TY - JOUR
T1 - Streptococcus agalactiae clones infecting humans were selected and fixed through the extensive use of tetracycline
AU - The DEVANI Consortium
AU - Da Cunha, Violette
AU - Davies, Mark R.
AU - Douarre, Pierre Emmanuel
AU - Rosinski-Chupin, Isabelle
AU - Margarit, Immaculada
AU - Spinali, Sebastien
AU - Perkins, Tim
AU - Lechat, Pierre
AU - Dmytruk, Nicolas
AU - Sauvage, Elisabeth
AU - Ma, Laurence
AU - Romi, Benedetta
AU - Tichit, Magali
AU - Lopez-Sanchez, Maria José
AU - Descorps-Declere, Stéphane
AU - Souche, Erika
AU - Buchrieser, Carmen
AU - Trieu-Cuot, Patrick
AU - Moszer, Ivan
AU - Clermont, Dominique
AU - Maione, Domenico
AU - Bouchier, Christiane
AU - McMillan, David J.
AU - Parkhill, Julian
AU - Telford, John L.
AU - Dougan, Gordan
AU - Walker, Mark J.
AU - Holden, Matthew T.G.
AU - Poyart, Claire
AU - Glaser, Philippe
AU - Melin, Pierette
AU - Decheva, Antoaneta
AU - Petrunov, Bogdan
AU - Kriz, Paula
AU - Berner, Reinhard
AU - Buchele, Anna
AU - Hufnagel, Markus
AU - Kunze, Mirjam
AU - Creti, Roberta
AU - Baldassarri, Lucilla
AU - Orefici, Graziella
AU - Berardi, Alberto
AU - Granger, Javier Rodriguez
AU - Fraile, Manuel De La Rosa
AU - Afshar, Baharak
AU - Efstratiou, Androulla
N1 - Funding Information:
This work was supported by the French National Research Agency (Grant ANR-08-GENM-027-001 and 2010-PATH-004-02) and by the Labex IBEID. The Institut Pasteur Genopole is a member of France Génomique (ANR10-IBNS-09-08). M.R.D. is supported by the National Health and Medical Research Council of Australia (565526 and 635250). M.T.G.H. and J.P. were supported by Wellcome Trust grant 098051. This study was in part supported by the European Commission Seventh Framework (grant agreement number 200481) as part of the DEVANI program. We would like to acknowledge Dr Sri Sriprakash and Ms Karen Taylor for their involvement with the Australian GBS strain collection and Alexandre Almeida for critical reading of the manuscript.
PY - 2014/8/4
Y1 - 2014/8/4
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84905454531&partnerID=8YFLogxK
U2 - 10.1038/ncomms5544
DO - 10.1038/ncomms5544
M3 - Article
C2 - 25088811
AN - SCOPUS:84905454531
SN - 2041-1723
VL - 5
JO - Nature Communications
JF - Nature Communications
M1 - 4544
ER -
