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Slippery Characters

Biofilms--slimy layers of bacteria that antibiotics don't fully kill--are in hospitals, kitchens, even your mouth. Scientists are on the attack.

June 11, 2007|Erin Cline | Special to The Times

WHETHER on a contact lens or a catheter, in your lungs or in your ears, a few bacterial invaders can set up a slimy fortress that can prove almost impossible to demolish. All it takes is a wet surface and a few days.

The sticky mess is called a biofilm, a slick layer of bacteria that is one of the biggest problems facing medicine today. Biofilms are forcing scientists to reevaluate their view of bacteria as free-floating bugs to one of sophisticated communities stuck on surfaces.

The National Institutes of Health estimates that more than 80% of microbial infections in the human body are caused by biofilms, many of them creating chronic and reoccurring problems. Two of the most serious: The layer of Pseudomonas aeruginosa that forms in the trachea of cystic fibrosis patients and the hospital-acquired infections resulting from biofilm formation on implanted medical devices.

Even the healthiest among us deals with biofilms on a daily basis in the form of dental plaque. And biofilms containing a pathogenic strain of E. coli were behind the spinach recall in October.

The problem with biofilms is that, because of their tightknit structure, they are resistant to traditional disinfectants and antibiotics. New research is aimed at finding ways to battle these goo-covered conglomerates. By understanding how biofilms thrive, scientists are devising new strategies for defeating them.

Biofilms form in a series of steps that scientists are just starting to understand. Step one occurs when a few bacteria attach to a surface. They activate certain genes within their genomes and inactivate others, starting their transformation from free-floaters to biofilm.

The bacteria begin to secrete polymers that hold aggregates of cells together. Then, as the biofilm grows, it becomes more complex and even starts to act like a multicellular organism.

Structures arise -- such as channels to bring in nutrients and take away wastes.

Bacteria in different areas of the biofilm take on different roles. Some cells secrete enzymes, while others continue to make sticky matrix proteins. Some bacteria continue to rapidly divide, while others enter a dormant state.

The heterogeneity of biofilms is part of what makes them so robust, says Phil Stewart, director of the Center for Biofilm Engineering at Montana State University in Bozeman. A drug that can kill some of the bacteria in the biofilm might be useless against some of their neighbors.

The final step in the biofilm life cycle is dispersion. As conditions get crowded and resources become scarce, groups of cells detach and float away -- potentially setting up new biofilms if they happen to land in a good spot.

"It's a little bit like seeds," Stewart says.

In many chronic and recurring infections -- such as ear infections, prostatitis in men, urinary tract infections and endocarditis -- these biofilm seeds set off the immune system and cause symptoms such as fever and inflammation that signal to doctor and patient that something's amiss.

When antibiotics are administered, the free-floating bacteria are killed. But the original biofilm remains unscathed. Although the infection appears to be cured, it is only a matter of time before another chunk of biofilm is set free and the symptoms return.

There are no good ways to fight biofilms because an awareness of their importance has only emerged in the last decade, Stewart says. Before that, research on bacteria focused on homogeneous cultures of fast-growing cells in flasks. Tools that fight these kinds of bacteria are great for acute infections in which bacteria are freely floating in the body. But they are almost useless against biofilms.

The Center for Biofilm Engineering is trying to change this by developing standardized methods for working with biofilms that the whole research community can use. A few companies and academic scientists are already exploring new avenues in treating and preventing biofilms.

One of the problems with today's antibiotics is that many only attack bacteria that are actively growing. This means that the dormant cells in a biofilm will escape treatment and be left behind to regrow the biofilm. So one approach to fighting biofilms is to come up with drugs that can kill all the biofilm residents.

Cubist Pharmaceuticals in Lexington, Mass., developed an antibiotic called daptomycin (marketed as Cubicin) that is able to do just that, enabling doctors to eradicate a biofilm with drug treatment.

But even if you could use antibiotics to kill all the bacteria in a biofilm, that might not be the best idea, says Wenyuan Shi, professor of oral biology and medicine at UCLA's School of Dentistry.

"Think of a lawn infested with dandelions," he says. "If you kill everything, the dandelions will come back first. But if you use a dandelion-specific killer and the grass fills in the lawn, the dandelions won't come back."

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