Role of Intraspecies Recombination in the Spread of Pathogenicity Islands within the Escherichia coli Species

Abstract

Horizontal gene transfer is a key step in the evolution of bacterial pathogens. Besides phages and plasmids, pathogenicity islands (PAIs) are subjected to horizontal transfer. The transfer mechanisms of PAIs within a certain bacterial species or between different species are still not well understood. This study is focused on the High-Pathogenicity Island (HPI), which is a PAI widely spread among extraintestinal pathogenic Escherichia coli and serves as a model for horizontal transfer of PAIs in general. We applied a phylogenetic approach using multilocus sequence typing on HPI-positive and -negative natural E. coli isolates representative of the species diversity to infer the mechanism of horizontal HPI transfer within the E. coli species. In each strain, the partial nucleotide sequences of 6 HPI–encoded genes and 6 housekeeping genes of the genomic backbone, as well as DNA fragments immediately upstream and downstream of the HPI were compared. This revealed that the HPI is not solely vertically transmitted, but that recombination of large DNA fragments beyond the HPI plays a major role in the spread of the HPI within E. coli species. In support of the results of the phylogenetic analyses, we experimentally demonstrated that HPI can be transferred between different E. coli strains by F-plasmid mediated mobilization. Sequencing of the chromosomal DNA regions immediately upstream and downstream of the HPI in the recipient strain indicated that the HPI was transferred and integrated together with HPI–flanking DNA regions of the donor strain. The results of this study demonstrate for the first time that conjugative transfer and homologous DNA recombination play a major role in horizontal transfer of a pathogenicity island within the species E. coli.

Survival of Escherichia coli in the environment: fundamental and public health aspects

“…An investigation of online genomic data taught us that this operon was actually spread across the different E. coli subgroups in both pathogenic and commensal forms (Figure 3). The operon may be considered to represent an environmentally relevant trait that is transferable by horizontal gene transfer given its occurrence in many species and genera in the family Enterobacteriaceae (Schubert et al, 2009). However, we do not know what it adds to the already substantial iron-scavenging capabilities of E. coli.…”

UPEC strain characterization isolated from Mexican patients with recurrent urinary infections

“…The presence of the genes associated with toxicity (cnf1, sat, uspA, hly) in the cystitis strains showed difference in frequency of them between those strains isolated from prostatitis. Various epidemiological studies support the notion that specific subsets of genes are characteristic of each of the E. coli uropathogenic subtypes involved in the development of cystitis, pyelonephritis, and urosepsis [10,11,24,25]. There are reports showing that cystitis isolates differ specifically from prostatitis isolates due to the lower prevalence of hlyA and cnf1 [26,27,28] and that prostatitis isolates have significantly higher aggregate virulence factors scores than cystitis isolates.…”

“…The foc operon encoding F1C fimbria and yad for Yad fimbriae are common to CFT073, EDL933, and MG1655 strains, both genes play an essential role in the pathogenesis of urinary tract infection [14,25]. The presence of the genes associated with toxicity (cnf1, sat, uspA, hly) in the cystitis strains showed difference in frequency of them between those strains isolated from prostatitis.…”

“…The ability to inhabit different niches during an ascending urinary tract infection and to cause particular pathologies at each site resides largely in the island genes specific to Uropathogenic E. coli [24,25]. However, the importance of other virulence factors should also be regarded.…”

Interplay between pathogenicity island carriage, resistance profile and plasmid acquisition in uropathogenic Escherichia coli

“…It has been suggested that some plasmids, containing the FIB replicon, may be carriers of PAIs (Johnson & Nolan, 2009). Additionally, PAI IV 536 , also known as the high pathogenicity island (HPI), may be transferred by a conjugative F plasmid (Schubert et al, 2009), and PAI II 536 has also been shown to be transferred by conjugation (Schneider et al, 2011). The higher prevalence of the most common islands, including PAI IV 536 , among strains resistant to antibiotics, which are mainly associated with plasmidic resistance mechanisms, may suggest that these islands may be using resistance plasmids to potentiate their dissemination.…”