What is the primary mechanism of action of INH against Mycobacterium tuberculosis?

The primary mechanism of action of isoniazid (INH) against Mycobacterium tuberculosis is the inhibition of mycolic acid synthesis. Mycolic acids are essential components of the cell wall of Mycobacterium species, contributing to the bacteria's structural integrity and overall survival. By inhibiting the enzymes involved in the synthesis of mycolic acids, INH effectively compromises the cell wall, leading to cell lysis and ultimately the death of the bacteria.

This mechanism is particularly relevant for Mycobacterium tuberculosis, as the unique composition of its cell wall, enriched with mycolic acids, plays a crucial role in its virulence and resistance to host immune responses. The action of INH is selective for mycobacterial species due to the presence of specific pathways and enzymes (such as InhA and KatG) that are not found in human cells, making INH an effective treatment while minimizing damage to host cells.

Understanding this mechanism is vital for appreciating how INH fits into the larger context of anti-tuberculosis therapy, where targeting the unique features of bacterial cell walls can lead to effective treatment strategies against infections that are notoriously challenging to manage.