Streptococcus dysgalactiae subspecies equisimilis (SDSE) is a Gram-positive bacterium closely related to the human pathogen S. pyogenes (group A streptococcus, GAS). Whilst GAS has been recognised as a major human pathogen for over 100 years, SDSE has traditionally been considered a commensal organism, and cause of opportunistic infections. However multiple studies have now shown that SDSE causes disease amongst otherwise healthy individuals. Although generally less frequent, the disease spectrum of SDSE is similar to that of GAS, and includes pharyngitis, invasive disease and the post-infectious sequelae post-streptococcal glomerulonephritis. Additionally there is circumstantial evidence for a role for SDSE in rheumatic fever in Australia’s Indigenous population. In contrast to GAS, our knowledge of the epidemiology, molecular genetics and factors contributing to the pathogenesis of SDSE is very limited. Here we describe our latest understanding of the pathogenesis and biology of SDSE. Our data show that genetic diversity in the SDSE population is extensive, and that recombination plays a major role in the genomic diversity at population level in this species. Evidence for lateral gene transfer involving both GAS and Streptococcus agalactiae is apparent. As an example of differences in genetic structure between SDSE and GAS, a homologue of the virulence gene, sic, restricted to only four of 200 GAS emm-types in GAS, is found in a third of all SDSE emm-types. However unlike GAS, not all isolates within a drsG-positive emm-type possess this gene providing evidence of recent transfer of this gene within the SDSE population. Moreover antibodies to SIC from SDSE are positively associated with post-streptococcal glomerulonephritis and chronic kidney disease.