Pathogenicity Factors of Genomic Islands in Intestinal and Extraintestinal Escherichia coli

Abstract

Escherichia coli is a versatile bacterial species that includes both harmless commensal strains and pathogenic strains found in the gastrointestinal tract in humans and warmblooded animals. The growing amount of DNA sequence information generated in the era of "genomics" has helped to increase our understanding of the factors and mechanisms involved in the diversification of this bacterial species. The pathogenic side of E. coli that is afforded through horizontal transfers of genes encoding virulence factors enables this bacterium to become a highly diverse and adapted pathogen that is responsible for intestinal or extraintestinal diseases in humans and animals. Many of the accessory genes acquired by horizontal transfers form syntenic blocks and are recognized as genomic islands (GIs). These genomic regions contribute to the rapid evolution, diversification and adaptation of E. coli variants because they are frequently subject to rearrangements, excision and transfer, as well as to further acquisition of additional DNA. Here, we review a subgroup of GIs from E. coli termed pathogenicity islands (PAIs), a concept defined in the late 1980s by Jörg Hacker and colleagues in Werner Goebel's group at the University of Würzburg, Würzburg, Germany. As with other GIs, the PAIs comprise large genomic regions that differ from the rest of the genome by their G + C content, by their typical insertion within transfer RNA genes, and by their harboring of direct repeats (at their ends), integrase determinants, or other mobility loci. The hallmark of PAIs is their contribution to the emergence of virulent bacteria and to the development of intestinal and extraintestinal diseases. This review summarizes the current knowledge on the structure and functional features of PAIs, on PAI-encoded E. coli pathogenicity factors and on the role of PAIs in host-pathogen interactions.

The Role of OmpR in Bile Tolerance and Pathogenesis of Adherent-Invasive Escherichia coli

“…A panel of 8 diverse AIEC clinical strains isolated from 8 different CD patients was used to evaluate the clinical relevance of OmpR as a drug target ( Table 1 ). All the strains belonged to distinct sequence types and encoded different FimH variants, reflecting the genotypic variability of the AIEC group ( Desvaux et al, 2020 ). Except for the strain S179, all AIEC strains belonged to the S70/N78 FimH clade, conferring higher ability to adhere to intestinal epithelial cells ( Dreux et al, 2013 ).…”

Carbapenem Resistance Profiles of Pathogenic Escherichia coli in Uganda

“…This is in agreement with previous studies [24,60] which reported PAI IV536 as the most prevalent PAI. The main virulence genes residing in the PAI IV536 and PAI IICFT073 are yersiniabactin siderophore iron-uptake system and P. mbriae as well as iron regulated proteins respectively [61,63,64]. A previous study in Uganda reported high prevalence of E. coli with P. mbriae virulent factor encoded for by the pap gene in UPEC [65]indicating high prevalence of PAI IICFT073 pathotypes.…”

“…Furthermore, existence of virulence genes and genetic determinants of resistance in phylogenetic groups A and D where commensal mainly fall should be treated as a major threat as they are considered to reservoirs of genetic determinants of virulence and antibiotic resistance and they donate these traits to the pathogenic strains of phylogroups B1 and B2 through horizontal gene transfer, arbitrated regularly by plasmids and transposons [44]. Indeed, previous studies observed that PAIs are mobile genetic elements (transposons) that are transferred from one E. coli strain to another through horizontal gene transfer mediated by bacteriophages, conjugative plasmids, conjugation and homologous DNA recombination [64,81,82]…”

Carbapenem Resistance Profiles of Pathogenic Escherichia coli in Uganda

“…This is in agreement with previous studies [22,65] which reported PAI IV536 as the most prevalent PAI. The main virulence genes residing in the PAI IV536 and PAI IICFT073 are yersiniabactin siderophore iron-uptake system and P. fimbriae as well as iron regulated proteins respectively [66,68,69]. A previous study in Uganda reported high prevalence of E. coli with P. fimbriae virulent factor encoded for by the pap gene in UPEC [70]indicating high prevalence of PAI IICFT073 pathotypes.…”

“…Furthermore, existence of virulence genes and genetic determinants of resistance in phylogenetic groups A and D where commensal mainly fall should be treated as a major threat as they are considered to reservoirs of genetic determinants of virulence and antibiotic resistance and they donate these traits to the pathogenic strains of phylogroups B1 and B2 through horizontal gene transfer, arbitrated regularly by plasmids and transposons [49]. Indeed, previous studies observed that PAIs are mobile genetic elements (transposons) that are transferred from one E. coli strain to another through horizontal gene transfer mediated by bacteriophages, conjugative plasmids, conjugation and homologous DNA recombination [69,85,86].…”