Tigecycline, despite in vitro activity against MRSA, VRE and extended-spectrum beta-lactamase producers, is avoided as monotherapy for bloodstream infections. The reason is:

• A It is rapidly inactivated by serum beta-lactamases
• B It achieves very low peak serum concentrations because of rapid extensive tissue distribution ✓
• C It antagonizes the action of any concurrently given beta-lactam
• D It is exclusively bacteriostatic against Enterococcus and cannot kill organisms in blood

Explanation

Tigecycline has a large volume of distribution with rapid uptake into tissues, producing peak serum concentrations well below the MICs of many blood isolates. This pharmacokinetic profile led to higher mortality in pooled analyses of serious infections, and regulatory warnings followed. It is therefore reserved for intra-abdominal, skin-structure and community-acquired pneumonia indications rather than bacteremia. Its static activity alone does not explain the failure, since adequate exposure would still permit efficacy.

Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.