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A TOPOLOGY OF BIOFILMS:
Bacteria, as many as 600 cohabitating species // Autoinducers, the chemicals through which the beasties communicate // A polymeric matrix, the defense force that makes these gooey infections nearly impossible to subdue.

Slime and the City

By Wendy Orent // Illustrations by Skwak // Fall 2006
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Biofilms

The bottle looked perfectly ordinary. It contained a greenish, translucent liquid—jasmine tea. I had left it by my rowing machine a few days earlier. But when I opened it and took a swig, I nearly choked. The liquid had congealed into a jellylike ooze that slipped down my throat like an oyster, with shocking, nauseating ease. I had just swallowed a biofilm.

Most of us, including many scientists and physicians, think of bacteria as free-floating planktonic germs awash in a sea of solution—water, blood, pus, growth medium—or drifting in the air or buried in the soil. When researchers (or high school biology students) grow solutions of bacteria on dry or liquid media, they see generally unattached colonies, and studying germs in this way has probably conditioned us to think we are observing them in something like their natural state.

But during the past 10 years, bacteriologists have discovered that more than 99% of bacteria live enmeshed in a substance they produce, an extracellular polymeric matrix consisting of complex sugars known as exopolysaccharides, which may form as much as 85% of the biofilm’s entire volume. This matrix creates structures more akin to a gelatin of frog eggs than to a wash of plankton. A biofilm is actually a tiny ecosystem, composed sometimes of one species but often of many living together. In either case, bacteria in the biofilm both take from and contribute to their environment, as do the residents of any ecosystem.

In the 1980s, the pioneering researcher J. William Costerton, director of the Center for Biofilms at the University of Southern California in Los Angeles, dubbed these ecosystems biofilms, but you could also call them slime—and it is in the form of slime, as in that innocuous-looking bottle of tea, that we usually encounter them. The most complex examples, comprising many kinds of bacteria, form by adhering to a surface and then aggregating, piling up upon one another and communicating through chemicals called autoinducers. Biofilms may even contain pillars and channels through which water flows, bringing nutrients to microbes clinging to the pillars.

Biofilm architecture—“Biofilms: City of Microbes” was the title of a recent review article that Boston researchers Paula Watnick of Children’s Hospital and Roberto Kolter of Harvard Medical School published in the Journal of Bacteriology—is fascinating in itself. But as Watnick, among others, has shown, biofilms also play a significant—and until recently, largely unappreciated—role in human disease.

The germs that cause certain deadly infectious diseases, notably plague and cholera, form biofilms, an important phase in the germ’s life cycle. And in a particularly pernicious development, some bacteria have evolved the ability to occupy a recently created ecological niche, forming on hospital implants—ranging from simple urinary catheters to artificial hips to heart-valve implants—biofilms that are virtually impervious to antibiotics.

Learning how to treat diseases that, until recently, no one knew were caused by biofilms is daunting. Only by understanding how these structures work can scientists find ways to break through the exopolysaccharide matrix and assault the more vulnerable bacteria within biofilms.

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Danger by Degrees

The myriad threats posed by biofilms.

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1.Biofilms: City of Microbes, by Paula Watnick and Roberto Kolter, Journal of Bacteriology, May 2000. An unusually illuminating scientific review comparing biofilms to human cities—complete with suburbs, residential districts and “zoning regulations” governed by bacterial communication.

2. “Self-generated diversity produces ‘insurance effects’ in biofilm communities, by Blaise R. Boles, Matthew Thoendel and Pradeep Singh, Proceedings of the National Academy of Sciences, Nov. 23, 2004. Explains how rapidly developing genetic diversity in P. aeruginosa biofilms (one of the most harmful, in humans) acts as an “insurance policy” for the biofilm as a whole, in the same way that a diverse population of trees benefits all trees in a forest.

3.“Interspecies communication in bacteria,” by Michael J. Federle and Bonnie L. Bassler, The Journal of Clinical Investigation, November 2003. Difficult but fascinating reading on how autoinducers facilitate interspecies bacterial communication. Learning to interfere with the signal might produce novel therapies to prevent biofilm formation.

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