In order to be successful in the gut where there are literally trillions of bacteria competing for the nutrients their human host eats, the successful microbe must develop a system to determine what nutrients to go after and a strategy to capture them. B. thetaiotaomicron, says Gordon, has learned how to do this with great facility.
"This organism has an enormous capacity to grab the polysaccharides it encounters from our diet," he said. "It senses their presence and deploys the proper set of enzymes to harvest these nutrients as they enter its niche. This is beneficial to them, to other members of the gut's microbial community, and to us."
Bug Gone Bad
The bacterium Enterococcus faecalis is a relatively minor player in healthy human hosts and scientists can't say for sure what it does. "We don't know whether it's beneficial or whether it's just neutral in its interaction," said Ian Paulsen, a researcher at the Institute for Genomic Research in Rockville, Maryland.
But when the host becomes ill, new strains of the microbe have evolved an uncanny ability to attack the weakened immune system with fierce resistance to even the most potent of antibiotics, causing a range of maladies such as the heart disease infective endocarditis and urinary-tract infections.
Doctors often treat E. faecalis infections with the potent antibiotic vancomycin if other drugs fail to slow the infection's progress. But now there are more and more strains that have evolved resistance to the drug, making it more difficult for doctors to effectively treat infections.
Paulsen and his colleagues at the institute sequenced the genome of a strain of the bacterium that has developed a resistance to vancomycin. They discovered that more than a quarter of its genome consists of mobile, or foreign, DNA.
"They are bits of DNA that can move around, that can hop between different bacterial strains and species," said Paulsen. The drug resistance is found in the mobile DNA.
For this particular strain, the researchers identified two sites on the genome that are related to vancomycin resistance. These encoded genes allow the bacterium to alter its cell wall structure to prevent the drug from causing any damage.
Paulsen is not sure how the knowledge of this particular strain applies to the wider population of E. faecalis, but he does say that it gives researchers some information they can use to ask more focused questions on how best to treat E. faecalis infections.
"Having the genome doesn't give you all the answers to these sorts of problems," said Paulsen. "But it enables experiments and technologies to start trying to answer these questions."
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