We investigated the dissemination of pathogenicity island (PAI) II J96-like elements (hra, hly, cnf1, and pap) among 455 Escherichia coli isolates from children and adults with urinary tract infection (UTI), neonates with meningitis or colonized healthy neonates, and 74 reference strains by means of PCR phylogenetic grouping, ribotyping, and PCR analysis of virulence genes. Colocalization of these genes was documented by pulsed-field gel electrophoresis followed by Southern hybridization and long-range PCR (LRPCR) between the hra and the papG alleles. Site-specific insertion of the PAI was determined by LRPCR between hra and tRNA flanking sequences, hra, hly, and cnf1 were found in 113 isolates and consistently colocalized, constituting the backbone of PAI IIJ96-like domains. The prevalence of PAI II J96-like domains was significantly higher among UTI isolates than among neonatal meningitis and commensal isolates. These domains were restricted to a few ribotypes of group B2. In contrast to the consistent colocalization of hra, hly, and cnf1, the pap operon was varied: 12% of strains exhibited an allelic exchange of the papG class III allele (papGIII) for thepapG class II allele (papGII) (only UTI isolates), and the pap operon was deleted in 23% of strains. No strains harbored papGIII outside the PAI, which appears to be the only source of this allele. PAI IIJ96-like domains were inserted in the vicinities of three different tRNAs-pheU (54%), leuX (29%), and pheV (15%)-depending on the genetic backgrounds and origins of the isolates. Multiple insertional events restricted by the genetic background have thus led to PAI IIJ96 acquisition. Specific genetic backgrounds and insertion sites may have played a role in additional recombination processes for E. coli adaptation to different ecological niches. Copyright © 2005, American Society for Microbiology. All Rights Reserved.
CITATION STYLE
Bidet, P., Bonacorsi, S., Clermont, O., De Montille, C., Brahimi, N., & Bingen, E. (2005). Multiple insertional events, restricted by the genetic background, have led to acquisition of pathogenicity island IIJ96-like domains among Escherichia coli strains of different clinical origins. Infection and Immunity, 73(7), 4081–4087. https://doi.org/10.1128/IAI.73.7.4081-4087.2005
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