Escherichia coli is a Gram-negative, rod-shaped bacterium belonging to the Enterobacteriaceae family[1]. This microorganism was first described by Theodor Escherich in 1885. E. coli typically colonizes the gastrointestinal tract of human infants within a few hours after birth. Usually, E. coli and its human host coexist harmoniously and mutual benefit for decades[2]. E. coli includes not only commensal strains but also pathogenic ones, which cause a variety of human diseases, resulting in more than 2 million deaths each year. There are currently approximately 186 different E. coli O-groups and over 50 H-types, making serotyping highly complex.
The diversity between E. coli strains is driven by high genome plasticity, genes are regularly gained and lost, leading to high variability in gene content between lineages and isolates[3]. The combination of these factors, a large gene pool, genome plasticity, global distribution, and ubiquity across niches, make E. coli an important genetic storehouse for the spread and wider dissemination of genes, including those that confer resistance and virulence[4].
E. coli possesses various virulence factors (VFs), including toxins, adhesins, siderophores, and polysaccharide capsules. Many of these VFs are related to the pathogenicity of E. coli, with a wide range of pathogenic activities[5]. The pathogenic species encompass intestinal and extraintestinal pathogens. The intestinal pathogens, also known as diarrheagenic E. coli, are classified into seven categories: enteropathogenic E. coli (EPEC), enterohaemorrhagic E. coli (EHEC), enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), adherent invasive E. coli (AIEC), and diffusely adhering E. coli (DAEC)[6]. EHECs are the only diarrhoeagenic E. coli that pose a concern in developed countries, as their major reservoir is in the gastrointestinal tracts of cattle[7]. EHEC infections cause severe diarrhoea, and complications of an infection can cause haemolytic uraemic syndrome, a life-threatening condition that can lead to kidney failure[7]; ETEC strains are a global cause of acute diarrheal disease in both human and animals, responsible for a high rate of infantile mortality in developing countries. They are also an important agent of diarrhea among travelers from industrialized countries visiting tropical or subtropical areas of the world; EPEC was divided into two groups, typical EPEC (tEPEC) and atypical EPEC (aEPEC). The basic difference between the two groups is the presence of the EPEC adherence factor plasmid in tEPEC and its absence in aEPEC[8]. Extraintestinal pathogenic E. coli (ExPEC) strains cause diverse infections outside of the intestinal tract in humans and animals, represent a significant public health burden worldwide. Based on the host and the site of infection, different ExPEC strains are subclassified as neonatal meningitis E. coli (NMEC), sepsis-associated E. coli (SEPEC), uropathogenic E. coli (UPEC), which cause newborn meningitis, sepsis, and urinary tract infections, respectively; and avian pathogenic E. coli (APEC), which mainly causes respiratory and systemic disease in poultry[9]. The E. coli population is subdivided into phylogenetic groups A, B1, B2, C, D, F, and G, and cryptic clades, with ExPEC strains deriving predominantly from phylogroups B2 and D. Strains from phylogroups B2 and D typically have more virulence-associated genes than do those from phylogroups A and B1, which are associated with commensal and intestinal pathogenic E. coli[10].
E. coli has been designated a priority pathogen by the World Health Organization due to its high levels of drug resistance[11]. The most problematic mechanisms in E. coli correspond to the acquisition of genes coding for extended-spectrum β-lactamases (conferring resistance to broad-spectrum cephalosporins), carbapenemases (conferring resistance to carbapenems), 16S rRNA methylases (conferring pan-resistance to aminoglycosides), plasmid-mediated quinolone resistance genes (conferring resistance to [fluoro]quinolones), and mcr genes (conferring resistance to polymyxins)[12].
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