Pseudomonas aeruginosa and Acinetobacter Infections
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Direct answer
Pseudomonas aeruginosa and Acinetobacter infections are nosocomial infections caused by gram-negative bacilli with intrinsic and acquired resistance. Pseudomonas is oxidase-positive and produces pyocyanin, while Acinetobacter baumannii is oxidase-negative and survives for weeks on dry surfaces. Antipseudomonal therapy relies on beta-lactams, aminoglycosides or ciprofloxacin, and carbapenem-resistant Acinetobacter often needs colistin or a sulbactam-based regimen.
What you must remember
- Oxidase test: P. aeruginosa is oxidase-positive, while A. baumannii is oxidase-negative, a clean separation that exam stems rely on.
- Pigments and odour: pyocyanin gives blue-green pus and pyoverdine fluoresces under ultraviolet light, and a sweet, grape-like odour also suggests Pseudomonas.
- Ecthyma gangrenosum: a painless black necrotic skin lesion with surrounding erythema, classically from Pseudomonas bacteraemia in neutropenic patients.
- Cystic fibrosis: mucoid Pseudomonas is the main long-term lung pathogen, forming biofilms that persist despite repeated treatment.
- Intrinsic resistance: efflux pumps such as MexAB-OprM, low outer-membrane permeability and inducible AmpC beta-lactamase limit the drug list.
- Acinetobacter resistance: OXA-type carbapenemases are frequently reported in Indian intensive care units, leaving colistin and sulbactam-based options.
- Antipseudomonal drugs: piperacillin-tazobactam, ceftazidime, cefepime, meropenem, aztreonam, ciprofloxacin and aminoglycosides, with combination therapy sometimes used in severe infection.
Comparing the two hospital pathogens
The two organisms share wards and resistance problems, but the bench tests separate them cleanly. Exam stems usually give the oxidase result or the lesion, and that single clue names the organism. Both are opportunistic, so neutropenia, mechanical ventilation and indwelling catheters decide who gets infected.
| Feature | P. aeruginosa | A. baumannii |
|---|---|---|
| Oxidase | Positive | Negative |
| Motility | Motile, polar flagellum | Non-motile |
| Classic lesion | Ecthyma gangrenosum, malignant otitis externa | Pneumonia, wound and line infections |
| Key trait | Pyocyanin, pyoverdine | Survives on dry surfaces for weeks |
| Main resistance tool | Efflux pumps and AmpC | Carbapenemases and porin loss |
| Usual reserve drugs | Colistin, combinations | Colistin, sulbactam, tigecycline |
Carbapenem-resistant Acinetobacter is common in many Indian intensive care units, so colistin and sulbactam-based regimens appear often in management answers, since sulbactam is itself active against this organism. In serious Pseudomonas infection, textbooks traditionally combine an antipseudomonal beta-lactam with an aminoglycoside, although recent guidance favours monotherapy for susceptible isolates. Acinetobacter survives on hospital surfaces and equipment, so outbreaks are controlled with infection-control measures alongside antibiotics.
Traps in hospital pathogen stems
Most errors come from misreading the lesion or the lab result, rather than from the drug list.
- Trap: an oxidase-negative, non-motile coccobacillus from a ventilator is labelled Pseudomonas. Correct: Acinetobacter baumannii is oxidase-negative and non-motile, so the isolate is Acinetobacter and its carbapenem resistance is screened early.
- Trap: a black necrotic lesion in a neutropenic patient is called a fungal infection without thought. Correct: ecthyma gangrenosum is the classic Pseudomonas lesion, and it calls for antipseudomonal therapy and a skin biopsy.
- Trap: colistin is given first for every resistant gram-negative. Correct: colistin is reserved for multidrug-resistant isolates, because nephrotoxicity and neurotoxicity limit routine use.
Frequently asked questions
Which test separates Pseudomonas aeruginosa from Acinetobacter baumannii?
The oxidase test separates them, because Pseudomonas aeruginosa is oxidase-positive while Acinetobacter baumannii is oxidase-negative. Motility also differs, since Pseudomonas is motile and Acinetobacter is not.
What is ecthyma gangrenosum and which organism causes it?
Ecthyma gangrenosum is a painless black necrotic skin lesion with surrounding erythema, most often seen in neutropenic or bacteraemic patients. Pseudomonas aeruginosa is its classic cause, and early antipseudomonal treatment is needed.
Which drug is used for carbapenem-resistant Acinetobacter infections?
Colistin is a common last-line option for carbapenem-resistant Acinetobacter baumannii, often combined with another agent. Sulbactam-based regimens and tigecycline are also used, guided by susceptibility testing.
Why does Pseudomonas cause chronic lung infection in cystic fibrosis?
Thick mucus in cystic fibrosis impairs clearance, and Pseudomonas aeruginosa adapts by forming mucoid biofilms that persist in the airways. Chronic lung colonisation is a major cause of progressive lung damage in these patients.
How does Pseudomonas aeruginosa resist so many antibiotics?
Pseudomonas aeruginosa resists drugs through efflux pumps such as MexAB-OprM, low outer-membrane permeability and an inducible AmpC beta-lactamase. These mechanisms explain why only a limited set of beta-lactams and fluoroquinolones remains active.