Tigecycline is often called an expanded-broad-spectrum agent covering MRSA, VRE, ESBL producers, and anaerobes. Despite this profile, it is avoided empirically for ventilator-associated pneumonia caused by Pseudomonas aeruginosa because:

• A Pseudomonas aeruginosa lacks the ribosomal target site shared by other tetracycline-susceptible bacteria
• B Tigecycline is inactivated by the AmpC beta-lactamase constitutively expressed by Pseudomonas
• C Tigecycline cannot penetrate the Pseudomonas outer membrane owing to its bulky glycylamido side chain
• D Pseudomonas aeruginosa possesses chromosomal mexXY efflux pumps that extrude tigecycline efficiently ✓

Explanation

Pseudomonas aeruginosa and Proteus species are intrinsically resistant to tigecycline largely through chromosomally encoded multidrug efflux systems, principally MexXY-OprM in Pseudomonas, which actively pump the drug out before it reaches the 30S subunit. In addition, tigecycline achieves low peak serum concentrations because it is rapidly distributed into tissues, making it unsuitable for bloodstream and lower respiratory tract infections. AmpC is a beta-lactamase and irrelevant to a non-beta-lactam drug, and the ribosome target is universally present.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.