Streptococcus equi evolution
S. equi is a host-restricted pathogen of equids, thought to have evolved from the opportunistic pathogen Streptococcus equi subspecies zooepidemicus (S. zooepidemicus ) (Waller et al., 2011, Holden et al., 2009, Harris et al., 2015). S. equi andS. zooepidemicus are closely related, sharing over 97% of their DNA (Holden et al., 2009).
S. equi and S. zooepidemicus share a common phage pool that has enhanced their cross-species evolution: their divergent evolution is a result of functional loss, pathogenic adaptation, and genetic exchange (Holden et al., 2009). The deletion of the clustered regularly interspaced short palindromic repeats (CRISPR) locus inS. equi is thought to have favoured the acquisition of genetic elements, at the expense of genome stability (Waller and Robinson, 2013). S. equi and S. zooepidemicus have many structural and functional differences (Bannister et al., 1985, Holden et al., 2009, Lindmark et al., 2001), as S. equi has refined its requirements and capabilities similar to other host-restricted pathogens (Parkhill et al., 2003). A notable difference between the two genomes is the presence of the equibactin locus in S. equi , involved in iron acquisition (Heather et al., 2008). This species difference is indicative of how novel functions were introduced, at the expense of ancestral capabilities (Holden et al., 2009); indeed, its acquisition may have been the speciation event that distinguishes S. equi fromS. zooepidemicus (Holden et al., 2009, Heather et al., 2008, Harris et al., 2015).
The S. equi genome is larger than that of S. zooepidemicus , in-part because of its plasticity and the procurement of many mobile genomic elements (Holden et al., 2009). This has been crucial in the development of S. equi as a pathogen; although, the loss of genes not required to cause has resulted in host-restriction, only being able to cause disease in equids (Waller, 2016).