Pseudomonas aeruginosa

Lisa A. Spacek, M.D., Ph.D.
Pseudomonas aeruginosa is a topic covered in the Johns Hopkins ABX Guide.

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MICROBIOLOGY

  • Gram-negative non-fermenting, motile bacillus [Fig 1]; known for blue-green pus due to pyocyanin and pyoverdin pigments.
  • Non-fastidious organism; inhabits a variety of environments including soil and water, i.e., hot tubs, sinks, water faucets, respirators, disinfectants, and contact lens cleaning solution.
  • Grows on a wide variety of media. Clinical isolates usually render smooth colonies on plates [Fig 2].
  • Produces biofilm, toxins, and proteases.
  • Drug resistance mechanisms include multiple pathways: chromosomal and inducible beta-lactamases, active efflux pumps, acquired genes and plasmid-mediated ESBLs (TEM, SHV, CTX-M), and altered permeability.[8][13]
    • Carbapenem-resistance mechanisms include:
      • Loss of outer membrane porin D (OprD) results in resistance to carbapenems.
      • The combined loss of OprD in combination with another mechanism, i.e., overexpression of AmpC beta-lactamase OR overexpression of efflux pumps, is a major determinant of resistance to carbapenems.[12]
      • Production of carbapenemases, esp. Ambler class B metallo-beta-lactamases (NDM, VIM, IMP).[4]
    • Clinical utility of rapid molecular diagnostic platforms to detect genotype resistance to beta-lactam/beta-lactamase inhibitor combinations is limited by the complexity of non-tested determinants of beta-lactam resistance, such as OprD changes and drug efflux systems.[3]

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MICROBIOLOGY

  • Gram-negative non-fermenting, motile bacillus [Fig 1]; known for blue-green pus due to pyocyanin and pyoverdin pigments.
  • Non-fastidious organism; inhabits a variety of environments including soil and water, i.e., hot tubs, sinks, water faucets, respirators, disinfectants, and contact lens cleaning solution.
  • Grows on a wide variety of media. Clinical isolates usually render smooth colonies on plates [Fig 2].
  • Produces biofilm, toxins, and proteases.
  • Drug resistance mechanisms include multiple pathways: chromosomal and inducible beta-lactamases, active efflux pumps, acquired genes and plasmid-mediated ESBLs (TEM, SHV, CTX-M), and altered permeability.[8][13]
    • Carbapenem-resistance mechanisms include:
      • Loss of outer membrane porin D (OprD) results in resistance to carbapenems.
      • The combined loss of OprD in combination with another mechanism, i.e., overexpression of AmpC beta-lactamase OR overexpression of efflux pumps, is a major determinant of resistance to carbapenems.[12]
      • Production of carbapenemases, esp. Ambler class B metallo-beta-lactamases (NDM, VIM, IMP).[4]
    • Clinical utility of rapid molecular diagnostic platforms to detect genotype resistance to beta-lactam/beta-lactamase inhibitor combinations is limited by the complexity of non-tested determinants of beta-lactam resistance, such as OprD changes and drug efflux systems.[3]

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Last updated: May 5, 2021