Comparison of extraintestinal pathogenic Escherichia coli strains from human and avian sources reveals a mixed subset representing potential zoonotic pathogens

Abstract

Since extraintestinal pathogenic Escherichia coli (ExPEC) strains from human and avian hosts encounter similar challenges in establishing infection in extraintestinal locations, they may share similar contents of virulence genes and capacities to cause disease. In the present study, 1,074 ExPEC isolates were classified by phylogenetic group and possession of 67 other traits, including virulence-associated genes and plasmid replicon types. These ExPEC isolates included 452 avian pathogenic E. coli strains from avian colibacillosis, 91 neonatal meningitis E. coli (NMEC) strains causing human neonatal meningitis, and 531 uropathogenic E. coli strains from human urinary tract infections. Cluster analysis of the data revealed that most members of each subpathotype represent a genetically distinct group and have distinguishing characteristics. However, a genotyping cluster containing 108 ExPEC isolates was identified, heavily mixed with regard to subpathotype, in which there was substantial trait overlap. Many of the isolates within this cluster belonged to the O1, O2, or O18 serogroup. Also, 58% belonged to the ST95 multilocus sequence typing group, and over 90% of them were assigned to the B2 phylogenetic group typical of human ExPEC strains. This cluster contained strains with a high number of both chromosome- and plasmid-associated ExPEC genes. Further characterization of this ExPEC subset with zoonotic potential urges future studies exploring the potential for the transmission of certain ExPEC strains between humans and animals. Also, the widespread occurrence of plasmids among NMEC strains and members of the mixed cluster suggests that plasmid-mediated virulence in these pathotypes warrants further attention.

FIG. 1.

Two-way clustering of gene prevalence results among the ExPEC subpathotypes. A blue-gray-red heat map was constructed based upon the percentage of each gene examined among each of the subpathotypes. Clustering was performed to illustrate similarities between the prevalence of the genes examined and between the subpathotypes with regard to gene prevalence.

FIG. 2.

Results of cluster and discriminant analyses based on the traits examined. From left to right, the dendrogram was constructed based upon the cluster analysis of common traits, and cluster numbers (1 to 4) were discerned using a cutoff based upon overall virulence genotype; the source column indicates the origin of an isolate; the following columns depict individual PCR results for the presence (black) or absence (light green) of plasmid-carried genes, chromosomal genes, plasmid replicons, and phylogenetic type. ompTp, episomal ompT; iss, episomal iss; ompTc, chromosomal ompT.

FIG. 3.

Overview of isolates belonging to the mixed genotyping cluster. The 108 isolates from the mixed genotyping cluster shown in Fig. 1 are listed in order. For each isolate, the serogroup, pathotype (source), phylotype, and overall genotype are provided. For serogroup O1 (purple), O2 (olive), and O18 (salmon), isolates are colored. Isolates are also colored by source (APEC, sky blue; UPEC, yellow; NMEC, red). For genotype, black squares containing “+” represent a positive PCR, whereas open squares represent a negative PCR.