Rifampicin resistance in M. tuberculosis most commonly results from a point mutation in the gene encoding:

• A InhA (enoyl-ACP reductase)
• B embB (arabinosyltransferase)
• C pncA (pyrazinamidase)
• D rpoB (β-subunit of RNA polymerase) ✓

Explanation

Rifampicin inhibits bacterial DNA-dependent RNA polymerase by binding to the β-subunit (encoded by rpoB). Over 95% of rifampicin-resistant M. tuberculosis strains have mutations in the 81-bp rifampicin resistance-determining region (RRDR) of rpoB, which alters the drug binding site. rpoB mutations are used as a molecular surrogate for rifampicin resistance in GeneXpert MTB/RIF. InhA mutations confer isoniazid resistance; embB mutations confer ethambutol resistance; pncA mutations confer pyrazinamide resistance.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.