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Biofilm formation by Gardnerella vaginalis is a multicellular process by which the bacteria adhere to surfaces and aggregate in a structured, self-produced extracellular matrix. This process leads to increased resistance to antimicrobials and immune clearance, and is implicated as a central pathogenic mechanism in bacterial vaginosis (BV). Biofilms formed by G. vaginalis are tolerant of much higher concentrations of hydrogen peroxide and lactic acid, compared to planktonic bacteria, and can coaggregate with other vaginal species to form multispecies biofilms. Current antibiotic therapies (such as metronidazole and clindamycin) are unable to effectively eradicate these biofilms, resulting in frequent recurrence of BV. There are also phenotypic changes during biofilm formation: upregulation of genes for antimicrobial resistance, amino acid biosynthesis, DNA repair, efflux transporters, and adhesion proteins; and downregulation of metabolic genes, resulting in low metabolic activity and persistent infection. No drugs are specifically approved to treat biofilms in BV.
Direct antibiotic-mediated killing of planktonic bacteria (ineffective on mature biofilm); Disruption of biofilm matrix (e.g., proteolytic enzymes, D-amino acids, detergent-like molecules); Experimental agents target biofilm formation or promote biofilm disassembly
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