aeruginosa control several physiological aspects, such as expression of multiple virulence determinants, secondary metabolite production, swarming motility, biofilm formation, biodegradation of pollutants, and electricity generation ( 13).ĭuring chronic infections, P. The production of these virulence factors is in turn dependent on quorum sensing (QS), the ability to monitor and respond to changes in cell population density ( 11, 12). aeruginosa has an armory of cell-associated (flagella, pili, lectins, alginate/biofilm, and lipopolysaccharide) and extracellular (proteases, hemolysins, cytotoxin, pyocyanin, siderophores, exotoxin A, exoenzyme S, and exoenzyme U) virulence factors ( 11, 12). aeruginosa is controlled by several virulence factors that aid tissue invasion and damage ( 2, 11). It is a common cause of hospital- and community-acquired lung, skin, eye, wound, bloodborne, and urinary tract infections ( 4, 7, 8) and is particularly hazardous for immunocompromised patients and those with cystic fibrosis (CF), burns, open fractures, or implanted medical devices such as catheters ( 4, 9, 10).
aeruginosa is responsible for 10–20% of nosocomial infections ( 3) and has been ranked by the World Health Organization as the priority-one human pathogen requiring development of novel antibacterial agents ( 4, 5, 6). aeruginosa may be functionally equivalent in several traits relevant for their virulence or environmental properties ( 1, 2). Therefore, environmental and clinical strains of P. The environmental strains express typical virulence factors and multidrug resistance determinants, while the clinical strains can use oil hydrocarbons as a carbon source. Pseudomonas aeruginosa is an opportunistic pathogen that exists in various eukaryotic hosts, as well as in host-free environments ( 1).