Biofilms

A biofilm is a structured community of microorganisms adherent to a surface (biological or inert) and to each other, embedded within a self-produced extracellular polymeric matrix.

Biofilms may be single-species or, more commonly in clinical settings, polymicrobial, with multiple organisms coexisting within the same matrix.

1. Initial adhesion: free-floating (planktonic) organisms attach reversibly to a surface, mediated by surface adhesins, fimbriae, and nonspecific physicochemical forces. This attachment is initially weak and reversible.
2. Microcolony formation: attachment becomes irreversible as the organisms multiply locally, forming small clusters (microcolonies) on the surface.
3. Extracellular matrix production: organisms secrete an extracellular polymeric substance (EPS), composed of polysaccharides, proteins, and extracellular DNA, forming the structural scaffold that binds the community together and to the surface.
4. Maturation: the biofilm develops into a complex three-dimensional structure with channels allowing nutrient and waste diffusion, and internal microenvironments with differing oxygen tension and metabolic activity between the biofilm's surface and its deeper layers.
5. Dispersal: individual cells or clusters detach from the mature biofilm and return to a planktonic state, capable of seeding new sites of colonisation or infection elsewhere in the host or environment.

• Increased antimicrobial tolerance: biofilm organisms tolerate antibiotic concentrations many times higher than the same organism in planktonic (free-living) form. Mechanisms include restricted antibiotic penetration through the matrix, reduced metabolic activity in deeper biofilm layers (many antibiotics require active growth/division to act), and the presence of persister cells, a small dormant subpopulation that survives antibiotic exposure through metabolic inactivity rather than genetic resistance.
• Reduced immune clearance: the extracellular matrix physically impedes phagocyte access and antibody/complement penetration, allowing the organism to persist despite an intact host immune response.
• Persistent infection: the combination of antimicrobial tolerance and immune evasion makes biofilm-associated infections characteristically difficult to eradicate with antibiotics alone, frequently requiring removal of the underlying surface (device removal, debridement) for cure.
• Surface adherence: biofilms form on both biological surfaces (native heart valves, respiratory epithelium in cystic fibrosis, teeth) and inert medical surfaces (catheters, prosthetic joints, heart valves, endotracheal tubes).

• Catheters: intravascular and urinary catheters are classic biofilm sites; catheter-associated bloodstream infection and catheter-associated urinary tract infection are both biofilm-mediated processes, frequently requiring catheter removal alongside antibiotic therapy for resolution.
• Prosthetic devices: prosthetic joints, heart valves, and pacemaker leads are all susceptible to biofilm formation; prosthetic joint infection in particular is notoriously difficult to cure with antibiotics alone and often requires surgical removal/exchange of the device.
• Dental plaque: a naturally occurring biofilm on tooth surfaces, the substrate for dental caries (via acid-producing bacteria within the biofilm) and periodontal disease.
• Chronic wounds: biofilm formation within chronic wound beds (diabetic foot ulcers, pressure ulcers, venous ulcers) impairs healing and antibiotic efficacy, a major contributor to wound chronicity.