Group B Streptococcus (GBS) is the leading cause of neonatal sepsis and a significant human pathobiont causing invasive disease in non-pregnant adults. Opportunistic by nature, healthy pregnant women colonised by GBS will receive antibiotic prophylaxis prior to delivery to prevent vertical transmission. Our studies have shown that this equates to a quarter of all pregnant women receiving antibiotics before giving birth due to this single species of bacteria.
Across multiple studies, both phenotypic and genotypic traits have been assessed to understanding the epidemiology of GBS in both colonisation and disease states, such as antibiotic susceptibility testing, whole genome sequencing and prophage detection. The collective findings demonstrate a rising rate of antimicrobial resistance in GBS isolates from neonatal disease over time, with up to 45.8% clindamycin resistance in Western Australian isolates. In adults, up to 32% of both colonising and invasive disease were resistant to clindamycin in a New South Wales cohort.
Of a subset (n=95), in silico prophage analysis using PhiSpy highlighted their prevalence, with 86.3% (n = 82) of GBS genomes carrying at least one complete or defective prophage. Phenotypic analyses are underway to functionally assess these genetic features, however, this highlights the genetic information bacteriophages contribute to GBS genomes.
Highlighting GBS as opportunists, we describe GBS in Australia with a focus on the perinatal context. The rising rates of resistance to macrolide antibiotics require our attention particularly with current prophylaxis in pregnancy, and consideration of the contribution of phages in this species in both colonisation and virulence states.