Indian scientists find chink in superbug armour

TV Jayan New Delhi | Updated on July 24, 2019

An electron micrograph shows a white blood cell that eats the antibiotic-resistant bacteria MRSA   -  National Institute of Allergy and Infectious Diseases

Drug molecules developed with this frame work is likely to develop delayed antibiotic resistance

Indian scientists may have hit upon a novel way to destroy superbugs, which are becoming increasingly resistant to most known antibiotics.

The strategy, devised by researchers at the Indian Institute of Technology (IIT) Kanpur and the Lucknow-based Central Drug Research Institute (CDRI), is very attractive because it makes it possible to destroy these bacteria with the same class of drugs to which they have developed resistance.

For the study, the scientists used staphylococcus aureus, bacteria frequently found in the nostrils, upper respiratory tract and on the skin of nearly 30 per cent of people. While they are innocuous in healthy people, in those with low immunity levels, the bugs cause many infections, some of them lethal. Over the years, they have become resistant to most drugs that are commonly used in clinics. It is feared that these multidrug-resistant superbugs may kill as many as 10 million people worldwide by 2050.

Molecular framework

Working on an idea conceived by Sandeep Verma, professor of chemistry at IIT Kanpur, the scientists designed a novel molecular framework that would help drugs latch on to the germs and prevent them from multiplying. “The novelty of this molecule is its structural design,” said Nisanth N Nair, another chemist at IIT, whose computational biology expertise came in handy in designing the molecule.

“If the energy production in the bacteria is stopped for 20 minutes, the bacteria cannot divide and multiply. The molecule we designed just does that,” Nair said.

According to Sidharth Chopra, microbiologist at CDRI, a constituent laboratory of the Council of Scientific and Industrial Research, a substance called gyrase is essential for bacteria’s survival and multiplication. In most organisms, there are two types of gyrases — gyrase A and gyrase B.

“Almost all of the antibacterial drugs in use currently work by targeting gyrase A. Ever evolving, these bugs have a way with the drugs, modifying gyrase A in a such a way that the drugs fail to bind to them,” said Chopra, a co-author of the work.

The new molecule on the other hand targets gyrase B, which is more conserved in organisms and hence difficult to mutate. They showed that when used in combination with fluoroquinolone drugs, the first line of antibiotic drugs, both gyrase A and gyrase B are attacked, making them more effective.

Though still in a proof-of-concept stage, the scientists have found it to be effective in lab-grown bacterial cells. More importantly, they found that the bacteria do not develop resistance to the new molecule that easily.

“Given the dire need of novel therapeutic interventions and alternative mechanisms to counter the emerging threat of antimicrobial resistance, we surmise that our results may open up new opportunities in designing unique scaffolds to fend off S. aureus-based infections,” said Verma, chief author of the study.

Published on July 24, 2019

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