Since its first report in the United Kingdom in 2008 as an extended spectrum beta lactamase (ESBL) producing pathogenic Escherichia coli, E. coli sequence type 131 (ST131) has become the predominant fluoroquinolone resistant (FQR) E. coli clone world-wide. While previous genomic studies have explored the ST131 clonal structure [1, 2], and established the major impact of recombination in shaping the evolution of distinct lineages [1], neither could resolve the temporal or geographical origin of FQR E. coli ST131. In the present study, we reconstructed the putative evolutionary scenario of the emergence of FQR E. coli ST131, using the combined genomic data of 188 strains from two previously published studies [1, 2], spanning the years 1967 to 2011 and from 9 geographical regions.
We confirmed that the global phylogeny of E. coli ST131 separates the strains into 4 distinct lineages, namely clades A (H41), B (H22), C1 (H30-R, FQR) and C2 (H30-Rx, FQR, CTX-M-15). Divergence time estimation using Bayesian Evolutionary Analysis by Sampling Trees(BEAST) revealed that FQR clades C1 and C2 originated around 1987, coincidently following the first clinical usage of fluoroquinolone in 1986. Rather than mobile genetic elements acquisitions (plasmid excepted) and recombination events, which likely occurred prior to 1987, point mutations conferring FQR seem to have been the pivotal events leading to a rapid population expansion in the early 1990’s, followed by stabilization around the 2000’s. This work highlights how efficiently combining publicly available genomic datasets can synergistically provide better resolution into the temporal and geographical emergence of multi-drug resistant bacteria.