Similarly, EPEC are commonly found in the intestines and faeces of normal animals, but may cause disease in immunocompromised animals.
Top of page. Classification Diseases Pathogenesis Virulence factors and serogroups Diagnostic strategies. Sub-sets of clones differentiated by their ability to cause disease Most E. Sub-sets of pathogenic E.
Transmission of STEC infection mainly occurs through contaminated food or water and contact with animals. Person-to-person transmission is also possible among close contacts families, childcare centres, nursing homes, etc.
A wide variety of food has previously been implicated in outbreaks as suspected sources, including raw unpasteurised raw milk and cheese, undercooked beef, a variety of fresh produce e. Various types of animals, in particular cattle and other ruminants, can be healthy carriers of human-pathogenic STEC that can be spread to humans through faecal contamination.
The infective dose is very low. The incubation period ranges from three to eight days. The typical. The typically bloody diarrhoea is in most cases mild and self-limiting and most people recover within five to seven days. Most varieties of E. Shiga toxin-producing E. STEC strains can cause serious illness in humans by producing toxins that can severely damage the lining of your intestines and kidneys. Complete this free online training and the Minnesota Department of Health will provide certification that your venue has learned about these issues.
Turkey: Safe Thawing and Cooking Food safety tips for handling, thawing, roasting, storing, and reheating turkey. Anderson, G. Intracellular bacterial biofilm-like pods in urinary tract infections. Svanborg-Eden, C. Escherichia coli pili as possible mediators of attachment to human urinary tract epithelial cells.
Korhonen, T. Localization of binding sites for purified Escherichia coli P fimbriae in the human kidney.
Trifillis, A. Binding to and killing of human renal epithelial cells by hemolytic P-fimbriated E. Kidney Int. Uhlen, P. Guyer, D. Identification of Sat, an autotransporter toxin produced by uropathogenic Escherichia coli.
Describes the identification of a new toxin of uropathogenic E. Unhanand, M. Gram-negative enteric bacillary meningitis: a twenty-one-year experience. Dawson, K. Fifteen years of experience with bacterial meningitis. Stoll, B. Changes in pathogens causing early-onset sepsis in very-low-birth-weight infants. Dietzman, D. Neonatal Escherichia coli septicemia-bacterial counts in blood. Stins, M. Bacterial invasion and transcytosis in transfected human brain microvascular endothelial cells.
Escherichia coli binding to and invasion of brain microvascular endothelial cells derived from humans and rats of different ages. Kim, K. The K1 capsule is the critical determinant in the development of Escherichia coli meningitis in the rat. Recognition of the importance of capsule for virulence of MNEC.
Rode, C. Type-specific contributions to chromosome size differences in Escherichia coli. Bonacorsi, S. Identification of regions of the Escherichia coli chromosome specific for neonatal meningitis-associated strains. Badger, J. Application of signature-tagged mutagenesis for identification of Escherichia coli K1 genes that contribute to invasion of human brain microvascular endothelial cells.
Parkkinen, J. Binding sites in the rat brain for Escherichia coli S fimbriae associated with neonatal meningitis. Invest 81 , — Prasadarao, N. Escherichia coli translocation at the blood—brain barrier.
Environmental growth conditions influence the ability of Escherichia coli K1 to invade brain microvascular endothelial cells and confer serum resistance. Hoffman, J. The capsule supports survival but not traversal of Escherichia coli K1 across the blood—brain barrier.
Reddy, M. Involvement of focal adhesion kinase in Escherichia coli invasion of human brain microvascular endothelial cells. Khan, M. Identification of Escherichia coli genes that are specifically expressed in a murine model of septicemic infection. Darfeuille-Michaud, A. Adherent-invasive Escherichia coli : a putative new E. Panigrahi, P. Escherichia coli transcytosis in a Caco-2 cell model: implications in neonatal necrotizing enterocolitis.
Elliott, S. Toth, I. Production of cytolethal distending toxins by pathogenic Escherichia coli strains isolated from human and animal sources: establishment of the existence of a new cdt variant type IV. Janka, A. Cytolethal distending toxin gene cluster in enterohemorrhagic Escherichia coli OH- and OH7: characterization and evolutionary considerations. Otto, B. Escherichia coli hemoglobin protease autotransporter contributes to synergistic abscess formation and heme-dependent growth of Bacteroides fragilis.
McVeigh, A. IS , an Escherichia coli insertion sequence with a heat-stable enterotoxin gene embedded in a transposase-like gene. Hacker, J. Pathogenicity islands and the evolution of microbes. Dobrindt, U. Characterization and evidence of mobilization of the LEE pathogenicity island of rabbit-specific strains of enteropathogenic Escherichia coli. Torres, A. Pathogenicity islands of intestinal E. Ingersoll, M. Pathogenicity islands of Shigella.
Redford, P. Extraintestinal Escherichia coli as a model system for the study of pathogenicity islands. Schubert, S. High-pathogenicity island of Yersinia pestis in enterobacteriaceae isolated from blood cultures and urine samples: prevalence and functional expression. Maurelli, A. USA 95 , — Casalino, M. CadC is the preferential target of a convergent evolution driving enteroinvasive Escherichia coli toward a lysine decarboxylase-defective phenotype.
Weissman, S. Enterobacterial adhesins and the case for studying SNPs in bacteria. Analysis of genome plasticity in pathogenic and commensal Escherichia coli isolates by use of DNA arrays. Mellies, J. The Per regulon of enteropathogenic Escherichia coli : identification of a regulatory cascade and a novel transcriptional activator, the locus of enterocyte effacement LEE -encoded regulator Ler.
Xia, Y. Regulatory cross-talk between adhesin operons in Escherichia coli : inhibition of type 1 fimbriae expression by the PapB protein. Wagner, P. Bacteriophage control of Shiga toxin 1 production and release by Escherichia coli. Zhang, X. Quinolone antibiotics induce Shiga toxin-encoding bacteriophages, toxin production, and death in mice.
Sperandio, V. Quorum sensing controls expression of the type III secretion gene transcription and protein secretion in enterohemorrhagic and enteropathogenic Escherichia coli. USA 96 , First report that enteric bacterial virulence factors are regulated by quorum sensing. Bacteria—host communication: the language of hormones.
Abraham, J. An invertible element of DNA controls phase variation of type 1 fimbriae of Escherichia coli. USA 82 , — Kuehn, M. P pili in uropathogenic E. Bustamante, V. Friedberg, D. Hierarchy in the expression of the locus of enterocyte effacement genes of enteropathogenic Escherichia coli. Role of the nucleoid-associated protein Fis in the regulation of virulence properties of enteropathogenic Escherichia coli.
Grant, A. Quorum-sensing Escherichia coli regulator A: a regulator of the LysR family involved in the regulation of the locus of enterocyte effacement pathogenicity island in enterohemorrhagic E. Quorum sensing Escherichia coli regulators B and C QseBC : a novel two-component regulatory system involved in the regulation of flagella and motility by quorum sensing in E. A plasmid-encoded regulatory region activates chromosomal eaeA expression in enteropathogenic Escherichia coli.
Cloning and characterization of bfpTVW , genes required for the transcriptional activation of bfpA in enteropathogenic Escherichia coli. Shin, S. An activator of glutamate decarboxylase genes regulates the expression of enteropathogenic Escherichia coli virulence genes through control of the plasmid-encoded regulator, Per. Download references. Work in the authors' laboratories is supported by the National Institutes of Health.
We thank J. We apologize to the numerous investigators whose papers could not be cited due to space constraints. You can also search for this author in PubMed Google Scholar. Correspondence to James B. Shigella flexneri 2a. Shiga toxin. James Kaper's laboratory. James Nataro's laboratory. A group of strains of a single species that cause a common disease using a common set of virulence factors. An antigenically distinct variety within a bacterial species.
For E. A plasma membrane protein, also called CD55, that regulates the complement cascade by interfering with the formation of the C3bBb complex. A homologue of MHC major histocompatibility complex I molecules. A nucleolar protein that functions as a shuttle protein between the nucleus and the cytoplasm and is also found on the cell surface. GTPase-activating protein. A family of eukaryotic proteins that modulate the activity of Rac, Rho and Cdc A neuropeptide that is widely distributed in the central nervous system and the gastrointestinal tract.
Binding to the galanin-1 receptor can alter intestinal ion flux. A device that is used to measure ion flow across an epithelium. Bacterial enterotoxins that induce ion fluxes are frequently studied in Ussing chambers. A technique to screen large numbers of distinct mutants for those that fail to survive an animal infection.
Each mutant is tagged with a unique DNA sequence called a signature tag , which allows a specific mutant to be tracked within a large pool of bacteria. In vivo expression technology is a promoter trap technique that uses cloned promoters fused to a reporter gene. A library of such constructs is introduced into an animal model to detect promoters that are activated in vivo. Reprints and Permissions. Kaper, J.
Pathogenic Escherichia coli. Nat Rev Microbiol 2, — Download citation. Issue Date : February Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. BMC Microbiology Irish Veterinary Journal Annals of Clinical Microbiology and Antimicrobials Bulletin of the National Research Centre Advanced search.
Skip to main content Thank you for visiting nature. Download PDF. Key Points In addition to being an important member of the normal intestinal microflora of humans and other mammals, the species Escherichia coli contains many pathotypes that cause a variety of diseases.
Abstract Few microorganisms are as versatile as Escherichia coli. Main Escherichia coli typically colonizes the gastrointestinal tract of human infants within a few hours after birth. Figure 1: Pathogenic schema of diarrhoeagenic E. Full size image. Table 1 E. Figure 2: Colonization factors of E. Table 2 E. Figure 4: Pathogenesis of urinary tract infection caused by uropathogenic E.
Figure 5: Contribution of mobile genetic elements to the evolution of pathogenic E. Figure 6: Expression of virulence factors in pathogenic E. Box 1 Questions for future research What are the best methods for the diagnosis of intestinal E.
What other pathotypes of E. References 1 Sweeney, N. Google Scholar 5 Cassels, F. Google Scholar 13 De Rycke, J. Google Scholar 76 Zychlinsky, A. Google Scholar Korhonen, T. Acknowledgements Work in the authors' laboratories is supported by the National Institutes of Health.
Nataro Authors James B. Kaper View author publications. View author publications. Ethics declarations Competing interests The authors declare no competing financial interests. IVET In vivo expression technology is a promoter trap technique that uses cloned promoters fused to a reporter gene.
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