# Pseudomonas aeruginosa

> Pseudomonas aeruginosa for NEET-PG Microbiology covering pyocyanin and other pigments, exotoxin A, burn and cystic fibrosis infections, and drug choice.

- Canonical URL: https://prepelephant.com/topics/neet-pg/microbiology/pseudomonas-aeruginosa
- Exam / course: NEET-PG · Subject: Microbiology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-08
- Last updated: 2026-10-08
- Reference basis: Ananthanarayan and Paniker's Textbook of Microbiology; Jawetz, Melnick and Adelberg's Medical Microbiology
- How to cite: "Pseudomonas aeruginosa", PrepElephant, https://prepelephant.com/topics/neet-pg/microbiology/pseudomonas-aeruginosa

## Direct answer

Pseudomonas aeruginosa is an oxidase-positive, non-lactose-fermenting Gram-negative bacillus that causes opportunistic infection in burns, catheterised patients, ventilated patients and people with cystic fibrosis. Its defining features are blue-green pyocyanin pigment, a grape-like odour and intrinsic resistance to many antibiotics. Treatment depends on susceptibility testing, and serious infections are treated with antipseudomonal agents chosen by local antibiogram, with combinations used selectively.

## What you must remember

- **Morphology and growth:** Motile Gram-negative rod with a polar flagellum that grows at 42 degrees Celsius, a feature used to separate it from other pseudomonads.
- **Pigments:** Pyocyanin is blue-green, pyoverdine is yellow-green and fluorescent under UV, pyorubin is red and pyomelanin is brown.
- **Exotoxin A:** ADP-ribosylates elongation factor 2, the same mechanism as diphtheria toxin, and blocks host protein synthesis.
- **Other virulence factors:** Exoenzyme S, elastase, phospholipase C and a type III secretion system that injects effector proteins into host cells.
- **Mucoid phenotype:** Alginate-producing strains colonise cystic fibrosis airways chronically and resist phagocytosis.
- **Ecthyma gangrenosum:** Haemorrhagic, necrotic skin lesion with a black centre, classically seen in neutropenic patients with bacteraemia.
- **Intrinsic resistance:** Low outer membrane permeability and efflux pumps such as MexAB-OprM limit many antibiotics.
- **Laboratory clues:** Oxidase positive, enhanced pigment production on cetrimide agar, and a grape-like odour on culture.

## Choosing an antipseudomonal drug by class

Antipseudomonal activity is not one property shared by all antibiotics, so the drug class matters. Each group has a distinct role in empirical and definitive therapy.

| Class | Examples | Role in practice |
| --- | --- | --- |
| Antipseudomonal penicillins | Piperacillin, ticarcillin | Empirical cover, often with a beta-lactamase inhibitor |
| Antipseudomonal cephalosporins | Ceftazidime, cefepime | Serious hospital-acquired infection and febrile neutropenia |
| Carbapenems | Imipenem, meropenem | Reserve agents for resistant or severe infection |
| Aminoglycosides | Gentamicin, tobramycin, amikacin | Synergy in combination therapy; nephrotoxic and ototoxic |
| Fluoroquinolones | Ciprofloxacin, levofloxacin | Oral option with good activity; resistance rises with use |
| Polymyxins | Colistin, polymyxin B | Last line for multidrug-resistant isolates; nephrotoxic |

Combination therapy is sometimes used in severe infection, although recent guidance favours a single active agent in many settings. Piperacillin-tazobactam and cefepime are often chosen for hospital-acquired infection, but local antibiogram data decide the first choice.

The final regimen should always follow the culture and susceptibility report rather than the empirical table. Susceptibility results override the table at every review, not only at the start.

## Where the exam tries to catch you

Pseudomonas questions usually hinge on intrinsic resistance and on the typical clinical picture.

- **Trap:** Choosing ampicillin or a first-generation cephalosporin for a burn-wound infection — **Correct:** Pseudomonas is intrinsically resistant to these drugs, so an antipseudomonal agent is needed.
- **Trap:** Attributing green pus or a sweet smell to Staphylococcus — **Correct:** Blue-green pigment and a grape-like odour point to Pseudomonas aeruginosa.
- **Trap:** Treating chronic cystic fibrosis lung infection without considering Pseudomonas — **Correct:** Chronic colonisation with mucoid Pseudomonas aeruginosa is the classic picture, and long-term inhaled antibiotics are used per current guidance.

## Frequently asked questions

### Which pigment gives Pseudomonas aeruginosa its blue-green colour?

Pyocyanin, a phenazine pigment, gives Pseudomonas aeruginosa its blue-green colour. Pyoverdine adds a yellow-green fluorescence visible under ultraviolet light, which helps in laboratory recognition. Cetrimide agar enhances pigment production during culture.

### Which toxin of Pseudomonas aeruginosa acts like diphtheria toxin?

Exotoxin A of Pseudomonas aeruginosa acts like diphtheria toxin by ADP-ribosylating elongation factor 2. This blocks protein synthesis in host cells and contributes to tissue necrosis in burns and systemic infection.

### Why do cystic fibrosis patients become chronically colonised by Pseudomonas aeruginosa?

Thick, dehydrated airway secretions in cystic fibrosis impair mucus clearance and trap bacteria. Pseudomonas aeruginosa then shifts to alginate-producing mucoid forms that resist phagocytosis and antibiotics, so colonisation becomes long-term.

### What is ecthyma gangrenosum and when is it seen?

Ecthyma gangrenosum is a haemorrhagic, necrotic skin lesion with a black centre. In Pseudomonas aeruginosa bacteraemia it is classically seen in neutropenic patients, and it serves as a bedside clue to disseminated infection.

### Why is Pseudomonas aeruginosa difficult to treat?

Pseudomonas aeruginosa combines low outer membrane permeability, efflux pumps such as MexAB-OprM, and the ability to acquire resistance during therapy. These features limit the number of effective drugs, so therapy must be guided by susceptibility testing, with combinations used selectively.