Despite a risk-based peripartum chemoprophylaxis approach in Iceland since 1996, Streptococcus agalactiae [group B streptococci (GBS)] remains an important cause of early-onset [<7 days, early-onset disease (EOD)] and late-onset disease (LOD; 7 days to 3 months).
We studied GBS invasive disease in children <1 year in Iceland in 1976–2015. Bacteria (n = 98) were characterized by susceptibility to a panel of antimicrobials, capsular serotyping, resistance genes, surface protein and pilus-locus profiling and multilocus sequence typing.
Both EOD and LOD increased during the early years, but while EOD subsequently decreased from 0.7/1000 live births in 1991–1995 to 0.2/1000 in 2011–2015, LOD showed a nonsignificant decrease from its peak value of 0.6/1000 in 2001–2005 to 0.4/1000 in 2006–2015. Serotype III was the most frequently found (n = 48), represented mostly by the hypervirulent lineage CC17/III/rib/PI-1+PI-2b (62%), but also by CC19/III/rib/PI-1+PI-2a (35%) frequently associated with colonization. Serotype Ia (n = 22) was represented by CC23/Ia/eps/PI-2a (68%) and CC7/Ia/bca/PI-1+PI-2b (23%) of possible zoonotic origin. Resistance to erythromycin and clindamycin was increasingly detected in the last years of the study (5 of the 9 cases were isolated after 2013), including representatives of a multiresistant CC17/III/rib/PI-2b sublineage described recently in other countries and expressing resistance to erythromycin, clindamycin and streptomycin.
The risk-based chemoprophylaxis adopted in Iceland possibly contributed to the decline of EOD but has had limited effect on LOD. GBS causing neonatal and early infancy invasive infections in Iceland are genetically diverse, and the recent emergence of antimicrobial resistant lineages may reduce the choices for prophylaxis and therapy of these infections.
From the *Department of Clinical Microbiology, Landspitali University Hospital, Reykjavik, Iceland
†BioMedical Centre of the University of Iceland, Reykjavik, Iceland
‡Instituto de Microbiologia, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Accepted for publication July 18, 2018.
This work was partially funded by a grant from the Governments of Iceland, Lichtenstein and Norway (EEA-PT06). E.S.B. was partially funded by a grant from Landspitali University Hospital Research Fund. E.R.M. was supported by a grant from Fundação para a Ciência e a Tecnologia (SFRH/BPD/80038/2011). Reagents for serotyping the isolates were a kind gift from the Statens Serum Institute.
J.M.-C. received research grants administered through his university and received honoraria for serving on the speakers bureaus of Pfizer, Bial, GlaxoSmithKline and Novartis. M.R. received honoraria for serving on speakers bureau of Pfizer and for consulting for GlaxoSmithKline and Merck Sharp and Dohme. The other authors have no conflicts of interest to disclose. No company or financing body had any interference in the decision to publish.
Part of this work was presented at the 26th European Congress of Clinical Microbiology and Infectious Diseases (ECCMID), 2016, Amsterdam, the Netherlands.
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Address for correspondence: Mario Ramirez, PhD, Instituto de Microbiologia, Faculdade Medicina, Universidade de Lisboa, Avenida Professor Egas Moniz, PT 1649-028 Lisboa, Portugal. E-mail: firstname.lastname@example.org.