US scientists believe they may have found a way to stop the growing problem of bacteria becoming resistant to current drug treatments.
They have found drugs called bisphosphonates block an enzyme used by bacteria to swap genes, and acquire or spread resistance to antibiotic drugs.
They also showed that interfering with the enzyme could destroy drug resistant bacteria cultured in the lab.
The study appears in Proceedings of the National Academy of Sciences.
"It's promising, but they have certainly got a long way to go"
Lead researcher Professor Matt Redinbo, of the University of North Carolina at Chapel Hill, said: "Our discoveries may lead to the ability to selectively kill antibiotic-resistant bacteria in patients, and to halt the spread of resistance in clinical settings."
In the last decade almost every type of bacteria has become more resistant to antibiotic treatment, rendering many deadly infections such as tuberculosis more difficult to treat effectively.
Every time someone takes an antibiotic, the drug kills the weakest bacteria in the bloodstream. Any bug that has a protective mutation against the antibiotic survives.
Bacterial 'mating'
These drug-resistant microbes quickly accumulate useful mutations and share them with other bacteria through conjugation - the microbe equivalent of mating.
Conjugation starts when two bacteria smooth their membranes together. After each opens a hole in their membrane, one squirts a single strand of DNA to the other.
This movement of DNA is stopped and started by an enzyme called DNA relaxase.
The Chapel Hill team analysed the structure of the enzyme, and identified a weakness which could potentially be exploited.
They found that by using bisphosphonate drugs, widely prescribed for bone loss, they could plug the site at which the enzyme usually binds to DNA.
Tests on E. coli bacteria, which can cause severe food poisoning, showed the bisphosphonate drugs wreaked havoc inside bacteria that were preparing to transfer their genes.
Exactly how bisphosphonates destroy each bacterium is still unknown, but the drugs were potent, wiping out any E. coli carrying relaxase.
The researchers plan to carry out further tests to establish whether bisphosphonates also attack similar species, such as those responsible for hospital-acquired pneumonia, and other lung infections.
Professor Redinbo said: "We hope this discovery will help existing antibiotics or offer a new treatment for antibiotic-resistant bacteria."
Professor Kevin Kerr, a consultant microbiologist at Harrogate and District NHS Foundation Trust, said other drugs had also been tested for their anti-conjugation properties, including the schizophrenia drug chlorpromazine.
He stressed the latest study was at a very early stage, and that bisphosphonates had only been shown to have an effect against one type of bacterium - E. coli.
"This the latest in a long series of potential candidates," he said.
"It's promising, but they have certainly got a long way to go."
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