New Study to boost antibiotic treatment

The schematic representation of possible binding events occurring between antibiotics in solution and membrane bound targets. This is consistent with the picture that following the application of a lethal antibiotic dose, the insertion of drug molecules into bacterium cell wall can induce a local strain which grows as the number of reacted regions grow until a deleterious strain is generated, weakening overall mechanical strength as well as the ability for the cell to counteract high internal osmotic pressure (yielding cracks on the cell wall – yellow depression) which bacteria cannot ultimately withstand, leaving bacterium susceptible to lysis and death."

The schematic representation of possible binding events occurring between antibiotics in solution and membrane bound targets. This is consistent with the picture that following the application of a lethal antibiotic dose, the insertion of drug molecules into bacterium cell wall can induce a local strain which grows as the number of reacted regions grow until a deleterious strain is generated, weakening overall mechanical strength as well as the ability for the cell to counteract high internal osmotic pressure (yielding cracks on the cell wall – yellow depression) which bacteria cannot ultimately withstand, leaving bacterium susceptible to lysis and death.” (Picture: Courtesy)

Scientists at Britain’s University College London (UCL) are excited following new and promising studies likely to lead to new ways of developing resistance free antibiotics.  The study, pioneered by Dr. Joseph Ndieyira and published in U.K based journal Nature Scientific Reports, has established that antibiotics have the ability to use brute-mechanical forces to penetrate and destroy microorganisms.

Antibiotics, the study finds could still kill drug-resistance bacteria if they ‘push’ hard enough into bacterial cells.   Dr. Ndeiyira explains that while antibiotics worked in different ways, they nevertheless needed to bind to bacterial cells as a way of killing them. “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 anymore.”

According to Dr. Ndeiyira, formerly a Senior Lecturer at Jomo Kenyatta University of Agriculture and Technology, Department of Chemistry, the encouraging results revealed that certain antibiotics could still ‘force’ the lock, ‘allowing them to bind to and kill resistant bacteria because they are able to push hard enough’. A group of antibiotics were, according to the findings so strong to the extent that ‘they tore the door off its hinges, killing the bacteria instantly”

The researchers used sensitive equipment to measure the mechanical forces that four different antibiotics exerted on bacterial cells. They tested bacteria that were susceptible to antibiotics and those that had developed resistance.

The antibiotics all exerted similar forces on susceptible bacteria, but the forces they exerted on resistant bacteria varied significantly. The antibiotics tested included vancomycin, a powerful antibiotic used as a last resort treatment for MRSA and other infections, and Oritavancin, a modified version of vancomycin used against complex skin infections.

“We found that Oritavancin pressed into resistant bacteria with a force 11,000 times stronger than vancomycin,” says Dr Ndieyira. “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 suggests that the forces it generates can actually tear holes in the bacteria and rip them apart.”

The research was primarily funded by the EPSRC, with additional support from UCL, the European Union and the National Institute for Health Research University College London Hospital’s Biomedical Research Centre.

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