Evaluating Fluoxetine's Growth-Inhibitory Impact on Clinical Isolates of Enteric Bacteria: Harnessing Repurposing Potential

Abstract

The over-the-counter use and imprudent utilization of antibiotics in recent times have led to the emergence of microbial resistance. This has given rise to an alarming situation, prompting researchers to explore novel strategies for managing infections induced by antibiotic-resistant species. However, the process of drug discovery is time-consuming and expensive, which makes it a challenging endeavor. In recent years, drug repurposing has gained significant attention as an alternative strategy. Notably, several antidepressants have piqued interest as potential candidates for repositioning as antibiotics. Thus, the present study was aimed at investigating the anti-bacterial potential of different classes of antidepressants i.e., fluoxetine, venlafaxine, and phenelzine in clinical isolates of Escherichia coli, Enterobacter aerogenes, Enterococcus faecalis, Klebsiella pneumonia, Pseudomonas aeruginosa, Proteus mirabilis, Salmonella typhi, Shigella dysenteriae, and Staphylococcus aureus. The strains were cultivated on Mueller Hinton agar, with the aforementioned antidepressants or conventional antibiotics. Following a 24-hour incubation period, the extent of growth inhibition was assessed by measuring the zone of inhibition, serving as an indicator of their inhibitory potential. The findings showed that fluoxetine arrested the growth of almost all isolates with maximal effect against Pseudomonas aeruginosa. The impact of venlafaxine was exclusively observed in Enterobacter aerogenes, with phenelzine demonstrating complete ineffectiveness in bacterial growth suppression. In conclusion, the current study elucidates the efficacy of fluoxetine in clinical isolates, thereby positioning it as a promising contender for the advancement of novel antimicrobial agents. Additionally, our data raises questions regarding the proposed mechanisms of antibacterial action for selective serotonin reuptake inhibitors (SSRIs) and challenges the notion of dysbiosis as a potential mode of action for antidepressants.