Bacteria in slimy biofilms are able to spread rapidly over surfaces such as catheters by building a transport network with DNA for tracks, say Australian researchers.
Microbiologist Associate Professor Cynthia Whitchurch from the University of Technology, Sydney and colleagues report their findings today in the journal Proceedings of the National Academy of Sciences.
“By following each other along this network and behaving the rules they can move quite efficiently through the system and out to the front of the biofilm,” says Whitchurch.
“We believe this is the equivalent to how a bacterial biofilm would expand up a catheter.”
Bacteria colonise the surfaces of our body, and the environment, in communities held together with slime.
These “biofilms” are a real problem because they make the bacteria resistant to antibiotics and disinfectants, and to the immune systems of organisms.
“They’re really resistant to everything we can throw at them, pretty much,” says Whitchurch.
“Probably half of hospital-acquired infections are due to biofilms forming on implanted medical devices … like catheters.”
If a biofilm establishes on a catheter, it can migrate and spread infection up to the bladder and kidneys, says Whitchurch.
To investigate how biofilms form and expand into new areas she and colleagues studied Pseudomonas aeruginosa, a bacteria that commonly causes urinary tract and respiratory infections.
The researchers used a technique called high-resolution phase-contrast time-lapse microscopy to track the movement of thousands of individual bacterial cells on computer.
“For the first time we could get quantitative data of individual cell movements during the process of biofilm expansion,” says Whitchurch.
She and colleagues were able to show the cells lining up in co-ordinated fashion to blaze new trails.
Atomic force microscopy revealed that the advancing bacteria were forging furrows, which constituted the edges of the network.
Fluorescence microscopy revealed that DNA excreted by the bacteria provided the network “tracks” that organised the flow of bacterial traffic.
“You have long ropes of DNA that the bacteria are aligning themselves to,” says Whitchurch.
To demonstrate the role of the DNA the researchers used an enzyme to chew up the DNA.
“When we remove the DNA, the bacteria completely lose their ability to co-ordinate their behaviours. They start bouncing around as individual cells and end up in traffic jams and the whole rate of expansion of the biofilm seizes up.”
Importantly, Whitchurch and colleagues also found that the DNA was also helping to glue together individual bacteria, called “bulldozer aggregates”, which collectively forged new furrows ahead of them.
“They can’t move out into new territory individually. They have to act as a collective to do that,” says Whitchurch.
She says if this is indeed how bacterial biofilms colonise, it suggests ways of controlling biofilms on medical devices such as catheters.
“One opportunity is to build our own networks that tell the bacteria to go in a way that doesn’t enable their biofilm to expand,” says Whitchurch.
Whitchurch suggests it might be possible to insert small furrows on the devices using microfabrication that would limit the spread of the biofilm.
“We could build our own furrows and get the bacteria running around in futile circles instead of co-ordinating themselves to move along the device,” she says.
Abc.net.au [en línea] Sydney (AUS): abc.net.au, 22 de julio de 2013 [ref. 25 de junio de 2013] Disponible en Internet: http://www.abc.net.au/science/articles/2013/06/25/3788443.htm?topic=health