Pseudomonas aeruginosa: Difference between revisions
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Pseudomonas aeruginosa
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*Broad intrinsic and acquired antibiotic resistance[[CiteRef::livermore2002mu]] |
*Broad intrinsic and acquired antibiotic resistance[[CiteRef::livermore2002mu]] |
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*Membrane impermeability |
*Membrane impermeability |
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**Decreased or absent OprD porin: resistance to carbapenems ([[imipenem]] and [[meropenem]]) |
**Decreased or absent OprD porin: resistance to [[carbapenems]] ([[imipenem]] and [[meropenem]]) |
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**Membrane changes: resistance to polymixins ([[colistin]]) |
**Membrane changes: resistance to polymixins ([[colistin]]) |
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**Reduced aminoglycoside transport: resistance to [[aminoglycosides]] |
**Reduced aminoglycoside transport: resistance to [[aminoglycosides]] |
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*Efflux pumps |
*Efflux pumps |
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**MexAB-OprM: resistance to fluoroquinolones and all β-lactams except [[imipenem]] |
**MexAB-OprM: resistance to [[fluoroquinolones]] and all [[β-lactams]] except [[imipenem]] |
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**MexCD-OprJ: resistance to fluoroquinolones and most β-lactams ([[cefoperazone]], [[cefpirome]], [[cefepime]], [[meropenem]]) but not [[imipenem]] |
**MexCD-OprJ: resistance to [[fluoroquinolones]] and most [[β-lactams]] ([[cefoperazone]], [[cefpirome]], [[cefepime]], [[meropenem]]) but not [[imipenem]] |
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**MexEF-OprN: resistance to fluoroquinolones and all β-lactams |
**MexEF-OprN: resistance to [[fluoroquinolones]] and all [[β-lactams]] |
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**MexXY-OprM: resistance to fluoroquinolones, most β-lactams (but not [[imipenem]]), and [[aminoglycosides]] |
**MexXY-OprM: resistance to [[fluoroquinolones]], [[tetracyclines]] including [[tigecycline]], most [[β-lactams]] (but not [[imipenem]] or [[ceftazidime]]), and [[aminoglycosides]] |
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*β-lactamases |
*β-lactamases |
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**Derepressed AmpC β-lactamase: resistance to penicillins and cephalosporins (except [[ceftolozane]]) |
**Derepressed AmpC β-lactamase: resistance to [[penicillins]] and [[cephalosporins]] (except [[ceftolozane]]) |
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**Acquired carbapenemases such as NDM-1: resistance to essentially all β- |
**Acquired [[carbapenemases]] such as NDM-1: resistance to essentially all [[β-lactams]] |
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*Aminoglycoside-modifying enzymes: resistance to [[aminoglycosides]] |
*Aminoglycoside-modifying enzymes: resistance to [[aminoglycosides]] |
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*Target site mutations |
*Target site mutations |
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**Topoisomerase II (gyrA) or IV (parC) point mutations: resistance to fluoroquinolones |
**Topoisomerase II (gyrA) or IV (parC) point mutations: resistance to [[fluoroquinolones]] |
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===Epidemiology=== |
===Epidemiology=== |
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Revision as of 14:45, 21 September 2020
Background
Microbiology
- Oxidase positive, non-fermenting Gram-negative bacillus
Mechanisms of Resistance
- Broad intrinsic and acquired antibiotic resistance1
- 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, tetracyclines including tigecycline, most β-lactams (but not imipenem or ceftazidime), 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-lactams
- 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.
