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Biofilms, for instance, fog your contacts, help to rot your teeth and cause or complicate outcomes in a host of diseases from ear infections and ulcers to colitis and cystic fibrosis. They are a leading cause of hospital infections and non-healing wounds, and were even at the root last summer of corrosion that forced the replacement of 16 miles of the Alaska pipeline. As a result of that incident, 400,000 barrels a day of production from the largest oil field in the United States was suspended. The indefinite shutdown, at a cost equal to 8 percent of U.S. petroleum output, led to immediate increases in the price of crude oil, and drove up fuel oil and gasoline prices.

The annual worldwide costs of biofilm infection and remediation are in the high billions of dollars, even according to the most modest estimates, and they are costs borne by industries and consumers alike. Name a manufacturing process and biofilms are probably a serious and costly issue. They have even been discovered in pipes at factories producing prepadine, the anti-bacterial, iodine-based solution that doctors swab on patients to “prep“ them for surgery.

Biofilms’ resilience and unusual resistance to remediation stem from a combination of mechanisms, including such things as restricted transport of antibiotics through the biofilm, reduced metabolic activity of biofilm bacteria and such physiological resistance mechanisms as the use of membrane pumps to remove antibiotics from inside the cell, Davies said.

But even in nature, biofilms will disperse when environmental conditions become adverse. If sources of nutrition run low or waste products build up, bacteria within a biofilm community “save“ themselves by breaking free of the bad situation, turning on some genes and turning off others, and returning to a planktonic state.

By homing in on the regulatory device that he thinks leads to their natural dispersion, Davies not only seems to have found the key to inducing biofilm dispersion at will, but might also have solved one of the older mysteries in microbiology.

Biofilms will not grow in a flask — no matter how many bacteria you put there. They require a flowing system — water, tears, saliva, a pipeline, etc. — and nutrients. But against all intuition and previous thinking, turning up the flow in a pipe or stream doesn’t shear off or break up biofilms. It only produces more robust biofilms. And Davies now thinks he knows why. “I think this dispersion molecule is just something naturally produced with growth. And the idea is that the flowing liquid will wash out the dispersion-inducer molecule, so the faster the flow rate, the less the inducer molecule builds up in the biofilm, and the biofilm gets bigger and bigger and bigger,“ he says.

“So, in fact, if you have a batch system, like in a flask, the inducer molecule can’t get washed away. Instead it builds up so much that you can’t grow any biofilm at all.“

Davies feels certain his discovery will dramatically change the way infections are treated. “I think people will start inducing dispersion to disaggregate biofilms and, then, treat them concurrently, and with significantly greater efficacy, with antibiotics.“

He envisions his discovery first making its way to market as a topical treatment for cuts, lacerations and minor burns, perhaps even as an additive in adhesive bandages.

But his major interest, and something he hopes to turn his attention toward in earnest in the coming year, is the area of non-healing wounds. Davies watched his diabetic great-aunt lose both of her feet to amputation after bacterial biofilm infections set in.

“If we can treat those kinds of wounds and clear up the infection, they will heal. We know that from wound debridement studies,“ he said. “I really think we can make a difference with these people, and if that was the only thing we did, it would be worth everything we’re doing.“

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