Pictured above is an electron micrograph of methicillin-resistant Staphylococcus aureus, or MRSA, and a dead human neutrophil. Researchers at the University College of London have discovered a new method to fight antibiotic resistance in bacteria. (Flickr/NIAID)
Feb. 3 (UPI) -- Researchers at the University College London have developed a new method that may overcome antibiotic resistance in bacterial cells.
The team used sensitive equipment to measure the mechanical forces that four different antibiotics, including vancomycin, used to treat MRSA and oritavancin, exerted on bacterial cells that were susceptible to antibiotics and those that had developed resistance.
The antibiotics exerted similar forces on susceptible bacteria, but exerted significantly varied force on antibiotic-resistant bacteria.
"We found that oritavancin pressed into resistant bacteria with a force 11,000 times stronger than vancomycin," Dr. Joseph Ndieyira of the University College of London and lead author of the study, said in a press release. "Even though it has the same 'key' as vancomycin, oritavancin was still highly effective at killing resistant bacteria. Until now it wasn't clear how oritavancin killed bacteria, but our study suggest that the forces it generates can actually tear holes in the bacteria and rip them apart."
Vancomycin takes 6 to 24 hours to kill bacteria, but oritavancin can kill bacteria in just 15 minutes.
"Oritavancin molecules are good at sticking together to form clusters, which fundamentally changes how they kill bacteria," Ndieyira said. "When two clusters dig into a bacterial surface they push apart from each other, tearing the surface and killing the bacteria. Remarkably, we found that conditions at the bacterial surface actually encourage clustering which makes antibiotics even more effective."
The research team created a mathematical model to explain how antibiotics behave at the surface of bacterial cells, which could be used to screen new antibiotics to treat drug resistance.
"Antibiotics work in different ways, but they all need to bind to bacterial cells in order to kill them," Ndieyira said. "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 locks so the key won't fit any more. Incredibly, we found that certain antibiotics can still 'force' the lock, allowing them to bind to 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 study was published in Scientific Reports.