Last updated on May 30th, 2021
Pseudomonas aeruginosa is a gram-negative rod. Pseudomonas aeruginosa can resist high concentrations of salt, dyes, weak antiseptics, and many commonly used antibiotics. Most pseudomonads known to cause disease in humans are associated with opportunistic infections. Pseudomonas aeruginosa and Pseudomonas maltophila are mostly responsible for disease conditions.
This opportunistic pathogen may infect virtually any tissue. Infection is facilitated by the presence of an underlying disease. It is a major threat to hospitalized patients, particularly those with serious underlying diseases such as cancer and burns (burning causes breakdown of nonspecific host defenses).
Sites of infection by P. aeruginosa
- Central nervous system infections
- Localized infections of ear and sinus
- Skin and musculoskeletal tissues, burn wounds, surgical wounds
- Respiratory tract: chronic infections in cystic fibrosis patients, acute pneumonia in other patients
- Urinary tract infections
Mortality in P. aeruginosa infection
Infections with P. aeruginosa are associated with high mortality rate. This is because of the combination of
- Bacterial resistance to antibiotics
- Weakened host defenses
- Production of extracellular bacterial enzymes and toxins.
Pathogenesis of P. aeruginosa
Pseudomonas aeruginosa produces many factors that may contribute to its virulence. Some of them are
- Hemolysins: Glycolipid hemolysin may play a role in P. aeruginosa pulmonary infections.
- Extracellular polysaccharide: They may impede phagocytosis and impair diffusion of antibiotics and thus facilitate colonization and persistence. These mucoid strains usually are isolated only from patients with cystic fibrosis.
- Pigments: Pyocyanin (a phenazine pigment) and fluorescein are two common pigments produced by P. aeruginosa. Pyocyanin retards the growth of some other bacteria and thus may facilitate colonization by P. aeruginosa.
- Extracellular protease: May play role in the formation of hemorrhagic lesions and tissue destruction.