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  • 1
    Publication Date: 2010-01-23
    Description: Current methods for differentiating isolates of predominant lineages of pathogenic bacteria often do not provide sufficient resolution to define precise relationships. Here, we describe a high-throughput genomics approach that provides a high-resolution view of the epidemiology and microevolution of a dominant strain of methicillin-resistant Staphylococcus aureus (MRSA). This approach reveals the global geographic structure within the lineage, its intercontinental transmission through four decades, and the potential to trace person-to-person transmission within a hospital environment. The ability to interrogate and resolve bacterial populations is applicable to a range of infectious diseases, as well as microbial ecology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821690/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821690/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harris, Simon R -- Feil, Edward J -- Holden, Matthew T G -- Quail, Michael A -- Nickerson, Emma K -- Chantratita, Narisara -- Gardete, Susana -- Tavares, Ana -- Day, Nick -- Lindsay, Jodi A -- Edgeworth, Jonathan D -- de Lencastre, Herminia -- Parkhill, Julian -- Peacock, Sharon J -- Bentley, Stephen D -- 076964/Wellcome Trust/United Kingdom -- Department of Health/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2010 Jan 22;327(5964):469-74. doi: 10.1126/science.1182395.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 15A, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20093474" target="_blank"〉PubMed〈/a〉
    Keywords: Asia/epidemiology ; Bacterial Typing Techniques ; Cross Infection/epidemiology/*microbiology/transmission ; Europe/epidemiology ; Evolution, Molecular ; *Genome, Bacterial ; Genomics/methods ; Humans ; Likelihood Functions ; Methicillin-Resistant Staphylococcus aureus/*classification/*genetics/isolation & ; purification ; Molecular Epidemiology ; Molecular Sequence Data ; Phylogeny ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; South America/epidemiology ; Staphylococcal Infections/epidemiology/*microbiology/transmission ; Time Factors ; United States/epidemiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2011-01-29
    Description: Epidemiological studies of the naturally transformable bacterial pathogen Streptococcus pneumoniae have previously been confounded by high rates of recombination. Sequencing 240 isolates of the PMEN1 (Spain(23F)-1) multidrug-resistant lineage enabled base substitutions to be distinguished from polymorphisms arising through horizontal sequence transfer. More than 700 recombinations were detected, with genes encoding major antigens frequently affected. Among these were 10 capsule-switching events, one of which accompanied a population shift as vaccine-escape serotype 19A isolates emerged in the USA after the introduction of the conjugate polysaccharide vaccine. The evolution of resistance to fluoroquinolones, rifampicin, and macrolides was observed to occur on multiple occasions. This study details how genomic plasticity within lineages of recombinogenic bacteria can permit adaptation to clinical interventions over remarkably short time scales.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648787/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Croucher, Nicholas J -- Harris, Simon R -- Fraser, Christophe -- Quail, Michael A -- Burton, John -- van der Linden, Mark -- McGee, Lesley -- von Gottberg, Anne -- Song, Jae Hoon -- Ko, Kwan Soo -- Pichon, Bruno -- Baker, Stephen -- Parry, Christopher M -- Lambertsen, Lotte M -- Shahinas, Dea -- Pillai, Dylan R -- Mitchell, Timothy J -- Dougan, Gordon -- Tomasz, Alexander -- Klugman, Keith P -- Parkhill, Julian -- Hanage, William P -- Bentley, Stephen D -- 076962/Wellcome Trust/United Kingdom -- 076964/Wellcome Trust/United Kingdom -- G0800596/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Jan 28;331(6016):430-4. doi: 10.1126/science.1198545.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21273480" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptation, Physiological ; Anti-Bacterial Agents/pharmacology ; Antigenic Variation ; DNA Transposable Elements ; Drug Resistance, Multiple, Bacterial ; *Evolution, Molecular ; Genome, Bacterial ; Humans ; Molecular Epidemiology ; Phylogeny ; Phylogeography ; Pneumococcal Infections/drug therapy/*microbiology ; Pneumococcal Vaccines/immunology ; Polymorphism, Single Nucleotide ; Prophages/genetics ; *Recombination, Genetic ; Selection, Genetic ; Serotyping ; Streptococcus Phages/genetics ; Streptococcus pneumoniae/classification/drug effects/*genetics/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2013-09-14
    Description: The global epidemic of multidrug-resistant Salmonella Typhimurium DT104 provides an important example, both in terms of the agent and its resistance, of a widely disseminated zoonotic pathogen. Here, with an unprecedented national collection of isolates collected contemporaneously from humans and animals and including a sample of internationally derived isolates, we have used whole-genome sequencing to dissect the phylogenetic associations of the bacterium and its antimicrobial resistance genes through the course of an epidemic. Contrary to current tenets supporting a single homogeneous epidemic, we demonstrate that the bacterium and its resistance genes were largely maintained within animal and human populations separately and that there was limited transmission, in either direction. We also show considerable variation in the resistance profiles, in contrast to the largely stable bacterial core genome, which emphasizes the critical importance of integrated genotypic data sets in understanding the ecology of bacterial zoonoses and antimicrobial resistance.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4012302/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4012302/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mather, A E -- Reid, S W J -- Maskell, D J -- Parkhill, J -- Fookes, M C -- Harris, S R -- Brown, D J -- Coia, J E -- Mulvey, M R -- Gilmour, M W -- Petrovska, L -- de Pinna, E -- Kuroda, M -- Akiba, M -- Izumiya, H -- Connor, T R -- Suchard, M A -- Lemey, P -- Mellor, D J -- Haydon, D T -- Thomson, N R -- 098051/Wellcome Trust/United Kingdom -- 260864/European Research Council/International -- AI107034/AI/NIAID NIH HHS/ -- HG006139/HG/NHGRI NIH HHS/ -- R01 AI107034/AI/NIAID NIH HHS/ -- R01 GM086887/GM/NIGMS NIH HHS/ -- R01 HG006139/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2013 Sep 27;341(6153):1514-7. doi: 10.1126/science.1240578. Epub 2013 Sep 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24030491" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Resistance, Multiple, Bacterial/*genetics ; Epidemics ; Genome, Bacterial ; *Host-Pathogen Interactions ; Humans ; Molecular Sequence Data ; Phylogeny ; Salmonella Infections/epidemiology/*microbiology ; Salmonella Infections, Animal/epidemiology/*microbiology ; Salmonella typhimurium/*classification/drug effects/genetics ; Zoonoses/*microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2019
    Description: 〈p〉Models on how bacterial lineages differentiate increase our understanding of early bacterial speciation events and the genetic loci involved. Here, we analyze the population genomics events leading to the emergence of the tuberculosis pathogen. The emergence is characterized by a combination of recombination events involving core pathogenesis functions and purifying selection on early diverging loci. We identify the 〈i〉phoR〈/i〉 gene, the sensor kinase of a two-component system involved in virulence, as a key functional player subject to pervasive positive selection after the divergence of the 〈i〉Mycobacterium tuberculosis〈/i〉 complex from its ancestor. Previous evidence showed that 〈i〉phoR〈/i〉 mutations played a central role in the adaptation of the pathogen to different host species. Now, we show that 〈i〉phoR〈/i〉 mutations have been under selection during the early spread of human tuberculosis, during later expansions, and in ongoing transmission events. Our results show that linking pathogen evolution across evolutionary and epidemiological time scales points to past and present virulence determinants.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
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