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Nat Commun. 2014 Aug 4;5:4544. doi: 10.1038/ncomms5544.

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

Author information

1
Institut Pasteur, Unité de Biologie des Bacteries Pathogènes à Gram-positif, Paris 75015, France.
2
CNRS UMR3525, Paris 75015, France.
3
Institut Pasteur, Bioinformatics platform, Paris 75015, France.
4
The Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 15A, UK.
5
Australian Infectious Diseases Research Centre, School of Chemistry and Molecular Biosciences, University of Queensland, Brisbane, 4072 Queensland, Australia.
6
Novartis Vaccines and Diagnostics, Siena 53100, Italy.
7
Centre National de Référence des Streptocoques, Hôpitaux Universitaires, Paris Centre Cochin-Hôtel Dieu-Broca, Paris 75014, France.
8
Institut Pasteur Genomic platform, Paris 75015, France.
9
Institut Pasteur, Biologie des Bactéries Intracellulaires, Paris 75015, France.
10
CNRS ERL3526, Paris 75015, France.
11
Institut Pasteur, Collection de l'Institut Pasteur (CIP), Paris 75015, France.
12
QIMR Berghofer Medical Research Institute, Brisbane, 7006 Queensland, Australia.
13
Inflammation and Healing Research Cluster, University of the Sunshine Coast, Sippy Downs, 4556 Queensland, Australia.
14
Institut Cochin, Université Sorbonne Paris Descartes, Paris 75014, France.
15
INSERM, U1016, Paris 75014, France.
#
Contributed equally

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.

PMID:
25088811
PMCID:
PMC4538795
DOI:
10.1038/ncomms5544
[Indexed for MEDLINE]
Free PMC Article

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