GBS is a major cause of invasive infections in newborn babies. In the Netherlands, the incidence of GBS neonatal disease increased by 60% between 1987 and 2011, despite the introduction of disease prevention guidelines in 1999. This was associated with rise in number of cases caused by isolates belonging to clonal complex 17 (CC17). To investigate the changing genetic epidemiology of GBS neonatal infections in the Netherlands we whole genome sequenced isolates submitted to the Netherlands Reference Laboratory for Bacterial Meningitis between 1987 and 2016. A total of 1331 isolates derived from early and late-onset infections were analysed. The population consisted of 5 lineages representing CC17, CC19, CC23, CC10 and CC1. There was an increase in relative prevalence of CC17 and CC23 while CC19 remained stable. We inferred phylogenies for individual lineages and observed temporal trends for defined sub-lineages. The CC17 phylogeny revealed a major sub-population that increased rapidly in prevalence over time becoming dominant in early 2000s. Bayesian analysis of past population dynamics showed a major expansion in effective population size of this clade in mid 1990s. In contrast CC19 revealed a dropping prevalence of isolates representing a major clade while CC23 showed increasing frequency of isolates from a dominant cluster, which experienced population expansion in mid 1980s. Preliminary analysis shows emergence of a phage in GBS population in the mid 1990s, carrying a novel surface protein gene, that has spread rapidly in CC17 and was associated with clonal expansion events.