Abstract
A single extra-intestinal pathogenic Escherichia coli (ExPEC) clone, named sequence type (ST) 131, is responsible for millions of global antimicrobial-resistant (AMR) infections annually. Population genetics indicate that ST131 consists of different clades (i.e. A, B, and C); however, clade C is the most dominant globally. A ST131 subclade, named C1-M27, is emerging in Japan and has been responsible for the recent increase in AMR ExPEC in that country. The sequential acquisition of several virulence and AMR genes associated with mobile genetic elements during the 1960s to 1980s primed clade C (and its subclades C1 and C2) for success in the 1990s to 2000s. IncF plasmids with F1:A2:B20 and F2:A1:B replicons have shaped the evolution of the C1 and C2 subclades. It is possible that ST131 is a host generalist with different accessory gene profiles. Compensatory mutations within the core genome of this clone have counterbalanced the fitness cost associated with IncF plasmids. ST131 clade C had dramatically changed the population structure of ExPEC, but it still remains unclear which features of this clade resulted in one of the most unprecedented AMR successes of the 2000s.
Highlights
Extra-intestinal pathogenic Escherichia coli, or extra-intestinal pathogenic Escherichia coli (ExPEC), is a major human pathogen and is the most common cause of urinary tract infections and the most common Gram-negative bacterium associated with bloodstream infections in both developed and developing countries[1]
Of special concern is that fluoroquinolone resistance (FQ-R) is often accompanied by resistance to the cephs, which is mainly due to the production of extended-spectrum β-lactamases (ESBLs), especially an enzyme named CTX-M-154
A single ExPEC clone, sequence type (ST) 131, is predominantly responsible for this global FQ-R and cephalosporin resistance (ceph-R) pandemic causing millions of antimicrobial-resistant (AMR) infections annually[5]
Summary
Extra-intestinal pathogenic Escherichia coli, or ExPEC, is a major human pathogen and is the most common cause of urinary tract infections and the most common Gram-negative bacterium associated with bloodstream infections in both developed and developing countries[1]. The Brisbane study described a stepwise evolution process in which clade B was divided into five paraphyletic subclades and sequentially acquired several prophages (Phi), GIs, the fimH30 allele, and mutations within gyrA and parC and evolved into clade C8 Each one of these acquisitions increased the population size and extended the relational interactive field of the successive variants. The Oxford and Brisbane studies showed that clade C instantly divided into subclades C1 and C2 after the acquisition of the high-level FQ-R mutations (via selection) in parC (parC1aAB) and gyrA (gyrA1AB) that defined clade C (Figure 1) This process transpired during the mid–late 1980s and coincided with the introduction of the FQs (especially ciprofloxacin) in clinical medicine. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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