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Streptococcus agalactiae clones infecting humans were selected and fixed through the extensive use of tetracycline

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  • Violette Da Cunha

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    CNRS UMR3525
    Institut Pasteur, Bioinformatics platform)

  • Mark R. Davies

    (The Wellcome Trust Sanger Institute
    Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, University of Queensland)

  • Pierre-Emmanuel Douarre

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    CNRS UMR3525)

  • Isabelle Rosinski-Chupin

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    CNRS UMR3525)

  • Immaculada Margarit

    (Novartis Vaccines and Diagnostics)

  • Sebastien Spinali

    (Centre National de Référence des Streptocoques, Hôpitaux Universitaires, Paris Centre Cochin–Hôtel Dieu-Broca)

  • Tim Perkins

    (Novartis Vaccines and Diagnostics)

  • Pierre Lechat

    (Institut Pasteur, Bioinformatics platform)

  • Nicolas Dmytruk

    (Centre National de Référence des Streptocoques, Hôpitaux Universitaires, Paris Centre Cochin–Hôtel Dieu-Broca)

  • Elisabeth Sauvage

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    CNRS UMR3525)

  • Laurence Ma

    (Institut Pasteur Genomic platform)

  • Benedetta Romi

    (Novartis Vaccines and Diagnostics)

  • Magali Tichit

    (Institut Pasteur Genomic platform)

  • Maria-José Lopez-Sanchez

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    CNRS UMR3525)

  • Stéphane Descorps-Declere

    (Institut Pasteur, Bioinformatics platform)

  • Erika Souche

    (Institut Pasteur, Bioinformatics platform)

  • Carmen Buchrieser

    (CNRS UMR3525
    Institut Pasteur, Biologie des Bactéries Intracellulaires)

  • Patrick Trieu-Cuot

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    CNRS ERL3526)

  • Ivan Moszer

    (Institut Pasteur, Bioinformatics platform)

  • Dominique Clermont

    (Institut Pasteur, Collection de l'Institut Pasteur (CIP))

  • Domenico Maione

    (Novartis Vaccines and Diagnostics)

  • Christiane Bouchier

    (Institut Pasteur Genomic platform)

  • David J. McMillan

    (QIMR Berghofer Medical Research Institute
    Inflammation and Healing Research Cluster, University of the Sunshine Coast)

  • Julian Parkhill

    (The Wellcome Trust Sanger Institute)

  • John L. Telford

    (Novartis Vaccines and Diagnostics)

  • Gordan Dougan

    (The Wellcome Trust Sanger Institute)

  • Mark J. Walker

    (Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, University of Queensland)

  • Matthew T. G. Holden

    (The Wellcome Trust Sanger Institute
    Present address: School of Medicine, University of St Andrews, St Andrews KY16 9TF, Scotland, UK)

  • Claire Poyart

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    Centre National de Référence des Streptocoques, Hôpitaux Universitaires, Paris Centre Cochin–Hôtel Dieu-Broca
    Institut Cochin, Université Sorbonne Paris Descartes
    INSERM, U1016)

  • Philippe Glaser

    (Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif
    CNRS UMR3525
    Institut Pasteur, Bioinformatics platform)

Abstract

Streptococcus agalactiae (Group B Streptococcus, GBS) is a commensal of the digestive and genitourinary tracts of humans that emerged as the leading cause of bacterial neonatal infections in Europe and North America during the 1960s. Due to the lack of epidemiological and genomic data, the reasons for this emergence are unknown. Here we show by comparative genome analysis and phylogenetic reconstruction of 229 isolates that the rise of human GBS infections corresponds to the selection and worldwide dissemination of only a few clones. The parallel expansion of the clones is preceded by the insertion of integrative and conjugative elements conferring tetracycline resistance (TcR). Thus, we propose that the use of tetracycline from 1948 onwards led in humans to the complete replacement of a diverse GBS population by only few TcR clones particularly well adapted to their host, causing the observed emergence of GBS diseases in neonates.

Suggested Citation

  • Violette Da Cunha & Mark R. Davies & Pierre-Emmanuel Douarre & Isabelle Rosinski-Chupin & Immaculada Margarit & Sebastien Spinali & Tim Perkins & Pierre Lechat & Nicolas Dmytruk & Elisabeth Sauvage & , 2014. "Streptococcus agalactiae clones infecting humans were selected and fixed through the extensive use of tetracycline," Nature Communications, Nature, vol. 5(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5544
    DOI: 10.1038/ncomms5544
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    Cited by:

    1. Kevin S. Blake & Yao-Peng Xue & Vincent J. Gillespie & Skye R. S. Fishbein & Niraj H. Tolia & Timothy A. Wencewicz & Gautam Dantas, 2025. "The tetracycline resistome is shaped by selection for specific resistance mechanisms by each antibiotic generation," Nature Communications, Nature, vol. 16(1), pages 1-14, December.

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