Ciprofloxacin-induced mucoviscosity in ESBL-positive Escherichia coli carrying the Klebsiella pneumoniae K23 capsular structure hinders phagocytosis.

Abstract

Escherichia coli is a Gram-negative ubiquitous bacteria occurring in a diversity of environments including water, soil, and the gastrointestinal tract of humans and warm-blooded animals, being classified into commensal and pathogenic strains. While empirical antibiotic therapy with fluoroquinolones, such a ciprofloxacin and norfloxacin, has been a common practice, resistance to broad-spectrum cephalosporins, mediated by extended-spectrum β-lactamases (ESBLs), has been alerted as a critical priority by the World Health Organization. Additionally, the convergence of virulence and resistance has been observed in some E. coli strains, which enable these bacteria to infect humans and animals, and can jeopardize their health. Mucoviscosity phenotype has been frequently described in highly-virulent Klebsiella pneumoniae strains, whereas this phenotypic behavior remains rarely reported in E. coli. Herein, we report microbiological, genomic, and anti-phagocytic activity of ciprofloxacin-induced mucoviscosity in a CTX-M-15 (ESBL)-positive E. coli. Noteworthy, genomic analysis revealed virulence genes responsible for the synthesis of the K23 capsule type, previously described in hypermucoviscous K. pneumoniae lineages, whereas phagocytosis assays confirmed the ability of K23 E. coli strain to evade the immune system under mucoviscosity induction by ciprofloxacin treatment.