Pruritus (the itchy horse)

Pruritus can be defined as the (unpleasant) sensation that encourages the animal to itch and is one of the commonest dermatological clinical presentations. It is vitally important to recognize that pruritus is a phenomenon attributable to both central and peripheral neural mechanisms (Blood & Studdert 1988). Nerve endings in the region of the dermo-epidermal junction transmit the sensation of ‘itchiness’ via slow-conducting C-fibres to a central region where the itch sensation is modulated. ‘Scratching’ at the site of itch is transmitted via fast conducting fibres and results in a temporary suppression of the sensation by down-regulating the peripheral input (the so-called Wall’s gate phenomenon). Pruritus is a common symptom of local peripheral and central pathology and can be triggered by many factors. In addition pruritus such as that associated with insect bites in particular may continue until there is a marked local inflammatory response arising from self-trauma. Only then does the pruritus abate – preventing self-trauma can therefore prolong the ‘itchy’ state. A diagnostic complication can therefore arise when the pruritic state results in masking of the original signs and this aspect should not be forgotten.

The extent or severity of the pruritus exhibited by an individual animal is very variable – there is no consistent degree of pruritus for any particular condition. Some horses will show mild signs with severe disease and others will show marked pruritus with mild disease of the same type. This is possibly the main reason why grading pruritus has not gained any credibility in horses at least; however, a scale of 0 (no itch) to 10 (extreme itch) has been suggested and it can sometimes be helpful in assessing progression and the effects (positive or negative) of therapeutic interventions in a particular individual (Scott & Miller 2003). This can be difficult to apply when there is variability of signs at different sites and under different conditions such as warmth, cold, etc. Often the severity of the itching can be determined – sometimes simply by asking the owner and at other times by assessing the severity of the secondary changes. Thus, an animal with a severe localized allergic response to the bite of an insect may cause severe self-trauma at the site – often the induced skin damage and inflammation is more extensive than the original bite/sting or insult. Pruritus can therefore be self-perpetuating and triggered by a relatively minor episode of intense itchiness. This can be followed by rubbing, biting and self-mutilation which, in turn, cause further local inflammation and irritation. The instigating factor may not therefore be present at the time of the examination or may be significantly masked by the changes. Most pathologists do not relish the assessment of a chronically rubbed/itched and self-traumatized skin. The more prolonged the effects the more difficult it is for the clinician to be sure of the original cause and the more damaged the skin the less the pathologists will be able to glean from biopsies (Fig. 19.1).

Figure 19.1 This horse suffered a prolonged, severe self-trauma to the breast and anterior shoulder region of both sides. The location is unusual for any of the ‘common’ causes of pruritus but might be consistent with a contact irritation of some sort. It was impossible to get any meaningful information from biopsy of this case and only symptomatic treatment could be applied.

Figure courtesy of Dr Andrea Bertuglia.

The location of the ‘itching’ can, however, be a marker for the location of the pathology but there are some circumstances such as rabies, for example (see Fig. 15.2), when the clinical response can be referred, i.e. the pathology is in a different place to the itch. Similarly, head-shaker horses often rub the side of the face suggesting pruritus but this may be a response to pain or irritation within the nasal cavity, or to numbness or to ‘tingling’ sensations (see Fig. 15.3). If the horse could just tell us where and what it is feeling, the diagnosis of pruritus in horses would be far simpler!

It is helpful also to establish whether itching initially occurred in the absence of a perceived lesion (as might be indicated by an allergic response) or whether the itchiness followed the appearance of a distinct lesion. For example, a rabid horse may itch at the site of an original bite wound on the carpus while the pathology that results in this is within the central nervous system. In the same way many head-shaking syndrome cases rub their noses – often to the point of moderate to severe skin damage – it is difficult of course to differentiate between the response to a genuine pruritus (true itch) and nerve ‘tingling’ or numbness both of which can induce rubbing (false pruritus).

Pruritus is not commonly associated with deep ulceration of the skin. In a few cases pain will result in ‘directed attention’ at the site (licking and chewing responses) but clinically this is recognizably different from pruritus. However, ulcers may be painful and may induce self-inflicted trauma suggestive of pruritus.

Often the pruritic horse will show a ‘pleasure response’ when the affected area is gently rubbed while the palpation/touching of a painful area will be resented and the animal will show aversion behaviour. The horse that exhibits the rub-pleasure response in the absence of any defined cause usually has an underlying hypersensitivity problem.

Pruritus is a particular feature of parasitic infestations and allergic skin inflammation. It can also arise from hypersensitivity reactions of immediate or delayed responses. It may be due to a primary skin disease, usually related to insect bites, It may be related to immune-mediated diseases such as pemphigus foliaceus or to a wide variety of bacterial, fungal or parasitic diseases. It may also be due to direct irritation by chemicals or to photoactivated dermatoses. More rarely in the horse it may be a manifestation of a systemic disease – the paraneoplastic syndrome, for example, often includes episodes or persistence of pruritus. In the case of hepatocutaneous disease the itch may be less easy to explain – it may have a central or local origin.

Pruritus arises as a result of either physical skin irritation (such as occurs with ectoparasitic infestation, e.g. Werneckiella (Damalinia) equi spp. lice) or superficial skin irritation (such as occurs with mange mites, e.g. Chorioptes spp./Sarcoptes spp.), or as a result of an inflammatory response. The causes of an inflammatory response may be local or generalized, and in the former the responses can be local (restricted to the direct vicinity of the inciting cause) or can have a more widespread clinical effect. Thus an animal with a louse infestation may have no skin inflammation but severe pruritus can arise from the irritating effects of the movement of the parasites in the hair coat. Horses with chorioptic mange also itch and stamp (cardinal signs of limb pruritus in the horse) because of the irritation effects of parasite movement, but in this case the movement is much closer to the skin itself and the extent of movement of an individual parasite can be much more limited. Burrowing mites such as the sarcoptic mange mites have a dermal irritation effect and, while they do cause local inflammation, their movement is also responsible for the clinical responses. A single insect bite or sting may cause a prominent local inflammatory response but not all such responses are liable to induce pruritus (as opposed to pain). Even a small amount of venom may cause a serious systemic release of inflammatory mediators with systemic as well as (or without) dermatological signs including urticaria and possibly generalized pruritus. In the horse this response is somewhat less prominent than in other species.

Cutaneous infections may also cause self-itching – it is important to differentiate this from a pain response; some horses will bite or chew at a painful locus. Bacterial infections do rarely cause pruritus but the fungal infections (superficial dermatophytosis) or deep (mycetoma) are somewhat more likely to be pruritic. In the former case itch is not one of the main signs but gentle (and carefully protected) rubbing of the lesion may elicit the ‘pleasure’ response manifest by muzzle twitching, grimacing and arching of the back towards the site. Deep fungal conditions such as pythiosis (see p. 183) can cause enough irritation to cause severe self-trauma.

Although equine urticaria and most hypersensitivity reactions only rarely cause pruritus, insect bite hypersensitivity (IBHS) (most frequently due to Culicoides spp. hypersensitivity) is probably the commonest single pruritic disease. Horses suffering from even a single (or few) bites show a very significant extreme pruritic response. The response to masses of bites from the same insects in a non-sensitized horse can be very similar but is usually sporadic, more transient and more restricted anatomically to the preferred regions of insect activity.

The site of the itching is usually a really good indicator of the location of the problem. A horse affected by the spinose ear tick (Otobius megnini) or aural (Otodectes) spp. mites or the bites of the Simulium fly (see p. 210) or certain species of Culicoides may itch and worry at the ear and indeed an affected horse may develop a non-neurological head-shaking syndrome with rotatory movements of the head and ‘ear shaking’. A common symptom in equine practice is perineal itching. Here the differential diagnosis may include the insect bite hypersensitivity (‘sweet itch’) syndrome, lice (the tail base being one of the preferred sites for both the major species of louse), or oxyuriasis (due to the combined effects of adult worm activity in and around the anus and perineal skin as well as the presence of the eggs). There are several species of fly, such as Hippobosca equinum (see p. 210) and Haematobius spp., and some mosquitoes that prefer to feed at this site also. The physical presence of the insects may be enough to cause localized worry but there may also be some direct localized hypersensitivity responses.

Another quite common perineal or rump rubbing/’pruritic’ condition is associated with the accumulation of skin debris and grease in the intermammary region of mares. It is always therefore worth checking for this condition in a mare that rubs her rump region (Fig. 19.2).

Figure 19.2 This mare had been presented for investigation of perineal pruritus. A biopsy had been taken 3 days before referral presentation (left buttock site). The mare showed no other signs at other sites. Simply cleaning out her intermammary detritus resolved the issue. This pattern of pruritus is significantly different from that caused by insect bite hypersensitivity but is similar to that caused by Oxyuris equi infestation. However, in the investigation of pruritus no possibility should be ignored.

There are also a few conditions that are characterized by pruritus with minimal or at least easily overlooked reasons. For example, there are horses that have a psychogenic itch – these cases may be distracted from the ‘neurosis’ (see p. 331). A well-recognized form of this occurs in bored stallions where they develop a so-called ‘self-mutilation syndrome’; they will actively bite and chew at a defined location (often on the flank or stifle region). It is very important to investigate such cases very thoroughly because there are significant differences in management and treatment between the various diagnostic possibilities.

Investigation of the pruritic horse

The investigation will always involve a detailed history of the case and the specific history of the pruritus. As many horses will be presented in a chronic state, often having received all manner of medications and manipulations, obtaining an honest and complete history is sometimes very difficult. Usually the clinician will be able to consider the veracity of statements suggesting and reporting ‘acute onset’ when the skin is really thickened and lichenified! It is easy to be critical of this but it is far better to gradually extract the truth by careful questioning in a variety of ways than to directly confront the client.

A full general history should be obtained during which the presence of systemic disease or other chronic conditions and any concurrent medications that may mask or alter the clinical signs may be identified. For example, it might be possible to establish that the horse had been losing significant weight recently; the non-dermatological signs may be due to a second disease but they may be part of a wider syndrome. In the latter case the skin may be the best and possibly the only visible indication of a systemic disorder. A suggested list of preliminary questions is shown in Table 19.1.

Table 19.1 The significant aspects of the clinical investigation of a pruritic horse

1. Was pruritus the first sign? a Where was the first site affected? b Were lesions present before the itch or was the itch present before the lesion(s)? c Was the pruritus localized to one site or several defined sites or more general? 2. When did the pruritus first begin and how has it progressed since then? a Sudden/insidious onset b Gradual/rapid progression or static extent/severity c Alterations associated with management procedures/manipulations • Worse/better with different feeds or changes in management d Changes occurring naturally (seasonal/non-seasonal) e Changes occurring as a result of applied therapeutic measures 3. Are any exacerbating factors obvious? a Heat/cold b Exercise c Medications/feeds 4. What alleviating factors can be identified? (What makes it better?) a Management manipulations • Worse/better inside or outside b Medications 5. Are any other horses similarly affected? a Did they develop the signs at the same time or another time (before/after)? b Are any similarly affected horses in contact with each other or subjected to the same management? 6. Has the condition adversely affected the horse or not? a Affected prior to onset of pruritus b Affected after onset of pruritus

Possibly the most important historical step is to establish how long the horse has been itching and when, where and, if possible, why it started. An acute onset of generalized pruritus associated with a change in feed will clearly have a different implication from a recurrent summer seasonal onset closely related to turn-out. Aspects of contagion can be established from enquiry as to whether other horses in contact (directly or indirectly) are affected similarly.

A further fundamental question is related to the presence of a defined lesion prior to the onset of itching or whether any visible lesion actually developed after the pruritus. The latter may be due then to self-trauma and subsequent biopsy of this region may be very misleading (see Fig. 19.2). This can be very difficult to establish simply because the owner may not have examined the horse closely enough to detect a lesion before or soon after the horse started to rub or scratch the site. It is possibly unfair to expect owners to be able to answer this question but if it can be answered it is a big help.

The course of a pruritic lesion is unpredictable. It is well recognized in all species that a single focus of pruritus usually abates if the skin becomes inflamed – once the skin surface is broken and inflammation is induced the itch may either settle or at least reduce. Of course this may lead to superficial or in some cases deep infection and then the outward evidence may be masked or very different from the original or primary state.

As might be expected, a full dermatological examination must then be performed (see p. 25). This is particularly important because of the possibility of helpful signs in other body systems. An old horse affected, for example, by pituitary pars intermedia dysfunction (PPID/equine Cushing’s disease) may show characteristic features and this condition may suppress immune processes sufficiently for ectoparasites and bacterial skin diseases to develop. Failure to recognize the underlying primary condition may waste time, effort and money. It is often very helpful for the veterinarian to observe the responses that the horse shows; if this cannot be achieved within the normal time scale of a clinical visit a video recording taken by the owner may help enormously; there are ‘secret scratchers’ who only show the signs when they alone and others that only show the signs at night! Of course such a manifestation may be a strong indicator of possible causes also. A horse that rubs or scratches its legs and face when it is only in a stable may be exposed to biting or worrying parasites in the bedding.

As pruritus is simply a sign of many possible diagnostic options, further samples and diagnostic tests are commonly undertaken. The commonest overall cause of pruritus in the absence of a defined pre-existing lesion in the general population are the ectoparasitic conditions and so a common early test is the collection of brushings from both affected zones and from the animal generally (see p. 60).

Biopsy of pruritic skin lesions or areas affected by pruritus where no overt lesions are apparent is frequently disappointing. In the former case there may be too much secondary trauma and in the later the pathological evidence may be unremarkable or non-specific.

No diagnostic technique can be completely precluded from an investigation of the pruritic horse because some cases can arise from highly unusual disorders such as a cervical vertebral fracture (see p. 332) or a serious internal neoplasm. In some cases even rectal examination, ultrasonographic examinations, or radiography (conventional or computed tomography) may be justified.

Fortunately in some cases, such as insect bite hypersensitivity (IBHS/sweet itch) and atopy, a diagnosis can often be suggested by the detailed history alone. In the former the condition is highly seasonal and anatomically restricted (tail, mane and ventral midline most often), begins around 3–6 years, improves when the horse is brought inside and deteriorates each sequential year during the challenge season. In the latter, the onset is usually between 1 and 3 years, is much less anatomically restricted, is non-seasonal and is usually not improved by altered environmental management. In others, for example in Chorioptes spp. infestation, the clinical examination and further tests may help to establish the true cause. Sometimes the diagnostic process can be much more problematic and involved; for example, confirmation of an allergy may involve challenge/deprivation tests, skin or IgE-related blood tests.

There are, however, a few cases for which a working diagnosis cannot be achieved and these are clearly a problem. In these, test therapy may help to identify the type of pathology present and then some extrapolations can be drawn. For example, administration of an antihistamine or an analgesic may provide useful information whether they are effective at eliminating the itch or not.

A good working knowledge of the main and less common disorders associated with pruritus can help enormously. Table 19.2 and Fig. 19.3 outline the main diagnostic possibilities for the pruritic horse; there will, however, inevitably be some rare conditions that are not shown here.

Table 19.2 Differential diagnosis of pruritus

Figure 19.3 The relative prevalence of the various types of disease as a cause of pruritus in horses.

Alterations in hair quality and quantity (hair follicle disorders and alopecia)

Normal shedding of the body hair coat is governed by seasonal photoperiod factors. It is also true that other factors will alter the physical appearance and the length and density of the hair coat. Horses in very hot climates and those that are heavily rugged during winter months in cold climates do not usually grow a long winter coat. They will shed normally of course but the process is down-regulated by body and ambient temperature and the extent of photoperiodicity stimulus.

Alopecia is defined as the absolute loss of hairs or the reduction in hair length or diameter when the number of hairs per unit areas may be normal (Fig. 19.4). Alopecia can be congenital (and sometimes also hereditary), when it is termed hypotrichosis, or acquired. The name alopecia does not apply to the simple rubbing away of hairs to the extent of an apparently bald patch such as occurs when rugs or other tack/harness rub hairs away. In these cases the skin is normal and the hairs are themselves normal in number, density and quality (Fig. 19.5).

Figure 19.4 True alopecia. The hair density is very low and the hairs that are present are thin and shorter than the normal hair adjacent. (A) The mane and tail are largely spared. The apparently spared areas over the back and rostral areas of the face were easily depilated. Notice in this case that the hair loss is accompanied by scaling (seborrhoea) over the breast (B) and face (C) in particular – other changes are not always present. This was a case of pemphigus foliaceus.

Figure 19.5 This apparently bald patch over the breast and shoulders was easily explained by simple rubbing of a tightly fitted, heavy winter rug. This is not alopecia.

Alopecia can arise from a variety of primary and secondary diseases and is defined as a ‘deficiency of the hair coat’. It may be due to hair growth failure or to loss of hair. There is a significant difference between hair loss involving fracture of the shaft (stumps of hair fibres remain) and hair which is shed from the follicle, i.e. when the whole hair is shed.

Congenital hypotrichosis is very rare in horses but it does occur – of course there are some disorders that are hereditary and congenital where the alopecia becomes evident at a later age. There are some circumstances such as neonatal hypo­thyroidism and prematurity when an apparent hypo­trichosis/alopecia can be detected at birth but although these are therefore congenital they have no genetic foundation and are classified as acquired congenital disorders. Perhaps the best example of a true hereditary/genetic alopecia is the relatively common mane and tail dystrophy of the Appaloosa horse (see p. 245). Another syndrome of adult-onset facial hypotrichosis (often to the extent of complete hair loss) is recognized by clinicians but is poorly described (Fig. CD19 • 1A and B). There is no known aetiology and biopsies of the skin simply identify atrophic non-functional follicles.

Linear keratosis is another relatively well-recognized congenital (possibly heritable) cause of persistent alopecia. In disorders where there is a genetic reason for the alopecia the condition is most unlikely to improve and owners will need to be apprised of this.

Loss of hair without any other accompanying clinical signs such as pruritus, scaling, crusting, erosion or ulceration occurs in relatively few conditions (see Fig. 11.33). However, as these other clinical signs very frequently occur with loss of hair, they should always be considered as part of the hair loss syndrome. Acquired forms of alopecia have been divided into two groups depending on the cause and whether the hair will grow back once the condition has resolved (Stannard 2000):

Cicatricial alopecia

results when the hair follicles are completely destroyed by a pathological process such as physical, chemical or thermal injuries, infections or tumours and results in a complete and permanent alopecia. A typical example is a scar from a wound or chemical burn (Fig. 19.6 and Fig. CD19 • 2). This same effect is sometimes used to create identification marks on horses using thermal branding. The resulting alopecia and scarring enables firm identification to take place (Fig. 19.7 and Fig. CD19 • 3; see also Fig. 16.1A).

Figure 19.6 Scarring inevitably causes adnexal damage. Where a large wound occurs on the body trunk contraction limits the size of the scar and therefore the extent of the alopecia. This scar was the result of a chemical ‘burn’ during preparation for surgery.

Figure 19.7 This thermal burn resulted in a scar and a patterned alopecia that allowed permanent firm identification of this animal. Note that the alopecia is variable over the damaged skin.

Severe viral (see p. 129) or bacterial skin infections (see p. 141) and some tumour conditions such as the equine sarcoid (see p. 387) also cause localized alopecia in which there is seldom any recovery of hair growth.

In non-cicatricial alopecia

the hair is not permanently destroyed and will regrow once the instigating factors have been removed. So long as the hair follicles are uninjured or at least only mildly injured hair will regrow. There are many causes of this type of hair loss in horses including:

1. Traumatic injuries that result in epidermal and/or superficial dermal damage (as a result of either direct trauma, chemical or thermal injuries or self-inflicted trauma including the effects of pruritus and cutaneous ‘worry’). Even pressure applied to the skin under bandages, etc. can cause significant hair loss – sometimes with more overt epidermal or dermal damage but sometimes without these. Often there is a dramatic shedding of hair as a result of contact with urine, diarrhoeic faeces, saliva, wound exudate, etc.) (see p. 299).

2. Alterations in the function of hair follicles including several dystrophic conditions that incorporate the dramatic effluvium or gross shedding of hairs at defined stages in the growth cycle (see p. 346). Alopecia areata is also a good example of a sterile folliculitis resulting in localized or sometimes generalized alopecia (see p. 278).

3. Bacterial and fungal infections resulting in hair follicle suppression or hair shaft damage are important causes of alopecia – dermatophilosis, staphylococcal and streptococcal dermatitis and dermatophytosis are good examples of this type of response.

Abnormally long/dense hair coat

The hair coat quality and quantity varies widely between breeds and individuals. Most horses have a ‘typical’ pattern of hair growth with isolated whorls and increases and reductions in coat density at different sites. For example, the hair density on the side of the face is usually much less and the hairs are much shorter here than on the main body. Some horses have ‘unusual’ patterning of hair growth that can at first glance be misinterpreted as an abnormality. A good example is shown in Fig. 19.8, in which the lie of the hair creates an impression of abnormality. A brief examination will show that this is a normal healthy coat that has been present from birth. This is a relatively common occurrence but is very variable in extent.

Figure 19.8 (A) This Welsh pony gelding exhibited a very prominent patterning of a hair alignment over the neck and shoulder regions in particular. (B) Close examination showed the hair and skin were, as might be expected, totally normal.

There are individual horses that have hair length variations and some breeds that have longer hair coats than others. Some have isolated ‘tresses’ of longer hair in summer and these same sites usually have a normal length winter coat but sometimes a summer coat hair growth can be identified at these sites (Fig. 19.9).

Figure 19.9 (A) This pony regularly grew large numbers of isolated long ‘winter-type’‘tresses’ in its summer coat. (B) The hair was not noticeably abnormal in any way apart from its length. Although these areas were more obvious there was also a rather more diffuse, isolated distribution of long hairs over the body trunk and neck. The summer coat therefore lacked sheen/patina. In winter there was no detectable difference at these sites.

There are also some individuals that may have a very dense wavy, curly coat in winter and more normal hair coat in summer – the important point about all these animals is that they shed normally and usually have shown the same pattern of hair growth throughout their lives without any concurrent primary or secondary pathology. An interesting ‘curly coat’ genetic variation is being encouraged by some breed societies (see p. 233).

Sites of skin grafting can result in an abnormal hair growth pattern. The recipient site will adopt the characteristics of the donor site in terms of hair shedding and colour. The history and clinical features of these sites is easily recognized.

For all practical purposes the only disease that is characterized by acquired generalized hirsutism (overgrowth of hair) is pituitary pars intermedia dysfunction (PPID) (pituitary adenoma/equine Cushing’s disease) (see p. 322). This symptom is almost pathognomonic for the disease in older horses and occurs in a high proportion of cases.

Investigation of equine skin with either altered density or length of hair

As is usually the case, a full history will be very helpful. Indeed, in most of the major syndromes much of the differential diagnosis can be achieved directly from this. The full range of possible aetiological states also exists for cases showing hair loss and alteration in hair density and structure so it is in fact always wise to explore the history to the fullest possible extent. For example, diagnosis of a genetically based disorder occurring in a known specific breed, such as the mane and tail dystrophy condition in Appaloosa horses, can usually be assumed from the history and the physical appearance (Fig. 19.10). Of course such intuitive supposition can also be misleading. The loss of mane and tail hairs may simply be a matter of hair pulling by either another horse or even cattle (see Fig. 19.10A). Chronic ingestion of selenium (either in inorganic feed-supplement form, or in seleniferous plants and grains) may result in significant more-or-less symmetrical alopecia and hoof wall growth alterations (see Fig. 12.11). If the history includes dietary supplementation or the environmental conditions suggest that plant feeds might be involved, the process of diagnosis can be shortened dramatically. This also emphasizes the importance of understanding the local environmental conditions – are potentially toxic plants prevalent in the area and available to the horse? Has the horse received any abnormal nutrients? It is possible to draw effective diagnostic conclusions from the historical features and clinical appearance alone in most cases.

Figure 19.10 (A) This horse suffered from severe tail pulling by cattle in the same field. Once the cattle were removed the tail hair would regrow normally. This is false alopecia. (B) An over-tight tail bandage caused necrosis of the skin of the tail and much of its tail hair was shed. Regrowing hair was white but otherwise the individual hairs appeared normal. This is true cicatricial alopecia. (C) This Appaloosa gelding developed progressive thinning of his tail and mane. This is a congenital/hereditary condition and has no implication for the horse.

Having completed the history, a full clinical examination is important. The objective is to try to establish whether the hair loss is primary (true alopecia) or secondary (false alopecia). Skin rubbing by tack or harness or contact with walls and other solid objects can induce changes that closely resemble alopecia. Viewing the skin with an illuminated magnifying glass can usually confirm the nature of the problem. Furthermore, the correlation of the hair loss with obvious trauma is a key factor. Careful questioning can be very helpful (Table 19.3).

Table 19.3 Possible questions for the investigation of hair loss in horses

1. Has the alopecia been present from birth? If so was the foal otherwise normal? Congenital alopecia is usually associated with prematurity/dysmaturity, hypothyroidism or in rare cases congenital hypotrichosis. The possibility of congenital junctional disorders such as cutaneous agenesis, epidermolysis bullosa and heritable equine regional dermal asthenia can be considered where signs are obvious. 2. Has the horse been ill (febrile or non-febrile systemic disease) or had access to any possible toxic materials (such as selenium, mimosa, etc.)? Information on previous disease states is often very important. However, often there is no known/recognized/declared episode and so the answer can be a bit misleading. 3. Is there any correlation between the areas affected and the previous existence of any inflammatory or infectious process? Horses may develop alopecia at sites that have extensive oedema or localized infections – this applies particularly to the limbs but also occurs over developing abscesses and in areas that have body fluids such as plasma, pus, urine, diarrhoea, saliva in contact with the skin. 4. Was the hair loss preceded by pruritus? Hair loss preceded by pruritus might suggest that it is a secondary state and it is worth investigating causes of pruritus and establishing the nature of the hairs by using a trichogram (see p. 62). 5. Did pruritus develop after the hair loss or at the same time? Where hair loss precedes the development of pruritus, it is often safe to assume that the hair loss is the primary event. 6. Has any chemical wash or unusual skin dressing been used? Often it is possible to detect patterns of hair loss that are associated with applications of chemicals and in some cases simply wetting the skin can encourage infection such as Dermatophilus congolensis (see p. 156). 7. Did the alopecia start at one place and spread or did it develop simultaneously over several areas? Centrifugal ‘spread’ of alopecia is highly suggestive of infection – often fungal such as dermatophytosis (see p. 168). Simultaneous development of alopecia at several sites could of course be infectious also but in the absence of any other signs this may, for example, be typical of alopecia areata (see p. 278). 8. Is the alopecia restricted to any defined area? Loss of mane and tail hair has very different implications from loss of body hair because of the significant difference in growth patterns. Many alopecic disorders spare the mane and tail but some important ones such as selenium or heavy metal toxicity have a disproportionate effect on the mane and tail and possibly the hoof also. 9. Is the alopecia associated with normal skin or is the skin abnormally flaky (seborrhoeic, exudative) or are there palpable variations in the skin itself? In the former case alopecia areata might be considered – it is the most typical and symptomless defined primary cause of focal alopecia. Exudate and other body fluids are usually obvious but the alopecia can develop well after the event so that history is important. Variations in the skin (seborrhoea, micro-nodules or obvious thickening) are invariably detected clinically simply by palpation. Equine occult or verrucose sarcoid, for example (see p. 390), and the pemphigus conditions (see p. 264) are often associated with alopecia but the concurrent evidence is usually diagnostically very significant. 10. Is any other in-contact animal similarly affected? Where more than one animal has a similar state, contagious infection or common exposure to a toxic or contact insult should be considered. 11. Is there any obvious explanation for the hair loss? Rubbing of harness, rugs and contact with walls and trailer sides are often overlooked! Similarly chewing or licking of the skin by other in-contact animals occurs with some frequency. These are clearly false (secondary) hair loss conditions and should not be classified as alopecia (Fig. 19.12). Traumatic hair loss is usually obvious. Grazes and wounds, for example, are obvious; again this is not really alopecia. < div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Nutritional disorders Introduction Diagnostic/investigative procedures Iatrogenic and idiopathic disorders Stay updated, free articles. Join our Telegram channel Join Tags: Pascoes Principles and Practice of Equine Dermatology Jul 8, 2016 | Posted by admin in EQUINE MEDICINE | Comments Off on Syndromes in equine dermatology Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access