The diarrheic attaching and effacing (A/E) pathogen was first isolated from infants in Bangladesh in 1991, although the bacterium was initially classified as Subsequent genetic and biochemical interrogation of these isolates raised concerns about their initial taxonomic placement. It was not until 2003 that these isolates were reassigned to the novel taxon because they were genetically more closely related to , although they had diverged sufficiently to warrant a novel species name. Unfortunately, new isolates continue to be mistyped as enteropathogenic (EPEC) or enterohemorrhagic (EHEC) owing to shared traits, most notably the ability to form A/E lesions. Consequently, remains an underappreciated A/E pathogen, despite multiple reports demonstrating that many provisional EPEC and EHEC isolates incriminated in disease outbreaks are actually Metagenomic studies on dozens of isolates reveal a genetic architecture that boasts an arsenal of candidate virulence factors to rival that of its better-characterized cousins, EPEC and EHEC. Beyond these computational comparisons, studies addressing the regulation, structure, function, and mechanism of action of its repertoire of virulence factors are lacking. Thus, the paucity of knowledge about the epidemiology, virulence, and antibiotic resistance of , coupled with its misclassification and its ability to develop multidrug resistance in a single step, highlights the challenges in combating this emerging pathogen. This review seeks to synthesize our current but incomplete understanding of the biology of .
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http://dx.doi.org/10.1128/IAI.00254-18 | DOI Listing |
Gut Microbes
December 2024
Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Enteropathogenic (EPEC) is a bacterium that causes attaching/effacing (A/E) lesions and serious diarrheal disease, a major health issue in developing countries. EPEC pathogenicity results from the effect of virulence factors and dysregulation of host responses. Polyamines, including spermidine, play a major role in intestinal homeostasis.
View Article and Find Full Text PDFPLoS Pathog
December 2024
Department of Biochemistry and Molecular Biology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, United States of America.
Attaching and effacing (A/E) bacterial pathogens consist of human pathogens enteropathogenic Escherichia coli, enterohemorrhagic E. coli and their murine equivalent Citrobacter rodentium (CR). Emerging evidence suggests that the complex pathogen-microbiota-host interactions are critical in conferring A/E pathogen infection-induced severe symptoms and lethality in immunocompromised hosts; however, the precise underlying mechanisms remain enigmatic.
View Article and Find Full Text PDFMol Divers
November 2024
Department of Biotechnology, National Institute of Technology Durgapur, Durgapur, 713209, India.
Escherichia coli (E. coli), a gram-negative bacterium, quickly colonizes in the human gastrointestinal tract after birth and typically sustains a long-term, symbiotic relationship with the host. However, certain virulent strains of E.
View Article and Find Full Text PDFSci Rep
October 2024
National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, 102206, China.
PLoS Pathog
October 2024
School of Infection and Immunity, University of Glasgow, Glasgow, United Kingdom.
The ability of the attaching and effacing pathogens enterohaemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium to overcome colonisation resistance is reliant on a type 3 secretion system used to intimately attach to the colonic epithelium. This crucial virulence factor is encoded on a pathogenicity island known as the Locus of Enterocyte Effacement (LEE) but its expression is regulated by several core-genome encoded transcription factors. Here, we unveil that the core transcription factor PdhR, traditionally known as a regulator of central metabolism in response to cellular pyruvate levels, is a key activator of the LEE.
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