Common virulence factors and genetic relationships between O18:K1:H7 Escherichia coli isolates of human and avian origin

Abstract

Extraintestinal pathogenic (ExPEC) Escherichia coli strains of serotype O18:K1:H7 are mainly responsible for neonatal meningitis and sepsis in humans and belong to a limited number of closely related clones. The same serotype is also frequently isolated from the extraintestinal lesions of colibacillosis in poultry, but it is not well known to what extent human and avian strains of this particular serotype are related. Twenty-two ExPEC isolates of human origin and 33 isolates of avian origin were compared on the basis of their virulence determinants, lethality for chicks, pulsed-field gel electrophoresis (PFGE) patterns, and classification in the main phylogenetic groups. Both avian and human isolates were lethal for chicks and harbored similar virulence genotypes. A major virulence pattern, identified in 75% of the isolates, was characterized by the presence of F1 variant fimbriae; S fimbriae; IbeA; the aerobactin system; and genomic fragments A9, A12, D1, D7, D10, and D11 and by the absence of P fimbriae, F1C fimbriae, Afa adhesin, and CNF1. All but one of the avian and human isolates also belonged to major phylogenetic group B2. However, various subclonal populations could be distinguished by PFGE in relation to animal species and geographical origin. These results demonstrate that very closely related clones can be recovered from extraintestinal infections in humans and chickens and suggest that avian pathogenic E. coli isolates of serotype O18:K1:H7 are potential human pathogens.

FIG. 1.

Genetic relationships among 38 ExPEC isolates of human and avian origin. The PFGE profiles obtained by XbaI restriction were compared by using the Pearson similarity coefficient, and the resulting dendrogram was calculated by the UPGMA method. The origins of the isolates are indicated: Av, avian; Hu, human; FR, France; SP, Spain; NL, The Netherlands. Groups of strains showing the highest similarity are indicated with brackets.

FIG. 2.

PLS discrimination between PFGE profiles of E. coli strains of human origin (open triangles; n = 23) and of avian origin (black triangles; n = 16). The R²Y coefficients correspond to the part of the variation of the Y matrix, as explained by the PLS components, and the explanatory performance of the model is evaluated by adding the R²Y coefficients. The cross-validation led to three PLS components (only the results for t[1] and t[2] are represented here), and the corresponding PLS model explained 91.6% of the variation of the Y matrix. The 95% probability region defined by the model is delimited by the ellipse. Five groups of strains could be distinguished and are delimited by circles: 1a, human cdt-positive strains (except SP15); 1b, human cdt-positive and cdt-negative strains; 1c, human cdt-negative strains; 2a, avian cdt-positive strains; and 2b, avian cdt-negative strains.

FIG. 3.

PLS discrimination between PFGE profiles of avian E. coli strains of different geographical origins. The R²Y coefficients correspond to the part of the variation of the Y matrix, as explained by the PLS components, and the explanatory performance of the model is evaluated by adding the R²Y coefficients. The cross-validation led to two PLS components, represented here as t[1] and t[2]. The corresponding PLS model explained 97.5% of the variation of the Y matrix. The 95% probability region defined by the model is delimited by the ellipse. The 2a group of cdt-positive strains could be subdivided into two subgroups, according to the geographical origins of the strain: 2a1, avian cdt-positive strains from Spain, and 2a2, cdt-positive strains from France and Belgium. The 2b group comprised cdt-negative strains from Spain only.