Pseudomonas aeruginosa

MICROBIOLOGY

  • Gram-negative non-fermenting, motile bacillus [Fig 1]; known for blue-green pus due to pyocyanin and pyoverdin pigments.
  • This non-fastidious organism inhabits various environments, including soil and water, such as hot tubs, sinks, faucets, respirators, disinfectants, and contact lens cleaning solutions. It grows on a wide variety of media.
  • Clinical isolates usually render smooth colonies on plates [Fig 2].
  • P. aeruginosa produces biofilm, toxins, and proteases.[6]
  • Drug resistance mechanisms include multiple pathways, including chromosomal and inducible beta-lactamases, active efflux pumps, acquired genes and plasmid-mediated ESBLs (TEM, SHV, CTX-M), and altered permeability due to decreased expression of outer membrane porins.[15][19]
    • P. aeruginosa iteratively expresses alternative resistance strategies while exposed to antibiotics.[2]
    • Carbapenem-resistance mechanisms include:
      • Loss of outer membrane porin D (OprD) results in carbapenem resistance.
      • The combined loss of OprD with another mechanism, i.e., overexpression of AmpC beta-lactamase OR overexpression of efflux pumps, is a significant determinant of resistance to carbapenems.[18]
      • Production of carbapenemases, esp. Ambler class B metallo-beta-lactamases (NDM, VIM, IMP) are rare in US isolates and are estimated at 20% in global isolates.[10]
    • The 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.[16]

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Last updated: August 9, 2024