New research paves the way for reducing antibiotic resistance – University of Copenhagen

Health > News > News 2016 > New research paves the...

20 November 2016

New research paves the way for reducing antibiotic resistance


New research has created a breakthrough in our understanding of the evolution of staphylococci. A research group from the Faculty of Health and Medical Sciences at the University of Copenhagen has discovered how antibiotic resistance spreads in nature. The new knowledge can ultimately help reduce antibiotic resistance.

Research has shown that antibiotic resistance spreads amongst staphylococci rapidly and effectively. But until now, we have not been quite clear precisely how this happens.  New research by the Faculty of Health and Medical Sciences at the University of Copenhagen however, shows that resistance can spread between different staphylococcus/bacterial populations in a surprising and effective way.  The process has been called auto-transduction and may be highly significant for future research into reducing the spread of antibiotic resistance.

Imagine that you have a bacterial population of 1000 bacteria.  The bacteria contain a virus, a so-called bacteriophage. The bacteria sacrifice one or two bacteria that are used to make new bacteriophages. These bacteriophages are now discharged from the bacterium. The bacteriophages roam around the surrounding environment to identify any other bacteria they can steal from. The bacteriophages latch onto a bacterium, destroy it and appropriate its characteristics, which could for example be antibiotic resistance. They then return to their original population to share their new characteristics with the rest of the bacteria.

”It was previously known that bacteriophages play an important role in transferring genes, including resistance, but we did not know precisely how. In the new study, we have identified a process that may turn out to be an important driver in the evolution of staphylococci. This means we can now investigate and see more specifically whereabouts in the process we can intervene and hopefully, ultimately prevent bacteria from getting the opportunity to steal the resistance gene from other bacteria and hence spread," reports Assistant Professor Jakob Haaber, SUND, who is one of the driving forces in the project.

Click on the picture to see how auto-transduction works

Survival of the fittest
Using auto-transduction, the bacteria can intercept many different genes in a highly efficient manner. And particularly the ability to steal properties from surrounding bacteria makes the bacteria much more adaptable, and thereby also better equipped for the evolutionary race – also in terms of resistance to antibiotics, says Professor Hanne Ingmer from the Department of Veterinary Disease Biology at the Faculty of Health and Medical Sciences, where the study was conducted.

"We initially thought that it would be stressful for the bacteria to carry around bacterial viruses, but the new research shows that this is not the case. We thought that these bacterial viruses were parasites which entered the bacteria for their own gain, but we now know that the bacteria are able to efficiently use the virus to steal genes from surrounding bacteria. In other words, viruses and bacteria benefit from each other," she says.

The experiments were carried out in the laboratory, and the impact of the discovery on the transfer of resistance genes in animals and humans is yet to be studied. The results, however, make it possible to focus future research in the area. The researchers behind the study believe, for example, that it would be only natural to study whether the bacteria can be prevented from sending out spies. If they can, it would be possible to stop the spread already in the first stage.

The study 'Bacterial viruses enable their hosts to acquire antibiotic resistance genes from neighbouring cells' has recently been published in the prestigious journal Nature Communications. Read it here.

Professor Hanne Ingmer, Mail:, Telefon: +45 22 15 95 18
Assistant professor Jakob Haaber, Mail:, Telefon: +45 35 33 63 87