Pseudomonas aeruginosa: Difference between revisions
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Pseudomonas aeruginosa
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===Microbiology=== |
===Microbiology=== |
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===Mechanisms of Resistance=== |
===Mechanisms of Resistance=== |
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Revision as of 20:49, 14 September 2020
Background
Microbiology
- Oxidase positive, non-fermenting Gram-negative bacillus
Mechanisms of Resistance
- Broad intrinsic and acquired antibiotic resistance
- Membrane impermeability
- Decreased or absent OprD porin: resistance to carbapenems (imipenem and meropenem)
- Membrane changes: resistance to polymixins (colistin)
- Reduced aminoglycoside transport: resistance to aminoglycosides
- Efflux pumps
- MexAB-OprM: resistance to fluoroquinolones and all β-lactams except imipenem
- MexCD-OprJ: resistance to fluoroquinolones and most β-lactams (cefoperazone, cefpirome, cefepime, meropenem) but not imipenem
- MexEF-OprN: resistance to fluoroquinolones and all β-lactams
- MexXY-OprM: resistance to fluoroquinolones, most β-lactams (but not imipenem), and aminoglycosides
- β-lactamases
- Derepressed AmpC β-lactamase: resistance to penicillins and cephalosporins (except ceftolozane)
- Acquired carbapenemases such as NDM-1: resistance to essentially all β-lactam antibiotics
- Aminoglycoside-modifying enzymes: resistance to aminoglycosides
- Target site mutations
- Topoisomerase II (gyrA) or IV (parC) point mutations: resistance to fluoroquinolones
Epidemiology
- Loves moist and wet environments
- Causes healthcare-associated infections
- UTI, SSI, bacteremia, HAP, VAP
- Especially common in cystic fibrosis
Treatment
- Refer to antipseudomonal antibiotics for specific treatment options
- Double coverage (ß-lactam + non-ß-lactam) in cases of severe infection in order to ensure activity against the infection
References
- ^ D. M. Livermore. Multiple Mechanisms of Antimicrobial Resistance in Pseudomonas aeruginosa: Our Worst Nightmare?. Clinical Infectious Diseases. 2002;34(5):634-640. doi:10.1086/338782.
