Pseudomonas aeruginosa: Difference between revisions

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Pseudomonas aeruginosa
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== Background ==
==Background==
=== Microbiology ===
===Microbiology===
* [[Oxidase test::Oxidase-positive]], [[Has fermentation::non-fermenting]] [[Stain::Gram-negative]] [[Cellular shape::bacillus]]


*[[Oxidase test::Oxidase-positive]], [[Has fermentation::non-fermenting]] [[Stain::Gram-negative]] [[Cellular shape::bacillus]]
=== Mechanisms of Resistance ===
* Broad intrinsic and acquired antibiotic resistance
* Membrane impermeability
* MexAB-OprM efflux pump
* Acquired mutations
* Inducible AmpC β-lactamase
* Plasmid sharing


===Mechanisms of Resistance===
=== Epidemiology ===
* Loves moist and wet environments
* Causes healthcare-associated infections
** UTI, SSI, bacteremia, HAP, VAP
** Especially common in cystic fibrosis


*Broad intrinsic and acquired antibiotic resistance
== Treatment ==
*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===
* 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
*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


{{DISPLAYTITLE:''Pseudomonas aeruginosa''}}
{{DISPLAYTITLE:''Pseudomonas aeruginosa''}}

Revision as of 14:05, 15 August 2020

Background

Microbiology

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
  • 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

  1. ^  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.