General Characteristics and Properties
Pseudomonas aeruginosa belongs to the family Pseudomonadaceae. These are Gram-negative, non-spore-forming rods possessing pili and polar flagella, conferring motility. The bacterium is an obligate aerobe. To generate energy, it oxidizes carbohydrates without fermentation, a feature detected using the Hugh-Leifson oxidative-fermentative (OF) test.
On standard nutrient media, the organism forms colonies that frequently produce water-soluble pigments:
- Pyocyanin (blue-green);
- Fluorescein / pyoverdine (green, UV-fluorescent);
- Pyorubin (red) and pyomelanin (black).
The culture emits a characteristic sweet odor (resembling jasmine or strawberry soap) due to the production of trimethylamine. It is capable of growth at 42 °C, which differentiates it from other pseudomonads.
Pathogenicity Factors
The pathogenicity of P. aeruginosa is driven by numerous adhesion factors, toxins, and enzymes:
- Adhesion factors: Pili facilitate initial attachment to the epithelium. Extracellular slime (a glycolipoprotein) protects the bacterium against phagocytosis and promotes adhesion to mucin. Mucoid strains, which overproduce slime, commonly infect patients with cystic fibrosis.
- Exotoxin A: The primary virulence factor. Its mechanism of action resembles diphtheria toxin: it inhibits protein synthesis by ADP-ribosylating elongation factor 2 (EF-2), leading to cell death. Its regulation is controlled by iron levels.
- Endotoxin (LPS): A component of the cell wall that triggers fever, oliguria, and leukopenia.
- Aggressive enzymes: Elastase degrades elastin and casein, neuraminidase aids in mucous membrane colonization, and hemolysins break down pulmonary surfactant, contributing to atelectasis. IgA protease destroys secretory antibodies.
Resistance and Epidemiology
P. aeruginosa exhibits remarkable survival capabilities (oligotrophy)—it can multiply in distilled water and disinfectant solutions (e.g., furatsilin). However, the bacterium is susceptible to drying, boiling, and chlorine-based agents.
This bacterium is a classic pathogen responsible for healthcare-associated (nosocomial) infections. Sources of infection include infected individuals or contaminated environmental objects within healthcare facilities: sinks, mechanical ventilators, and catheters. Transmission occurs via contact, respiratory, and hematogenous routes.
High-risk groups include patients with severe burns, cystic fibrosis, diabetes mellitus, and immunodeficiencies (e.g., post-transplantation). P. aeruginosa causes wound infections, pneumonia, urinary tract infections, and, in severe cases, sepsis.
Diagnosis and Treatment
The primary diagnostic method is bacteriological culture. Selective media (e.g., cetrimide agar, malachite green agar) are used for isolation. Identification is based on:
- Pigment production and characteristic odor;
- Ability to grow at 42 °C;
- Positive oxidase test;
- Glucose oxidation under aerobic conditions.
Due to intrinsic porin mutations and the capacity to synthesize β-lactamases, the bacterium displays high natural resistance. Treatment is initiated only after obtaining susceptibility testing (antibiogram) results, often using combination therapy. Anti-pseudomonal cephalosporins (e.g., ceftazidime), carbapenems, aminoglycosides (e.g., amikacin), and fluoroquinolones are utilized. For local infections, antipseudomonal bacteriophages may be applied.