Abstract
Biofilms are characterized by high tolerance to antimicrobials. However, conventional antibiograms are performed on planktonic microorganisms. Through the clinical Biofilm Ring Test® (cBRT), initially aimed to measure the adhesion propensity of bacteria, we discerned a variable distribution of biofilm-producer strains among P. aeruginosa samples isolated from expectorations of cystic fibrosis (CF) patients. Despite a majority of spontaneous adherent isolates, few strains remained planktonic after 5 h of incubation. Their analysis by an adapted protocol of the cBRT revealed an induction of the biofilm early formation by sub-inhibitory doses of β-lactams. Microscopic observations of bacterial cultures stained with Syto 9/Propidium Iodide (PI) confirmed the ability of antimicrobials to increase either the bacterial biomass or the biovolume occupied by induced sessile cells. Finally, the cBRT and its derivatives enabled to highlight in a few hours the potential inducer property of antibiotics on bacterial adhesion. This phenomenon should be considered carefully in the context of CF since patients are constantly under fluctuating antimicrobial treatments. To conclude, assays derived from the Biofilm Ring Test® (BRT) device, not only define efficient doses preventing biofilm formation, but could be useful for the antimicrobial selection in CF, to avoid inducer molecules of the early biofilm initiation.
Highlights
Pseudomonas aeruginosa is highly resistant to antimicrobials and plays a major role in nosocomial infections leading to a high mortality rate [1,2]
We evaluated the biofilm formation ability of P. aeruginosa isolates that originated from the sputum of anonymized cystic fibrosis (CF) patients, by using the BioFilm Ring Test (BRT)
The clinical Biofilm Ring Test (cBRT) procedure allowed for the characterization of microbial cultures through the biofilm strength evaluation of the bacterial serial dilutions
Summary
Pseudomonas aeruginosa is highly resistant to antimicrobials and plays a major role in nosocomial infections leading to a high mortality rate [1,2]. Its survival ability is very complex and involves multifactorial mechanisms including the capacity to grow in biofilms. These structural organizations are defined as communities of microorganisms embedded in a self-produced matrix and adhering to surfaces. It is well recognized that Minimal Inhibitory Concentrations (MICs) and Minimal Bactericidal Concentrations (MBCs) of antimicrobials effective against bacteria in biofilms may be 10 to 1000-fold higher than those effective against the planktonic microorganisms [4,5]. This tolerance can be explained, at least partly, by the slower metabolism of sessile bacteria forming the biofilm, the hypoxic environment inside
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