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Pseudomonas AmpC During Therapy — SCE Infectious Diseases MCQ

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ModerateAntimicrobial StewardshipPseudomonas AmpC During TherapySCE Infectious Diseases

A 50-year-old man develops hospital-acquired pneumonia caused by Pseudomonas aeruginosa. He is treated with IV Piperacillin/Tazobactam. After 5 days, repeat sputum grows Pseudomonas now resistant to Piperacillin/Tazobactam but sensitive to Meropenem. What mechanism most likely explains this resistance emergence?

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Correct answer: E — Derepression of chromosomal AmpC beta-lactamase — Pseudomonas can develop resistance to antipseudomonal penicillins during therapy through AmpC upregulation

Pseudomonas aeruginosa has multiple intrinsic and inducible resistance mechanisms. AmpC derepression (stable overproduction of the chromosomal AmpC beta-lactamase) is a common mechanism for developing resistance to antipseudomonal penicillins and 3rd-generation cephalosporins during therapy. Additionally, loss of the OprD porin (leading to Imipenem resistance) and upregulation of efflux pumps (MexAB-OprM — affecting Meropenem) are other common acquired mechanisms. This highlights the importance of susceptibility testing on serial isolates and combination therapy for serious Pseudomonas infections.

Reference: BSAC 2023 – Pseudomonas resistance; EUCAST 2024