article · Microorganisms
Serratia marcescens is an opportunistic hospital-acquired pathogen known for antibiotic resistance and quorum sensing-regulated virulence factors. Rather than killing the bacterium directly, disrupting its communication network presents an alternative therapeutic strategy. Investigations into secnidazole, an imidazole compound, demonstrated that sub-inhibitory concentrations significantly decrease key virulence traits in a clinical isolate. In laboratory assays, the compound curbed biofilm formation, swarming motility, protease release, hemolysin activity, and prodigiosin synthesis. Animal trials in mice confirmed that secnidazole lowered pathogenesis and conferred protective effects against infection. In addition, computational docking models indicated that secnidazole competitively obstructs natural autoinducer binding to the bacterial SmaR quorum sensing receptor. These combined experimental and computational results suggest that secnidazole could serve as a viable anti-virulence candidate to help manage infections triggered by Serratia marcescens.
Hospital-acquired infections caused by drug-resistant bacteria like Serratia marcescens pose severe clinical challenges. Targeting bacterial communication and virulence mechanisms, rather than cell viability, provides an innovative pathway to control harmful infections while potentially reducing selective pressure for antibiotic resistance. Demonstrating that an existing compound can neutralise virulence factors offers a potential route toward alternative antimicrobial strategies.
This research presents early-stage preclinical evidence for repurposing secnidazole as an anti-virulence therapeutic against hospital-acquired Serratia marcescens infections. Potential users include pharmaceutical developers and clinical researchers focusing on antimicrobial resistance solutions. Because validation is currently limited to in vitro assays, mouse models, and molecular docking, substantial further development, including formulation optimisation and human clinical trials, is required before real-world clinical application.
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<i>Serratia marcescens</i> is an opportunistic pathogen that causes diverse nosocomial infections. <i>S. marcescens</i> has developed considerable resistance to different antibiotics and is equipped with an armory of virulence factors. These virulence factors are regulated in <i>S. marcescens</i> by an intercellular communication system termed quorum sensing (QS). Targeting bacterial virulence and QS is an interesting approach to mitigating bacterial pathogenesis and overcoming the development of resistance to antimicrobials. In this study, we aimed to evaluate the anti-virulence activities of secnidazole on a clinical isolate of <i>S. marcescens</i>. The effects of secnidazole at sub-inhibitory concentrations (sub-MICs) on virulence factors, swarming motility, biofilm formation, proteases, hemolysin activity, and prodigiosin production were evaluated in vitro. Secnidazole's protective activity against <i>S. marcescens</i> pathogenesis was assessed in vivo in mice. Furthermore, a molecular docking study was conducted to evaluate the binding ability of secnidazole to the <i>S. marcescens</i> SmaR QS receptor. Our findings showed that secnidazole at sub-MICs significantly reduced <i>S. marcescens</i> virulence factor production in vitro and diminished its pathogenesis in mice. The <i>insilico</i> docking study revealed a great ability of secnidazole to competitively hinder the binding of the autoinducer to the SmaR QS receptor. In conclusion, secnidazole is a promising anti-virulence agent that may be used to control infections caused by <i>S. marcescens</i>.
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DOI: 10.3390/microorganisms9112333
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