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described as a possible feature of the disease (Scott and others 2003, Stannard 1987)
and were found in one horse (Woods and others 1992). Nodules were identified in
one horse in this study but were presumed to be injection reactions rather than part
of the disease. This is in contrast to human medicine, where prevalent lesions are
papules, nodules, plaques, subcutaneous tumours and scaly erythema (Braverman
2003). Edema at various body sites (lips, eye lids, distal limbs, ventral abdomen and
prepuce) was reported previously (Anderson and others 1983, Heath and others
1990, Peters and others 2003, Woods and others 1992) and was noted in one of our
horses. Erosions and ulcers described in an earlier report (Sellers and others 2001)
were seen in 2 horses in our study. In human sarcoidosis, violaceous plaques are
commonly observed lesions. In some of these, large telangiectatic vessels are present
on the surface. Inflammatory changes involving these vessels may be the
pathomechanism responsible for the development of edema, erosions and ulcerative
lesions in horses. Depigmentation on the lips and eyelid margins was described
previously (Heath and others 1990). In one of our horses, depigmentation was
observed at the prepuce. Loss of skin pigmentation is an uncommon manifestation
in human sarcoidosis, reported to occur exclusively in black patients and may be
related to decreased melanization of the overlying epidermal cells (Braverman 2003).
In the literature only one report gives information about the localisation of the initial
skin lesions manifesting as a swelling around the lips (Anderson and others 1983).
One author describes the disease onset on the face or limb (Scott 1988, Scott and
others 2003). This could not be confirmed by the findings of our study, as all horses
exhibited initial lesions over the trunk and/or shoulder.
Equine sarcoidosis is reportedly characterized clinically by multifocal to generalized
exfoliative dermatitis with internal organ involvement and a poor to guarded
prognosis (Anderson and others 1983, Peters and others 2003, Scott and others
2003, Sellers and others 2001, von Tscharner and others 2000, Woods and others
1992). Granulomatous lesions have been reported in lymph nodes, lungs, heart, liver,
spleen, kidneys, gastrointestinal tract, adrenal and thyroid glands and brain. Affected
horses typically develop a wasting syndrome and signs of other organ involvement
such as dyspnoea, gastrointestinal or central nervous signs or lameness (Anderson
and others 1983, Heath and others 1990, Peters and others 2003, Rose and others
1996, Sellers and others 2001, Woods and others 1992). In this study, only one horse
exhibited clinical signs of systemic disease such as intermittent fever, prescapular
lymphadenopathy, depression, poor body condition, and nasal discharge. However,
no internal tissue specimens were taken to further investigate internal organ
involvement. As the horse actually responded clinically to glucocorticoid therapy, an
infectious origin seems unlikely, but confirmation of granulomatous changes in
organs other than the skin was not made.
The low incidence of systemic signs seen in horses included in this study could have
been influenced by our inclusion criteria. We contacted dermatologists rather than
internists with the request for participation, which may have led to a bias for horses
with predominant skin disease rather than horses affected with severe systemic
disease evaluated by internists rather than dermatologists and the search criterion in
ACVSC Proceedings Dermatology Chapter Science Week 2005 61