses showed that the mechanism of RrpA and RrpB DNA binding is likely a cysteine-based redox switch. Complete genome sequences analysis indicated that MdaB is predominant in Campylobacter spp. and the related Helicobacter spp., whilst NfrA is more often found in C. jejuni strains. Quinones and flavins are antimicrobial redox cycling agents secreted by a wide range of cell-types that can form damaging superoxide by one-electron reactions. We propose that MdaB and NfrA production allows a two-electron reduction mechanism to the less toxic quinol forms. These enzymes thus aid the survival and persistence of C. jejuni in the face of toxic compounds from competing microbes.
2021-11-02 | PXD025924 | Pride