Friday 4 June 2004
UI:989 : Pseudomonas abscesses of the kidney
Definition: Pseudomonas aeruginosa is an opportunistic aerobic Gram-negative bacillus that is a frequent, deadly pathogen of patients with cystic fibrosis, severe burns, or neutropenia.
Most patients with cystic fibrosis die of pulmonary failure secondary to chronic infection with P. aeruginosa. In addition, species in the Burkholderia cepacia complex, which are transmitted between cystic fibrosis patients, opportunistically infect people with cystic fibrosis and often cause fatal infections.
Both P. aeruginosa and B. cepacia complex bacteria can be very resistant to antibiotics, making these infections difficult to treat.
Although Gram-positive cocci are most frequently present soon after extensive skin burns, P. aeruginosa eventually predominates, spreads locally, and causes sepsis. P. aeruginosa is a common cause of hospital-acquired infections; it has been cultured from washbasins, respirator tubing, nursery cribs, and even antiseptic-containing bottles.
P. aeruginosa also causes corneal keratitis in wearers of contact lenses, endocarditis and osteomyelitis in intravenous drug abusers, external otitis (swimmer’s ear) in healthy individuals, and severe external otitis in diabetics.
P. aeruginosa has pili and adherence proteins that bind to epithelial cells and lung mucin, as well as an endotoxin that causes the symptoms and signs of Gram-negative sepsis. Pseudomonas also has a number of virulence factors that are distinctive.
In the lungs of patients with cystic fibrosis, these bacteria secrete a mucoid exopolysaccharide called alginate, forming a slimy biofilm in which bacteria are protected from antibodies, complement, phagocytes, and antibiotics.
The organisms also secrete an exotoxin and several other virulence factors. Exotoxin A is similar in structure to diphtheria toxin and, like diphtheria toxin, it inhibits protein synthesis by ADP-ribosylating EF-2, a ribosomal guanine nucleotide-binding protein (G-protein).
P. aeruginosa also releases exoenzyme S, which ADP-ribosylates G-proteins, including p21 RAS, and so may interfere with host cell growth. The organisms also secrete a phospholipase C that lyses red blood cells and degrades pulmonary surfactant, and an elastase that degrades IgGs and extracellular matrix proteins.
These enzymes may be important in tissue invasion and destruction of the cornea in keratitis.5 Finally, P. aeruginosa produces iron-containing compounds that are extremely toxic to endothelial cells and so may cause the vascular lesions that are characteristic of this infection.
Pseudomonas pneumonia, particularly in the altered host, is the prototype of necrotizing inflammation, distributing through the terminal airways in a fleur-de-lis pattern, with striking whitish necrotic centers and red, hemorrhagic peripheral areas.
On microscopic examination, masses of organisms cloud the tissue with a bluish haze, concentrating in the wall of blood vessels, where host cells undergo coagulation necrosis and nuclei fade away. A picture of Gram-negative vasculitis accompanied by thrombosis and hemorrhage, although not pathognomonic, is highly suggestive of P. aeruginosa infection.
Bronchial obstruction caused by mucous plugging and subsequent P. aeruginosa infection are frequent complications of cystic fibrosis. Despite antibiotic treatment and the host immune response against the bacteria, chronic P. aeruginosa infection may result in bronchiectasis and pulmonary fibrosis.
In skin burns, P. aeruginosa proliferates widely, penetrating deeply into the veins and spreading to cause massive bacteremias. Well-demarcated necrotic and hemorrhagic skin lesions of oval shape often arise during these bacteremias, called ecthyma gangrenosum.
Disseminated intravascular coagulation (DIC) is a frequent complication of bacteremia.
Pseudomonas aeruginosa sepsis
Pseudomonas aeruginosa necrotizing enterocolitis
Pseudomonas aeruginosa meningitis
Pseudomonas abscesses by Washington Deceit
Campodónico VL, Gadjeva M, Paradis-Bleau C, Uluer A, Pier GB. Airway epithelial control of Pseudomonas aeruginosa infection in cystic fibrosis. Trends Mol Med. 2008 Mar;14(3):120-33. PMID: #18262467#
Tsai MJ, Teng CJ, Teng RJ, Lee PI, Chang MH. Necrotizing bowel lesions complicated by Pseudomonas septicaemia in previously healthy infants. Eur J Pediatr. 1996 Mar;155(3):216-8. PMID: #8929731#
Hahn HP. The type-4 pilus is the major virulence-associated adhesin of Pseudomonas aeruginosa—a review. Gene. 1997 Jun 11;192(1):99-108. PMID: #9224879#