Scientists have successfully modified a ‘magical’ antibiotic to kill drug-resistant superbugs.
Vancomycin has been prescribed by doctors for 60 years, but bacteria are becoming increasingly resistant to it.
Researchers at The Scripps Research Institute in the United States (US) modified the drug so it works in three separate ways on bacteria, making it much harder for them to develop resistance.
The first tests on the drug showed it to be a success – in an advance which researchers hope will help fight the threat of antibiotic-resistant infections.
The World Health Organisation (WHO) warns antibiotic resistance is one of the biggest threats to global health, food security and development, with major diseases becoming harder to treat because the drugs used on them are becoming less effective.
The length of time it has taken for bacteria to become resistant to vancomycin suggests they have had a hard time overcoming the way the original drug worked, disrupting how bacteria form cell walls, the researchers said.
Previous studies by the team showed it was possible to add two modifications to vancomycin, a drug they labelled ‘magical’ because of its strength against infection, to make it even more potent and reduce the amount of the medicine needed to have the same effect.
The new study, published in the journal Proceedings of the National Academy of Sciences, reveals another modification, which interferes with bacteria cell walls in a different way.
Combined with the previous alterations, the latest modification gives vancomycin a 1,000-fold increase in activity, so doctors could use less of the antibiotic to fight infection, the researchers said.
It was tested on Enterococci bacteria and killed both vancomycin-resistant Enterococci – considered by the WHO to be one of the drug-resistant bacteria that pose the greatest threat to human health – and the original forms of Enterococci.
The research was led by Dale Boger, co-chair of TSRI’s Department of Chemistry, who said the discovery made the new version of vancomycin the first antibiotic to have three independent ‘mechanisms of action’ to kill bacteria.
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