A multidrug-resistant Acinetobacter isolate shows resistance to tigecycline-free tetracyclines mediated both by efflux pump genes and by the ribosomal protection protein Tet(O). Tigecycline retains activity against this organism because it:
- A Inhibits the efflux pump ATPase directly
- B Irreversibly acetylates the ribosomal binding site
- C Is not a substrate for classical tetracycline efflux pumps and still binds ribosomes protected by Tet(O) ✓
- D Acts on the 50S subunit rather than the 30S subunit
Explanation
As a glycylcycline derivative, tigecycline carries a bulky side chain at position 9 that prevents recognition by most classic tetracycline efflux pumps such as Tet(C) through Tet(E), and its binding affinity is sufficient that ribosomal protection proteins like Tet(M) and Tet(O) cannot displace it. Resistance therefore arises mainly via specific efflux pumps such as AdeABC in Acinetobacter. It still acts on the 30S subunit.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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