  High-throughput molecular screening is required to investigate the origin and
diffusion of antimicrobial resistance in pathogen outbreaks. The most frequent
cause of human infection is Escherichia coli, which is dominated by sequence
type 131 (ST131), a set of rapidly radiating pandemic clones. The highly
infectious clades of ST131 originated firstly by a mutation enhancing virulence
and adhesion. Secondly, single-nucleotide polymorphisms occurred enabling
fluoroquinolone-resistance, which is near-fixed in all ST131. Thirdly, broader
resistance through beta-lactamases has been gained and lost frequently,
symptomatic of conflicting environmental selective effects. This flexible
approach to gene exchange is worrying and supports the proposition that ST131
will develop an even wider range of plasmid and chromosomal elements promoting
antimicrobial resistance. To stymie ST131, deep genome sequencing is required
to understand the origin, evolution and spread of antimicrobial resistance
genes. Phylogenetic methods that decipher past events can predict future
patterns of virulence and transmission based on genetic signatures of
adaptation and gene exchange. Both the effect of partial antimicrobial exposure
and cell dormancy caused by variation in gene expression may accelerate the
development of resistance. High-throughput sequencing can decode measurable
evolution of cell populations within patients associated with systems-wide
changes in gene expression during treatments. A multi-faceted approach can
enhance assessment of antimicrobial resistance in E. coli ST131 by examining
transmission dynamics between hosts to achieve a goal of pre-empting resistance
before it emerges by optimising antimicrobial treatment protocols.
