Abstract
Although different strategies to control biofilm formation on endotracheal tubes have been proposed, there are scarce scientific data on applying phages for both removing and preventing Pseudomonas aeruginosa biofilms on the device surface. Here, the anti-biofilm capacity of five bacteriophages was evaluated by a high content screening assay. We observed that biofilms were significantly reduced after phage treatment, especially in multidrug-resistant strains. Considering the anti-biofilm screens, two phages were selected as cocktail components, and the cocktail’s ability to prevent colonization of the endotracheal tube surface was tested in a dynamic biofilm model. Phage-coated tubes were challenged with different P. aeruginosa strains. The biofilm growth was monitored from 24 to 168 h by colony forming unit counting, metabolic activity assessment, and biofilm morphology observation. The phage cocktail promoted differences of bacterial colonization; nonetheless, the action was strain dependent. Phage cocktail coating did not promote substantial changes in metabolic activity. Scanning electron microscopy revealed a higher concentration of biofilm cells in control, while tower-like structures could be observed on phage cocktail-coated tubes. These results demonstrate that with the development of new coating strategies, phage therapy has potential in controlling the endotracheal tube-associated biofilm.
Highlights
Ventilator-associated pneumonia (VAP) is a serious concern in critically ill patients occurring within the 48 h period following endotracheal intubation
Biofilm-covered areas showed a significant reduction after phage treatment in 4/15 P. aeruginosa strains (Table S1), in which three were classified previously as multidrug-resistant [25]
Even though phage infectivity had been previously determined, seven P. aeruginosa strains were not affected by the phage treatment
Summary
Ventilator-associated pneumonia (VAP) is a serious concern in critically ill patients occurring within the 48 h period following endotracheal intubation. VAP frequently involves high morbidity and excessive healthcare costs, and its incidence increases with the duration of ventilation [2,3,4]. The role of the endotracheal tube-associated biofilms in VAP etiology has been largely discussed. Biofilms on the device surface appear rapidly after intubation, promote a global covering of the internal side, and remain attached even after suctioning [2,5]. These biofilms represent a persistent source of pathogenic bacteria that can invade the lower airways, colonizing the lungs and causing VAP [6]
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