Superbug News: New Study Shows How Bacteria Resist 'Last Resort' Antibiotics
Over the past years, the world has faced various superbug outbreaks. Bacteria, which had been easy to treat in the past, are becoming more resistant, even to the last line of antibiotics developed today. A new study shows how these pathogens develop resistance to a "last resort" antibiotic.
An international team of researchers at the University of Bristol, Oxford, Cardiff, Diamond Light Source China and Thailand has shed light on how the mcr-1 gene protects bacteria from colistin, the last line antibiotic used to treat life-threatening bacterial infections, which did not respond to other treatments.
Since the discovery of penicillin in the 1920s, antibiotics revolutionized medicine by being able to save millions of lives by treating infections. However, with the discovery of various antibiotics and misusing them in treating diseases, bacteria has developed resistance to some of them.
Colistin was introduced in 1959 but its use has been limited due to nephrotoxicity. However, since some antibiotics became unable to treat resistant types of bacteria, colistin has become the last resort treatment.
The researchers identified mcr-1 as the first colistin-resistance gene that could be passed between bacteria. This can trigger resistance to spread quickly among bacteria in a population. In fact, this gene has been detected in common bacteria found in China, Europe and the United States. First, it has been detected among farm animals and now, in human patients.
When the spread of mcr-1 happened, there has been an increased use of colistin in farms. This could trigger a transmission between animals and humans, making China decide to ban the use of colistin in animal feed.
The team found that colistin acts by binding to and disrupting the outer surface of the bacteria. The bacteria which has the mcr-1 gene create a protein that tweaks the bacterial surface to reduce colistin binding, triggering resistance.
The study is the first one to provide clues as to how the gene acts and how it boosts resistance. The information is important to develop ways of blocking mcr-1 gene function that could restore the power of colistin against the bacteria.
"The importance of understanding colistin resistance can hardly be overstated: it is rapidly emerging threat to public health. Our results illuminate the structural and (for the first time) mechanistic basis of transferable colistin resistance conferred by mcr-1, thanks to the combination of biological, chemical and computational expertise brought to bear on this project," Adrian Mulholland, co-author of the study, said in a press release by the University of Bristol.
"We are confident that our findings will drive efforts to understand mcr-1-mediated resistance and ultimately help identify routes towards overcoming MCR-1 activity in harmful bacteria," he added.
The study was published in the journal Scientific Reports.