Complete genome sequence of Pseudomonas aeruginosa PA01
Pseudomonas aeruginosa PA01 Genome Page
Gene assigned a role category
Pseudomonas Genome Data Base
Genome Data base
PFGE
Pseudomonas aeruginosa PFGE protocol (HPA.UK)
ARPAC Pseudomonas aeruginosa Typing Database
PFGE method
Organism-------Pseudomonas aeruginosa
Recommended lysis enzyme--proteinase K
Restriction enzyme----------------SpeI,XbaI
Approximate no. of-----------20–25,40–50
restriction Fragments
Fragments size-------------10–700,10–300
range (kb)
Identification of glucose non-fermenting Gram-negative rods
Pseudomonas
Pseudomonas species is a ubiquitous, aerobic gram-negative bacillus.
Reservoirs in nature include soil, vegetation, and water.
Reservoirs in a hospital include sinks, toilets, mops, respiratory therapy, and dialysis equipment.
It exhibits intrinsic resistance to many antibiotics and disinfectants.
Pseudomonas adheres to host cells by pili and nonpili adhesins. It produces a polysaccharide capsule that allows the organism to adhere to epithelial cells, inhibits phagocytosis,and confers protection against antibiotic activity.
Patients with cystic fibrosis are more likely to be infected with a strain whose colony appears mucoid because of the presence of the capsule.
Pseudomonas produces multiple toxins and enzymes, which contribute to its virulence.Its lipopolysaccharide endotoxin and exotoxin A appear to cause most of the systemic manifestations of Pseudomonas disease. Exotoxin A blocks protein synthesis in host cells, causing direct cytotoxicity. It mediates systemic toxic effects as well. It is similar in function to diphtheria toxin but is structurally and immunologically distinct. Endotoxin contributes to the development of many of the symptoms and signs of sepsis, including fever, leukocytosis, and hypotension.
Antibiotic resistance is another important aspect of its virulence. It is intrinsically resistant to numerous antibiotics and has acquired resistance to others through various means. The polysaccharide capsule prevents the penetration of many antibiotics into Pseudomonas. Penetration of antibiotic into the Pseudomonas cell is usually through pores in the outer membrane. Mutation of these porin proteins appears to be a primary mechanism of its antibiotic resistance. Multidrug efflux pumps and b-lactamase production also contribute to the antibiotic resistance that so frequently complicates the treatment of Pseudomonas infections.
Some P. aeruginosa strains produce a diffusable pigment: pyocyanin, which gives the colonies a blue color; fluorescein, which gives them a yellow color; or pyorubin, which gives them a red-brown color. Pyocyanin also
seems to aid in the virulence of the organism by stimulating an inflammatory response and by producing toxic oxygen radicals.
Clinically significant infections with P. aeruginosa should not be treated with single-drug therapy, because the bacteria can develop resistance when single drugs are employed. The newer quinolones, including ciprofloxacin, are active against Pseudomonas. Quinolones inhibit bacterial DNA synthesis by blocking DNA gyrase. The fluorinated forms of ciprofloxacin and norfloxacin have low toxicity and greater antibacterial activity than the earlier forms. Plasmids code for enzymes that determine the active transport of various antimicrobials across the cell membrane.
