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The genome of Burkholderia cenocepacia J2315, an epidemic pathogen of cystic fibrosis patients
Authors:Holden Matthew T G  Seth-Smith Helena M B  Crossman Lisa C  Sebaihia Mohammed  Bentley Stephen D  Cerdeño-Tárraga Ana M  Thomson Nicholas R  Bason Nathalie  Quail Michael A  Sharp Sarah  Cherevach Inna  Churcher Carol  Goodhead Ian  Hauser Heidi  Holroyd Nancy  Mungall Karen  Scott Paul  Walker Danielle  White Brian  Rose Helen  Iversen Pernille  Mil-Homens Dalila  Rocha Eduardo P C  Fialho Arsenio M  Baldwin Adam  Dowson Christopher  Barrell Bart G  Govan John R  Vandamme Peter  Hart C Anthony  Mahenthiralingam Eshwar  Parkhill Julian
Institution:The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge CB10 1SA, United Kingdom. mh3@sanger.ac.uk
Abstract:Bacterial infections of the lungs of cystic fibrosis (CF) patients cause major complications in the treatment of this common genetic disease. Burkholderia cenocepacia infection is particularly problematic since this organism has high levels of antibiotic resistance, making it difficult to eradicate; the resulting chronic infections are associated with severe declines in lung function and increased mortality rates. B. cenocepacia strain J2315 was isolated from a CF patient and is a member of the epidemic ET12 lineage that originated in Canada or the United Kingdom and spread to Europe. The 8.06-Mb genome of this highly transmissible pathogen comprises three circular chromosomes and a plasmid and encodes a broad array of functions typical of this metabolically versatile genus, as well as numerous virulence and drug resistance functions. Although B. cenocepacia strains can be isolated from soil and can be pathogenic to both plants and man, J2315 is representative of a lineage of B. cenocepacia rarely isolated from the environment and which spreads between CF patients. Comparative analysis revealed that ca. 21% of the genome is unique in comparison to other strains of B. cenocepacia, highlighting the genomic plasticity of this species. Pseudogenes in virulence determinants suggest that the pathogenic response of J2315 may have been recently selected to promote persistence in the CF lung. The J2315 genome contains evidence that its unique and highly adapted genetic content has played a significant role in its success as an epidemic CF pathogen.
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