The ST131 Escherichia coli H 22 subclone from human intestinal microbiota: Comparison of genomic and phenotypic traits with those of the globally successful H 30 subclone

Abstract Background In 2006, we found healthy subjects carrying ST131 Escherichia coli in their intestinal microbiota consisting of two populations: a subdominant population of fluoroquinolone-resistant E. coli belonging to subclone H 30 ( H 30-R or subclade C1), the current worldwide dominant ST131 subclone, and a dominant E. coli population composed of antibiotic-susceptible E. coli belonging to subclone H 22 (clade B) , the precursor of subclone H 30. We sequenced the whole genome of fecal H 22 strain S250, compared it to the genomes of ExPEC ST131 H 30-Rx strain JJ1886 and commensal ST131 H 41 strain SE15, sought the H 22- H 30 genomic differences in our fecal strains and assessed their phenotypic consequences. Results We detected 173 genes found in the Virulence Factor Database, of which 148 were shared by the three ST131 genomes, whereas some were genome-specific, notably those allowing determination of virotype (D for S250 and C for JJ1886). We found three sequences of the FimH site involved in adhesion: two in S250 and SE15 close and identical, respectively, to that previously reported to confer strong intestinal adhesion, and one in JJ1886, corresponding to that commonly present in uropathogenic E. coli. Among the genes involved in sugar metabolism, one encoding a gluconate kinase lacked in S250 and JJ1886. Although this gene was also absent in both our fecal H 22 and H3 0-R strains, H 22 strains showed a higher capacity to grow in minimal medium with gluconate. Among the genes involved in gluconate metabolism, only the ghrB gene differed between S250/ H 22 and JJ1886/ H 30-R strains, resulting in different gluconate reductases. Of the genes involved in biofilm formation, two were absent in the three genomes and one, fimB , in the JJ1886 genome. Our fecal H 30-R strains lacking intact fimB displayed delayed biofilm formation relative to our fecal H 22 strains. The H 22 strains differed by subclade B type and plasmid content, whereas the H 30-R strains were identical. Conclusions Phenotypic analysis of our fecal strains based on observed genomic differences between S250 and JJ1886 strains suggests the presence of traits related to bacterial commensalism in our H 22 strains and traits commonly found in uropathogenic E. coli in our H 30-R strains.