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Escherichia coli sequence type 131 (ST131) is a pandemic multidrug resistant (MDR) strain that has had unprecedented global expansion in the last decade and is now the predominant resistant E. coli in both the adult and pediatric populations [1]. ST131 has been associated with a variety of invasive infections, resulting in higher healthcare costs and increased morbidity and mortality. These strains produce extended-spectrum β-lactamases (ESBLs), usually encoded by large plasmids, which can severely limit treatment options, delaying adequate therapy and increasing the use of last-resort antimicrobials such as carbapenems and colistin [2]. They are most commonly associated with CTX-M-15, a broad spectrum cephalosporinase. It is estimated that overall prevalence ranges from 12%–30% of all E. coli isolates, 70%–80% of fluoroquinolone-resistant E. coli isolates, and 50%–60% of all ESBL-producing E. coli isolates [3]. Rates of asymptomatic fecal carriage in the community are increasing worldwide, though the exact bacterial or host factors involved are not fully understood. Although ST131 strains are not thought to be hypervirulent, they are rapidly transmitted between hosts and are persistent gut colonizers [4–7]. In mouse models, they can out-compete commensal E. coli to colonize the gut [8]. The population structure of ST131 has recently been defined by using whole-genome sequencing (WGS) data, either with classification into clades A, B, or C or by the fimH alleles. Most ST131 strains fall with the 2 subclades of C1 and C2, corresponding to presence or absence of the CTX-M-15 beta-lactamase [9]. The most common fimH variants are fimH30 and fimH22 [9]. This article provides a broad overview of the ST131 colonization and transmission patterns, associated antimicrobial resistance (AMR) plasmid types, and current knowledge about its virulence and metabolism potential.

The pandemic Escherichia coli sequence type 131 strain is acquired even in the absence of antibiotic exposure