Biofilm Formation by Clinical Isolates of Pseudomonas aeruginosa and Its Correlation With Antibiotic Resistance

Abstract

Pseudomonas aeruginosa is an opportunist that causes stubborn infections in hospitals and in people with damaged airways, and two of its habits are blamed for much of that stubbornness: it forms biofilms, and it resists many antibiotics. It is often assumed that the isolates which build the thickest biofilms are also the most resistant. This narrative review asks how far that assumption can be defended. It draws on published work on biofilm development, on the genetics of resistance, and on the laboratory methods used to measure both, and it reports no new isolates and no new data. Biofilm growth protects cells through slow diffusion, oxygen limitation, dormant subpopulations, matrix components and biofilm-specific genes, while conventional resistance rests on efflux, enzymes, target changes and reduced permeability. The two sets of mechanisms overlap but are not the same, so a correlation across a collection of isolates is possible without being necessary, and its direction can depend on who is sampled. Differences in assay design, growth medium, plate surface and definitions of resistance make published comparisons hard to line up. The review concludes that biofilm capacity and resistance should be reported together but interpreted separately, and it sets out what a convincing comparison of clinical isolates would need to include.