Profile

This is an acquired depigmentation that possibly has an autoimmune basis relating to anti-melanocyte antibodies (Naughton 1986). However, the localized distribution of the condition is somewhat at odds with this theory. An auto-toxicity alternative has been proposed. Neural alterations and virus infections have also been proposed.

Depigmented spots and larger, poorly defined areas appear on the skin. They may be idiopathic or may follow primary damage to melanocytes (Meijer 1962, Pascoe 1973). They are usually restricted to horses over 4 years old. The condition may be heritable and is probably commonest in Shire and Arabian horses.

Clinical signs

Depigmented circular or irregular spots and bigger less well-defined areas up to (or over) 1 cm diameter which increase in number rather than size (Fig. 16.2) are typical. The lesions may be more or less symmetrical in distribution.

Figure 16.2 Vitiligo (idiopathic depigmentation): spotted, body form (spotted leukotrichia) which caused changes in the hair colour.

Key points: Vitiligo

1. An acquired depigmenting disorder of limited areas of theskin, possibly related to an autoimmune condition and frequently encountered around the eyes and face in particular.

2. Arabians, Thoroughbreds and Shire horses are possibly more prone to the condition. Grey horses may be more affectedbut this is possibly because the changes are more obvious in these. Horses of all ages can be affected. The condition is remarkably free of concurrent symptoms but some have associated hair loss.

3. Anular, more or less symmetrical, permanent, areas of depigmentation of varying extent develop without apparentsymptoms of inflammation or apparent causative insult.

4. The features are typical but biopsy can be used to confirmthe condition. There is a distinct lack of melanocytes but otherwise the skin is normal.

5. No treatment is possible although some reports suggest that copper and vitamin A are helpful.

On the body these seldom if ever cause alopecia, but around the eye where the hair coat is sparse in any case, hair loss is sometimes pronounced (Fig. 16.3). Leukoderma may or may not copy the associated leukotrichia.

Figure 16.3 Vitiligo (idiopathic depigmentation) around the eye.

Owners often become very concerned but can be reassured of the benign nature of the condition, although the progressive nature of some cases makes certain uses of the horse unrewarding. There is no associated pain, pruritus or any evidence of inflammatory responses (Figs 16.4 and 16.5 and Fig. CD16 • 3A and B).

Figure 16.4 This gelding developed bilateral extensive areas of vitiligo on its face (A) and around the eyelids (B) that progressed slowly for some years and then stabilized.

Figure 16.5 Vitiligo can also affect the perineal skin. The perineal skin of this grey horse had been completely black for many years and then over a period of about 6 months the pigment was lost. Note the two patches of vitiligo also on the lateral aspects of the tail base (arrows).

The depigmented areas may be more prone to actinic dermatitis (sunburn) and ultimately to squamous cell carcinoma.

Differential diagnosis

Diagnostic confirmation

Treatment

There is no remedy. Surgical removal of 3–5 mm spots where only 2–3 areas occur may be feasible but may cause more extensive depigmentation. It is best left alone. Cosmetic coverage is possible in show horses by dyes or stains.

Profile

Loss of pigment in hair and skin related to various factors such as pressure injury, cryosurgery, surgery, radiation or other skin disorders. The pathological consequence is exploited in freeze marking. Even minor insults to the melanocytes cause significant loss or in some cases malfunction. This means that even minor skin damage and some trivial infections such as coital exanthema (see p. 138) can result in depigmented scars. In some disease states the melanocyte loss is less easy to explain. For example, the condition known as pinnal acanthosis (see p. 136) often causes proliferation of the epidermis with loss of pigmentation.

Key points: Acquired persistent leukoderma/leukotrichia

1. An acquired, depigmenting disorder arising from skin damage or insult. In some cases the insult may be trivial. Trauma, radiation or freeze or thermal burns are common instigating factors.

2. The distribution of the white hair (and possibly the associated white skin) changes follow the pattern of the insult. Freeze branding illustrates clearly how the melanocytes are more sensitive to insult than the skin itself.

3. Diagnosis is usually simple and the pattern of leukoderma/ leukotrichia is typically associated with other skin damage. Usually by the time the hair colour changes are detected the original insult will have disappeared. Biopsy shows evidence of scarring and loss of melanocytes.

4. Treatment is not usually possible; cosmetic dyes can be used to mask the changes. More invasive ‘treatments’ such as excision or tattoo are probably contraindicated.

5. The prognosis is excellent – it is best regarded as a cosmetic problem (unless the extent of scarring and tissue damage is limiting)

Clinical signs

Ill-defined, irregular white patches of hair and skin appear corresponding to areas of skin damage by many factors such as skin trauma (Fig. 16.6) and freeze branding (Fig. 16.7). Even tight bandages can cause melanocyte damage and white hairs appear and these are particularly obvious on distal limbs – often the owners will deny any knowledge of any episode of over-tight bandages or any obvious trauma.

Figure 16.6 This horse was subjected to line and pin firing for a tendon disorder. The treatment has no merit but the scars remain obvious – usually as a combination of an alopecic scar and leukotrichia. Note also that the bandages applied to the limb at the time of the ‘treatment’ also resulted in leukotrichia on the more dorsal region of the cannon.

Figure 16.7 Leukoderma/leukotrichia (acquired vitiligo). Two forms of the condition are shown. Irregular ‘saddle (and girth) marks’ are usually accepted as being of traumatic origin. Freeze branding should result in a change in pigment without any other scarring, but in this case the ‘burn’ was less well judged and only limited pigment changes arose at the margins of the scars.

Cryosurgery or normal sharp surgery, irradiation (X-ray or gamma) (see Fig. CD16 • 1A), etc. can also cause changes in the melanocytes with local development of white hair. Freeze branding, which is used as a permanent means of identification, exploits this response. Where the freeze is superficial and transient only the hair becomes white; this implies that the follicular melanocytes are perhaps the most sensitive or that the process of pigmentary uptake in hair shafts is also affected. More extensive freezing causes more damage to the melanocytes in the treated area and so the skin becomes hairless and white. Even more extensive/severe freezing results in a scar formation and this may be darker or lighter in colour than the surrounding skin.

Melanocytes can be destroyed by contact with irritants, harness, rubber, bits, etc. Common sites include the saddle region and withers and girth where they arise from repeated minor or more severe trauma (Fig. 16.7). The changes that follow rubber contact in particular arise without any obvious inflammatory response at all. There may be an abrupt loss of pigment in the affected skin and hair in particular and the contact area is closely related to the pattern of leukoderma/leukotrichia (Fig. 16.8 and Fig. CD16 • 4A and B). These changes are poorly understood but alopecia is seldom encountered in these conditions.

Figure 16.8 This Friesian gelding carriage horse developed this dramatically localized leukotrichia without any associated leukoderma and without any apparent inflammation. Note the remarkable symmetry and obvious relationship to the harness contact points on its head (A) and the body (B, C). Its partner was unaffected. The changes were persistent (see also Fig. CD16 • 4).

Figures courtesy of Dr M. de Rijk.

There is often no apparent thickening or other cutaneous changes, but with injuries and surgical sites the skin is sometimes patently scarred and thickened. It is important to realize that the hair cannot change colour overnight! The change has to appear with the growth of the hair and so it may be possible to identify roughly when the insult took place by the position of the change in the hair shafts. Often, however, the changes are fastest when the new hair coat (either summer or winter) is being produced and the old coat is being shed. This may give a misleading impression of an abrupt/acute change.

Differential diagnosis

Diagnostic confirmation

Treatment

There is no known treatment. Attempts to surgically remove the affected area usually creates another similar (often bigger) problem area. By far the best approach is to leave the area alone and to apply suitably coloured dyes to mask the changes if that is what is necessary! It is important to emphasize to owners how the damage arises and ensure that the potential insults are not repeated. The prognosis is excellent for the horse even if the owner is annoyed/disappointed by the changes. Saddle marks and to a lesser extent girth marks are very common and viewed by most as a cosmetic nuisance.

The erasure or alteration of freeze branding scars is virtually impossible but can be attempted with laser surgery. However, it invariably leaves more white hairs and skin, but the number may be hidden.

Profile

The loss of pigment in traumatic injuries to the skin occurs when the pigment-containing cells of the epidermis are lost. The most obvious cases relate to grazes and superficial skin erosions and ulcerations. There is usually no long term scar but some injuries may have deeper wounds where scarring and long-term leukoderma/leukotrichia can develop.

Key points: Transient trauma-related pigmentary loss

1. A common transient pigmentary loss with only occasional permanent changes.

2. Area of transient depigmentation that follows bruising, erosion or ulceration of the skin. Signs of trauma may be obvious or may be less so. Sometimes the changes can become permanent and then there may be leukoderma and leukotrichia (see p. 341) .

3. History of superficial cutaneous bruising or grazes. The transient nature of the changes differentiates this from other persistent forms of pigmentary change such as vitiligo and the changes that follow more severe skin trauma and selective destruction of melanocytes (e.g. freeze band, saddle marks).

4. Treatment is limited to nursing care of the injured skin but recovery of pigment can take some weeks.

5. The prognosis is excellent.

Clinical signs

Following obvious trauma, the loss of the epidermis will inevitably result in exposure of the basal and germinal layers and possibly the dermis (Fig. 16.9). The episode of trauma is usually mild but the area involved will vary. A similar condition occurs when the skin is sunburnt or is excoriated with faeces/diarrhoea/urine or other discharges. It can also occur simply following swelling or localized inflammation with epidermal collarette formation. The pigment is gradually restored over some weeks, usually fully but sometimes to a lesser extent.

Figure 16.9 This horse suffered a graze to its upper eyelid (A) that caused a transient loss of skin pigmentation (B). Note the normal dark brown skin. The hair grew back normally after some weeks.

Hair loss as a result of the trauma or excoriation may occur – this is not really alopecia.

Differential diagnosis

Diagnostic confirmation

Treatment

Treatment is not necessary for the pigmentary problem but of course the quicker the skin is restored to normal the quicker the pigmentation will be restored. Often the hair loss that may have occurred takes longer to regrow so the site may remain ‘noticeable’ for some time. A few white hairs may develop in a few cases.

The prognosis is excellent.

Profile

Owners often report a variety of clinical signs on the skin of horses that have recently been clipped. Where actual trauma occurs from poor clipper technique or poor adjustment of the blades, the lesions are often obvious traumatic skin injuries. Other cases show nodules or areas of inflammation. It is thought that this might relate either to heat in the blades or to inflammatory responses to the oils and sprays used for lubrication.

Clinical signs

Following clipping, injury may be obvious with bleeding or serum exudation. Nodules or areas of inflammation following clipper tracks and strictly restricted to the clipped area are significant. The signs are usually more severe on the thin skin of the neck and withers regions.

Nodules often take some days to develop (Fig. CD16 • 5A and B).

Differential diagnosis

• Urticaria: oedematous raised plaques with an acute or peracute onset and usually a rapid resolution either spontaneously or following a single injection of dexamethasone.

Key points: Clipper rash

1. A common transient inflammatory skin condition occurring within hours or days of clipping sometimes as a result of heat or from oils or from sharp clipper trauma.

2. Skin trauma, multiple small focal non-painful nodules or more diffuse areas of mild inflammation following the pattern of clipping and strictly restricted to the clipped area are typical.

3. The transient nature of the changes differentiates this from other more persistent conditions. The history is typical.

4. Treatment is limited to nursing care of the injured skin but recovery can take some weeks. If oil is suspected as being involved this should be washed away carefully.

5. The prognosis is excellent but advice regarding clipping techniques and care of the clippers may need to be given.

• Eosinophilic dermatitis with collagen necrosis: usually slower to appear and seldom resolves. Not related to clipping but could be revealed by clipping.

• Dermatophilosis: usually related more to hair loss and characteristic bacteriology.

• Staphylococcal folliculitis/furunculosis: painful and exudative localized lesions with positive cultures. Could be related to clipping trauma also.

• Chemical burn/irritation: known exposure or suggestive pattern of lesions.

• Contact allergy: only the area exposed to allergen is affected.

Diagnostic confirmation

Treatment

Treatment is not necessary but extra care should be taken with hygiene, and a single antibacterial wash may be helpful. Usually the nodules and any associated skin trauma will heal in time. Some may persist, however, so the sites may remain ‘noticeable’ for some time. A few white hairs may develop in a few cases.

The prognosis is excellent but care must be taken to avoid repeating such episodes, and advice regarding the use of appropriate lubricants and avoidance of direct trauma and heat should be given.

Profile

Dorsal, bilateral, reticulated, white hair-striping is characteristic. Although the condition is reported to affect yearling Quarterhorses in particular in the USA, the condition also affects Thoroughbred and Standardbred horses in Australia. Other breeds and older animals can be affected in other countries also, but it is most often reported in older horses with an unknown earlier history. It has been suggested that it is a form of erythema multiforme. There is a suggested correlation between rhinopneumonitis (EHV) vaccine and the onset of the disease but cases occur in unvaccinated horses and in circumstances when exposure to herpesvirus is very unlikely. Hereditary aspects have been suggested (see Fig. CD16 • 6A–D) but this is not established.

Key points: Leukotrichia

1. A rare, sporadic pigmentary disorder mainly affecting the dorsum of young (1 – 3-year-old) horses of different breeds under different conditions. ‘Brindle’ Quarterhorses may be overrepresented. Several suggestions have been made concerningits possible genetic basis and it may represent a particular form of linear keratosis; some pain initially and scaling along the lines of pigment changes are common.

2. Linear crusting lesions develop along the back with limited pain at first. Some long-term discomfort may be present. The permanent ‘tiger striping’ /brindling develops along the lines of the crusting some weeks later.

3. The underlying skin is normal histologically but the earlystages have an ill-defined oedema and pigmentary incontinence.

4. There is no treatment for the condition.

5. Suggestions that it is sufficiently heritable to exclude breeding from affected horses are ill-founded.

Clinical signs

There is a sudden development of painless small vesicles and crusts arranged in a cross-hatched pattern along the dorsum between the tail and the withers. In some cases this stage passes unnoticed. In a few cases extreme pain can be encountered with resentment to both palpation and tack/harness placement; this may then be more akin to the hyperaesthetic leukotrichia disorder (described below). Temporary alopecia follows shedding of crusts. New hair is white but the skin retains its original pigmentation (Fig. 16.10).

Figure 16.10 Reticulated leukotrichia in a Quarterhorse. Note the obvious dorsal transverse striping.

The condition has a course of about 3 months. Repeated episodes have also been reported (Yu 1997).

Differential diagnosis

Diagnostic confirmation

Treatment

There is no known treatment; it is probably best left alone to settle with time. Attempts at local treatment may simply exaggerate the resentment of the horse until it becomes a serious management problem. Corticosteroids probably will not help, even at high doses. Treatment with aciclovir has been suggested followed by administration of the post-herpes-zoster neuralgia drug amitriptyline. There are no reports of the results of this approach.

The prognosis is good – most cases will eventually settle down and become a cosmetic curiosity.

Profile

This is a rare disease with highly characteristic signs restricted to the dorsum of mature horses and, as yet, only reported in some areas of the USA (Stannard 1987). It is possibly a variant of the reticulated leukotrichia condition (see above) but is associated with far more pain and obvious inflammation. Some cases are reported to follow the use of live or killed EHV (rhinopneumonitis/abortion) vaccine (Stannard 1987). The geographical restriction suggests that other factors are in fact involved and the vaccine relationship is likely to be coincidental/irrelevant.

Key points: Hyperaesthetic leuko(melano)trichia

1. A rare pigmentary disorder without known aetiology. Immunological changes are suspected but little is known about it. It may reflect an early or unusual form of reticulated leukotrichia in which cutaneous sensory nerve fibres are involved.

2. Multiple linear and focal, crusting, very painful lesions along the back predominately. Pain may precede the development of obvious skin lesions. The consequent pigmentary changes are persistent.

3. Biopsy is non-specific with variable evidence of perivascular superficial and deep inflammatory responses.

4. Treatment is largely symptomatic. Analgesia with nonsteroidal anti-inflammatory drugs and possibly corticosteroids may help but there are too few reported cases to be definitive.

5. The condition may last up to around 3 months and may recur.

Clinical signs

Single or multiple, very painful, non-pruritic, crusting dermatosis with small focal lesions, 1–4 mm in diameter, occur along the dorsum of the back and over the saddle area. Obvious (sometimes extreme) pain is usually manifest – horses react violently if the lesions are handled. (Note: in some cases the pain may precede the development of overt lesions and the horse may be presented for a ‘cold back’ or saddle resentment.)

Lesions remain for 1–3 months followed by spontaneous regression. Permanent white hair changes and sometimes limited alopecia are the norm (Fig. 16.11). In a few cases a similar clinical picture is seen but the skin darkens and the alopecia is more pronounced. This may or may not be a variation of the more regular but still rare hyperaesthetic leukotrichia (Fig. 16.12).

Figure 16.11 Hyperaesthetic reticulated leukotrichia in a cross-breed working horse in Ethiopia. This horse had severely resented palpation of the back for around 6 months and once the crusts were shed, the white hair appeared in its characteristic pattern and the pain subsided.

Figure 16.12 Hyperaesthetic melanotrichia. The sparsely haired pigmented areas were acutely painful and the hair colour changed to white over the following years.

Some cases will resolve completely (although some scarring usually remains), while in others it may recur or be persistent with variable degrees of hypersensitivity.

Differential diagnosis

Diagnostic confirmation

Treatment

There is no known effective treatment. Even high doses of corticosteroids and non-steroidal anti-inflammatory drugs may have no material effect. The pigmentary changes can be masked with cosmetic hair dyes.

The course is usually some weeks with gradual remission, but some horses remain ‘cold-backed’ or ‘saddle-shy’.

Profile

This uncommon but distinctive papular disorder with an unknown aetiology affects yearlings and 2-year-old Quarterhorses (and some Thoroughbreds); other breeds and other ages may also be affected. The aetiopathogenesis is unknown (Scott 1988a). Most lesions develop in spring/summer, suggesting an insect-related aetiology (Williams 1995) and a viral cause has been suggested also (see p. 133). The characteristic restriction of the lesions to one side of the body possibly relates to insect feeding access but the condition is not seasonal and recurrences are rarely reported.