Multilocus Sequence Typing and Evolutionary Relationships among the Causative Agents of Melioidosis and Glanders,
            <i>Burkholderia pseudomallei</i>
            and
            <i>Burkholderia mallei</i>

Godoy, Daniel; Randle, Gaynor; Simpson, Andrew; Aanensen, David M.; Pitt, T. L.; Kinoshita, R; Spratt, Brian G.

doi:10.1128/jcm.41.5.2068-2079.2003

Cited by 455 publications

(357 citation statements)

References 23 publications

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“…Before the sequencing of both genomes, DNA-DNA hybridization suggested that these two species were closely related (26). A recent multilocus sequence typing study of B. pseudomallei and B. mallei isolates from around the globe has revealed that B. mallei can be considered to be a clone of B. pseudomallei (27).…”

Section: Resultsmentioning

confidence: 99%

Genomic plasticity of the causative agent of melioidosis, Burkholderia pseudomallei

Holden

Titball

Peacock

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

680

690

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Burkholderia pseudomallei is a recognized biothreat agent and the causative agent of melioidosis. This Gram-negative bacterium exists as a soil saprophyte in melioidosis-endemic areas of the world and accounts for 20% of community-acquired septicaemias in northeastern Thailand where half of those affected die. Here we report the complete genome of B. pseudomallei, which is composed of two chromosomes of 4.07 megabase pairs and 3.17 megabase pairs, showing significant functional partitioning of genes between them. The large chromosome encodes many of the core functions associated with central metabolism and cell growth, whereas the small chromosome carries more accessory functions associated with adaptation and survival in different niches. Genomic comparisons with closely and more distantly related bacteria revealed a greater level of gene order conservation and a greater number of orthologous genes on the large chromosome, suggesting that the two replicons have distinct evolutionary origins. A striking feature of the genome was the presence of 16 genomic islands (GIs) that together made up 6.1% of the genome. Further analysis revealed these islands to be variably present in a collection of invasive and soil isolates but entirely absent from the clonally related organism B. mallei. We propose that variable horizontal gene acquisition by B. pseudomallei is an important feature of recent genetic evolution and that this has resulted in a genetically diverse pathogenic species.

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Section: Resultsmentioning

confidence: 99%

Genomic plasticity of the causative agent of melioidosis, Burkholderia pseudomallei

Holden

Titball

Peacock

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

680

690

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“…MLSA is widely used to understand the taxonomic relationships among bacterial populations (8,10,11), and it was the method we employed in an earlier study to suggest that M. ulcerans recently evolved from M. marinum (32). To improve genome coverage and increase resolution of the MLSA method for the present investigation, we added an eighth locus to create a 3,210-bp semantide (a large information-bearing molecule).…”

Section: Discussionmentioning

confidence: 99%

Evolution of Mycobacterium ulcerans and Other Mycolactone-Producing Mycobacteria from a Common Mycobacterium marinum Progenitor

et al. 2007

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It had been assumed that production of the cytotoxic polyketide mycolactone was strictly associated with Mycobacterium ulcerans, the causative agent of Buruli ulcer. However, a recent study has uncovered a broader distribution of mycolactone-producing mycobacteria (MPM) that includes mycobacteria cultured from diseased fish and frogs in the United States and from diseased fish in the Red and Mediterranean Seas. All of these mycobacteria contain versions of the M. ulcerans pMUM plasmid, produce mycolactones, and show a high degree of genetic relatedness to both M. ulcerans and Mycobacterium marinum. Here, we show by multiple genetic methods, including multilocus sequence analysis and DNA-DNA hybridization, that all MPM have evolved from a common M. marinum progenitor to form a genetically cohesive group among a more diverse assemblage of M. marinum strains. Like M. ulcerans, the fish and frog MPM show multiple copies of the insertion sequence IS2404. Comparisons of pMUM and chromosomal gene sequences demonstrate that plasmid acquisition and the subsequent ability to produce mycolactone were probably the key drivers of speciation. Ongoing evolution among MPM has since produced at least two genetically distinct ecotypes that can be broadly divided into those typically causing disease in ectotherms (but also having a high zoonotic potential) and those causing disease in endotherms, such as humans.

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“…In contrast, other genetically monomorphic lineages have been accorded species status because of the distinctive diseases they cause, e.g. the causes of plague (Y. pestis [23]), anthrax (Bacillus anthracis [24]), glanders (Burkholderia mallei [25]) and tuberculosis (Mycobacterium tuberculosis [20]), although each of them corresponds to a lineage within a species of greater diversity (Yersinia pseudotuberculosis, Bacillus cereus, Burkholderia pseudomallei and the M. tuberculosis complex, respectively). Finally, still other species also have similar properties, except that a parental species has not been identified, such as the causes of leprosy (Mycobacterium leprae [14]) and Buruli ulcer (Mycobacterium ulcerans [26]).…”

Section: Introductionmentioning

confidence: 99%

Insights from genomic comparisons of genetically monomorphic bacterial pathogens

Achtman

2012

Phil. Trans. R. Soc. B

116

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Some of the most deadly bacterial diseases, including leprosy, anthrax and plague, are caused by bacterial lineages with extremely low levels of genetic diversity, the so-called 'genetically monomorphic bacteria'. It has only become possible to analyse the population genetics of such bacteria since the recent advent of high-throughput comparative genomics. The genomes of genetically monomorphic lineages contain very few polymorphic sites, which often reflect unambiguous clonal genealogies. Some genetically monomorphic lineages have evolved in the last decades, e.g. antibiotic-resistant Staphylococcus aureus, whereas others have evolved over several millennia, e.g. the cause of plague, Yersinia pestis. Based on recent results, it is now possible to reconstruct the sources and the history of pandemic waves of plague by a combined analysis of phylogeographic signals in Y. pestis plus polymorphisms found in ancient DNA. Different from historical accounts based exclusively on human disease, Y. pestis evolved in China, or the vicinity, and has spread globally on multiple occasions. These routes of transmission can be reconstructed from the genealogy, most precisely for the most recent pandemic that was spread from Hong Kong in multiple independent waves in 1894.

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Multilocus Sequence Typing and Evolutionary Relationships among the Causative Agents of Melioidosis and Glanders, Burkholderia pseudomallei and Burkholderia mallei

Cited by 455 publications

References 23 publications

Genomic plasticity of the causative agent of melioidosis, Burkholderia pseudomallei

Genomic plasticity of the causative agent of melioidosis, Burkholderia pseudomallei

Evolution of Mycobacterium ulcerans and Other Mycolactone-Producing Mycobacteria from a Common Mycobacterium marinum Progenitor

Insights from genomic comparisons of genetically monomorphic bacterial pathogens

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