| March 22, 2001 Vol. 22, No. 25 |
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 CURRENT ISSUEBACK ISSUES
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David Davies explores ways to block communication in biofilm colonies
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| David Davies, assistant professor of biology, researches the evolutionary adaptability of bacterial colonies known as biofilms to discover ways of transforming their destructive properties into useful processes that can protect the environment from disasters such as oil spills. |
David Davies will never have to travel far to be near his research subjects. Nonetheless, he is learning a foreign language and studying new cultures as a way of understanding the objects of his scientific curiosity.
Davies, an assistant professor of biology, studies biofilms, the ubiquitous bacterial communities that live just about anywhere that water and solids, or solids and gases meet — from contact lenses to ship’s hulls and from hospitals to household plumbing. Davies wants to know what makes biofilms — more commonly known as “slime” — exist and thrive despite some very serious attempts to disperse them.
Among the oldest lifeforms on the planet, biofilms are communities of individual microorganisms that are created when bacteria on the surface of just about everything become embedded in a gelatinous structure of their own making. This “slime” is composed of organic polymers, which can grow to several centimeters thick and cover large areas. Dental plaque is one commonly encountered biofilm. And, anyone who has ever been up-ended by slippery rocks in a stream likely has had a close encounter with a biofilm.
If such minor calamities were the worst thing about biofilms, probably no one, including Davies, would pay much attention. But the negative effects of biofilms can be tallied in both dollars and lives. Biofilms account for a wide range of diseases from cystic fibrosis, an always-fatal condition in which the lungs are colonized
| More funding sought for biofilm research David Davies’ work is currently supported by $38,434 in National Science Foundation funds. He has applied for $451,000 from the Department of Health and Human Services Public Health Service for a project titled, “The Biofilm Development Cycle of Pseudomonas Aeruginosa,” and is a co-principal investigator on a multidisciplinary $1.1 million Binghamton University application to the National Science Foundation for a project titled, “Ecosystem-Level Selection.” Davies is also a collaborative investigator on a proposed $3.08 million project on “The Role of Biofilms in the Pathogenesis of Otorrhea.” |
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Biofilms are everywhere. They grow like wildfire in hospitals and are a leading cause of hospital-acquired infections.
“You’ve got biofilms, antibiotics and nutrient sources all in this one location and you end up with ‘super bugs’ that form biofilms in and on people,” Davies explains. "It’s a real problem and hospitals can’t get rid of them. If you’re not sick when you go to the hospital, you’ll definitely get sick while you’re in there, if you’re there long enough.”
Those who stay in an intensive care unit for seven days or longer have nearly a 100 percent chance of developing a hospital-acquired infection, the worst of which are almost always related to biofilms that develop in the tubing of respirators and catheters, Davies said.
Biofilms can wreak havoc in a broad spectrum of industries including petroleum recovery and refining, wood pulp and paper production, food and beverage manufacturing, processing and distribution, cosmetics, power generation, aerospace, pharmaceuticals and health care. Name a manufacturing process and biofilms are probably an issue.
Biofilms have been discovered in the pipes at factories that produce prepadine, the iodine-based pre-surgery disinfectant swabbed on patients. “They treat and they disinfect and they dose with antibiotics, but they don’t kill off the biofilms,” Davies said. “And if you don’t kill them, you make them stronger.”
Biofilms are so difficult to control because they have had the benefit of 3.5 billion years of adaptive evolution to fine tune their strategies for successful living. Chief among those strategies seems to be the formation of communities that enhance the life expectancy of individual organisms while imbuing the group with something akin to supernatural powers. When living in close contact, bacteria are able to exchange genetic material with organisms other than their biological descendents through horizontal gene transfer, a process in which even highly unrelated organisms can swap genes.
One result of this process is antibiotic resistance, Davies said. Because bacteria don’t have to wait through biological generations to proliferate antibiotic resistant genes, but can instead pass them on to their generational peers, they are better able to confound the development of new drugs to treat bacterial infections.
“Any experience that a microbe can have, it can share with another microbe,” Davies said. “If humans could do that, when you passed somebody in the hallway who had read a certain book, they could simply bump into you and you would gain their memory for that experience and would know whatever they knew about the book.”
What’s more, bacteria can share information in this way with very distantly related microbial species. “They can get information or pass information to a microorganism that is more distantly related to them than a monkey or a tree would be to us,” he said.
Given these benefits, it’s no surprise that most bacteria seem to gravitate toward communal living. “The numbers of bacteria living in biofilm communities have been estimated at between 1,000 to 10,000 times greater than the numbers of planktonic bacteria in any given environment,” said Davies.
Until recently, almost all research into ways to control and remediate bacteria was conducted in laboratories where bacteria were studied in test tubes or petri dishes. But trying to extrapolate how to treat microorganisms in a medical or industrial environment from the results of work with planktonic or free-floating bacteria in liquid broths or pure cultures is like trying to assess the strength of lions or grizzly bears by studying a book in which the animals are pictured.
“In those test-tube conditions, you add a little bleach to the culture and the bacteria are all killed,” Davies said. “Then you go to an industrial system where you have biofilms growing on the walls of the pipes in a soft drink manufacturing facility or a milk production facility and you find that these organisms living in a biofilm community just don’t behave the same way.”
In a stunning display of the old adage “United we stand, divided we fall,” biofilms and their resident microorganisms are unfazed by antibiotic doses 1,000 times greater than the concentration that would kill the laboratory version in a liquid culture.
Davies’ work primarily focuses on Pseudomonas aeruginosa, arguably the most common organism on the planet. P. aeruginosa is everywhere, from the soil beneath our feet to the air we breathe. Although notorious because of its link to cystic fibrosis and a host of hospital-acquired or injury-related infections, P. aeruginosa is a normal microorganism that is only an “accidental pathogen” in humans, Davies notes.
“It doesn’t go through its entire life-cycle living in or on people," he said. “When people catch an infection from P. aeruginosa, they get it from the environment, not from another person. Most P. aeruginosa never see a host.”
Davis is focusing his research in several areas. Before coming to Binghamton from Montana State University in 1999, Davies and collaborators at the Center for Biofilm Engineering demonstrated that biofilm development is mediated by cell-to-cell signals, using chemical signaling agents to “talk” to one another much like pheromones orchestrate community behavior in ways that help ensure survival.
By discovering ways that leave the bacteria either “mute” or “deaf” to such cell-to-cell communication, Davies hopes to block their ability to form stable communities and make them more susceptible to antibiotics and immune system functions. The principal inventor of a method to inhibit the development of biofilms in response to this chemical communication, he has a patent pending on the technology.
He is also working to isolate a factor that will cause existing biofilms to disperse, leaving individual bacteria easier prey to disinfectants, antibiotics and immune function. Preliminary studies in Davies lab have found that when a non-toxic medium containing a natural dispersion factor is introduced prior to antibiotic treatment, the effectiveness of the antibiotics increases up to five times. The market potential for a non-toxic biofilm-dispersing agent is enormous. The technology to induce biofilm “autodis-persion” will be owned by Binghamton University and will be licensed to New York industries once the technology is developed.
Davies’ efforts to better understand the underlying molecular interactions of biofilms aren’t all aimed at their destruction, however. “Biofilms aren’t all bad," he said. "Under the right circumstances, they are and can be very beneficial.”
Antibiotics, for instance, are actually derived from bacteria, and certain processes, from the brewing of beer to the treatment of sewage, depend on them. Davies says that by increasing our ability to control biofilm development, we could harness bacteria beneficially. If bacteria are deprived of nutrients, for instance, they will stop producing slime and shrink. The starved bacteria could then be introduced at the site of an oil spill, where they would find nutrients and start growing, effectively walling off the spill.
Davies earned his doctorate and conducted postdoctoral research at the Center for Biofilm Engineering at Montana State University. He has worked with many industrial collaborators, including S. C. Johnson and Son, Inc., ARCO, Chevron, Dupont, Unilever, NALCO, SGM Biotech and others. During his work there, he also developed an in situ biofilm monitoring device, patented by Montana State University.