The integumentary system

The skin is a large, diverse organ, and diseases and conditions may be primarily of dermatological origin or may be secondary manifestations of disease in other organs. Whilst the clinical signs may be obvious on the surface of the skin some are the result of underlying disorders of metabolism and organ dysfunction. Of all equine diseases, those of the skin are amongst the most difficult to diagnose and treat.

Congenital/developmental disorders

Hereditary equine regional dermal asthenia (HERDA; hypoelastosis cutis; cutaneous asthenia/Ehlers-Danlos syndrome) (Figs. 9.8 & 9.9)

This is an inherited defect of connective tissue which results in abnormal folding of the skin, particularly of the shoulders, body and upper limbs. This usually causes considerable, abnormal local folding of the skin which is noticeably thin on palpation. The skin is excessively fragile and is liable to trauma. Healed lesions involving this skin show abnormally prominent scarring. The condition is most frequently seen in Quarterhorses (especially descendants of Poco Bueno) but has been seen in other breeds.

Diagnosis and treatment

• DNA testing is available and will also differentiate carriers.

• Affected horses have an elevation of their urine deoxypyridinoline (DPD):pyridinoline (PYD) ratios which is diagnostic of the disease, from birth, but this testing may not be readily available.

• Currently, there is no effective therapy for HERDA. Affected horses are often euthanized due to the severity of lesions and associated discomfort.

Dermoid cysts (Fig. 9.10)

Single or multiple dermoid cysts are found on the skin of the dorsal midline, particularly in Thoroughbred horses between 6 months and 3–4 years of age. These contain coiled hair and a cheesy, caseous, sterile material. They are seldom painful unless they burst and become infected.

Diagnosis and treatment

• Close examination is usually sufficient for diagnosis and differentiation from inflammatory, neoplastic and parasitic lesions which sometimes occur in the same vicinity.

• Incision and removal of the contents is normally all that is required to treat this condition with minimal aftercare.

Hypotrichosis/mane and tail dystrophy (follicular dysplasia) (Fig. 9.11)

This is a rare condition in which there is less than normal density of hair. It is most commonly seen affecting mane and tail hair but can affect other areas of the body. It is frequently seen in Arabians and Appaloosas.

Diagnosis and treatment

• Diagnosis is usually made based on clinical signs and breed, but histopathology of biopsy samples may help to demonstrate the lack of functional hair follicles.

• It is important to differentiate from selenium poisoning.

• No treatment is possible and it does not affect the horse clinically, being more of a cosmetic defect.

Arabian fading syndrome (pinky Arab syndrome) (Fig. 9.12)

This is a common condition that primarily affects gray Arabian horses but has also been seen in Welsh Mountain ponies and Clydesdales. The skin in affected areas loses its pigmentation and may also lose the hair. It is found most frequently on the face and in the perineal region.

Diagnosis and treatment

• Diagnosis is normally based on clinical signs, but biopsy will confirm the loss of melanocytes.

• There is no effective treatment.

• Tattooing has been used in some Arabian show horses in which the loss of pigmentation is regarded as undesirable cosmetically.

Non-infectious disorders

Calcinosis circumscripta (Figs. 9.13 & 9.14)

This is a rare condition of young horses (1–4 years) of unknown etiology although it is thought that in many cases there may be a relation to previous trauma. It presents as a firm swelling which is sometimes mobile over the underlying tissue and is most frequently seen over the lateral aspect of the stifle.

Diagnosis and treatment

• Clinical signs are usually diagnostic, but radiography or ultrasonography can be used to confirm.

• Biopsy shows multinodular deposits of minerals within fibrous and granulomatous tissue.

• Complete surgical removal is the treatment of choice, but depending on the area affected and the size of the lesion may be difficult to achieve.

Equine axillary nodular necrosis (Fig. 9.15)

This is a rare disorder that is characterized by the development of an irregular number of firm, well-defined skin nodules of varying size which are particularly distributed in the girth and axillary regions. The lesions do not at first involve the loss of overlying hair but latterly they may become larger and usually show a focal area of alopecia. The lesions are painless and are not associated with local inflammatory responses.

Diagnosis and treatment

• Clinical signs are suggestive but definitive diagnosis requires biopsy (excisional biopsy is required).

• Eosinophilic granulomatous inflammation is detected histologically.

• Surgical excision is curative but diagnosis should be definitive prior to excision. In many cases no treatment is pursued due to the benign nature of the condition.

Wounds

The scope for damage to the skin of horses is extensive. An almost infinite variety of injuries may occur. Trauma to the skin of horses is frequently directly attributable to their lifestyle or to their excitable nature when confronted by unusual events such as storms, transport, strange horses, new paddocks, etc. In many cases the more serious consequences of the injury involve underlying structures such as tendons, ligaments, nerves or blood vessels.

Healing of limb wounds is often slow, particularly if the injury, such as deep wire cuts, involves deeper tissues. Where the periosteal blood supply is disrupted sequestration of the underlying bone frequently occurs (see Fig. 7.121). Failure of even relatively minor wounds to heal at sites subjected to trauma involving (even minor) periosteal damage should be investigated carefully in case such sequestration has occurred. These wounds invariably completely fail to heal until either the sequestrum has been spontaneously reabsorbed or surgically removed. Other reasons for the failure of wounds to heal include excessive movement at the site, inadequate wound contraction, infection (bacterial and parasitic), poor or interrupted blood supply, foreign bodies, excessive blood loss and underlying systemic disease.

Wounds in some areas such as the thorax and neck often heal rapidly, relying on a combination of wound contracture and effective spontaneous drainage of exudates and inflammatory debris. Wounds involving the eyelids (see p. 358) or the margins of the mouth, nose and vulva, may heal effectively by second intention healing but may result in a possibly more serious secondary effect after cicatrization (scarring) has taken place.

Non-healing wounds of the lower limb (or elsewhere) which produce large accumulations of exuberant granulation tissue (proud flesh) create a considerable problem for the clinician. Repeated debridement of the granulation tissue and subsequent skin grafting (usually pinch grafting) is required, but such wounds should first be explored by all possible means (including radiography and ultrasonography) to ensure that there is no obvious reason for the failure to heal. Careful handling of wounds in these areas will ensure that healing when it finally occurs will contain the minimum amount of unsightly fibrous and/or osseous tissue. Wounds which fail to heal should also be examined carefully for the possibility that the apparent granulation tissue is not in fact sarcoid.

Foreign body wounds

Foreign bodies which are introduced through skin wounds may lead either to a persistently discharging non-healing wound or to discharging sinuses in the skin. The latter may discharge a considerable distance from the original site and this may be misleading when such wounds and sinuses are examined. Radiography (using probes and/or contrast media if necessary), ultrasonography and careful exploratory surgery under general anesthetic may be required in order to locate and remove such foreign bodies.

Self-inflicted trauma (Fig. 9.16)

Self-inflicted injury also occurs as a result of irritation from biting insects such as Stomoxys spp. Skin mutilation can also occur as a result of the self-mutilation syndrome in stallions; horses bite severely at flanks, ribs and pectoral areas, causing patchy alopecia, leukotrichia and scarring. The use of aluminum muzzles or neck cradles, which allow the horse to eat and drink normally but prevent self-molestation, may be necessary in this and in other skin conditions accompanied by self-mutilation. It is unusual for horses to chew or lick at open wounds unless they are associated with nerve damage or foreign bodies, but they do occasionally chew dressings and bandages where these are poorly applied or where there is an excessive exudation.

Pressure sores (Fig. 9.17)

A more chronic type of skin trauma occurs from poorly applied plaster casts or from localized pressure over bony prominences during prolonged recumbency. These wounds and decubital (pressure) sores are notoriously slow to heal. Residual slow healing occurs only if the pressure is relieved and appropriate treatment applied.

Where skin trauma is prolonged but intermittent, and/or is not severe enough to cause circulation problems, the skin reacts to form a callus. These are common over joints and bony protuberances, especially at the knee, fetlock, elbow, hock and tuber ischia. False or acquired bursae are often encountered where the pressure is applied, such as over the carpus in horses which habitually kneel. Skin thickening and lichenification are common sequels to such injuries. Embedded foreign bodies are also a possible cause of such thickened skin but the history of the lesion is notably different. In all these conditions the lesions are usually cold and non-painful. Prevention of pressure and local irritation may improve the condition but, again, the total resolution is often disappointing.

Thermal injury (Fig. 9.18)

Thermal injury may occur as a result of either heat loss as in frost bite, cryotherapy or heat excess such as sunburn, photosensitization, thermocautery or accidental fire burns. Skin injury caused by exposure to extremely cold environmental conditions appears to be particularly unusual in horses and where it does occur it primarily affects the tail and ears. Even very low environmental temperatures appear to have little effect upon the limbs. Application of severe heat, such as used in the firing of horses’ legs, causes swelling, exudation and residual scarring in much the same fashion as freezing injuries.

Horses trapped in fires may sustain very severe skin damage. The most common sites for severe burns are around the head and dorsum. Horses with burns which cover more than 50% of the body surface almost invariably die from the secondary circulatory, renal and cardiovascular effects. The extent of involvement of the layers of the skin is used to classify burns into four degrees with the most severe, fourth-degree burns involving the entire depth of the skin and underlying tissues. The deeper the skin involvement the more plasma protein is lost in the acute stage and the more severe the consequent scarring. The typical thick, coagulated crusts which develop following thermal (or chemical or physical) cauterization of the skin are called eschars. Severe exudation, loss of body fluids and extremely slow healing of up to 12 months or more, with extensive hairless scarring commonly follows burns of third or fourth degree. The treatment of extensive or localized burns of any degree should be oriented toward controlling the loss of plasma as well as toward pain relief and the limitation of subsequent sloughing. Skin grafting may be an effective method of speeding the naturally slow healing process. Secondary complications, including severe pneumonia due to inhalation of smoke and/or noxious chemicals released from fires (such as burnt plastic), may result in death during the 24–48 hours after the incident.

Endocrine diseases with cutaneous manifestations

Horses with equine Cushing’s disease (see Chapter 6, p. 227) have a wide range of endocrine abnormalities but frequently the first signs to be noted by owners are the changes in coat (hirsutism), excessive sweating and abnormal fat deposits.

Nutritional diseases with cutaneous manifestations

These are infrequent conditions in horses. Nutritional diseases are poorly differentiated and have non-specific skin changes more related to general health than specific deficiency. However, specific mineral deficiencies including zinc, iodine and copper may be associated with skin disorders.

• Zinc (Fig. 9.19). Zinc has a major influence on skin health and adult daily requirements are 500 mg. Deficiency causes a generalized alopecia and flaking of the superficial skin layers giving a dandruff-like appearance. Dietary supplementation with zinc methionine or other zinc salts is curative over a number of weeks.

Figure 9.19 Zinc deficiency with severe exfoliative non-inflammatory shedding of the hair and hyperkeratosis. Reproduced from Knottenbelt D, *Pascoe’s Principles & Practice of Equine Dermatology*, second ed. (2009), with permission from Elsevier.

• Iodine. Young foals born to mares with sub-optimal iodine diets during pregnancy may be born with an obvious goiter (see p. 221) and such foals are often weak and have a very poor coat quality. On occasion they may be almost hairless. Iodine poisoning (iodism) results from ingestion of abnormal amounts of iodine (usually from supplements). Cutaneous findings are heavy surf/seborrhea mostly on the mane and tail base but it can also be seen on the body. Diagnosis is normally based on a history of iodine supplementation and treatment involves removal of the supplement.

• Copper. Copper deficiency is particularly unusual in horses, even in areas with a primary copper-deficient soil or in areas with high soil molybdenum concentrations, but in the event that the animal is unable to maintain its copper status, alteration in the color of the hair (hypochromotrichia) is usually all that is seen. Dark-pigmented hair may become obviously russet in color. Other more serious consequences of copper deficiency are a tendency to arterial rupture and chronic anemia. Diagnosis can be made by blood and liver analysis of copper levels but frequently response to supplementation is used. It is important to remember that not all forms of copper are bioavailable and if deficiency is suspected consultation with an equine nutritionist is valuable in selecting or developing supplementation.

• Selenium poisoning (Fig. 9.20). Selenium causes toxicity either in metallic base form (usually following over-enthusiastic feed supplementation) or from plants which either concentrate selenium or have increased selenium levels as a result of seleniferous soils. Loss of mane and tail hair occurs, as well as the prominent signs of laminitis. In some cases the laminitis may be severe enough to result in separation of the coronary band and sloughing of the hoof. Long-term toxicity or repeated episodes may result in obvious laminitic deformities of the hoof walls with converging growth lines.