Sub-minimal inhibitory concentrations of fluoroquinolones in the environment: A trigger for the emergence of drug-resistant bacteria

Fluoroquinolones represent a significant class of antimicrobial agents. These compounds are effective in the treatment of various enteric infections in veterinary medicine. The primary bacterial targets of quinolones are topoisomerase IV and DNA gyrase, enzymes essential for DNA replication and repair. A major public health concern is the potential transmission of fluoroquinolone-resistant bacteria from livestock to humans. The development of antimicrobial resistance in both animals and humans is interconnected. Multiple observational studies and randomized trials have established an association between the use of antibiotics in food animals and the emergence of antimicrobial-resistant bacteria. Fluoroquinolones induce DNA damage, leading to DNA strand breaks that activate the SOS response and various DNA repair pathways. The SOS system, a key component of the DNA repair machinery, plays a critical role in cell cycle regulation. Activation of this system initiates a cascade of signals within bacteria, resulting in enhanced pathogenicity. Through these signaling pathways, bacteria have evolved diverse mechanisms such as pathogenicity islands, biofilm formation, and toxin production. The presence of residual fluoroquinolones in livestock environments and animal production systems following veterinary use is associated with increased bacterial virulence. This review focuses on the impact of fluoroquinolone exposure at sub-minimal inhibitory concentrations on bacterial virulence and pathogenicity.