A boy with cystic fibrosis develops a chronic and potentially deadly Burkholderia dolosa infection in his lungs. Varieties of genetic mutations allow some strains of the bacteria to survive the dual assaults from his immune system and antibiotics, while others perish. Eventually, the strongest mutant dominates the B. dolosa colony.

Right?

Maybe not, say the authors of a new study. Examining sputum samples from infected patients, they found that dozens of different kinds of B. dolosa may coexist in that boy’s lungs. Instead of a majority genome representing the “best” way to survive in their combative environment, groups of B. dolosa exhibit different genetic variations that have helped them adapt in different ways.

“We found that when a pathogen like B. dolosa infects us, it diversifies. Many cells discover ways to survive, and these successful mutants coexist,” said Roy Kishony, professor of systems biology at Harvard Medical School and senior author of the study. “This suggests we can reject the model in which a single mutant starts to grow better than everyone else and takes over.”

Published online Dec. 8 in Nature Genetics, the findings not only reveal new insights into human infection, bacterial evolution and B. dolosa biology, they also provide a warning about possible shortfalls in current methods of testing and treatment.

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