A team from University College London has demonstrated that it’s possible for antibiotics to effectively kill resistant bacteria through sheer “brute force.”

It’s a promising step forward in counteracting antibiotic resistance, which is a growing problem worldwide.

“Antibiotics work in different ways, but they need to bind to bacterial cells in order to kill them,” Joseph Ndieyira, lead study author, and senior research associate at University College London (UCL) Medicine, said in a release. “Antibiotics have ‘keys’ that fit ‘locks’ on bacterial cell surfaces, allowing them to latch on. When a bacterium becomes resistant to a drug, it effectively changes the lock so the key won’t fit anymore. Incredibly, we found that certain antibiotics can still ‘force’ the lock, allowing them to bind and kill resistant bacteria because they are able to push hard enough. In fact, some of them were so strong they tore the door off its hinges, killing the bacteria instantly.”

The team published their findings in the journal Scientific Reports.

Experts say the research is welcome, but there’s still a lot of work to be done.

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A growing problem

Antibiotics can be extremely useful, but overuse has led to a rise of antibiotic resistant bacteria.

The medical community has been sounding the alarm on the rise of antibiotic resistant bacteria for years. In 2014 then-President Barack Obama signed an executive order acknowledging the threat.

Ndieyira outlined some other ways the international health community is working to combat the issue, noting that a 2016 United Nations conference called for a coordinated plan of action.

In an email to Healthline, he added, “The World Health Organization, together with partners, has developed a global action plan to mitigate the problem of drug resistant bacteria by strengthening surveillance to better inform strategies on health interventions and detection of new trend resistance evolution, as well as the threat posed by the new strains of bacteria.”

Others also see the threat.

“Antibiotic resistant bacteria are a worldwide threat,” Daniel Wozniak, Ph.D., professor in the department of microbial infection and immunity at The Ohio State University College of Medicine, told Heathline in an email. “There are some infections caused by these bacteria that simply cannot be treated with conventional antibiotics, putting us in a position where we were almost 75 years ago. Without effective antibiotics, people can succumb to infections during routine surgery or chemotherapy. Unfortunately, new resistance strategies are emerging and spreading at a pace faster than we are developing means to combat infection.”

David S. Weiss, Ph.D., director of the Emory University Antibiotic Resistance Center, acknowledged the issue in an email to Healthline.

“Carefully studying the characteristics of known antibiotics is of great interest as it may broadly guide the enhancement of antibiotic activity and efficacy,” he wrote. “This would likely be a faster process than the development of new antibiotics. Given the dire situation we currently face, it is critical to explore all paths and leave no stone unturned.”

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Forcing the lock

Ndieyira’s team at UCL studied the effects of two antibiotics.

One was vancomycin, a powerful antibiotic typically used to treat MRSA and other dangerous infections.

The other was oritavancin, a modified version of vancomycin that can be used to treat skin infections.

In addition to working more quickly — oritavancin begins killing bacteria in 15 minutes, while vancomycin takes hours — oritavancin has some properties that could make it a game-changer when it comes to killing powerful antibiotic resistant bacteria.

“There are three properties that make oritavancin unique,” wrote Ndieyira. “First, its molecules are good at sticking together at the surface of bacteria to form clusters. Second, its clusters bind very strongly to the surface of bacteria, and third, the clusters consequently generate the largest mechanical forces against drug resistant and drug-susceptible bacteria, which can lead to bacteria cells being killed more rapidly compared to vancomycin.”

In short, these unique clusters literally tear the surface of the bacteria apart.

Wozniak applauded the research.

“I found the work quite compelling and interesting,” he wrote. “The multidisciplinary approach involving biological, physical, and mathematical sciences to tackle this problem was impressive. The authors bring a new perspective on drug-bacteria interactions by studying mechanobiology, the forces at play during antibiotic-target binding. For me, the most important advance was the premise to utilize mathematical modelling prior to, or integrated with, the synthesis of new antibiotics to help ensure potent activity of drugs. This work also has implications outside of antibiotic development, since the concept applies potentially to any drug-target interaction.”

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A fine balance

Medical experts acknowledge that combating antibiotic resistant bacteria can create an “arms race” when bacteria grows stronger and more resistant as the medication used to combat it becomes more effective.

“There has to be a balance between the need and usage, so as to avoid a future arms race,” acknowledged Ndieyira. “For example, overuse of oritavancin when it is not absolutely necessary, or using it in agriculture, might lead to the evolution of antibiotic resistant bacteria.”

“We frankly have been in an arms race with microorganisms throughout history,” wrote Wozniak. “Because bacteria can grow to such high numbers, and because they grow much faster than our cells, acquisition of resistance is an evolutionary inevitable outcome, I’m afraid. The trick is to use antibiotics prudently and often in combination with other drugs that target different bacterial processes, and for us to remain healthy so that our immune systems can fight infections during antibiotic treatment.”

Ndieyira says his team will continue their research.

“Our next step is to use these findings to develop new antibiotics, and modify existing antibiotics, so that they are effective against multi-drug resistant bacteria,” he wrote.