ena-STUDY-STATENS SERUM INSTITUT-08-06-2018-08:41:21:064-413
Emergence of enteroaggregative Escherichia coli within the ST131 lineage as a cause of extraintestinal infections
Escherichia colisequence type 131 (ST131) is a major cause of urinary and bloodstream infections and its association with extended-spectrum ß-lactamases (ESBL) significantly complicates treatment. Most notorious is its rapidly expanding H30-Rx clade (named for containing allele 30 of the type-1 fimbrial adhesin gene fimHand extensive antimicrobial resistance), which appears to have emerged in the United States due in part due to acquisition of the ESBL-encoding blaCTX-M-15 gene and resistance to fluoroquinolones. However, non-H30 ST131 lineages with acquired CTX-M-type resistance genes also are emerging. Based on whole-genome analyses, we describe here the presence of an (fimH) H27 E. coliST131 lineage that currently is causing an outbreak of community-acquired bacteremia and recurrent urinary tract infections (UTIs) in Denmark. This lineage has acquired both a virulence plasmid (pAA) that defines the enteroaggregative E. coli(EAEC) diarrheagenic pathotype and multiple genes associated with extraintestinal E. coli(ExPEC) that combined has made this particular ST131 lineage highly successful at colonizing its human host and cause recurrent UTI. Moreover, using a historic World Health Organization E. coli collection and publically available genome sequences, we identify a global H27 EAEC ST131 lineage dating back as far as 1998. Most H27 EAEC ST131 isolates harbor pAA or pAA-like plasmids, which analysis strongly imply was caused by a single ancestral acquisition. These findings illustrate the profound plasticity of this important pathogenic E. coliH27 lineage in general, and the genetic acquisitions of EAEC-specific virulence traits that likely confer an enhanced ability to cause intestinal colonization.
Escherichia colisequence type 131 (ST131) is a major cause of urinary and bloodstream infections and its association with extended-spectrum ß-lactamases (ESBL) significantly complicates treatment. Most notorious is its rapidly expanding H30-Rx clade (named for containing allele 30 of the type-1 fimbrial adhesin gene fimHand extensive antimicrobial resistance), which appears to have emerged in the United States due in part due to acquisition of the ESBL-encoding blaCTX-M-15 gene and resistance to fluoroquinolones. However, non-H30 ST131 lineages with acquired CTX-M-type resistance genes also are emerging. Based on whole-genome analyses, we describe here the presence of an (fimH) H27 E. coliST131 lineage that currently is causing an outbreak of community-acquired bacteremia and recurrent urinary tract infections (UTIs) in Denmark. This lineage has acquired both a virulence plasmid (pAA) that defines the enteroaggregative E. coli(EAEC) diarrheagenic pathotype and multiple genes associated with extraintestinal E. coli(ExPEC) that combined has made this particular ST131 lineage highly successful at colonizing its human host and cause recurrent UTI. Moreover, using a historic World Health Organization E. coli collection and publically available genome sequences, we identify a global H27 EAEC ST131 lineage dating back as far as 1998. Most H27 EAEC ST131 isolates harbor pAA or pAA-like plasmids, which analysis strongly imply was caused by a single ancestral acquisition. These findings illustrate the profound plasticity of this important pathogenic E. coliH27 lineage in general, and the genetic acquisitions of EAEC-specific virulence traits that likely confer an enhanced ability to cause intestinal colonization.