Targeting TB Bacteria’s Fatty Outer Coat May Boost Drug Effectiveness: IIT Bombay–Monash Study

Researchers from IIT Bombay and Monash University have discovered that the fatty outer coat of Mycobacterium tuberculosis—the bacteria that causes TB—plays a crucial role in helping it evade antibiotics. By altering this lipid-rich membrane, TB bacteria can survive drug treatment, especially when they enter a dormant state.

Despite over a century of research, tuberculosis remains a major global threat. In 2023, 10.8 million people fell ill and 1.25 million died from the disease, with India recording more than 2.6 million cases in 2024.

One of the biggest hurdles in treatment is the bacteria’s ability to slip into dormancy shortly after infection. In this phase, the bacteria remain alive but inactive, causing no symptoms and unable to spread. However, if a person’s immunity drops—due to HIV, illness or immunosuppressive medication—the bacteria can reactivate.

Since standard TB drugs mainly target bacteria that are actively growing, dormant cells are far less affected and often survive long treatment cycles.

The new study led by Prof Shobhna Kapoor of IIT Bombay and Prof Marie-Isabel Aguilar of Monash University examined how TB bacteria survive this drug assault. The researchers found that the dormant bacteria’s outer membrane undergoes changes that make it harder for antibiotics to penetrate. Drug concentrations needed to inhibit these dormant cells were up to ten times higher than those needed for active ones.

Advanced mass spectrometry allowed the team to map more than 270 lipid molecules in the bacterial membranes, revealing significant differences between active and dormant bacterial states.

According to the researchers, weakening this lipid barrier could make existing drugs far more effective. Instead of relying solely on new antibiotics, combining current treatments with molecules that disrupt the outer membrane could help kill persistent bacteria without promoting genetic resistance.

Prof Kapoor noted that such an approach could shorten therapy durations and restore drug sensitivity, giving TB bacteria little room to adapt permanently.

Source: PTI