Pseudomonas aeruginosa
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Pseudomonas Aeruginosa Key Points
- Motile aerobic gram-negative bacillus causing opportunistic infection.
- It is not normally part of human bacterial flora. Hospitalisation increases exposure.
- It is resistant to many antibiotics. Fluoroquinolones and carbopenems are often used for treatment. The bacteria thrives in moist environments.
- Pathogenic effect is via protease and exotoxin production.
- It is associated with ecthyma gangrenosum.
Background
Pseudomonas aeruginosa is an encapsulated rod-shaped Gram-negative bacteria that is primarily aerobic but can function as a facultative anaerobe. Pseudomonas is widely found in soil, water, and hospital environments. Among its species, Pseudomonas aeruginosa is the most clinically significant and is recognised as a major opportunistic pathogen, especially in immunocompromised individuals. It is particularly notorious for causing healthcare-associated infections.
Lab features
- Gram-negative rod
- Non-lactose fermenting
- Oxidase positive
Pseudomonas aeruginosa is the most important human pathogen in the Pseudomonas genus. It is responsible for a broad range of infections, especially in those with weakened immune systems, such as ICU patients, burn victims, and individuals with cystic fibrosis. Its adaptability, virulence, and resistance mechanisms make it a challenging pathogen to treat and control.
Role of moist environments in hospitals
P. aeruginosa thrives in moist environments. In hospitals, it is frequently found in sinks, showers, taps, respiratory equipment, and other wet surfaces. These settings provide ideal reservoirs for colonisation and transmission, particularly when infection control practices are insufficient. Contaminated water systems have been implicated in outbreaks, especially in neonatal and intensive care units.Pathophysiology
Pseudomonas aeruginosa has an array of features that enhance its virulence:- Exotoxins such as exotoxin A inhibit host cell protein synthesis.
- Endotoxins are part of the cell wall specifically lipopolysaccharide (LPS)
- Proteases such as elastase degrade host tissues and immune components.
- Biofilm formation enhances resistance to antibiotics and immune responses.
- Pili and flagella facilitate adhesion and motility.
These mechanisms lead to cellular damage, immune evasion, and persistent infection, especially in compromised tissues.
Pathophysiology
Pseudomonas aeruginosa produces both an endotoxin (causes fever and shock) and exotoxin A (inhibits protein synthesis by catalysing ADP-ribosylation of elongation factor EF-2)Clinical Features
Features depend on the site of infection- Eye: keratitis, endophthalmitis (especially contact lens wearers)
- Ear: otitis externa (including 'swimmer’s ear') and malignant otitis externa (most commonly in diabetics)
- Skin: wound infections, especially in burns. Often malodorous with a green superficial crust.
- Bone: osteomyelitis (e.g., following puncture wounds)
- CNS: meningitis, usually post-surgical or post-trauma
- Chest: pseudomonas infections are particularly common in patients with cystic fibrosis
- Urinary tract infections: particularly in long term catheters
- Bloodstream: bacteraemia and sepsis, especially in neutropenic or ICU patients
Diagnosis
The diagnosis of pseudomonas infections relies primarily on microbiological culture. Identification includes:
- Growth on selective media (e.g., cetrimide agar)
- Typical colonies producing a grape-like odour and blue-green pigment (pyocyanin)
- Sensitivity testing due to variable antibiotic resistance
Principles of treatment
Treatment is often complicated by high levels of intrinsic and acquired resistance:
- First-line antibiotics often include anti-pseudomonal beta-lactams e.g., ceftazidime, piperacillin-tazobactam, carbapenems e.g., meropenem, aminoglycosides and fluoroquinolones.
- Dual therapy may be used for serious infections or to prevent resistance.
- Local susceptibility patterns guide antibiotic selection.
- Chronic infections (e.g., in cystic fibrosis) may require long-term suppressive therapy.
Pseudomonas antibiotic resistance
Pseudomonas aeruginosa has a high level of intrinsic and acquired antibiotic resistance. Key resistance mechanisms include:
This makes infections difficult to treat and often requires combination therapy with anti-pseudomonal agents.
Pseudomonas aeruginosa has a high level of intrinsic and acquired antibiotic resistance. Key resistance mechanisms include:
- Efflux pumps that expel antibiotics
- Porin channel mutations reducing antibiotic entry
- Biofilm formation, which protects bacterial communities from immune responses and antimicrobials
- Production of antibiotic-inactivating enzymes such as beta-lactamases
This makes infections difficult to treat and often requires combination therapy with anti-pseudomonal agents.
Implications in hospital settings
P. aeruginosa poses a significant threat in healthcare environments:- Associated with prolonged hospital stays, increased morbidity, and higher mortality.
- Its ability to survive in water systems and form biofilms makes eradication difficult.
- Outbreaks are particularly concerning in high-risk units like NICUs and ICUs.
- Infection control measures include regular water system maintenance, hand hygiene, and equipment sterilisation.