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Pathogen biofilms are complex, multicellular communities of microorganisms, such as bacteria or fungi, that adhere to surfaces and are encased within a self-produced matrix of extracellular polymeric substances (EPS) composed of polysaccharides, proteins, and extracellular DNA [1, 3]. This structural arrangement provides a significant survival advantage by shielding the pathogens from the host immune system and increasing their tolerance to conventional antibiotics by up to 1,000-fold compared to their planktonic counterparts [6, 11]. Biofilms are central to the pathogenesis of chronic and recurrent infections, including those associated with cystic fibrosis, chronic wounds, endocarditis, and medical implants like catheters and prosthetic joints [3, 12]. Therapeutic strategies targeting biofilms focus on disrupting the EPS matrix, inhibiting cell-to-cell communication known as quorum sensing, or inducing the dispersal of sessile cells into their more vulnerable planktonic state [5, 13]. Effective management often requires combination therapies that pair biofilm-disrupting agents with traditional antimicrobials to ensure the eradication of released pathogens and prevent systemic dissemination [1, 13].
Biofilm disruption, inhibition of quorum sensing, degradation of extracellular polymeric substance (EPS), inhibition of adhesion, and induction of dispersal to enhance antimicrobial susceptibility.
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