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

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Author(s)

Violette Da Cunha, Mark R Davies, Pierre-Emmanuel Douarre, Isabelle Rosinski-Chupin, Immaculada Margarit, Sebastien Spinali, Tim Perkins, Pierre Lechat, Nicolas Dmytruk, Elisabeth Sauvage, Laurence Ma, Benedetta Romi, Magali Tichit, Maria-José Lopez-Sanchez, Stéphane Descorps-Declere, Erika Souche, Carmen Buchrieser, Patrick Trieu-Cuot, Ivan Moszer, Dominique Clermont & 11 others Domenico Maione, Christiane Bouchier, David J McMillan, Julian Parkhill, John L Telford, Gordan Dougan, Mark J Walker, Matthew T G Holden, Claire Poyart, Philippe Glaser, DEVANI Consortium

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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.
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Original languageEnglish
Pages (from-to)4544
JournalNature Communications
Volume5
DOIs
Publication statusPublished - 2014

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