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Watching bacteria evolve into problems

The rise of antibiotic resistance is old news by now—everyone knows that bacteria evolve in response to their surroundings to maintain, and enhance, their pathogenicity. What's less clear is exactly how this happens. Although we can identify genetic mutations in bacteria, it has been difficult to determine which of those mutations are adaptive and which are just random and neutral. Such knowledge would be mighty useful for identifying the biochemical pathways that are important for disease and can be targeted by therapies.

People with cystic fibrosis are highly prone to long-term bacterial infections. In the 1990s, a rare pathogen called Burkholderia dolosa infected 39 people with cystic fibrosis in a hospital in Boston. Tami Lieberman and her colleagues collected bacterial isolates from the airways and blood of 14 of these people over 16 years. These 112 isolates allowed them to analyze the bacteria's evolution in each individual. Results are reported in this week’s issue of Nature Genetics.

To investigate the pathogen’s evolution, the researchers first looked for isolates with known pathogenic behaviors and then correlated those behaviors with genetic changes. So those isolates that were resistant to the antibiotic ciprofloxacin all shared the same mutation, which occurred after the initial infection in six different subjects. Separately, isolates that were highly virulent had altered structures in their outer membranes. There were two different genetic mutations that yielded the same structure; these mutations arose independently in nine subjects.

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