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).