<it>Pseudomonas aeruginosa </it>Cystic Fibrosis isolates of similar RAPD genotype exhibit diversity in biofilm forming ability <it>in vitro</it>

• Main Authors: Elborn Stuart J, Moore John E, Haylock Richard W, Ternan Nigel G, Berrar Daniel, Pattison Sally, Deligianni Elena, Dooley James SG
• Format: Article
• Language: English
• Published: BMC 2010-02-01
• Series: BMC Microbiology
• Online Access: http://www.biomedcentral.com/1471-2180/10/38

<p>Abstract</p> <p>Background</p> <p><it>Pseudomonas aeruginosa </it>is considered to grow in a biofilm in cystic fibrosis (CF) chronic lung infections. Bacterial cell motility is one of the main factors that have been connected with <it>P. aeruginosa </it>adherence to both biotic and abiotic surfaces. In this investigation, we employed molecular and microscopic methods to determine the presence or absence of motility in <it>P. aeruginosa </it>CF isolates, and statistically correlated this with their biofilm forming ability <it>in vitro</it>.</p> <p>Results</p> <p>Our investigations revealed a wide diversity in the production, architecture and control of biofilm formation. Of 96 isolates, 49% possessed swimming motility, 27% twitching and 52% swarming motility, while 47% were non-motile. Microtitre plate assays for biofilm formation showed a range of biofilm formation ability from biofilm deficient phenotypes to those that formed very thick biofilms. A comparison of the motility and adherence properties of individual strains demonstrated that the presence of swimming and twitching motility positively affected biofilm biomass. Crucially, however, motility was not an absolute requirement for biofilm formation, as 30 non-motile isolates actually formed thick biofilms, and three motile isolates that had both flagella and type IV pili attached only weakly. In addition, CLSM analysis showed that biofilm-forming strains of <it>P. aeruginosa </it>were in fact capable of entrapping non-biofilm forming strains, such that these 'non-biofilm forming' cells could be observed as part of the mature biofilm architecture.</p> <p>Conclusions</p> <p>Clinical isolates that do not produce biofilms in the laboratory must have the ability to survive in the patient lung. We propose that a synergy exists between isolates <it>in vivo</it>, which allows "non biofilm-forming" isolates to be incorporated into the biofilm. Therefore, there is the potential for strains that are apparently non-biofilm forming <it>in vitro </it>to participate in biofilm-mediated pathogenesis in the CF lung.</p>