TY - JOUR
T1 - Streptococcus agalactiae clones infecting humans were selected and fixed through the extensive use of tetracycline
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 - DEVANI Consortium
PY - 2014
Y1 - 2014
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.
U2 - 10.1038/ncomms5544
DO - 10.1038/ncomms5544
M3 - Article
C2 - 25088811
SN - 2041-1723
VL - 5
SP - 4544
JO - Nature Communications
JF - Nature Communications
ER -