The in vitro mechanisms of isoniazid and ethionamide resistance poorly reflect those in vivo in Mycobacterium tuberculosis

To be active against Mycobacterium tuberculosis, isoniazid (INH) and ethionamide (ETH) need to be activated by the catalase/peroxidase KatG for INH and by the mono-oxygenase EthA (regulated by EthR) for ETH [1]. ETH and INH both target the enzyme InhA involved in the cell wall biosynthesis [2]. Clinical isolates resistant (R) to INH and ETH display a wide range of mutations altering KatG (mutation S315T in 70% of INH-R isolates), EthA (in 50% of ETH-R isolates) and, InhA and the inhA promoter (in 25% of INH-R and 65% of ETH-R isolates) [1,3].

Source: Tuberculosis - September 28, 2016 Category: Respiratory Medicine Authors: Florence Brossier, Emmanuelle Cambau, Emilie Tessier, Vincent Jarlier, Wladimir Sougakoff Tags: Letter to the Editor Source Type: research