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dbGaP phs001248 Gene Array to Predict Bacterial Infection with in Respiratory Illness - Eligibility

- 12/5/23 - 5 formularios, 1 itemgroup, 10 items, 1 idioma

Itemgroup: IG.elig

Principal Investigator: Ann Falsey, MD, University of Rochester, Rochester, NY, USA MeSH: Respiratory Tract Infections https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001248 Accurate tests for microbiologic diagnosis of lower respiratory tract infections (LRTI) are needed. Gene expression profiling of whole blood represents a powerful new approach for analysis of the host response during respiratory infection that can be used to supplement pathogen detection testing. Using qPCR, we prospectively validated the differential expression of 10 genes previously shown to discriminate bacterial and non-bacterial LRTI confirming the utility of this approach. In addition, a novel approach using RNAseq analysis identified 141 genes differentially expressed in LRTI subjects with bacterial infection. Using "pathway-informed" dimension reduction, we identified a novel 11 gene set (selected from lymphocyte, α-linoleic acid metabolism, and IGF regulation pathways) and demonstrated a predictive accuracy for bacterial LRTI (nested CV-AUC=0.87). RNAseq represents a new and an unbiased tool to evaluate host gene expression for the diagnosis of LRTI.

Respiratory Tract Infections

pht006092.v1.p1

1 itemgroup 4 items

pht006093.v1.p1

1 itemgroup 5 items

pht006094.v1.p1

1 itemgroup 23 items

pht006095.v1.p1

1 itemgroup 5 items

dbGaP phs001347 Prematurity, Respiratory Outcomes, Immune System, and Microbiome Study (PRISM) - Eligibility

- 11/11/24 - 5 formularios, 2 itemgroups, 20 items, 1 idioma

Itemgroups: IG.0, IG.5

Principal Investigator: Gloria Pryhuber, University of Rochester Rochester, Rochester, NY, USA MeSH: Infant, Premature,Infant, Newborn,Premature Birth,Term Birth,Microbiota,Gastrointestinal Microbiome,T-Lymphocytes,Bronchopulmonary Dysplasia,Respiratory Tract Diseases https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001347 *Public health importance*: Babies born preterm, approximately 1 out of every 9 live births in the United States, have significant respiratory morbidity over the first two years of life, exacerbated by respiratory viral infections. Many (50%) return to pediatricians, emergency rooms and pulmonologists with symptoms of respiratory dysfunction (SRD): intermittent or chronic wheezing, poor growth and an excess of upper and lower respiratory tract infections (LRTI). SRD correlate inversely with gestational age and weight at birth and is more common in those with chronic lung disease of prematurity, yet its incidence and severity varies widely among both the prematurely born and those born at term. There is evidence from clinical studies and animal models that risks of LRTI and recurrent wheezing is influenced by gut and respiratory flora and by T cell responses to infection. Information gained from this study will be used to identify characteristics, risk factors and potential mechanisms for early and persistent lung disease in children born at term and born preterm. This Clinical Research Study will investigate the relationships between sequential respiratory viral infections, patterns of intestinal and respiratory bacterial colonization, and adaptive cellular immune phenotypes which are associated with increased susceptibility to respiratory infections and long term respiratory morbidity in preterm and full term infants. We hypothesize that the timing and acquisition of specific viral infections and bacterial species are directly related to respiratory morbidity in the first year of life as defined by SRD and by measures of pulmonary function. We hypothesize that cellular and molecular immuno-maturity are altered due to factors presented by premature birth in such a way as to promote chronic inflammatory and cytotoxic damage to the lung, with subsequent enhanced, damaging responses to infectious agents and environmental irritants. Our preliminary studies demonstrate both feasibility and expertise in mutiparameter immunophenotyping of small volume peripheral blood samples obtained from premature infants including gene expression arrays of flow cytometry sorted cells. We will use new technologies for known viral identification, as well as high-throughput metagenome sequencing of RNA and DNA virus like particles (VLP) to be used for viral discovery in infant respiratory sample and use of high-throughput pyrosequencing (454T) of bacterial 16S rRNA to determine shifts in bacterial community structure, occurring in pre-term (PT) as compared to full term (FT) infants, over the first year of life. Finally, we present statistical approaches to stratify disease risk predictors using multivariate logistic regression modeling approaches. We propose to evaluate T cell phenotypic and functional profiles relative to viral and predominant bacterial exposures according to highly complementary, but independent, Specific Objectives. *Objective 1*: To determine if viral respiratory infections and patterns of respiratory and gut bacterial community structure (microbiome) in prematurely born babies predict the rate and degree of immunologic maturation, and pulmonary dysfunction, measured from birth to 36 weeks corrected gestational age (CGA). *Objective 2*: To determine the relationship between respiratory viral infections and disease severity up to one year CGA, and the lymphocyte (Lc) phenotypes documented at term gestation (birth for term infants and 36 wks/NICU discharge in preterm infants) and at one year CGA. Three secondary outcomes of this objective will be to a) relate the quantity, type and severity of viral infections with pulmonary function at one and three years of life, b) relate the viral community structure to severity of viral infections and c) to seek evidence of modulation of viral susceptibility by bacterial respiratory and gut community structure (microbiome). The relationship of colonization with known and non-identified bacterial species in both the respiratory tract and the gut will be evaluated. Flow cytometry data corresponding to this study can be found within Immport study SDY1302. Positive and negative controls for microbiome samples are uploaded under SRA bioproject PRJNA474485. Microbiome samples corresponding to PRISM2 are distinguished from PRISM1 via "_PRISM2" appended to the sample name. Within the positive and negative controls, PRISM1 controls are uploaded as bam files and PRISM2 controls are uploaded as paired fastq. Samples ending in -08 correspond to TLDA qPCR results for a given sample. There is a column for each pathogen tested and a column to indicate where that pathogen was bacteria or virus.

pht006796.v3.p2

1 itemgroup 32 items

pht006794.v3.p2

1 itemgroup 7 items

pht006795.v3.p2

1 itemgroup 2 items

pht006797.v3.p2

1 itemgroup 94 items

dbGaP phs000896 Functional Dynamics of the Elderly Gut Microbiome During Probiotic Consumption - pht005123.v1.p1

- 2/4/24 - 6 formularios, 1 itemgroup, 4 items, 1 idioma

Itemgroup: pht005123

Principal Investigator: Patricia L. Hibberd, Division of Global Health, Massachusetts General Hospital for Children, Boston, MA, USA MeSH: Human Microbiome https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000896 A mechanistic understanding of the health benefits conferred by consumption of probiotic bacteria has been limited by our knowledge of the resident gut microbiota and its interaction with the host. We used fecal samples from a study of twelve healthy individuals aged 65-80 to characterize the structure and functional dynamics of the gut microbiota associated with consumption of the single-organism probiotic, Lactobacillus rhamnosus GG ATCC 53103 (LGG). Samples were collected prior to probiotic consumption (day 0), on day 28 immediately after consuming 10^10 CFU of LGG twice daily for 28 days and day 56, one month after stopping LGG consumption. Our integrative approach incorporated bacterial 16S rRNA gene sequencing, whole-community expression profiling using RNA-seq, and metagenomic sequencing. We highlight the value of combinatorial 'omics methods and concomitant high-resolution informatics to probe the role that probiotics may play on the structure and function of the resident microbiota.

Microbiota

pht005124.v1.p1

1 itemgroup 5 items

pht005125.v1.p1

1 itemgroup 5 items

pht005126.v1.p1

1 itemgroup 5 items

pht005127.v1.p1

1 itemgroup 3 items

Eligibility

1 itemgroup 1 item

dbGaP phs000659 Mount Sinai Hospital (MSH, Toronto, CANADA) pelvic pouch microbiome study - pht003521.v1.p1

- 24/1/23 - 5 formularios, 1 itemgroup, 2 items, 1 idioma

Itemgroup: pht003521

Principal Investigator: Mark Silverberg, MD., PhD, Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, ON, CANADA MeSH: Inflammatory Bowel Diseases,Crohn Disease,Colitis, Ulcerative,Pouchitis,Adenomatous Polyposis Coli https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000659 This study involved evaluation of the tissue associated microbiome of the ileal pouch following surgery for ulcerative colitis (UC) or familial adenomatous polyposis (FAP). Individuals were recruited, with biopsies taken from the ileal pouch and the pre-pouch ileum, microbial DNA was extracted and sequenced using 454 pyrosequencing. Total bacterial community structure and abundance were evaluated to determine which changes were characteristic of inflammatory phenotypes including pouchitis (inflammation of the ileal pouch) and a Crohn's disease-like phenotype.

Eligibility

1 itemgroup 7 items

pht003522.v1.p1

1 itemgroup 3 items

pht003523.v1.p1

1 itemgroup 6 items

pht003524.v1.p1

1 itemgroup 5 items

dbGaP phs000735 The Placenta Harbors a Unique Microbiome - Eligibility

- 20/12/22 - 5 formularios, 1 itemgroup, 3 items, 1 idioma

Itemgroup: IG.elig

Principal Investigator: Aagaard, Kjersti, M.D., Ph.D, Baylor College of Medicine, Houston, TX, USA MeSH: Bacterial Infections https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000735 This study is to investigate placental microbiome through 16S rDNA-based and whole genome shotgun metagenomic sequencing. Identified taxa and their gene carriage patterns were compared to other human body sites niches. The placental microbiome profiles were most akin to the human oral microbiome.

Bacterial Infections

pht003796.v1.p1

1 itemgroup 3 items

pht003798.v1.p1

1 itemgroup 7 items

pht003795.v1.p1

1 itemgroup 2 items

pht003797.v1.p1

1 itemgroup 3 items

dbGaP phs000633 Enrichment of Lung Microbiome Associated with Pulmonary Inflammation - pht003623.v1.p1

- 25/11/22 - 4 formularios, 1 itemgroup, 5 items, 1 idioma

Itemgroup: pht003623

Principal Investigator: Leopoldo Nicolas Segal, PhD, New York University, School of Medicine, New York, NY, USA MeSH: Pneumonia https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000633 *Background*: The lung microbiome of healthy individuals frequently harbors oral organisms. Despite evidence that micro-aspiration is commonly associated with smoking-related lung diseases, the effects of lung microbiome enrichment with upper airway taxa on inflammation has not been studied. We hypothesize that the presence of oral microorganisms in the lung microbiome is associated with enhanced pulmonary inflammation. *Methods*: We sampled bronchoalveolar lavage (BAL) from the lower airways of 29 asymptomatic subjects (9 never-smokers, 14 former-smokers and 6 current-smokers). We quantified, amplified, and sequenced 16S rRNA genes from BAL samples by qPCR and 454 sequencing. Pulmonary inflammation was assessed by exhaled nitric oxide (eNO), BAL lymphocytes and neutrophils. *Results*: BAL had lower total 16S than supraglottic samples and higher than saline background. Bacterial communities in the lower airway clustered in two distinct groups that we designated as pneumotypes. The rRNA gene concentration and microbial community of the first pneumotype was similar to that of the saline background. The second pneumotype had higher rRNA gene concentration and higher relative abundance of supraglottic-characteristic taxa (SCT), such as Veillonella and Prevotella, and we called it pneumotypeSCT. Smoking had no effect on pneumotype allocation, alpha or beta diversity. PneumotypeSCT was associated with higher BAL lymphocyte-count (p = 0.007), BAL neutrophil-count (p = 0.034) and eNO (p = 0.022). *Conclusion*: A pneumotype with high relative abundance of supraglottic-characteristic taxa is associated with enhanced subclinical lung inflammation.

Pneumonia

pht003624.v1.p1

1 itemgroup 5 items

pht003625.v1.p1

1 itemgroup 2 items

pht003626.v1.p1

1 itemgroup 5 items

dbGaP phs000258 Human Gut Microbiome in Amish Obesity - pht001240.v2.p1

- 12/10/22 - 3 formularios, 1 itemgroup, 5 items, 1 idioma

Itemgroup: pht001240

Principal Investigator: Claire Fraser-Liggett, University of Maryland School of Medicine, Baltimore, MD, USA MeSH: Obesity,Obesity, Morbid https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000258 Emerging evidence that the gut microbiota may contribute in important ways to human health and disease has led us and others to hypothesize that both symbiotic and pathological relationships between gut microbes and their host may be key contributors to obesity and the metabolic complications of obesity. Our "Thrifty Microbiome Hypothesis" poses that gut microbiota play a key role in human energy homeostasis. Specifically, constituents of the gut microbial community may introduce a survival advantage to its host in times of nutrient scarcity, promoting positive energy balance by increasing efficiency of nutrient absorption and improving metabolic efficiency and energy storage. However, in the presence of excess nutrients, fat accretion and obesity may result, and in genetically predisposed individuals, increased fat mass may result in preferential abdominal obesity, ectopic fat deposition (liver, muscle), and metabolic complications of obesity (insulin resistance, hypertension, hyperlipidemia). Furthermore, in the presence of excess nutrients, a pathological transition of the gut microbial community may occur, causing leakage of bacterial products into the intestinal lymphatics and portal circulation, thereby inducing an inflammatory state, further aggravating metabolic syndrome traits and accelerating atherosclerosis. This pathological transition and the extent to which antimicrobial leakage occurs and causes inflammatory and other maladaptive sequelae of obesity may also be influenced by host factors, including genetics. In the proposed study, we will directly test the Thrifty Microbiome Hypothesis by performing detailed genomic and functional assessment of gut microbial communities in intensively phenotyped and genotyped human subjects before and after intentional manipulation of the gut microbiome. To address these hypotheses, five specific aims are proposed: (1) enroll three age- and sex-matched groups from the Old Order Amish: (i) 50 obese subjects (BMI 30 kg/m2) with metabolic syndrome, (ii) 50 obese subjects (BMI 30 kg/m2) without metabolic syndrome, and (iii) 50 non-obese subjects (BMI 25 kg/m2) without metabolic syndrome and characterize the architecture of the gut microbiota from the subjects enrolled in this study by high-throughput sequencing of 16S rRNA genes; (2) characterize the gene content (metagenome) to assess the metabolic potential of the gut microbiota in 75 subjects to determine whether particular genes or pathways are correlated with disease phenotype; (3) characterize the transcriptome in 75 subjects to determine whether differences in gene expression in the gut microbiota are correlated with disease phenotype, (4) determine the effect of manipulation of the gut microbiota with antibiotics on energy homeostasis, inflammation markers, and metabolic syndrome traits in 50 obese subjects with metabolic syndrome and (5) study the relationship between gut microbiota and metabolic and cardiovascular disease traits, weight change, and host genomics in 1,000 Amish already characterized for these traits and in whom 500K Affymetrix SNP chips have already been completed. These studies will provide our deepest understanding to date of the role of gut microbes in terms of 'who's there?', 'what are they doing?', and 'how are they influencing host energy homeostasis, obesity and its metabolic complications? PUBLIC HEALTH RELEVANCE: This study aims to unravel the contribution of the bacteria that normally inhabit the human gastrointestinal tract to the development of obesity, and its more severe metabolic consequences including cardiovascular disease, insulin resistance and Type II diabetes. We will take a multidisciplinary approach to study changes in the structure and function of gut microbial communities in three sets of Old Order Amish patients from Lancaster, Pennsylvania: obese patients, obese patients with metabolic syndrome and non-obese individuals. The Old Order Amish are a genetically closed homogeneous Caucasian population of Central European ancestry ideal for genetic studies. These works have the potential to provide new mechanistic insights into the role of gut microflora in obesity and metabolic syndrome, a disease that is responsible for significant morbidity in the adult population, and may ultimately lead to novel approaches for prevention and treatment of this disorder.

Obesity

pht001242.v2.p1

1 itemgroup 12 items

pht001241.v2.p1

1 itemgroup 4 items

dbGaP phs000259 Urethral Microbiome of Adolescent Males - pht001244.v2.p1

- 12/10/22 - 7 formularios, 1 itemgroup, 2 items, 1 idioma

Itemgroup: pht001244

Principal Investigator: J. Dennis Fortenberry, Indiana University School of Medicine, Indianapolis, IN, USA MeSH: Genitalia, Male,Urethritis,Sexually Transmitted Diseases, Bacterial,Circumcision, Male,Dysuria,Prostatitis https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000259 Urethral microbiome of adolescent males is designed to characterize the microbial communities resident in the urethra of young men, to identify differences in these communities as a function of race/ethnicity, circumcision status, sexual exposures, and uro-genital symptoms. We collect detailed sexual behavior and symptoms data using cellular telephones with Internet access. Specimens are routinely collected at monthly intervals, and intermittently following reported symptoms, specific sexual exposures, or identification of a sexually transmitted infection. We also collect periodic samples from the penile coronal sulcus to better characterize its relationship to the urethral micriobial communities. Participants are ages 14 - 17 at enrollment, and prior history of sexual exposure is not required for participation. Parental permission is obtained for each participant. The planned duration of followup is up to 4 years allowing for prospective observation of both physical and behavioral maturation from middle adolescence into young adulthood. The overall objectives of the project are to better characterize the healthy male urethral microbiome, and to use this information to better understand acquisition of urethritis and sexually transmitted infections, as well as chronic genital pain and prostatitis syndromes that become common among young adults.

pht001243.v2.p1

1 itemgroup 2 items

pht001245.v2.p1

1 itemgroup 17 items

pht001246.v2.p1

1 itemgroup 6 items

pht001247.v2.p1

1 itemgroup 17 items

Eligibility

1 itemgroup 5 items

pht001416.v1.p1

1 itemgroup 2 items

dbGaP phs000263 Metagenomic Study of the Human Skin Microbiome Associated with Acne - Eligibility

- 29/1/25 - 6 formularios, 1 itemgroup, 12 items, 1 idioma

Itemgroup: IG.elig

Principal Investigator: Huiying Li, PhD, David Geffen School of Medicine, University of California, Los Angeles, CA, USA MeSH: Acne Vulgaris https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000263 Acne vulgaris affects 17 million Americans, more than 80% of the people of age 12-24. The goal of this study is to investigate the relationship between acne pathogenesis and the skin microbiota residing in the microcomedones. This study will enroll approximately 100 healthy individuals and acne patients, both male and female with age 13 or older. Data obtained from this study will help better understand the disease pathogenesis and may lead to the development of new effective therapeutic strategies for treatment of acne.

Acne Vulgaris

pht001233.v1.p1

1 itemgroup 4 items

pht001234.v1.p1

1 itemgroup 13 items

pht001235.v1.p1

1 itemgroup 3 items

pht001236.v1.p1

1 itemgroup 2 items

pht001428.v1.p1

1 itemgroup 3 items

dbGaP phs000266 Skin Microbiome in Disease States: Atopic Dermatitis and Immunodeficiency - pht001264.v4.p1

- 29/1/25 - 6 formularios, 1 itemgroup, 5 items, 1 idioma

Itemgroup: pht001264

Principal Investigator: Julia Segre, PhD, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA MeSH: Dermatitis, Atopic,Job's Syndrome,Wiskott-Aldrich Syndrome https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000266 The NIH Intramural Skin Microbiome Consortium (NISMC) is a collaboration of investigators with primary expertise in genomics, bioinformatics, large-scale DNA sequencing, dermatology, immunology, allergy, infectious disease, and clinical microbiology. Atopic dermatitis (AD, "eczema") is a chronic relapsing skin disorder that affects ~15% of U.S. children and is associated with $1 billion of medical costs annually. AD is characterized by dry, itchy skin, infiltrated with immune cells. Colonization by Staphylococcus aureus (S. aureus) is ten-fold more common in AD patients and is associated with disease flares. We hypothesize that, in addition to S. aureus, AD may also be associated with additional novel microbes and/or selective shifts of commensal microbes that are relevant to disease progression. The NISMC seeks to define the microbiota that resides in and on the skin and nares of three patient groups, all of whom have eczematous lesions and are currently seen at the NIH Clinical Center: (1) AD patients; (2) Wiskott-Aldrich syndrome (WAS) patients; and (3) Hyper IgE syndrome (HIES) syndrome patients. Examination of the microbiome of patients with WAS or HIES syndromes, both rare immunodeficiencies, will advance our understanding of how an individual's immune system shapes their cutaneous microbial community. We are performing a prospective longitudinal study that follows these groups of patient thorough the cycles of eczema flares, ascertaining clinical data and samples at each stage.

Dermatitis, Atopic

pht001265.v4.p1

1 itemgroup 5 items

Eligibility

1 itemgroup 27 items

pht001266.v4.p1

1 itemgroup 10 items

pht001446.v4.p1

1 itemgroup 2 items

pht002360.v3.p1

1 itemgroup 7 items

dbGaP phs000970 Mercury and Gut Microbiota - Eligibility

- 1/12/23 - 5 formularios, 1 itemgroup, 2 items, 1 idioma

Itemgroup: IG.elig

Principal Investigator: Sarah E. Rothenberg, D.Env, University of South Carolina, Department of Environmental Health Sciences, Columbia, SC, USA MeSH: Methylmercury Compounds https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000970 There are few studies that have characterized maternal gut microbiota and fetal methylmercury exposure, yet microbes likely modulate this relationship. The primary objective of our pilot study was to determine associations between gut microbial taxa and mercury concentrations in multiple biomarkers (stool, hair, and cord blood). Our secondary objective was to determine the contribution of gut microbial mercury methylation to stool methylmercury.

Methylmercury Compounds

pht005017.v1.p1

1 itemgroup 3 items

pht005019.v1.p1

1 itemgroup 3 items

pht005016.v1.p1

1 itemgroup 2 items

pht005018.v1.p1

1 itemgroup 9 items

dbGaP phs001260 Metagenomic Epidemiology of Antibiotic Resistance in Infectious Diarrhea - pht006054.v1.p1

- 5/5/23 - 5 formularios, 1 itemgroup, 15 items, 1 idioma

Itemgroup: pht006054

Principal Investigator: Sarah Highlander, PhD, J Craig Venter Institute, La Jolla, CA, USA MeSH: Diarrhea,Escherichia coli,Salmonella,Campylobacter,Norovirus,Astroviridae,Adenoviridae,Gastroenteritis,Rotavirus https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001260 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. 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.

Eligibility

1 itemgroup 20 items

pht006051.v1.p1

1 itemgroup 5 items

pht006052.v1.p1

1 itemgroup 5 items

pht006053.v1.p1

1 itemgroup 16 items

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