Diarrhea, bacteremia and multiorgan dysfunction due to an extraintestinal pathogenic Escherichia coli strain with enteropathogenic E. coli genes.
Ontology highlight
ABSTRACT:
SUBMITTER: Kessler R
PROVIDER: S-EPMC4622172 | biostudies-literature | 2015 Nov
REPOSITORIES: biostudies-literature
Publications
Diarrhea, bacteremia and multiorgan dysfunction due to an extraintestinal pathogenic Escherichia coli strain with enteropathogenic E. coli genes.
Kessler Robert R Nisa Shahista S Hazen Tracy H TH Horneman Amy A Amoroso Anthony A Rasko David A DA Donnenberg Michael S MS
Pathogens and disease 20150926 8
A 55-year-old man with well-controlled HIV had severe diarrhea for 3 weeks and developed multiorgan dysfunction and bacteremia due to Escherichia coli. The genome of the patient's isolate had features characteristic of extraintestinal pathogenic E. coli and genes distantly related to those defining enteropathogenic E. coli. ...[more]
Similar Datasets
Project description:OBJECTIVE:Extraintestinal Pathogenic E. coli (ExPEC), are responsible for host diseases such as Neonatal Meningitis Escherichia coli (NMEC), the second-leading cause of neonatal bacterial meningitis, Avian Pathogenic E. coli (APEC), a cause of extraintestinal disease in poultry, and Uropathogenic E. coli (UPEC), the most common cause of urinary tract infections. Virulence factors associated with NMEC include outer membrane protein A (OmpA) and type I fimbriae (FimH), which also occur in APEC and UPEC. OmpA contributes to NMEC's ability to cross the blood-brain barrier, persist in the bloodstream and has been identified as a potential vaccine target for ExPEC, however the protein has amino acid variants, which may influence virulence of strains or alter vaccine efficacy. Although OmpA is present in virtually all E. coli, differences in its amino acid residues have yet to be surveyed in ExPEC. RESULTS:Here the ompA gene (n?=?399) from ExPEC collections were sequenced and translated in silico. Twenty-five different OmpA polymorphism patterns were identified. Seven polymorphism patterns were significantly associated with an ExPEC subpathotype, but chromosomal history most likely accounts for most differences found. The differences in OmpA protein sequences suggest that OmpA may influence variation in virulence and host specificity within ExPEC subpathotypes.
| S-EPMC6995065 | biostudies-literature
Project description:Evolutionary trade-offs occur when selection on one trait has detrimental effects on other traits. In pathogenic microbes, it has been hypothesized that antibiotic resistance trades off with fitness in the absence of antibiotic. Although studies of single resistance mutations support this hypothesis, it is unclear whether trade-offs are maintained over time, due to compensatory evolution and broader effects of genetic background. Here, we leverage natural variation in 39 extraintestinal clinical isolates of Escherichia coli to assess trade-offs between growth rates and resistance to fluoroquinolone and cephalosporin antibiotics. Whole-genome sequencing identifies a broad range of clinically relevant resistance determinants in these strains. We find evidence for a negative correlation between growth rate and antibiotic resistance, consistent with a persistent trade-off between resistance and growth. However, this relationship is sometimes weak and depends on the environment in which growth rates are measured. Using in vitro selection experiments, we find that compensatory evolution in one environment does not guarantee compensation in other environments. Thus, even in the face of compensatory evolution and other genetic background effects, resistance may be broadly costly, supporting the use of drug restriction protocols to limit the spread of resistance. Furthermore, our study demonstrates the power of using natural variation to study evolutionary trade-offs in microbes.
| S-EPMC5817949 | biostudies-literature
Project description:Large-scale bacterial genome sequencing efforts to date have provided limited information on the most prevalent category of disease: sporadically acquired infections caused by common pathogenic bacteria. Here, we performed whole-genome sequencing and de novo assembly of 312 blood- or urine-derived isolates of extraintestinal pathogenic (ExPEC) Escherichia coli, a common agent of sepsis and community-acquired urinary tract infections, obtained during the course of routine clinical care at a single institution. We find that ExPEC E. coli are highly genomically heterogeneous, consistent with pan-genome analyses encompassing the larger species. Investigation of differential virulence factor content and antibiotic resistance phenotypes reveals markedly different profiles among lineages and among strains infecting different body sites. We use high-resolution molecular epidemiology to explore the dynamics of infections at the level of individual patients, including identification of possible person-to-person transmission. Notably, a limited number of discrete lineages caused the majority of bloodstream infections, including one subclone (ST131-H30) responsible for 28% of bacteremic E. coli infections over a 3-yr period. We additionally use a microbial genome-wide-association study (GWAS) approach to identify individual genes responsible for antibiotic resistance, successfully recovering known genes but notably not identifying any novel factors. We anticipate that in the near future, whole-genome sequencing of microorganisms associated with clinical disease will become routine. Our study reveals what kind of information can be obtained from sequencing clinical isolates on a large scale, even well-characterized organisms such as E. coli, and provides insight into how this information might be utilized in a healthcare setting.
| S-EPMC4317167 | biostudies-literature
Project description:To test the canine reservoir hypothesis of extraintestinal pathogenic Escherichia coli (ExPEC), 63 environmental canine fecal deposits were evaluated for the presence of ExPEC by a combination of selective culturing, extended virulence genotyping, hemagglutination testing, O serotyping, and PCR-based phylotyping. Overall, 30% of canine fecal samples (56% of those that yielded viable E. coli) contained papG-positive E. coli, usually as the predominant E. coli strain and always possessing papG allele III (which encodes variant III of the P-fimbrial adhesin molecule PapG). Multiple other virulence-associated genes typical of human ExPEC were prevalent among the canine fecal isolates. According to serotyping, virulence genotyping, and random amplified polymorphic DNA analysis, over 50% of papG-positive fecal E. coli could be directly correlated with specific human clinical isolates from patients with cystitis, pyelonephritis, bacteremia, or meningitis, including archetypal human ExPEC strains 536, CP9, and RS218. Five canine fecal isolates and (clonally related) archetypal human pyelonephritis isolate 536 were found to share a novel allele of papA (which encodes the P-fimbrial structural subunit PapA). These data confirm that ExPEC representing known virulent clones are highly prevalent in canine feces, which consequently may provide a reservoir of ExPEC for acquisition by humans.
| S-EPMC98021 | biostudies-literature
Project description:Escherichia coli is a major cause of life-threatening infections in patients with neutropenia, particularly those receiving chemotherapy for the treatment of cancer. In most cases, these infections originate from opportunistic strains living within the patient's gastrointestinal tract which then translocate to major organ systems. There are no animal models that faithfully recapitulate these infections, and, as such, the host or bacterial factors that govern this process remain unidentified. We present here a novel model of chemotherapy-induced bacterial translocation of E. coli. Oral gavage of BALB/c mice with a clinical isolate of extraintestinal pathogenic E. coli (ExPEC) leads to stable and long-term colonization of the murine intestine. Following the induction of neutropenia with the chemotherapeutic drug cyclophosphamide, ExPEC translocates from the intestine to the lungs, liver, spleen, and kidneys with concomitant morbidity in infected animals. Translocation can also occur in mice bearing mammary tumors, even in the absence of chemotherapy. Translocation of ExPEC is also associated with an increase of the diversity of bacterial DNA detected in the blood. This is the first report of a chemotherapy-based animal model of ExPEC translocation in cancerous mice, a system that can be readily used to identify important virulence factors for this process.
| S-EPMC4496622 | biostudies-other
Project description:Diarrheagenic Escherichia coli is the major bacterial etiological agent of severe diarrhea and a major concern of public health. These pathogens have acquired genetic characteristics from other pathotypes, leading to unusual and singular genetic combinations, known as hybrid strains and may be more virulent due to a set of virulence factors from more than one pathotype. One of the possible combinations is with extraintestinal E. coli (ExPEC), a leading cause of urinary tract infection, often lethal after entering the bloodstream and atypical enteropathogenic E. coli (aEPEC), responsible for death of thousands of people every year, mainly children under five years old. Here we report the draft genome of a strain originally classified as aEPEC (BA1250) isolated from feces of a child with acute diarrhea. Phylogenetic analysis indicates that BA1250 genome content is genetically closer to E. coli strains that cause extraintestinal infections, other than intestinal infections. A deeper analysis showed that in fact this is a hybrid strain, due to the presence of a set of genes typically characteristic of ExPEC. These genomic findings expand our knowledge about aEPEC heterogeneity allowing further studies concerning E. coli pathogenicity and may be a source for future comparative studies, virulence characteristics, and evolutionary biology.
| S-EPMC8070890 | biostudies-literature
Project description:The role of atypical enteropathogenic Escherichia coli (EPEC) in childhood diarrhea is controversial. The aim of the present study was to search for genes linked with diarrhea in atypical EPEC strains from a case-control study among Norwegian children. Using DNA microarray analysis, genomic DNAs from strains isolated from children with (n = 37) and without (n = 20) diarrhea were hybridized against 242 different oligonucleotide probes specific for 182 virulence genes or markers from all known E. coli pathotypes. PCR was performed to test the strains for seven putative virulence genes not included in the microarray panel. The OI-122 gene efa1/lifA was the gene with the strongest statistical association with diarrhea (P = 0.0008). Other OI-122 genes (set/ent, nleB, and nleE) and genes with other locations (lpfA, paa, ehxA, and ureD) were also associated with diarrheal disease. The phylogenetic marker gene yjaA was negatively associated with diarrhea (P = 0.0004). Atypical EPEC strains could be classified in two main virulence groups based on their content of OI-122, lpfA, and yjaA genes. Among children with diarrhea, atypical EPEC isolates belonging to virulence group I (OI-122 and lpfA positive, yjaA negative) were the most common, while the majority of isolates from healthy children were classified as virulence group II strains (OI-122 negative, lpfA and yjaA positive; P < 0.001). In conclusion, using DNA microarray analysis to determine the virulence gene profile of atypical EPEC isolates, several genes were found to be significantly associated with diarrhea. Based on their composition of virulence genes, the majority of strains could be classified in two virulence groups, of which one was seen mainly in children with diarrhea.
| S-EPMC1594803 | biostudies-literature
Project description:Extraintestinal pathogenic Escherichia coli (ExPEC) is a common bacterial strain causing diverse diseases in humans and animals. To analyse the detailed mechanisms underlying ExPEC-mediated sepsis in humans, the transcriptome response of mice at 3h,6h, and 12h after ExPEC infection was analyzed by RNA-seq of mouse spleen samples.
2022-11-11 | GSE140637 | GEO
Project description:Interactions between humans and pets are increasingly valued in western countries, leading to more extensive contact between humans and their pets within households. Although the magnitude of the risk of transfer of Escherichia coli between humans and their companion animals is undefined, that such transmission occurs has been established and warrants attention. This study examined 186 fresh faecal samples from companion dogs visiting 22 municipal dog parks in the Minneapolis/Saint Paul metropolitan area, Minnesota, USA. Samples were processed to isolate 3rd-generation cephalosporin-resistant E. coli, which were further characterized using PCR-based virulence genotyping, antimicrobial susceptibility profiling and whole-genome sequencing. Of the 186 faecal samples, 29% yielded cephalosporin-resistant E. coli, and 2.2% yielded extended-spectrum beta-lactamase producers. Co-resistance to sulfonamides was typical (77.3% of isolates), and multidrug resistance (i.e. to ≥3 antimicrobial classes), including to combinations of tetracyclines, phenicols, quinolones and aminoglycosides, was substantial (18.9% of isolates). Identified beta-lactamase genes included blaCMY-2 , blaTEM-1B , blaTEM-1 , blaCTX-M-24 , blaCTX-M-15 and blaOXA-1 . Genome sequencing of 14 isolates identified genes typical of extraintestinal pathogenic E. coli or enteropathogenic E. coli. In three instances, closely related isolates were recovered from different dogs, within either the same park-suggesting transfer of E. coli between dogs within the park-or different parks-suggesting that dogs may be pre-disposed to carry certain E. coli types, such as those from serogroups O4, O71 and O157. This study adds to the existing evidence that companion dogs can harbour and share antimicrobial-resistant E. coli with presumed intestinal or extraintestinal pathogenic potential.
| S-EPMC9796152 | biostudies-literature
Project description:Multilocus sequence typing (MLST) is usually based on the sequencing of 5 to 8 housekeeping loci in the bacterial chromosome and has provided detailed descriptions of the population structure of bacterial species important to human health. However, even strains with identical MLST profiles (known as sequence types or STs) may possess distinct genotypes, which enable different eco- or pathotypic lifestyles. Here we describe a two-locus, sequence-based typing scheme for Escherichia coli that utilizes a 489-nucleotide (nt) internal fragment of fimH (encoding the type 1 fimbrial adhesin) and the 469-nt internal fumC fragment used in standard MLST. Based on sequence typing of 191 model commensal and pathogenic isolates plus 853 freshly isolated clinical E. coli strains, this 2-locus approach-which we call CH (fumC/fimH) typing-consistently yielded more haplotypes than standard 7-locus MLST, splitting large STs into multiple clonal subgroups and often distinguishing different within-ST eco- and pathotypes. Furthermore, specific CH profiles corresponded to specific STs, or ST complexes, with 95% accuracy, allowing excellent prediction of MLST-based profiles. Thus, 2-locus CH typing provides a genotyping tool for molecular epidemiology analysis that is more economical than standard 7-locus MLST but has superior clonal discrimination power and, at the same time, corresponds closely to MLST-based clonal groupings.
| S-EPMC3294456 | biostudies-literature