Pseudomonas aeruginosa is notoriously difficult to treat due to its high intrinsic resistance to many antibiotics. This intrinsic resistance is primarily mediated by its low outer membrane permeability, which restricts antibiotic entry, and the presence of multiple active efflux pump systems that actively pump out various classes of antibiotics, including beta-lactams. While P. aeruginosa can acquire resistance mechanisms like ESBLs (A) or carbapenemases, and PBP alterations (C) are relevant for beta-lactam resistance in some bacteria, the fundamental and most common reason for its broad resistance profile, even to anti-pseudomonal beta-lactams like piperacillin-tazobactam, is its intrinsic resistance mechanisms. Target site modification of ribosomal subunits (D) is a mechanism for resistance to antibiotics like aminoglycosides or macrolides, not typically beta-lactams.
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