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]