IIT Bombay Study Reveals How TB Bacteria Shield Themselves From Antibiotics and Survive Longer

New Delhi: A new study by researchers at the Indian Institute of Technology (IIT) Bombay has uncovered how Mycobacterium tuberculosis — the bacterium responsible for Tuberculosis (TB) — survives antibiotic treatment by altering the fat-based outer layer of its cell membrane.

Despite effective antibiotics and vaccination efforts, TB remains the world’s deadliest infectious disease. In 2024, an estimated 10.7 million people developed TB globally, and 1.23 million died. India alone reported over 2.71 million cases.

Published in Chemical Science, the study shows that the bacteria’s drug tolerance comes from changes in their cell membranes — protective barriers composed mostly of lipids.

Researchers examined the bacteria in two states:

• Active phase (rapidly dividing, resembling active infection)

• Dormant phase (slow-growing, mimicking latent TB)

When exposed to four common TB drugs — rifabutin, moxifloxacin, amikacin, and clarithromycin — dormant bacteria required two to ten times higher drug concentrations to halt 50% of their growth compared to active bacteria.

According to lead researcher Prof. Shobhna Kapoor (Department of Chemistry, IIT-B), this reduced sensitivity is not due to genetic mutations typically associated with antibiotic resistance. Instead, it is linked to the bacteria’s shift into a dormant state and the resulting changes in their membrane structure.

The team identified over 270 different lipid molecules in the bacterial membranes. Active bacteria had more fluid, flexible membranes, while dormant bacteria developed rigid, tightly packed membranes, forming a stronger shield against antibiotics.

The study also revealed that rifabutin, an important TB drug, could easily penetrate active bacterial cells but struggled to pass through the rigid membranes of dormant ones.

“The rigid outer layer becomes the main barrier — the bacterium’s first and strongest line of defence,” Prof. Kapoor said.

The findings suggest that weakening the outer membrane could make existing drugs more effective. Pairing standard antibiotics with molecules that loosen this membrane could help kill even dormant TB bacteria without triggering permanent drug resistance.

With inputs from IANS