Group B Streptococcus (GBS) is a gram-positive bacterium that can cause invasive infections in immunocompromised, elderly, pregnant, or neonatal patients. The invertebrate model, Galleria mellonella, has emerged as an effective tool to study GBS-host interactions; specifically, those conserved within the innate arm of the immune system. We sought to determine the role of metal homeostasis functions in GBS infections of G. mellonella larvae and to validate this model as a tool to study GBS-host interactions. Our results indicate that wild-type GBS infects G. mellonella in a dose-dependent manner, replicates in the invertebrate host, induces larval melanization and larval killing. These results were significantly abrogated in cohorts of larvae infected with the isogenic cadD deletion mutant. Additionally, complementation restored GBS-dependent infection, bacterial burden, larval melanization, and killing to wild-type levels. Together, these results indicate that the G. mellonella model is a useful tool for studying GBS pathogenesis.
Keywords: Streptococcus; innate immunity; metal homeostasis; pathogenesis.