Among Caucasians, cystic fibrosis is the most common autosomal recessive inherited disease. It is a multisystem disease caused by a genetic mutation of the cystic fibrosis transmembrane conductance regulator (CFTR). As a consequence, a thick mucus layer coating the surface of airway epithelium is formed, disabling normal mucocilliary clearance. Pseudomonas aeruginosa is an ubiquitous opportunistic pathogen, with the ability to survive in hospital environment. By early childhood, it colonizes the airways of most cystic fibrosis patients. If it is not promptly treated by aggressive antibiotic therapy at that stage, the acute intermittent infections become chronic, with a gradual decrease in pulmonary function leading to respiratory failure. This is perpetuated by a strong polimophonuclear inflammatory response, with production of oxygen radicals which cause mutations in Pa genome, and induce the mucoid phenotype, characterized by alginate overproduction and biofilm formation. Biofilm is a bacterial consortium, embedded in an exopolysaccharide matrix, within which the bacteria have reduced virulence and metabolic activity, but are protected against the activities of host immune system and the effects of antibiotic substances. This allows pseudomonas to survive and persist in the cystic fibrosis lung. Conventional chronic pulmonary infection therapy is chronic suppressive therapy, via inhaled antibiotics, with the primary goal of maintaining lung function in patients. Due to emergence of high antibiotic resistance, development of new drugs is focused on producing different antibiotic fomulations and combinations, and towards investigation of substances which can prevent biofilm formation (quorum sensing inhibitors, antioxidants, ion chelators), or achieve its disintegration.