Antibiotic Gets Supercharged To Stop Resistant Bacteria In Their Tracks
The rise of antibiotic-resistant bacteria, also known as superbugs, has got researchers worried about a return to the pre-antibiotic era and the fatal infections supposedly long wiped out. The U.S. Centers for Disease Control and Prevention (CDC), for instance, estimates that over 2 million in the country each year gets these antibiotic-resistant infections, with at least 23,000 dying.
Now scientists are structurally modifying an antibiotic known as vancomycin to produce a more potent version of an already-powerful medicine.
“Doctors could use this modified form of vancomycin without fear of resistance emerging,” said lead researcher Dale Boger of The Scripps Research Institute in a statement.
Doctors have become wary of antibiotic use due to fear of resistance, but for Boger’s team, restricting use only slows down the whole process. The key, they believe, is to engineer antibiotic drugs to anticipate as well as prevent resistance in the first place.
Vancomycin has been prescribed for six decades now, and bacteria have only begun developing resistance to the drug. What this means is they may have difficulties overcoming its mechanism of action, which works through disrupting how bacteria create cell walls.
Based on the team’s previous studies, one could add two modifications to vancomycin to make it more powerful, requiring less of the drug to have the same effect, Boger explained.
In this new research, a third modification meddled with bacteria’s cell wall in a novel way, as tested against Enterococci bacteria. Combined with the first two techniques, it gives the antibiotic 1,000 times more activity.
This way, physicians would need to use less of it for battling infection.
“Even if [the bacteria] found a solution to one of those [three mechanisms], the organisms would still be killed by the other two,” Boger added.
Next Steps Against Superbugs
This modified vancomycin still needs to be further developed to be tested in people for gauging safety and effectiveness. Furthermore, the team is looking to shorten the lengthy 30-step process that limits drug yield.
In 2015, medicinal chemist Derek Lowe lauded the previous study that introduced the two deadly modifications. In an email to the San Diego Union Tribune, he explained that the drug’s original mechanism of action has made it last so long: it does not directly bind to a bacterial protein but instead “vacuums up” a key oligopeptide needed by the bacteria to function.
“Throw these new functions in on top of that, and you not only get a big boost in potency, which this (latest) paper demonstrates,” Lowe said. “But you make it far, far less likely that a bacterium will emerge that will be able to deal with all of this at once.”
Vancomycin-resistant enterococci (VRE) have recently started to incite horror in hospital staff worldwide, spreading relentlessly despite medical experts’ best efforts. The enterococci group is known for its hardiness and dates as far back as 425 to 450 million years, as well as survive multiple catastrophes that have struck Earth.
The breakthrough on modified vancomycin, as Boger’s team and other professionals hope, offers a positive answer.