Understanding pneumococcal serotype 1 biology through population genomic analysis

BMC Infectious Diseases

Research Article

Madikay Senghore¹  Martin Antonio²  Chinelo Ebruke³  Paul Turner⁴  Betuel Sigauque⁵  Laura Bricio-Moreno⁶  Marie Yang⁶  Aras Kadioglu⁶  Cheryl P. Andam⁷  Anmol M. Kiran⁸  Dean B. Everett⁸  Chrispin Chaguza⁸  Jennifer E. Cornick⁸  Neil French⁸  Stephen D. Bentley⁹  William P. Hanage^1,10  Jukka Corander^1,11  Keith P. Klugman^1,12  Robert S. Heyderman^1,13  Shanil Govindpersad^1,14  Mignon Du Plessis^1,14  Anne von Gottberg^1,15  Julian Parkhill^1,16  Simon R. Harris^1,16  Feyruz Yalcin^1,16  Lesley McGee^1,17  Gerd Pluschke^1,18  Jean-Marc Collard^1,19  Sani Ousmane^1,19 

[1] Bacterial Diseases Programme, Medical Research Council (MRC), Banjul, The Gambia;Division of Translational and Systems Medicine, Warwick Medical School, University of Warwick, CV4 7AL, Coventry, UK;Bacterial Diseases Programme, Medical Research Council (MRC), Banjul, The Gambia;Division of Translational and Systems Medicine, Warwick Medical School, University of Warwick, CV4 7AL, Coventry, UK;Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, WC1E 7HT, London, UK;Bacterial Diseases Programme, Medical Research Council (MRC), Banjul, The Gambia;Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, WC1E 7HT, London, UK;Cambodia Oxford Medical Research Unit, Angkor Hospital for Children, Siem Reap, Cambodia;Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, OX3 7FZ, Oxford, UK;Centro de Investigação em Saúde da Manhiça, Maputo, Mozambique;Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, L69 7BE, Liverpool, UK;Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, L69 7BE, Liverpool, UK;Department of Epidemiology, Center for Communicable Disease Dynamics, Harvard T. H. Chan School of Public Health, 02115, Massachusetts, MA, USA;Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, L69 7BE, Liverpool, UK;Malawi-Liverpool-Wellcome Trust Clinical Research Programme, Queen Elizabeth Central Hospital, Blantyre, Malawi;Department of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, L69 7BE, Liverpool, UK;Pathogen Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, CB10 1SA, Cambridge, UK;Department of Epidemiology, Center for Communicable Disease Dynamics, Harvard T. H. Chan School of Public Health, 02115, Massachusetts, MA, USA;Department of Mathematics and Statistics, University of Helsinki, Helsinki, Finland;Hubert Department of Global Health, Rollins School of Public Health, Emory University, 30322, Atlanta, GA, USA;Bill and Melinda Gates Foundation, 98109, Seattle, WA, USA;Malawi-Liverpool-Wellcome Trust Clinical Research Programme, Queen Elizabeth Central Hospital, Blantyre, Malawi;Division of Infection and Immunity, University College London, WC1E 6BT, London, UK;National Institute for Communicable Diseases (NICD), Johannesburg, South Africa;National Institute for Communicable Diseases (NICD), Johannesburg, South Africa;School of Pathology, University of the Witwatersrand, Johannesburg, South Africa;Pathogen Genomics, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, CB10 1SA, Cambridge, UK;Respiratory Diseases Branch, Centers for Disease Control and Prevention, GA 30329, Atlanta, Georgia, USA;Swiss Tropical and Public Health Institute, Basel, Switzerland;Unité de Biologie, Centre de Recherche Médicale et Sanitaire (CERMES), Niamey, Niger;

关键词: Pneumococcal serotype 1;    ST217;    Phylogeography;    Evolution;    Antibiotic resistance;   

DOI  :  10.1186/s12879-016-1987-z

 received in 2016-05-25, accepted in 2016-10-30,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundPneumococcus kills over one million children annually and over 90 % of these deaths occur in low-income countries especially in Sub-Saharan Africa (SSA) where HIV exacerbates the disease burden. In SSA, serotype 1 pneumococci particularly the endemic ST217 clone, causes majority of the pneumococcal disease burden. To understand the evolution of the virulent ST217 clone, we analysed ST217 whole genomes from isolates sampled from African and Asian countries.MethodsWe analysed 226 whole genome sequences from the ST217 lineage sampled from 9 African and 4 Asian countries. We constructed a whole genome alignment and used it for phylogenetic and coalescent analyses. We also screened the genomes to determine presence of antibiotic resistance conferring genes.ResultsPopulation structure analysis grouped the ST217 isolates into five sequence clusters (SCs), which were highly associated with different geographical regions and showed limited intracontinental and intercontinental spread. The SCs showed lower than expected genomic sequence, which suggested strong purifying selection and small population sizes caused by bottlenecks. Recombination rates varied between the SCs but were lower than in other successful clones such as PMEN1. African isolates showed higher prevalence of antibiotic resistance genes than Asian isolates. Interestingly, certain West African isolates harbored a defective chloramphenicol and tetracycline resistance-conferring element (Tn5253) with a deletion in the loci encoding the chloramphenicol resistance gene (catpC194), which caused lower chloramphenicol than tetracycline resistance. Furthermore, certain genes that promote colonisation were absent in the isolates, which may contribute to serotype 1’s rarity in carriage and consequently its lower recombination rates.ConclusionsThe high phylogeographic diversity of the ST217 clone shows that this clone has been in circulation globally for a long time, which allowed its diversification and adaptation in different geographical regions. Such geographic adaptation reflects local variations in selection pressures in different locales. Further studies will be required to fully understand the biological mechanisms which makes the ST217 clone highly invasive but unable to successfully colonise the human nasopharynx for long durations which results in lower recombination rates.

【 授权许可】

CC BY   
© The Author(s). 2016