A toxin found in sugar that wipes out superbugs has been dubbed the ‘most exciting antibiotic candidate’ in decades.
Albicidin is a toxin produced by the plant pathogen that causes the devastating leaf scald disease in sugar cane.
Researchers found it was effective against six antibiotic-resistant bacteria in a new laboratory study.
Scientists hope it will help fight against antibiotic-resistant superbugs. The bugs are estimated to contribute to around seven million deaths a year and experts have warned they should be taken as seriously as global warming.
The antibiotic – called albicidin – is made by the plant pathogen which causes the devastating leaf scald disease in sugar cane, bacterial disease which can ruin crops
Dr Dmitry Ghilarov, head of the research group examining albicidin at the John Innes Centre in Norwich, UK, said: ‘We believe this is one of the most exciting new antibiotic candidates in many years.
‘It has extremely high effectiveness in small concentrations and is highly potent against pathogenic bacteria – even those resistant to the widely used antibiotics.’
Albicidin is used by the pathogen Xanthomonas albilineans to enable the spread of the disease throughout the plant.
The disease, called leaf scald disease in sugar cane, withers the leaves and renders crops unusable.
The development of albicidin has been slow because scientists could not work out exactly how it engaged with its target – the bacterial enzyme DNA gyrase.
Gyrase binds to DNA and twists it into a coil called supercoiling, which is crucial for cells to operate.
But gyrase has a moment of weakness as it needs to briefly break the DNA in the process.
The bacteria is usually quick to join the two pieces of bacteria back together, but albicidin prevents it, leading to broken DNA and bacterial death.
In the latest study, scientists used a powerful microscope to discover that albicidin takes an L-shape, blocking the gyrase from bringing the DNA together, like ‘a spanner thrown between two gears’.
The way albicidin interacts is sufficiently different from existing antibiotics, meaning it will likely work against many of the current antibiotic-resistant bacteria.
Through laboratory tests, the scientists found it to be effective against some of the most dangerous bacterial infections, which are often contracted in hospitals, including, salmonella, E. coli and pneumonia.
Those three antibiotic-resistant bugs are estimated to kill more than 50,000 Americans every year.
When antibiotics are taken unnecessarily, bacteria can develop the ability to defeat them and gradually become drug-resistant.
Dr Ghilarov said: ‘It seems by the nature of the interaction, albicidin targets a really essential part of the enzyme and it’s hard for bacteria to evolve resistance to that.
‘Now that we have a structural understanding, we can look to further exploit this binding pocket and make more modifications to albicidin to improve its efficacy and pharmacological properties.’
New lab tests have found the antibiotic is effective against bacterial infections often contracted in hospitals including salmonella, E. coli and pneumonia.
Now the researchers will seek funding for human clinical trials, which they hope will lead to the creation of a new class of antibiotics.
The findings were published in the journal Nature Catalysis.
Figures estimate that superbugs will kill 10 million people each year by 2050, with patients succumbing to once harmless bugs.
Around 700,000 people already die yearly due to drug-resistant infections including tuberculosis (TB), HIV and malaria across the world.
Concerns have repeatedly been raised that medicine will be taken back to the ‘dark ages’ if antibiotics are rendered ineffective in the coming years.
In addition to existing drugs becoming less effective, there have only been one or two new antibiotics developed in the last 30 years.
In 2019, the WHO warned antibiotics are ‘running out’ as a report found a ‘serious lack’ of new drugs in the development pipeline.
Without antibiotics, C-sections, cancer treatments and hip replacements will become incredibly ‘risky’, it was said at the time.