Drug shows no sign of inducing resistance and can kill superbugs
A turning point in the war against superbugs may have been reached with the discovery of a potent antibiotic that shows no sign of inducing drug resistance.
The drug, named teixobactin, has the ability to kill many types of harmful bacteria, including the superbug MRSA, by breaking down their cell walls.
Because it targets fatty molecules in the cell wall instead of proteins, it is also much less likely than most antibiotics to induce microbial resistance.
In tests, scientists found no evidence of bugs evolving ways to cheat death by teixobactin, which proved harmless to the cells of mammals.
Experts have hailed the research as a “game-changer” and “very exciting”.
Professor Kim Lewis, from Northeastern University in Boston, who led the US team, said: “No resistance normally means that we discovered a new detergent, which is a molecule that will destroy the membrane of the bacterial cell but also will destroy the membranes of our cells, so these are toxic compounds.
“That was my first reaction; that we found another boring molecule. But then in parallel we tested that compound against mammalian cells, and found it was not toxic against mammalian cells.
“So we have something very intriguing. Here is a new molecule that hits bacterial cells, does not hit mammalian cells, and there’s no resistance. That was unique and very exciting.”
Organisms vulnerable to teixobactin include some very nasty examples, such as MRSA, the TB bug mycobacterium tuberculosis, and Clostridium difficile (C. diff).
The drug will not work against other bacteria such as E.coli which have a kind of molecular armour plating protecting their cell membranes.
However, the research goes much further than identifying one promising new drug.
It potentially opens the door to further discoveries that could boost the world’s antibiotic arsenal and turn the tide against the superbugs.
In mice, the drug proved highly effective against MRSA and Streptococcus pneumoniae, which causes major infections of the lungs and blood poisoning.
The drug works in a similar way to the “last resort” antibiotic vancomycin, discovered in 1953, which also breaks down the cell walls of gram positive bacteria.
It took almost 40 years for bacteria to start becoming resistant to vancomycin. Because of its mode of action, which involves binding to multiple molecular targets, scientists believe it will take even longer for genetic resistance to teixobactin to emerge.
Prof Neil Woodford, head of Public Health England’s Antimicrobial Resistance and Healthcare Association Infections Reference Unit, said this discovery could help bridge the ever increasing gap between infections and the medicines available to treat them.
“Taking any potential antibacterial compound from discovery to successful licensing is a long, costly, and difficult process.
However, it is one that needs to be encouraged while we tackle other elements that contribute to the development of antibiotic resistance and seek to preserve the antibiotics we do have,” he said
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