Furanones have a unique advantage in that they act differently to other antibiotics. Unlike antibiotics, they don't kill bacteria. This means that the furanone compounds should not cause bacterial resistance, according to microbiologists.
"When bacteria sit on the surface, they first anchor themselves individually and then send out signalling molecules called homoserine lactones to other bacteria, which do the same, talking to each other via these signalling molecules until they reach sufficient density as a group on the surface. The bacteria then change their metabolism and start producing a slimy biofilm that protects them from antibiotics. Sitting under the protective biofilm, the bacteria multiply and grow, and that's what causes infection," Professor Griesser said.
Professor Griesser likens this process, called quorum sensing, to the example of soccer hooligans who on their own are quite ineffective but when they group together, can be a powerful force that creates havoc of disastrous proportions.
It's the furanones that come to the rescue by irreversibly switching off the bacterial signalling mechanism. Without the signal, the bacteria think that they are alone; they don't start producing the biofilm and eventually die on the surface.
"We attach the furanones by covalent bonding to our biomedical devices. We stress covalent bonding because it is important that we anchor them very firmly to the surface, making it impossible for them to break away and travel into remote organs such as the brain or liver," Professor Griesser said.
UniSA PhD student