In like a lion, out like a lamb...

University of Washington genome scientist, Maynard Olson, spoke this weekend at a symposium at Cold Spring Harbor Laboratory in honor of the 60th anniversary of the phage course, where he discussed molecular evolution in chronic bacterial infections. Analysis of whole genome sequences of Pseudomonas aeruginosa, a pathogen responsible for chronic lung colonization in patients with cystic fibrosis, reveals an evolutionary ?weakening? of the bacterium over time, resulting in a much less virulent or

By | June 27, 2005

University of Washington genome scientist, Maynard Olson, spoke this weekend at a symposium at Cold Spring Harbor Laboratory in honor of the 60th anniversary of the phage course, where he discussed molecular evolution in chronic bacterial infections. Analysis of whole genome sequences of Pseudomonas aeruginosa, a pathogen responsible for chronic lung colonization in patients with cystic fibrosis, reveals an evolutionary ?weakening? of the bacterium over time, resulting in a much less virulent organism. Comparing sequences from P. aeruginosa isolates obtained from a patient at 6 months and 96 months of age, with a 97% detection rate, found that 68 mutations had occurred in the late isolate compared to the original wild type. Many mutations were found in virulence genes. One large deletion removed 139 genes. Furthermore, the mutant isolate was sickly and difficult to grow in vitro. ?You overwhelmingly see loss of function mutations,? says Olson. ?There is positive selection to get rid of genes not selected for in the environment.? The findings suggest a microenvironmental heterogeneity, with increasing homogeneity occurring as infection progresses. Several of the genes mutated in this patient were also found to be mutated frequently in other patients as well. Nevertheless, progressive lung destruction continues despite the presence of a less virulent strain. The damage stems from the lungs being caught in the crossfire between infection and host immune responses. These unexpected findings may prove useful for developing novel therapies - desperately needed given high rates of antibiotic resistance among P. aeruginosa. Olson says exploiting new genotypic vulnerabilities in bacteria that are capable of establishing chronic infection may prove highly useful for identifying novel drug targets.
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