Commensal Escherichia coli isolates are phylogenetically distributed among geographically distinct human populations

Abstract

An intraspecies phylogenetic grouping of 168 human commensal Escherichia coli strains isolated from the stools of three geographically distinct human populations (France, Croatia, Mali) was generated by triplex PCR. The distributions of seven known extraintestinal virulence determinants (ibeA, pap, sfa/foc, afa, hly, cnf1, aer) were also determined by PCR. The data from the three populations were compiled, which showed that strains from phylogenetic groups A (40 %) and B1 (34 %) were the most common, followed by phylogenetic group D strains (15 %). Strains of the phylogenetic group B2 were rare (11 %). However, a significant specific distribution for strains of groups A, B1 and B2 within each population was observed, which may indicate the influence of (i) geographic/climatic conditions, (ii) dietary factors and/or the use of antibiotics or (iii) host genetic factors on the commensal flora. Virulence determinants were rarely detected, with only 256 % of the strains harbouring at least one of the virulence genes tested. The strains with virulence factors most frequently belonged to phylogenetic group B2. The commensal strains of phylogenetic groups A, B1 and D had fewer virulence determinants than pathogenic strains of the corresponding groups when these data were compared with those for previous collections of virulent extraintestinal infection strains studied using the same approach. However, the virulence patterns of commensal and pathogenic B2 phylogenetic group strains were the same. The data thus suggest that strains of the A, B1 and D phylogenetic groups predominate in the gut flora and that these strains must acquire virulence factors to become pathogenic. In contrast, commensal phylogenetic group B2 strains are rare but appear to be potentially virulent. Keywords : Escherichia coli, phylogeny, commensal, virulence INTRODUCTIONEscherichia coli is a normal inhabitant of the gut flora and is also the Gram-negative bacillus most frequently isolated in cases of human infection (Eisenstein & Zaleznick, 2000). Commensal enteric E. coli may therefore be the natural reservoir of pathogenic strains (Falkow, 1996). Intestinal or extraintestinal E. coli infections are caused by strains harbouring numerous virulence factors located on plasmids, bacteriophages, or the bacterial chromosome (Mu$ hldorfer & Hacker, 1994). Several studies have shown that pathogenic E. coli strains may be derived from commensal strains by the acquisition of chromosomal or extra-chromosomal virulence operons (Finlay & Falkow, 1997 ;Ochman et al., 2000). ' Black hole ' genomic deletions that enhance pathogenicity (Maurelli et al., 1998) or random functional point mutations that are adaptive for pathogenic environments (Sokurenko et al., 1998) may also represent additional strategies of genome plasticity by which a commensal strain may become virulent. Many of these observations were made possible by the fact that E. coli populations have a clonal structure (Selander & Levin, 1980). Four main phylogenetic groups, A, B1, B2 and D, were describ...

Expression of cellulose and curli fimbriae by Escherichia coli isolated from the gastrointestinal tract

“…Phylogenetic grouping placed the majority of isolates into phylogenetic group A (55 %), with a significant number of isolates in group B2 (21 %). While this frequency of strains of phylogenetic group A is characteristic for faecal E. coli from a middle-European population, the frequency of phylogenetic group B2 strains is higher than in the middle-European population (Duriez et al, 2001). Earlier studies showed that commensal and virulent strains are gathered in group B2 and that potentially virulent strains of group B2 had gathered several virulence factors (Duriez et al, 2001).…”

“…TOB1 belongs to the phylogenetic group B2, which harbours pathogenic as well as non-pathogenic strains (Duriez et al, 2001). However, PCR tests showed that TOB1 did not harbour common virulence factors, did not express haemolytic activity and was a prototroph (Table 2, data not shown).…”

Extra-intestinal pathogenic Escherichia coli (ExPEC): Disease, carriage and clones

“…Over the last decade, a number of authors have sought to establish the prevalence of E. coli with ExPEC potential colonising the gut by performing microbiological screening studies on the stool of healthy individuals that delineate resident E. coli strains based on their phylogroup (58)(59)(60)(61)(62)(63). Results of these studies have demonstrated that 11-48% of healthy individuals are colonised with E. coli belonging to phylogroup B2, which is traditionally associated with virulence and ExPEC infections.…”

Phylogenetic Grouping of Dominant Fecal Escherichia coli Isolates from Healthy Males and Females in Al-Kut/Wasit Province/Iraq

“…The virulent extraintestinal E. coli strains belong mainly to group B2 and, to a lesser extent, to group D, whereas most commensal strains belong to group A [10]. Numerically, group A is the dominant group among normal fecal E. coli but relative percent distribution of these groups differs from one country to another [11,12]. In comparison with ExPEC, the human commensal fecal strains had fewer virulence factors [11,13].…”

“…Numerically, group A is the dominant group among normal fecal E. coli but relative percent distribution of these groups differs from one country to another [11,12]. In comparison with ExPEC, the human commensal fecal strains had fewer virulence factors [11,13]. Such VFs induce disease through their ability to help the organisms to avoid or subvert host defenses, colonize key anatomical sites, perturb host physiology, invade host tissues, and/or incite a noxious host inflammatory response [9,[13][14][15].…”