Tigecycline is a glycylcycline antibiotic derived from minocycline with activity against tetracycline-resistant organisms. Its main mechanism overcoming tetracycline resistance is:
- A It inhibits efflux pumps that expel tetracyclines from the bacterial cell
- B It binds a different ribosomal site (23S rRNA) compared to tetracyclines (30S subunit)
- C It is metabolically stable to bacterial tetracycline-inactivating enzymes
- D It is not recognized by Tet(M) ribosomal protection proteins due to its bulkier glycylamino substituent at position 9 ✓
Explanation
Tigecycline bypasses the two main tetracycline resistance mechanisms: (1) Its bulky glycylamino side chain at C-9 prevents displacement by Tet(M) and Tet(O) ribosomal protection proteins that normally mimic EF-G to dislodge tetracyclines from the ribosome. (2) It evades many efflux pumps. Tigecycline retains 30S binding (same site as tetracyclines). It has broad-spectrum activity including MRSA, VRE, ESBL, and carbapenem-resistant organisms but lacks activity against Pseudomonas aeruginosa and Proteus. It has a boxed warning for increased all-cause mortality in severe infections.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.