Pseudomonas aeruginosa

General Characteristics and Properties

Pseudomonas aeruginosa belongs to the family Pseudomonadaceae. These are Gram-negative, non-spore-forming rods possessing pili and polar flagella, which ensure their motility. The bacterium is an obligate aerobe. To obtain energy, it oxidizes carbohydrates without resorting to fermentation, which is detected in the OF test (Hugh–Leifson medium).

On simple nutrient media, the microorganism forms colonies that often secrete water-soluble pigments:

• Pyocyanin (blue-green);
• Fluorescein / pyoverdine (green, fluorescent under UV light);
• Pyorubin (red) and pyomelanin (black).

The culture has a specific sweetish odor (resembling jasmine or strawberry soap) due to the production of trimethylamine. It is capable of growing at 42 °C, which distinguishes it from other pseudomonads.

Pathogenicity factors

The pathogenicity of P. aeruginosa is due to numerous adhesion factors, toxins, and enzymes:

1. Adhesion factors: Pili provide initial attachment to the epithelium. Extracellular slime (glycolipoprotein) protects the bacterium from phagocytosis and promotes adhesion to mucin. Mucoid strains, which abundantly produce slime, frequently affect patients with cystic fibrosis.
2. Exotoxin A: The main virulence factor. By its mechanism of action, it is similar to diphtheria toxin—it blocks protein synthesis by inhibiting elongation factor EF-2, leading to cell death. It is regulated by iron ions.
3. Endotoxin (LPS): A cell wall component. Causes fever, oliguria, and leukopenia.
4. Aggressive enzymes: Elastase breaks down elastin and casein, neuraminidase helps colonize mucous membranes, and hemolysins destroy surfactant in the lungs, contributing to the development of atelectasis. IgA protease destroys secretory antibodies.

Resistance and Epidemiology

P. aeruginosa exhibits incredible survival capacity (oligotrophy)—it can multiply in distilled water and disinfectant solutions (e.g., furacilin). At the same time, the bacterium is killed by drying, boiling, and exposure to chlorine-containing agents.

This bacterium is a typical causative agent of nosocomial (hospital-acquired) infections. The source of infection can be sick individuals or contaminated environmental objects in the hospital: sinks, ventilators, catheters. The infection is transmitted via contact, respiratory, and blood-borne routes.

Patients with burn disease, cystic fibrosis, diabetes mellitus, and immunodeficiencies (e.g., post-transplantation) are at high risk. P. aeruginosa causes wound infections, pneumonia, urinary tract infections, and, in severe cases, sepsis.

Diagnostics and treatment

The main diagnostic method is bacteriological. Selective media (cetrimide agar, malachite green agar) are used for inoculation. Identification is based on:

• pigment production and specific odor;
• ability to grow at 42 °C;
• positive oxidase test;
• glucose oxidation under aerobic conditions.

Due to an innate porin defect and the ability to synthesize β-lactamases, the bacterium possesses high natural resistance. Treatment is prescribed only after obtaining an antibiotic susceptibility test (antibiogram), combining drugs. Anti-pseudomonal cephalosporins (ceftazidime), carbapenems, aminoglycosides (amikacin), and fluoroquinolones are used. For local infections, anti-pseudomonal bacteriophage is applied.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanism of action of exotoxin A at the cellular level
• Specifics of pseudomonal infection in cystic fibrosis
• Typing methods for P. aeruginosa (pyocin typing, phage typing)
• Types of pseudomonal vaccines and immunotherapy
• Mechanisms of biofilm formation and their role in chronic persistence

Other topics in the section «Gram-negative aerobic rods (Pertussis, Brucella, Tularemia, Legionella, Coxiella/Q fever, Bartonella, Pseudomonas, Burkholderia, Acinetobacter, etc.)»

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.