Superbugs could lead to next-gen plastics


What makes them hard to kill may also make them highly useful. Mark Bruer reports.


A highly magnified cluster of Acinetobacter baumannii bacteria, which use a protein pump to resist the powerful hospital-grade antiseptic chlorhexidine.

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Antiseptic-resistant bacteria may hold the key to producing greener plastics such as petroleum-free nylon, researchers have found.

That’s the good news. The bad news is that these “superbugs” are equipped with ancient defences that will make them resistant to many new drugs.

Bacteria that are unaffected by antiseptics and antibiotics are a growing problem, but exactly how they acquire resistance is not fully understood.

Australian and British scientists wanted to find out why one such superbug, Acinetobacter baumannii, is so hard to kill and has become a major cause of hospital infections worldwide.

A. baumannii is a short, rod-shaped bacterium with a cell membrane. It is an opportunistic pathogen in humans, affecting people with compromised immune systems, and is resistant to chlorhexidine, a widely-used hospital antiseptic.

In a paper published in Proceedings of the National Academy of Sciences, the team explains how this superbug fends off chlorhexidine.

Its secret weapon is a protein called AceI, which acts as an “efflux pump”, sitting on the surface of the bacterium cell and expelling any chlorhexidine that gets inside.

This seems to be a stroke of good fortune for A. baumannii, as chlorhexidine was only introduced last century and the bacterium would not have had time to develop this defence in response. In other words, the AceI efflux pump is a primordial feature that just happens to purge one of modern medicine’s best antiseptics.

"Resistance to artificial antiseptics appears to be a lucky accident for the bacteria, and it could also be useful for humans," says Professor Ian Paulsen of Australia's Macquarie University, one of the leaders of the research group.

Paulsen and colleagues looked at what other compounds are pumped out by AceI and its relations, collectively known as Proteobacterial Antimicrobial Compound Efflux (PACE) proteins.

“We made several major advances in understanding the function of the prototypical PACE family protein,” the researchers write. These include working out the role played by AceI in pumping out substances such as cadaverine and putrescine, toxic compounds which are produced by the breakdown of living and dead organisms.

They found that the ability of AceI to transport these compounds, which can also be used in the production of polymers, could be harnessed to help make the building blocks for materials such as nylon.

“The discovery that AceI is a novel secondary transport system for these compounds adds potential for developing new biological platforms for their large-scale biotechnological production, which would provide much needed “green” alternatives to petroleum-based precursors,” they write.

On the other hand, the new research demonstrates that PACE proteins and efflux pumps expel a wide range of compounds from bacteria, and are therefore likely to limit the success of new drugs in fighting superbugs.

"These PACE proteins are very promiscuous in the compounds that they transport and are a likely cause of future resistance to new antimicrobials that are currently being developed," says Professor Peter Henderson at the University of Leeds, a senior researcher on the team.

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Mark Bruer is a freelance journalist based in Adelaide, Australia. He is a former Features Editor of The Age newspaper in Melbourne, and Online Editor of The Australian and news.com.au in Sydney.
  1. http://www.pnas.org/cgi/doi/10.1073/pnas.1901591116
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