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| Archive : Fall
2006 |
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 [page 2]
 By Wendy Orent
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The plague germ Yersinia pestis forms biofilms of the single-species variety—in the gut of carrier fleas. When an uninfected flea bites an infected mammal, the flea swallows a few plague germs that lodge in its midgut and then creep back into the proventriculus (a section of the foregut that leads to the midgut). As the bacteria multiply, according to plague expert Joseph Hinnebusch of the National Institutes of Health Rocky Mountain Laboratories in Hamilton, Mont., they exude an exopolysaccharide, forming a sticky matrix. The resultant biofilm seals off the proventriculus, trapping the blood the flea has ingested in the foregut. In short, its foregut is bulging, but the flea is starving. So it bites another mammal—this time an uninfected one—and part of the biofilm is injected into that host, where the mammal’s higher body temperature halts production of the sugar matrix. New bacterial cells, no longer confined to the matrix, are free to travel into the mammal’s deep tissue, causing another deadly infection.
While plague forms simple structures, multiple-species biofilms such as dental plaque are actually microbial cities, as Watnick and Kolter note. According to Watnick, these metropolises arise from a single layer of cells adhering to a surface. Once this monolayer has established itself, other bacteria are drawn to nutrients that the early arrivals release. After several layers of interacting bacteria have formed, says Watnick, you have a biofilm, whether it’s composed of a single clone or of many interacting species.
Some bacteria prefer to live attached to the substrate, which can be metal, plastic or cellular, while others live adjacent to channels of water that move nutrients through the biofilm. Bacteria don’t typically eat one another or any other intact organism—they acquire nutrients from their environment, often in the form of particles of DNA or other chemicals such as polysaccharides. Sometimes, though, bacteria within a biofilm kill and degrade other bacterial cells, yielding nutrients the predatory bacteria need. Some members of a biofilm community may be overtly predatory—for example, protozoa may graze on fields of biofilm like cows in a pasture.
On occasion, biofilms, especially those found in polluted water (“pond scum”) or in the lungs of cystic fibrosis patients, may become thick. But based on her research, Watnick suspects that healthy biofilms tend to be thin—like a film. “A thick biofilm may be a sick biofilm,” she says, “quite different from the balanced ecosystem existing in an unpolluted environment.” In a thick biofilm, cells in the middle die for want of nutrients. That means not all biofilm development is beneficial to all denizens of the microbe city.
Further demonstrating the extraordinary complexity of biofilms—and adding to the difficulty in treating diseases linked to them—some bacteria can exist both as environmental biofilms and as pathogens. For example, scientists have discovered that Vibrio cholerae, the germ that causes cholera, can float for years in both fresh water and seawater enmeshed in a biofilm, possibly associated with tiny crustaceans or blue-green algae. Cholera infects only humans, but its ability to survive outside the body and longer than any epidemic outbreak makes the disease almost impossible to eradicate.
According to Watnick’s experiments, when nutrients are plentiful, cholera germs form a biofilm by coating themselves with an exopolysaccharide matrix. Watnick thinks this matrix may serve as an extracellular nutrient-storage system, like fat cells in mammals. When environmental nutrients run out, the cells draw upon the matrix, and eventually the matrix dissolves. It’s possible that cholera germs then take refuge elsewhere. Watnick thinks V. cholerae may inhabit the intestinal tracts of flies or other arthropods, perhaps forming a biofilm as plague germs do in fleas. This raises the intriguing possibility that cholera may be spread by flies as well as through contaminated water or fecal-to-oral contact, long thought to be the only routes of transmission. It also suggests that cholera may have a complex life cycle—in biofilms, flies and people—that would make it all the more difficult, if not impossible, to banish from the environment. |
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Illustrations by SKWAK |
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