A 70-year-old man with a urinary catheter for 5 days develops fever and rigors. Blood cultures ×2 grow Pseudomonas aeruginosa (non-mucoid, oxidase positive, grape-like odour, produces pyocyanin). Disc diffusion shows resistance to piperacillin, imipenem, and gentamicin; sensitive only to colistin (polymyxin E) and ceftazidime-avibactam. What resistance mechanism would explain combined imipenem and piperacillin resistance in P. aeruginosa?
- A Acquisition of KPC (K. pneumoniae carbapenemase); common in P. aeruginosa causing multi-drug resistance
- B Loss of OprD (outer membrane porin D) reduces imipenem uptake; overexpression of MexAB-OprM efflux pump expels piperacillin/tazobactam; together these confer combined carbapenem + anti-pseudomonal penicillin resistance without carbapenemase production ✓
- C Plasmid-mediated ESBL production hydrolyses both imipenem and piperacillin equally
- D Biofilm formation physically prevents all antibiotics from reaching bacteria, explaining pan-resistance
Explanation
P. aeruginosa has multiple intrinsic and acquired resistance mechanisms operating simultaneously. OprD is an outer membrane protein that specifically allows carbapenem (particularly imipenem) entry; loss of OprD by mutation selectively raises imipenem MIC. MexAB-OprM is a constitutive efflux pump overexpressed in many resistant strains that expels penicillins, fluoroquinolones, and carbapenems. Together these two mechanisms (porin loss + efflux overexpression) commonly produce imipenem + piperacillin co-resistance without requiring carbapenemase production. KPC is predominantly found in Klebsiella, not P. aeruginosa (NDM/VIM are the common MBLs in Pseudomonas). ESBLs do not hydrolyse carbapenems. Biofilm is clinically important but does not explain the molecular disc-diffusion pattern.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.