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Pseudomonas aeruginosa

Pseudomonas aeruginosa

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Pseudomonas
General characteristics:
Gram-negative, straight or slightly curved rods.
"Non-fermenters": they do not catabolize glucose.
Aerobes – However, in the lungs of patients with cystic fibrosis, research indicates that formation of biofilms may facilitate anaerobic respiration.
Ubiquitous in the environment: they are often found in soil and water.
Flagellar and pili twitching motility
Oxidase-positive (aids in laboratory identification)
Fruity, grape-like aroma
Survive on trace nutrients – for example, they've even been found in distilled water.
Pseudomonas aeruginosa
Causes opportunistic infections; as we'll see, it is especially well-adapted for survival in patients with cystic fibrosis.
Produces two pigments that produce a distinctive appearance in culture: Pyocyanin, which is a bluish color Pyoverdine, which is a yellowish-green color (occaisionally spelled "pyoverdin")
Virulence Factors
Some virulence factors are regulated by quorum sensing, and some factors work together in disease pathogenesis.
Adhesins and pili facilitate adherence to host cells.
Biofilm production facilitates immune system evasion and, as mentioned earlier, plays an important role in infection of cystic fibrosis patients.
Endotoxin, which comprises lipopolysaccharide; as in other Gram-negative bacteria, endotoxin produces symptoms of sepsis and shock.
Polysaccharide capsule with alginate. – Capsule is anti-phagocytic and prevents clearance by antibodies, and is upregulated in patients with cystic fibrosis.
Exotoxins and enzymes are injected into host cells by Type III secretion systems, or into the tissues by Type II secretion systems.
Exotoxin A inhibits protein synthesis and contributes to tissue necrosis.
Pyoverdine, which, as described above, lends the bacteria a yellow-green hue, regulates secretion of Exotoxin A. Also acts as a siderophore to "steal" iron from the host.
Pyocyanin, the blue pigment, increases intracellular levels of cytotoxic superoxide and hydrogen peroxide. – Also promotes apoptosis of neutrophils, which inhibits the innate immune response. – Interferes with respiratory cilia and damages mucosal cells, which are otherwise important mechanisms of microbe clearance.
Alkaline protease inhibits complement and contributes to tissue destruction.
Exoenzymes S, T, U, and Y: – Exoenzymes S and T disrupt host cell actin cytoskeletons and promote cell death. – Exoenzyme U is cytotoxic, particularly to alveolar epithelial cells and macrophages. – Exoenzyme Y causes edema.
Elastases degrade complement and elastin, which is an important component of lung tissue. – LasA and LasB. – Host produces anti-elastase antibodies that form immune complexes; their deposition in tissues contributes to damage and malfunction.
Opportunistic infections
Infections are associated with hospital settings, especially in wet or moist areas.
Innate immune deficiencies or trauma, especially burn wounds, promote Pseudomonas infections.
Pulmonary infections range from mild tracheobronchitis to severe pneumonia with necrosis. – Patients with cystic fibrosis are particularly vulnerable. – Patients who rely on mechanical ventilation are also at a higher risk of infection.
Skin and soft tissue infections, particularly from burn wounds, are common. – Pseudomonas aeruginosa can also cause folliculitis and nail infections; cases have been linked to contaminated water in hot tubs, spas, and salons.
Urinary tract infections, particularly in patients with in-dwelling catheters.
Osteochondritis can develop after puncture wound infection; This is common in foot wounds caused by stepping on contaminated nails or other sharp objects. – Be aware that osteochondritis can also occur when infection spreads from other sites.
Otitis externa ranges from mild cases, aka, Swimmer's ear, to more severe cases, which are associated with diabetics and elderly people.
Corneal infections, which can produce ulcers, can occur after trauma; for example, corneal scratches caused by contact lenses.
Bacteremia with a high mortality rate, often because of multi-drug resistant strains and the fact that infected patients tend to be immunocompromised. – Ecthyma gangrenosum is characterized by necrotic and hemorrhagic skin lesions.
Antibiotic resistance:
– Intrinsic properties of their cell walls. – Acquired resistance via horizontal gene transfer. – Adaptive resistance; for example, environmental triggers in the lungs of cystic fibrosis patients induces upregulation of resistant mechanisms.
Additional Bacteria
Many of these were considered members of Pseudomonas until recently.
Burkholderia cepacia Complex comprises multiple species that are associated with Pulmonary infections, urinary tract infections, and bacteremia; they are generally susceptible to treatment with Trimethoprim-sulfamethoxazole (TMP-SMX).
Burkhoderia pseudomallei causes melioidosis, aka, Whitmore's disease; cutaneous and pulmonary infections can be treated with TMP-SMX.
Stenotrophomonas maltophilia causes pneumonia and bacteremia, and can also be treated with TMP-SMX. (formerly known as Xanthomonas maltophilia)
Acinetobacter species are associated with infections of the respiratory tract, urinary tract, and wounds; unfortunately, these species are resistant to many antibiotics.
Moraxella catahrralis is associated with Bronchial infections, sinusitis, and otitis; it is penicillin-resistant, but susceptible to other types of antibiotics.

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