A Pseudomonas aeruginosa isolate from a bronchoalveolar lavage is resistant to imipenem but susceptible to meropenem. No carbapenemase is detected by phenotypic testing. Which mechanism best explains this pattern?
- A Loss of the OprD porin channel ✓
- B Production of PER-type extended-spectrum beta-lactamase
- C Overexpression of AmpC cephalosporinase alone
- D Mutation of DNA gyrase conferring cross-resistance
Explanation
Imipenem enters Pseudomonas aeruginosa almost exclusively through the OprD porin. Loss or downregulation of OprD therefore selectively raises the imipenem MIC while meropenem, which uses alternative entry pathways, remains active. This is the classic non-enzymatic carbapenem resistance phenotype. AmpC overexpression and ESBL production primarily affect cephalosporins and antipseudomonal penicillins, and gyrase mutations confer fluoroquinolone resistance, none of which explains isolated imipenem resistance.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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