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.