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).