We were able to use WGS to identify the major events during the evolution of this lineage prior to, and after, its introduction into a new setting. Our data imply that the acquisition of a class 2 integron and a spA plasmid, together with the rapid accumulation of mutations associated with fluoroquinolone resistance, rendered the Bhutanese S. sonnei MDR by 2006. Furthermore, a fluoroquinolone-resistant subclade within the Central Asia clade was predicted to have arisen between 1999 and 2006. In addition, the fixation of a novel recombinant colicin E plasmid (pSSE3) may have offered this group of pathogens a competitive advantage over other enteric bacteria, similar to the colicin-associated selective sweep observed in S. sonnei in Vietnam (Holt et al., 2013). These data suggest that whilst antimicrobial resistance is clearly important, it is not sufficient in itself for driving the spread of new clones and anticompetitive functions appear to be key themes in the spread of MDR S. sonnei.