228 DISC

Veterinary Dermatology 2000, 11, 217223

Miscellaneous
Abstract This section includes clinical conditions which have unique characteristics which make them
unsuitable for inclusion in the rst six sections. The clinical description, aetiology and histopathologic ndings
of the unusual ear lesion, aural plaques, are described. Dermatoses complicated by, or caused by,
photosensitivity are discussed in regards to their aetiology and pathogenesis as well as clinical features. The
suggestion that photosensitization plays a role in the development of the lesions seen in pastern
leukocytoclastic vasculitis is made. This section ends with an in depth discussion of the various causes of
the nonspecic clinical entity known as `grease heel', a chronic and often painful condition of the equine foot.
Keywords: aural at warts, grease heel, pastern leukocytoclastic vasculitis, photo-induced dermatoses,
scratches.

AURAL FLAT WARTS

(Aural plaques)
General considerations
1 This is a common skin disease of horses.
2 There is no known breed or sex predilection.
Aetiology and pathogenesis
1 The aetiology of this condition has recently been
shown to be a papilloma virus.1,2
2 Black ies (Simulium spp.) may serve as a vector
for the virus.3

does not lead to the induction of resolution of

remaining lesions.
PASTERN LEUKOCYTOCLASTIC
VASCULITIS
General considerations
1 Pastern leukocytoclastic vasculitis is a specic

Ref start

Clinical signs
1 Lesions consist of one to several grey or white
plaques involving the inner surface of the pinna
(Fig. 1).
2 They tend to coalesce.
3 Lesions occasionally occur around the anus, vulva
and inguinal region.4
4 The plaques appear to be asymptomatic in most
horses but can cause pruritus in some animals.
5 Lesions usually persist indenitely.
Histological ndings
1 Compact hyperkeratosis, parakeratosis and severe
regular hyperplasia of the epidermis is noted (Fig. 2).
Diagnosis
1 The disease has a characteristic clinical appearance.
2 In horses that are exhibiting pruritus or head
shaking, there should be a thorough search for other
causes of ear irritation.
Clinical management
1 Aside from the unsightly appearance of this
condition, it is of little consequence.
2 A variety of topical medications have been used
without success.
3 In young horses, lesions may spontaneously
regress. Surgical resection of a few of the lesions
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Ahed
Bhed
Ched
Dhed
Ref marker
Fig marker
Table
marker
Ref end

Figure 1. Aural at warts. Coalescing white plaques on the inner

surface of the pinna (Case material: Stannard).
217

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A. A. Stannard

Figure 2. Aural at warts. Compact

hyperkeratosis and regular hyperplasia
of the epidermis. (H & E.
Magnication636.5.)

clinico-pathological entity unique to the horse that

aects only unpigmented distal extremities.5
2 The disease is relatively common, aects mature
horses and there is no known sex predilection.
3 The only breed predilection relates to the frequency
of nonpigmented extremities. The clinical signs
suggest that it is photo-activated.6
4 The disease primarily occurs during the summer
months in regions with abundant sunlight.
Aetiology and pathogenesis
1 This is believed to be a vasculitis.
2 The pathogenesis of the vasculitis is uncertain. In a
few horses, direct immunouorescence studies have
demonstrated deposition of IgG and/or the C-3
portion of complement in the walls of aected
vessels. Whether this represents evidence of an
immune-complex disease or is simply nonspecic
deposition remains to be determined.
3 The restriction of the lesions to the lower legs requires
explanation. If the disease does involve circulating
immune-complexes, their deposition in this region may
reect regional dierences in the vasculature.
4 Percutaneous absorption of some compound/agent
or a triggering lesion cannot be ruled out.
5 The restriction of lesions to unpigmented skin in the
vast majority of cases suggests a role of ultraviolet
radiation in the pathogenesis. However, the disease is
not a form of photosensitization. Aected horses have
had no known exposure to recognized photosensitizing compounds and their liver function is normal.
6 Some of these cases may be drug induced.

Figure 3. Pastern leukocytoclastic vasculitis. Haemorrhagic papular to

nodular lesions on leg lacking pigment (Case material: Stannard).

Clinical signs
1 The disease is almost exclusively limited to lower
extremities that lack pigment (Figs 3 and 4).The
lesions are usually limited to one leg even though
multiple extremities lack pigment. Rarely, horses with
pigmented legs have been seen with identical lesions
both clinically and histologically.

2 The disease occurs sporadically, only aecting an

individual animal. Other susceptible horses on the
premises, i.e. those with nonpigmented extremities,
remain unaected.
3 The lesions are usually multiple and reasonably
well demarcated. The medial and lateral aspects of
the pastern are the favoured sites.

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228 DISC
Miscellaneous

Figure 4. Pastern leukocytoclastic vasculitis. Erosions, supercial

ulceration and oedema of an aected limb (Case material: Stannard).

4 In the initial acute phase, erythema, oozing and

crusting predominate.
5 Erosions and supercial ulcerations may develop
(Fig. 5). An important, but not consistent, feature of
the disease is oedema of the aected limb(s). In
general, the oedema is more extensive than would be
expected with the degree of skin involvement.
6 In chronic cases the lesions usually develop a rough
`warty' surface that resists mechanical removal.
7 The lesions are painful rather than pruritic.7
Histological ndings
1 The primary changes involve small vessels in the
supercial papillary dermis (Fig. 6).
2 Acute changes include leukocytoclastic vasculitis,
vessel wall necrosis, and thrombosis (Fig. 7).
3 Chronic changes include thickening and hyalinization of the vessel walls (Fig. 8).
4 The epidermis exhibits a variety of hyperplastic
and degenerative changes depending on the stage of
the disease (Figs 9 and 10). In chronic cases,
papillomatosis is a relatively common feature and
reects the `warty' clinical appearance.
5 The dermis contains a mixed perivascular inltrate.
It must be stressed that the vascular changes, especially
the acute ones, are not uniform nor necessarily
widespread and thus can be missed or overlooked.

219

Figure 5. Pastern leukocytoclastic vasculitis. Both rear legs in this

chronic case have developed oedema (Case material: Rosenkrantz).

6 The failure to demonstrate an active vasculitis in

many cases leads some to prefer the term `vasculopathy'.
Diagnosis
1 Pastern leukocytoclastic vasculitis must be considered in the dierential diagnosis of any inammatory
skin disease limited to a nonpigmented extremity.
2 The major dierential diagnoses are the conventional forms of photosensitization, especially contact
photosensitization due to various plants (phytophotodermatitis). A careful history should be taken for
possible exposure to incriminated vegetation.
3 Liver function tests will rule out hepatogenous
photosensitization.
4 When the leg is swollen, all possible dierentials
for leg oedema should be considered.
Clinical management
1 Management consists of preventing further exposure of the aected area(s) to ultraviolet radiation
and reducing the inammation. Simple avoidance of
sunlight is usually not sucient.
2 Ideally, the patient should be stalled during the
daylight hours. Alternatively, leg wraps may be used.
3 Systemic administration of corticosteroids is required to reduce the inammation. Relatively large
doses of corticosteroids are given daily for the rst
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A. A. Stannard

Figure 8. Pastern leukocytoclastic vasculitis. In chronic lesions,

aected vessels are thick walled and may contain nuclear debris and
extravasating erythrocytes (arrow). (H & E. Magnication6226.)

Figure 6. Pastern leukocytoclastic vasculitis. Lesions aect

supercial capillaries and venules. Note the acute haemorrhage
from the damaged vessel. (H & E. Magnication6103.)

Figure 7. Pastern leukocytoclastic vasculitis. Fibrinoid vasculitis in

an acute lesion. (H & E. Magnication6170.)

two weeks. The dosage is then gradually reduced over

the following two to four weeks. Topical or systemic
corticosteroid and antibiotic preparations are of
limited value.
4 In the acute phase, symptomatic therapy may
include clipping any excess hair in the region,
hydrotherapy to facilitate gentle removal of crusts,
debris and exudate.
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Figure 9. Pastern leukocytoclastic vasculitis. Acute lesions may be

heavily crusted. (H & E. Magnication627.)

Figure 10. Pastern leukocytoclastic vasculitis. In chronic lesions,

the low power view is often unremarkable. (H & E.
Magnication627.)

5 Irritating topical preparations should be avoided.

6 The majority of cases, if treated as outlined, will
respond favourably and require no further therapy.
7 Occasionally, the lesions will recur following
cessation of corticosteroid therapy. If so, the treatment regimen should be repeated. In rare instances
the disease has recurred in subsequent year(s).

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Miscellaneous
PHOTO-INDUCED DERMATOSES
General considerations
1 Actinic dermatoses are the result of ultraviolet
radiation. For cutaneous damage to occur, the UV
radiation must be absorbed. This is greatly facilitated
by a lack of pigmentation and hair coat.
2 Skin disease can be produced by either acute
(hours) or chronic (years) exposure.
3 The primary problem associated with chronic
exposure is the development of preneoplastic and
neoplastic processes.
4 Actinic dermatoses resulting from acute exposure
can be divided into those in which the damage:
a. results from excessive exposure and is expected
(i.e. sunburn)
b. results from normal exposure and is greater
than expected (i.e. photosensitization).
5 Photodynamic agents can reach the skin either via
the circulation (systemic) or by percutaneous absorption (contact).
6 Photodynamic agents absorb specic wavelengths
of light, become activated and pass the extra energy
to the surrounding cells, resulting in their damage.
7 Supercial blood vessels and the epidermis are
primarily aected.
8 There are two basic types of photodynamic agents,
phototoxic and photoallergic.
a. There is no immunological mechanism involved
with phototoxic agents, i.e. they are capable of
producing photosensitization in nearly all animals
under suitable conditions. The vast majority of
photosensitization in animals is of this type.
b. For photosensitization to occur with photoallergic agents, the animal must be sensitized to the
compound. Such cases are well documented in
humans, but poorly understood in horses.
Aetiology and pathogenesis
1 Three features are basic to all types of photosensitization:
a. The presence of a photodynamic agent within
the skin.
b. A concomitant exposure to a sucient amount
of certain wave lengths of light.
c. Cutaneous absorption of this ultraviolet radiation.
2 Systemic photosensitization
a. Primary
i In this type, the photodynamic agent is ingested
and then absorbed directly from the digestive
tract, reaching the skin via the circulation.
ii A classic but rare example is seen in horses
grazing pastures containing Hypericum spp. (St
John's wort) which contains a photodynamic
agent, hypericin.
b. Hepatogenous.
i Phylloerythrin is a degradation product of
chlorophyll that is formed in the alimentary
tract of herbivores.
ii Some phylloerythrin is normally absorbed by
the portal system and subsequently excreted in

221

the bile (enterohepatic circulation).

iii When liver function has been deranged, the
phylloerythrin, which is a photodynamic agent,
accumulates in the animal's tissues.
1 Contact photosensitization
a. Most recognized cases of contact photosensitization have occurred in horses grazing in pastures
containing clover. Why clover plants sometimes
produce a photodynamic agent is unknown.
Clinical signs
1 The most severe lesions will involve unpigmented
skin that lacks hair (lips, eyelids, etc.).
2 The lesions can involve lightly pigmented, haired
regions. The most severe lesions, however, still occur
in the nonhaired, nonpigmented skin.
3 In hepatogenous and photoallergic types of photosensitization the occurrence of the disease is sporadic
(unless dealing with an epidemic of liver disease).
4 In contact photosensitization, only areas of contact
are involved. Lesions tend to be limited to nonpigmented portions of the lower extremities and the muzzle.
5 The lesions vary tremendously from urticarial to areas
of erythema and scaling with severe necrosis of the skin.
Histological ndings
1 These lesions are rarely biopsied.
2 Chronic lesions may have a lymphocytic perivascular dermatitis, epidermal hyperplasia and hyperkeratosis, with serous crust formation.
3 Apoptotic keratinocytes, sometimes known as
`sunburn' cells may be present.
Diagnosis
1 Any inammatory disease that primarily involves
the unpigmented areas of the body is suspect.
2 Involvement of some pigmented areas can occur.
3 Liver function tests are advised on all suspect cases
of photosensitization.
Clinical management
1 The primary goal is to prevent further damage and
involves:
a. Remove the animal from exposure to sunlight.
b. Prevention of re-exposure to the photodynamic
agent:
i change feed/pasture,
ii drugs?
2 Symptomatic therapy
a. Reduce inammation with corticosteroids.
This is of greatest value if utilized early in the
course of the disease.
GREASE HEEL/SCRATCHES
General considerations
1 The term `grease heel' is used by veterinarians and
laymen to refer to a variety of inammatory skin
conditions involving the horse's pastern region.
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A. A. Stannard

2 Unfortunately, many believe `grease heel' to be a

specic disease entity.
3 This partially explains the present confusion
regarding the `disease's' pathogenesis and the inconsistency of response to any given form of therapy.
Clinical signs
1 Regardless of the cause, most of the diseases have
similar clinical features.
2 Frequently only a single extremity is involved and
more often the rear leg(s). There is a tendency for
unpigmented skin to be predisposed.
3 The initial lesions may involve the posterior aspect
of the pastern region. With time, the lesions may
extend proximally and anteriorly involving the front
of the pastern and fetlock regions (Fig. 11).
4 The nature of the lesions varies depending on the
cause, duration and past therapy. Erythema, oozing
and alopecia are frequently the rst signs. Crust
formation is common. In diseases with a vasculitis as
the underlying cause, ulceration is common. With
chronicity the skin becomes thickened and, due to the
constant exion in this region, ssures may develop.
5 The lesions are frequently painful and may result in
lameness.
6 A sequela in draft breeds involves broblastic
proliferation in the area of damage leading to
multifocal circumscribed masses. These have been
referred to as `grapes.'
Underlying causes
1 Contact dermatitis
a. Primary irritant and allergic contact dermatitis
may involve the pastern region.
b. The vast majority of contact dermatitis in horses
is of the irritant type.
c. Chronic exposure to moisture is the most frequent
cause (wet bedding, muddy pastures, etc.). Draft
breeds with long hair in the fetlock and pastern
region are predisposed due to prolonged retention of
the moisture and maceration of the skin.
d. Most cases of contact dermatitis can be
diagnosed on the basis of the medical history,
environmental conditions and the fact that all four
limbs are usually involved.
2 Pastern folliculitis/pyoderma are caused by two
types of bacterial infections: Staphylococcus aureus
and Dermatophilus congolensis.
a. Staphylococcal infection is characterized initially by a papular eruption. Frank pustules are
rarely seen. A denitive diagnosis requires skin
biopsies for bacterial culture. Smears and cultures
of surface exudate and crusts are dicult to
interpret because of contamination.
b. Dermatophilus congolensis is the causative agent
of the second type of bacterial infection causing `grease
heel'. Circumstances must be present to provide
constant/frequent wetting of the aected areas.
Microscopic examination and/or cultures of crusts
should reveal the organism. It has been suggested that
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 217223

Figure 11. Grease heel. Typical chronicity of grease heel with

involvement of the anterior as well as posterior region of the foot
(Case material: Stannard).

dermatophilosis may be limited to nonpigmented

areas and thus be confused with photosensitization.
3 Dermatophytosis lesions, on rare occasions may be
limited to the pastern region. Denitive diagnosis
requires visualization and/or isolation of the causative organism. Biopsy and/or fungal cultures are
usually necessary.
4 Chorioptic mange
a. Long hairs in this region predispose draft horses
most commonly to Chorioptes infestation.
b. The condition is very pruritic and aected horses
are constantly rubbing the area and stamping their feet.
c. The diagnosis is made based on the breed
involved, the pruritus, the contagious nature of
the disease and the relative ease with which the
mites are found.
5 Photosensitization. Both systemic and contact
forms of photosensitization may involve the pastern
region in horses with white extremities. In contact
photosensitization only the muzzle and lower extremities are involved. Exposure to certain clover
pastures at specic times of the year is the most
frequently reported cause of equine contact photosensitization.
6 Pastern leukocytoclastic vasculitis (photoaggravataed vasculitis).
a. This is a poorly understood syndrome discussed
earlier in this section.
b. This syndrome should be considered in any case
of `grease heel' which is limited to nonpigmented
extremities and a conventional form of photosensitization cannot be documented.
c. This apparent disease entity may be responsible
for the majority of cases of `idiopathic grease heel'
that aect unpigmented extremities.
7 Idiopathic pastern dermatitis.

228 DISC
Miscellaneous

223

a. There will be many cases of `grease heel' in which

a more denitive diagnosis can't be made. It would
appear appropriate to simply call them idiopathic
pastern dermatitis, admit defeat and treat them
symptomatically. Using the term `grease heel' would
imply you have made a denitive diagnosis!

6 Simple cleansing and protective measures combined

with systemic corticosteroid therapy may be the best
approach to many cases of idiopathic grease heel.

Diagnosis
1 A complete medical history is necessary.
2 Liver function tests are indicated in any case in which
the lesions are limited to unpigmented areas of skin.
3 Dermatophilus preparations and fungal cultures
may be of value on occasion.
4 Biopsies are indicated in any unusual or refractory
case of `grease heel'. The skin biopsies can be
submitted for conventional histopathology, direct
immunouorescence, bacterial and fungal cultures.

1. Williams, A.M. Papillomatosis: warts and aural

plaques. In: Robinson, N.E. ed. Current Therapy in
Equine Medicine 4. Philadelphia: W.B. Saunders, 1997:
38990.
2. Fairley, R.A., Haines, D.M. The electron microscopic
and immunohistochemical demonstration of a
papillomavirus in equine aural plaques. Veterinary
Pathology, 1992; 29: 7981.
3. Perris, E.E. Parasitic dermatoses that cause pruritus in
horses. Veterinary Clinics of North America Equine
Practice 1995; 11(1): 1128.
4. Fadok, V.A. Update on four unusual equine
dermatoses. Veterinary Clinics of North America
Equine Practice 1995; 11(1): 1067.
5. Logas, D.B., Barbet, J.L. Diseases characterized by
ulceration, exudation, and crusting of the distal
extremities. In: Colahan, P.T., Merritt, A.M., Moore,
J.N., Mayhew, I.G. eds. Equine Medicine and Surgery
5th edn, St. Louis: Mosby, 1999: 192931.
6. Stannard, A.A. Photoactivated vasculitis. In:
Robinson, N.E. ed. Current Therapy In Equine
Medicine 2nd edn, Philadelphia: W.B. Saunders, 1987:
pp 6456.
7. Pascoe, R.R.R., Knottenbelt, D.C. Manual of Equine
Dermatology. London: W.B. Saunders, 1999.

Clinical management
1 Correct therapy obviously depends on the disease
involved.
2 Crusts should be removed and the aected area
thoroughly cleaned.
3 Further exposure to moisture, irritants and sunlight (in cases in which a photosensitive component is
thought to exist) should be avoided.
4 Above all, do no harm! Many of the concoctions
recommended are irritating astringent and/or caustic
compounds. Topical preparations with anti-inammatory, antibacterial and antifungal activities are
frequently utilized.
5 Vigorous systemic corticosteroid therapy is indicated
in cases where a vasculitis is the primary problem.

REFERENCES

Zusammenfassung Dieses Kapitel umfat klinische Beschwerden, deren einzigartige Eigenschaften eine
Einbeziehung in die ersten sechs Kapitel nicht erlaubt. Die klinische Beschreibung, die Atiologie und die
histopathologischen Befunde einer ungewohnlichen Ohrmuschelerkrankung, ``aural plaques'', werden
beschrieben. Dermatosen, die durch Lichtempndlichkeit erschwert oder verursacht werden, werden bezuglich
ihrer Atiologie und Pathogenese sowie ihrer Symptome diskutiert. Es wird vorgeschlagen, dass
Lichtempndlichkeit eine Rolle in der Entwicklung der Lasionen spielt, die in der leukozytoklastischen
Fesselvaskulitis gesehen werden. Dieses Kapitel endet mit einer ausfuhrlichen Diskussion uber die verschiedenen
Ursachen des unspezischen, chronischen und haug mit Schmerzen verbundenen klinischen Syndroms des
Pferdefusses, das als Fesselekzem oder Mauke bekannt ist. [Stannard A. A. Miscellaneous. (Verschiedene andere
Erkrankungen.) Veterinary Dermatology 2000; 11: 217223.]
Resume Ce chapitre comprend des maladies qui presentent des caracteristiques uniques, qui justient de ne
pas les inclure dans les six premiers chapitres. L'auteur decrit les aspects cliniques, etiologiques, et
histopathologiques des lesions atypiques des oreilles, les plaques auriculaires. Les dermatoses compliquees
par ou dues a une photosensibilisation sont egalement envisagees, en fonction de leur etiologie et de leur
pathogenie, ainsi que de leurs signes cliniques. L'auteur suggere qu'une photosensibilisation est responsable
de l'apparition de lesions de vasculite des paturons. Ce chapitre se termine par une discussion detaillee des
causes possibles du `grease heel', une entite clinique non specique, caracterisee par des lesions chroniques et
douloureuses des pieds du cheval. [Stannard A. A. Miscellaneous. (Divers.) Veterinary Dermatology 2000;
11: 217223.]
Resumen Esta seccion incluye entidades cl nicas con caracter sticas unicas que las hacen inclasicables en las
seis secciones anteriores. Se detalla la descripcion cl nica, la etiolog a y los hallazgos histopatologicos de la
lesion inusual de la oreja y las placas. Se discuten las dermatosis complicadas o causadas por la
fotosensibilidad con respecto a su etiolog a y patogenesis as como sus caracter sticas cl nicas. Se sugiere que la
fotosensibilizacion juega un papel en el desarrollo de las lesiones observadas en la vasculitis leucocitoclastica
de la cuartilla. Esta seccion naliza con una discusion en profundidad sobre las diferentes causas de la entidad
cl nica conocida como `talon sensible' (Grease Heel), una enfermedad cronica y a menudo dolorosa del pie
equino. [Stannard A. A. Miscellaneous. (Miscelanea.) Veterinary Dermatology 2000; 11: 217223.]
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