The Virulence of Pigmented and Non-Pigmented Pseudomonas Aeruginosa in Mice with Antibiotics Susceptibility

Pseudomonas aeruginosa, is an opportunistic pathogen that causes extensive morbidity and mortality in individuals who are immunocompromised or have underlying medical conditions such as, urinary tract, respiratory tract and skin infections and primarily causes of nosocomial infections [1,2]. Its anon sporulating, gram negative, oxidase positive motile bacterium with a polar flagellum [3], P. aeruginosa is a common nosocomial pathogen because it is capable of thriving in a wide variety of environmental niches [4]. It is a leading cause of hospital associated infections in the seriously ill, and the primary agent of chronic lung infections in cystic fibrosis patients [5] .They exist in very large numbers in the human environment and animal gut, they are capable of inhabiting/contaminating water, moist surface and sewage ,hospital environment usually have resident P. aeruginosa [6]. Despite the apparent ubiquity of P. aeruginosa in the natural environment and the vast array of potential virulence factors, the incidence of community-acquired infections in healthy subjects is relatively low. However, in the hospital environment, particularly in immunosuppressed, debilitated and burns patients, the incidence of P. aeruginosa infection is high [7]. It produces many numbers of extracellular toxins, which include phytotoxic factor, pigments, hydrocyanic acid, proteolytic enzymes, phospholipase enterotoxin, exotoxin and slim [1]. P. aeruginosa grows well on media and most strains elaborate the blue phenazine pigment pyocyanin and fluorescein (yellow), which together impart the characteristic blue –green coloration to agar cultures [6]. Pyocyanin is a blue redox-active secondary metabolite [8], which induces rapid apoptosis of human neutrophils, with a10 fold acceleration of constitutive neutrophil apoptosis in vitro but no apoptosis of epithelial cell or macrophages [9]. The redox active exotoxin pyocyanin is produced in the concentration up to 100 mol/l during the infection of CF patients and other bronchiectasis airways .The contribution of pyocyanin during infection of bronchiectasis airways are not appreciated [10]. Notably pyocyanin mediated ROS inhibit catalase activity, deplete cellular antioxidant reduced glutathione and increased the oxidized reduced glutathione in the bronchiolar epithelial cell [11,12]. Excessive and continuous producing of ROS and inhibit of antioxidant mechanisms overwhelm the antioxidant capacity, leading to tissue damage, also pyocyanin inhibit ciliary beating of the airway epithelial cell [13] pyocyanin. Also increases apoptosis and inactivates 1-protease inhibitor [14] reducing agents such as GSH and NADPH can reduce pyocyanin to pyocyanin radical, which then mono-or divalently reduce O2 to form superoxide anion O2or H2O2 [15]. Pyoverdine per contra is the main siderophore in iron gathering capacity its function as a powerful iron chelator, solubilizing and transporting iron through the bacterial membrane via specific receptor proteins at the level of outer membranes (Herinrichetal,1991). Pyoverdine is important because it has a high affinity for iron, with an affinity constant of 10(32) [16]. And has been shown to remove iron from transferrin in serum, probably assisting growth within, and ultimate colonization of the human host by P. aeruginosa (Cox and Adams,1985). Moreover experiments studying the burned models of P. aeruginosa infections have shown that ferric-pyoverdine is required infection and /or colonization, underlining the importance of ferric-pyoverdine to virulence of P. aeruginosa [16]. P. aeruginosa it is highly resist to antibiotics this resistance can be conferred by the outer membrane which provides an effective intrinsic barrier in the cell wall (or) cytoplasmic membrane (or) Abstract