JERUSALEM, Sept. 11 (Xinhua) -- Israeli scientists have developed a method to damage the salmonella and Escherichia coli (E. coli) bacteria's defense mechanism, using substances originally developed against Alzheimer's disease, the northern Israel Institute of Technology (Technion) reported on Wednesday.
The researchers' discovery is expected to lead to the development of innovative treatments that inhibit antibiotic resistance of violent bacteria.
The researchers have been able to damage the production of salmonella biofilm, a durable membrane which is a serious medical and environmental problem.
The biofilm protects the bacteria and allows them to stick to tissues, tubes, surfaces, medical devices and more.
In the new study published in the journal PLOS Pathogens, the Technion researchers found that the damage to stable and durable fibers produced by salmonella and E. coli, which are involved in food contamination, harms the bacteria's defense mechanisms and their ability to stick to tissues and medical devices.
These are amyloid fibers, which are proteins related to neurodegenerative diseases such as Alzheimer's and Parkinson's, but are structurally different.
The scientists harmed the defense mechanisms of salmonella and E. coli by repurposing substances that have already undergone clinical trials for Alzheimer's.
The great advantage of repurposing is that the approval process is much shorter and cheaper than that of a new drug.
The team estimates that damaging the biofilm will not lead to the development of resistance, because it does not force the bacteria to protect their lives as opposed to antibiotic drugs, the use of which causes increased bacterial resistance and violence.
The researchers hope the study will also help fight against other bacteria, including the violent staphylococcus aureus, because the toxic fibers secretes are similar to the studied amyloid fibers.
This bacterium has developed resistance to many strains of antibiotics and is responsible for many infections occurring in hospitals and the community.
