Biofilm

A biofilm forms when microbes attach to a surface and secrete an extracellular matrix of polysaccharide, extracellular DNA and protein. The matrix slows diffusion of some agents, and steep oxygen and nutrient gradients leave cells deep in the film metabolically dormant, removing the active targets most antibiotics depend on. The resulting survival is tolerance rather than resistance: it comes from the state of the community, not from a mutation in a drug target.

Biofilms account for a large share of chronic and device-associated infection, including prosthetic joints, catheters, endocarditis, chronic wounds and the cystic fibrosis airway. The minimum biofilm eradication concentration for an isolate commonly runs ten to a thousand times its planktonic minimum inhibitory concentration for the same drug. That gap is why infected hardware is usually removed rather than treated through, and why rifampin combinations are used against staphylococcal device infection when it must stay.

The tolerance is phenotypic and reversible, so cells recovered from a biofilm and regrown in suspension test fully susceptible again. A susceptibility report can be entirely correct and still fail to predict cure, because the assay measured a state the organism is not in. It also reframes what an anti-biofilm agent should be judged on, since dispersing the matrix as an antibiotic adjunct is a different objective from killing.

Almost all anti-biofilm claims for peptides rest on crystal violet staining of a twenty-four hour biofilm grown on a polystyrene plate. That stain measures retained biomass, not viable organisms. Preventing formation and eradicating an established biofilm are separate experiments with different potency requirements, and results from the easier one are routinely presented as if they answered the harder one.