Page 1271 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

1246 CHAPTER 12

VetBooks.ir SELENIUM TOXICOSIS Differential diagnosis
Mimosine toxicity; coronary band dystrophy; other
Definition/overview
dystrophy.
Ingestion of Morinda reticulata or Neptunia amplexi- causes of laminitis; other causes of mane and tail
caulis, both of which accumulate selenium, may cause
selenium toxicosis. Diagnosis
Hair, hooves, liver and kidney can be tested for sele-
Aetiology/pathophysiology nium levels.
Selenium toxicosis is related to high levels of
selenium in the soil or the presence of selenium- Management
accumulating plants. Levels are highest in low- Affected animals should be placed on a daily
rainfall areas with alkaline soil. high-protein supplement and given 2–3 g of
DL-methionine orally per day. Feed additives, such
Clinical presentation as sodium arsenate, arsenilic acid and copper supple-
Lameness, including acute and chronic laminitis, ments, have been reported as treatments. Access to
loss of hooves and loss of mane and tail hairs will be implicated plants should be restricted.
present.
Prognosis
The prognosis is fair in early cases, but very poor
when foot changes occur.

SEBORRHOEIC DISEASES

Primary sebaceous gland dysfunction is rare in in a 7-year-old Arabian gelding with progressive
horses. Seborrhoeic disease seems more likely to be patches of non-pruritic crusting, scaling, alopecia and
related to abnormal cornification resulting in scaling leucoderma. The lesions began in the periocular and
and crusting than to sebaceous gland dysfunction. muzzle regions and became generalised to include
Secondary seborrhoea is usually related to a skin the face, thorax, abdomen and rump. Although rare,
response to some other injury (e.g. ‘greasy heel’ in it is easily characterised by lymphoid destruction of
heavy horses), allergic, immune-mediated or meta- sebaceous ducts with subsequent complete loss of the
bolic disease. Sebaceous adenitis has been described sebaceous gland on dermatohistopathology.

NODULAR DISEASES

INTRODUCTION will vary from blood and tissue fluid through to
neutrophils, lymphocytes, histiocytes, plasma cells
The development of a solid skin swelling of >1 cm, and eosinophils. Visible nodules develop from this
which exceeds the dimensions of a papule, can be substrate as the infiltrating cells begin to aggregate
included in the category of nodular skin disease. Many to wall off the injury or the infective process. As the
forms of skin disease may originate as macules or pap- lesion enlarges, the dermis and subcutis become com-
ules, but progressively increase in size, either singly or pletely infiltrated by the above cells and the overlying
in numbers, and so become included in this category. epidermis may become atrophic, leading to erosion,
Nodules can be subdivided into inflammatory and ulceration and possible exudation of contents.
neoplastic lesions. The inflammation may be due to Most neoplasms of the skin and subcutaneous
injury or infection and the inflammatory infiltrate tissue originate as nodules and then increase by