Enteroaggregative Escherichia coli

Abstract

Enteroaggregative Escherichia coli (EAEC, formerly known as "EAggEC") cause acute or persistent watery diarrhoea (with or without mucus) in children, predominantly in low-income countries, and are associated with travellers' diarrhoea in children and adults in middle and high income countries. The diverse nature of EAEC is such that not all strains cause disease. Conversely, certain strains of EAEC possess additional virulence determinants associated with the ability to cause severe diarrhoea and other symptoms, which might be life-threatening in vulnerable patients. The EAEC virulence factors described to date are either encoded on the large virulence plasmid of EAEC (plasmid of aggregative adherence) or on pathogenicity islands on the chromosome. Testing of food and faecal samples involves the detection of EAEC-associated traits in the matrix followed by isolation of the organism and confirmation of the presence of EAEC-associated genes using PCR. The variability of the plasmid structure and virulence gene sequences and the possibility that this mobile genetic element may be lost has necessitated the inclusion of chromosomal markers in the molecular screening assays. There is evidence in the literature of foodborne transmission of EAEC, but currently no evidence of a zoonotic reservoir. Fimbriae-mediated adhesion and biofilm formation are likely to be involved in both clinical manifestations of infection and attachment to foodstuffs. Multidrug resistance appears to be common in EAEC and geographically widespread. Whole-genome sequencing has revealed the mosaic genomic structure of EAEC and provided evidence that horizontal gene transfer and recombination are the driving force for acquisition of novel genome features and potentially novel pathogenic mechanisms. This has significant public health implications in terms of the diversity and pathogenesis of EAEC and its ability to colonise and cause disease in the human host.

Pathogenicity Factors of Genomic Islands in Intestinal and Extraintestinal Escherichia coli

“…After ETEC, EAEC is the second most common cause of tourista that causes acute and sometimes persistent diarrhea (Jenkins, 2018). The diarrhea is typically non-bloody and without inflammation or emetic symptoms.…”

“…EAEC form a loose biofilm at the mucosal surface involving pili and especially AAF (aggregative adhesion fimbriae, encoded by a large plasmid pAA) (Kaper et al, 2004;Ageorges et al, 2020). Additional virulence factors include the pAA-encoded enterotoxins EAST1 and Pet (plasmid-encoded toxin) and the chromosome-encoded ShET1 (Shigella enterotoxin 1) and Pic (protein involved in intestinal colonization) (Chaudhuri et al, 2010;Jenkins, 2018). However, the molecular basis that mediates diarrhea upon infection by EAEC remains to be elucidated.…”

Antibacterial Activity of Bacteriocinogenic Commensal Escherichia coli against Zoonotic Strains Resistant and Sensitive to Antibiotics

“…The action of these inhibitory molecules, which affects phylogenetically related bacteria, can be vital for the health of the host organism. E. coli occurs not only as a commensal organism in the intestines of warm-blooded animals but also as six well-studied pathotypes causing morbidity and mortality [ 18 , 19 , 20 , 21 , 22 ]. What is more, E. coli bacteria in their primary intestinal environments are exposed to the antibiotics consumed by their host, so as a consequence, the high selection pressure results in the emergence of resistant strains [ 16 ].…”

Human microbiota modulation via QseC sensor kinase mediated in the Escherichia coli O104:H4 outbreak strain infection in microbiome model

“…AggR has been described in EAEC as an important transcriptional activator of at least 44 virulence genes, such as those encoding AAFs and a dispersin (antiaggregation protein) [ 19 – 24 ]. Nonetheless, this pathotype is a genetically very heterogeneous bacterial group, whereas recent studies have found virulence factors statistically correlated with disease, although EAEC complete pathogenesis process remain unclear [ 25 , 26 ].…”