The resistance mechanisms of bacteria against ciprofloxacin and new approaches for enhancing the efficacy of this antibiotic

Abstract

For around three decades, the fluoroquinolone (FQ) antibiotic ciprofloxacin has been used to treat a range of diseases, including chronic otorrhea, endocarditis, lower respiratory tract, gastrointestinal, skin and soft tissue, and urinary tract infections. Ciprofloxacin's main mode of action is to stop DNA replication by blocking the A subunit of DNA gyrase and having an extra impact on the substances in cell walls. Available in intravenous and oral formulations, ciprofloxacin reaches therapeutic concentrations in the majority of tissues and bodily fluids with a low possibility for side effects. Despite the outstanding qualities of this antibiotic, Salmonella typhi, Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa have all shown an increase in ciprofloxacin resistance over time. The rise of infections that are resistant to ciprofloxacin shows that new pharmacological synergisms and derivatives are required. To this end, ciprofloxacin may be more effective against the biofilm community of microorganisms and multi-drug resistant isolates when combined with a variety of antibacterial agents, such as antibiotics from various classes, nanoparticles, natural products, bacteriophages, and photodynamic therapy. This review focuses on the resistance mechanisms of bacteria against ciprofloxacin and new approaches for enhancing its efficacy.

Multidrug-Resistant Methicillin-Resistant Staphylococcus aureus Associated with Hospitalized Newborn Infants

“…Fluoroquinolone resistance in S. aureus is due to mutations in the target DNA topoisomerase II-encoding genes gyrA and gyrB , and the parC / grlA gene encoding DNA topoisomerase IV. Known mutations (i.e., S84L in GyrA and S80F in ParC) were detected in both sequenced MRSA isolates [ 63 , 66 ]. The fusA gene encodes the prokaryotic elongation factor G (EF-G) which is essential in protein translation and is a target for fusidic acid.…”

Identification and targeting of microbial putrescine acetylation in bloodstream infections

“…These findings were consistent with a recent report focused on repurposing old antimicrobials similar to pentamidine 69,72 , which found synergy between diminazene and streptomycin or chloramphenicol in some strains of drug resistant E. coli, K. pnuemoniae, and S. aureus, although the mechanism underlying this observation was not elucidated 66 . In our MDR strains, synergistic interactions were directly associated with increased intracellular accumulation of antibiotics (Figure 6B and Figure S9B) suggesting that diminazene treatment was improving cellular access of these drugs 74,75 .…”

Evaluation of Neisseria gonorrhoeae Isolates Susceptibility to Antibiotics in Zhejiang Province Since 2007

“…The main mechanism of fluoroquinolone resistance is mutations in gyrA and parC genes, which produce one or more specific concurrent mutations in gyrA and ParC proteins. 21 These mutations can be easily transferred to other gonococci and spread in the population. Therefore, the resistance rate of ciprofloxacin has remained high for many years.…”