Abstract
Strangles caused by the host adapted Lancefield group C Streptococcus equi subspecies equi (S. equi) is a frequently diagnosed infectious disease of horses worldwide. Critical to the global success of S. equi is its ability to establish persistent infections within the guttural pouches of recovered apparently healthy horses that can result in transmission to in-contact animals. Recent research has identified key events in the S. equi genome, which occurred during its evolution from an ancestral strain of S. equi subspecies zooepidemicus, that may enhance its ability to evade host innate immune responses and rapidly multiply in the tonsillar complex and draining lymph nodes. This review discusses the role of these genetic events on the evolution and emergence of this important host-restricted pathogen.
Highlights
Strangles caused by the bacterium Streptococcus equi subspecies equi (S. equi) continues to be the most frequently diagnosed infectious disease of horses worldwide
Extrapolation based on figures in the Equine Quarterly Disease Surveillance Reports and data from a recent study of UK strangles outbreaks (Ivens et al, 2011) suggests there were over 700 outbreaks of strangles in the UK during 2008
The global success of S. equi has likely stemmed from its ability to rapidly proliferate in tonsil tissue and draining lymph nodes, subsequently leading to abscesses that drain into the guttural pouches where infection persists
Summary
Strangles caused by the bacterium Streptococcus equi subspecies equi (S. equi) continues to be the most frequently diagnosed infectious disease of horses worldwide. A second gene encoding a putative phospholipase A2 toxin, SlaB, sharing 70 % amino acid sequence identity with SlaA and associated with a phage remnant, suggesting horizontal acquisition, was identified in all strains of S. equi and S. zooepidemicus examined by sequencing or quantitative PCR (Holden et al, 2009). The contribution of these toxins to both S. equi and S. zooepidemicus virulence is unknown (Fig. 1)
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