Pathogenesis
S. equi has been shown to persist in the environment for up to 34 and 13 days in wet and dry sites, respectively (Durham et al., 2018). Equids become infected via the oronasal route, likely through ingestion of contaminated material (Boyle et al., 2018). Upon entry, S. equi attaches to the crypt cells of the lingual and palatine tonsillar tissue, before translocating to regional lymph nodes (Timoney and Kumar, 2008).
Virulence factors act to mitigate the effects of the host immune response: the hyaluronic acid capsule aids immune evasion (Woolcock, 1974), IgG endopeptidases are secreted to cleave antibodies (Lannergard and Guss, 2006), and antiphagocytic binding proteins such as Se18.9 are secreted (Tiwari et al., 2007) Additionally, SeM surface proteins block immune activity by binding to fibrinogen and immunoglobulin (Timoney et al., 1997, Meehan et al., 2009). High morbidity is achieved through this antiphagocytic activity, resulting in intra and extracellular multiplication in tonsillar and lymphoid tissue, including regional lymph nodes (Timoney and Kumar, 2008). Additionally, S. equi can produce a microscopic biofilm with potential adhesive functions (Steward et al., 2017) that may play a role in persistence.
Abscessation of the lymph nodes is not visible until 3-5 days after their infiltration, as large numbers of neutrophils are attracted to the site through the interaction of complement-derived factors and pathogen-associated molecular patterns such as peptidoglycan (Muhktar and Timoney, 1988). The ability of S. equi to import iron has been linked to its growth within these abscesses, with the secreted molecule equibactin facilitating this acquisition (Heather et al., 2008, Harris et al., 2015). Abscesses commonly rupture into the airways, guttural pouches or through the skin 7-28 days after initial infection (Waller, 2014): abscesses of the retropharyngeal lymph nodes typically rupture into the guttural pouches, draining into the nasopharynx and subsequent nasal passages resulting in copious mucopurulent discharge.
Severity is dose-dependent with around 10,000 colony-forming units required to cause disease in a mature and immunocompetent equid (Boyle et al., 2018). Increasing the number of colony-forming units will result in more severe disease and a shorter incubation period, which can vary from 1-28 days (Boyle et al., 2018, Judy et al., 1999).
Shedding of S. equi typically commences 1-2 days after the onset of pyrexia and persists for 2-3 weeks; equids remain infectious for over six weeks after purulent nasal discharge has dried up (Boyle et al., 2018).