Phylogenetic Comparisons Reveal Multiple Acquisitions of the Toxin Genes by Enterotoxigenic Escherichia coli Strains of Different Evolutionary Lineages

Abstract

Escherichia coli is a diverse bacterial species which is widely distributed in the environment but also exists as a commensal and pathogen of different host species. Human intestinal pathogenic E. coli causes over 160 million cases of diarrhea and an estimated 1 million deaths per year. The majority of deaths are attributable to one pathovar of E. coli, namely, enterotoxigenic E. coli. The pathogenesis of enterotoxigenic E. coli is dependent on the production of a colonization factor to promote adhesion to the intestinal epithelium and the elaboration of heat-labile or heat-stable toxins which induce a secretory diarrhea. Despite the high morbidity and mortality associated with enterotoxigenic E. coli infection, little is known of the genetic background of this global pathogen. Here we demonstrate by multilocus sequence typing that enterotoxigenic E. coli isolates are present in all phylogenetic lineages of E. coli, indicating that acquisition of the toxin genes may be sufficient to generate an enterotoxigenic E. coli strain. In addition, screening of diarrheal isolates for the presence of additional genes previously associated with the virulence of enterotoxigenic E. coli revealed that they were not abundant. These observations have significant implications for disease epidemiology and for the design of effective vaccines.

Biochemical characterization of the enterotoxigenic Escherichia coli LeoA protein

“…Thus, in addition to roles in LT secretion and modulation of OMP composition, LeoA may in some way contribute to the formation of motility structures. However, it is unlikely that LeoA is generally important to ETEC motility, as the vast majority of characterized isolates are leoA 2 (see below; Turner et al, 2006). Our observations may instead result from the apparent pleiotropic nature of the leoA mutation on H10407 proteins associated with the periplasm or bacterial membranes.…”

“…The findings described here are of note because leoA is not typically found in ETEC isolates characterized to date. Turner et al (2006) analysed the distribution of leoA by multilocus sequence typing of 209 different ETEC isolates and found that leoA was present in only 3 % of the tested strains. These authors speculate that because numerous isolates possessing LT do not encode leoA, this gene is not generally required for ETEC pathogenicity (Turner et al, 2006).…”

“…Turner et al (2006) analysed the distribution of leoA by multilocus sequence typing of 209 different ETEC isolates and found that leoA was present in only 3 % of the tested strains. These authors speculate that because numerous isolates possessing LT do not encode leoA, this gene is not generally required for ETEC pathogenicity (Turner et al, 2006). Ongoing and future experiments may elucidate how LeoA might contribute to the disease severity associated with H10407 and whether similar functions might be imparted by related virulence factors in isolates that have been less well characterized.…”

Phylogenetic and pathotype analysis of Escherichia coli swine isolates from Southern Brazil

“…In the phylogenetic analysis, 65.6% (23/35) of the isolates were classiϐied in groups A or B1. The same results were described by Picard et al (1991) and Chapman et al (2006), which can reϐlect a preference of speciϐic virulence factor coded by plasmids from certain genetic groups (Turner et al 2006). A total of 34.4% were placed into groups B2 (6/35) and D (6/35).…”

Diversity of CRISPR loci in Escherichia coli

“…However, such a similarity cannot be due to a common origin, since Shigella species derive from lineages that are independent of B2 (Fricke et al, 2008;Ogura et al, 2009;Pupo et al, 2000;Turner et al 2006). Moreover, the closely related ECOR strains carry a complete CRISPR2/CAS-E system (our unpublished results) and the deletions in CRISPR2.1/CAS-E are unrelated, entailing distinct genes and sequences (Supplementary Fig.…”