222 DISC

Veterinary Dermatology 2000, 11, 163178

Immunologic diseases
Abstract Selected equine cutaneous diseases for which there is strong evidence of an immunological
aetiology are discussed in this section. The reactive disorders of urticaria, Culicoides hypersensitivity,
erythema multiforme, drug eruptions and systemic granulomatous disease are included. The autoimmune
diseases of the horse with cutaneous manifestations (pemphigus foliaceus, pemphigus vulgaris, bullous
pemphigoid and cutaneous lupus erythematosus) are discussed. The clinical signs and diagnostic features of
these immunologically induced equine dermatoses are dened, and the challenges in making a denitive
diagnosis and managing the clinical signs are conrmed.
Keywords: Culicoides, drug eruption, erythema multiforme, hypersensitivity, lupus, pemphigus, urticaria

URTICARIAL DISEASES
General considerations
1 Among all the species of domestic animals urticaria
is most common in horses.
2 It is most important to remember that urticaria is
not a diagnosis, but rather a clinical skin lesion
representing many causes. Nevertheless, it is usually
discussed as a single entity.
3 Urticarial diseases and syndromes vary in severity
from the minor and inconsequential to systemic
problems of a life-threatening nature.
Aetiology and pathogenesis
1 The basic pathogenesis of urticaria is presumed to
be due to the degranulation of mast cells followed by
the liberation of chemical mediators of inammation,
resulting in the subsequent development of dermal
oedema. Urticaria may result from immunological
and nonimmunological causes.
2 Regarding immunological causes, most involve a
hypersensitivity response. In almost all such cases
the antigen/allergen is thought to reach the skin via
the systemic route. The antigen reaches the
systemic circulation usually via injection (drugs),
ingestion (chemicals, feed), or possibly via inhalation or percutaneous penetration (chemicals, pollens, moulds, etc.). `Contact urticaria' is believed to
be rare.
3 Allergic urticaria is classied into the following
categories:
a. Drug eruptions (all chemical compounds can be
considered `drugs'; routine prophylactics, such as
deworming agents should not be ignored)
b. Insect allergies (including mosquitoes and chiggers)
c. Food allergies
d. Atopic disease
e. `Contact' allergy (Type I) is very rare and not
analogous to allergic contact dermatitis (Type IV).
4 Regarding nonimmunologic causes, most involve a
`physical trigger' The three most common causes are:
a. Dermatographism essentially a pressure urticaria
b. Cold urticaria
# 2000 Blackwell Science Ltd

c. Exercise induced urticaria

5 Most urticarias are idiopathic.
Clinical signs
1 The characteristic lesion is a wheal a at topped
papule/nodule with steep-walled sides. It is the
result of localized transient oedema within the
dermis. Because of the lesion's oedematous nature,
it pits on pressure.
2 Many wheals have a slightly depressed centre
giving them an annular conguration.
3 The onset of the lesions is acute to peracute with
the wheals developing within minutes to hours after
exposure to the trigger.
4 The size of the individual wheals can vary
considerably. Based on their size, a clinical classication can be used:
a. Conventional: The size of the wheals varies
from 23 mm to 35 cm in diameter (Figs 1 and 2).
b. Papular: The size of the wheals is rather uniform
and small, and varies from around 36 mm in
diameter. Papular urticaria frequently is associated
with biting insects, in particular, mosquitoes.
c. Giant: Either single or multiple wheals that are
very large up to 2040 cm in diameter. There is
no particular signicance associated with this type
of urticaria as compared to conventional urticaria.
5 Aside from size, there are several other varieties of
urticaria.
a. Oozing (transudative/exudative) urticaria: In
cases of severe dermal oedema, especially in the
upper dermis, serum may ooze to the skin surface
and mat/crust the hair coat. This is in contrast to
typical urticaria in which the skin surface appears
normal. The serum transudation may mask the
urticarial nature of the lesions suggesting other
processes, e.g. suppuration (pyoderma). In areas
where the skin is tightly adherent to the underlying
tissues, e.g. the face, alopecia may follow oozing
urticaria and the eruption be mistaken for pyoderma
or dermatophytosis. Crusting can be the presenting
clinical sign in some cases of oozing urticaria.
b. Gyrate or polycyclic urticaria: This form of
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A. A. Stannard

Figure 1. Urticaria. Urticarial lesions on the face of horse (Case

material: University of Florida).

Figure 2. Urticaria. Wheals on the trunk of same horse as in Fig. 1.

Thought to be drug (butazolidine) induced (Case material:
University of Florida).

urticaria has erroneously been referred to as the dermal

form of `erythema multiforme'. Drug reactions are a
common cause of this form of urticaria. This eruption,
the gyrate form, can persist for months.
c. Angioedema (angioneurotic oedema). This is an
oedematous lesion similar in pathology and pathogenesis to urticaria, except the oedema involves large
areas of subcutaneous tissues. The lesions are much
more diuse because there is no localization of
oedema in the dermis. Angioedema usually involves
the head and/or the extremities and signies a more
systemic and serious disease than urticaria.
Histological ndings
1 Dermal oedema is usually severe (Fig. 3), but may
be mild in chronic cases (Fig. 4).
2 There is moderate to severe supercial and/or deep
perivascular dermatitis. In some lesions, inammation may be diuse.
3 Most inltrates are primarily eosinophilic; others
have a fairly large lymphocytic component (Fig. 5).
Whether this merely represents age of the lesion
biopsied or has correlation to the aetiology or
pathogenesis is unknown. Some wheals have little
inammation. The epidermis is unaected in most
cases of urticaria.
4 The exception is in the case of `exudative oozing'
urticaria where the epidermis exhibits intra- and
intercellular oedema leading to microvesiculation
(Fig. 6). These vesicles are often subcorneal in location.
5 Extensive subepidermal oedema may lead to
subepidermal vesiculation.
Diagnosis
1 The diagnosis of urticaria is usually obvious based
on the acute onset of typical lesions.
2 When the character of the lesions is questionable,
the most important criterion is the presence of pitting
oedema.
3 Special characteristics of the lesions should be
noted, especially angioedema, papular lesions and
gyrate lesions.
4 Currently, the value of biopsies for histopathology
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 163178

Figure 3. Urticaria. In this example of acute urticaria, the dermal

oedema is extreme, causing marked separation of the dermal collagen
and secondary epidermal vesiculation. (H & E. Magnication660).

is uncertain, but it may be helpful in dierentiating

cases of dermatophytosis and pemphigus foliaceus.
5 The medical history is the most important tool for
determining the cause. Is this the rst episode? The
number of episodes and seasonality should be noted.
A complete drug history is mandatory especially
regarding medications that have been given in the
past two weeks. In addition to drug usage, an attempt
should be made to associate the onset of urticaria to
other events (especially in recurrent/chronic cases)
such as exercise, `cold weather', etc.
6 Dermatographism is easily determined by `writing'
on the horse with a blunt instrument (e.g. haemostat
tip, ball-point pen with the cap) putting a fair degree
of pressure on the skin. A positive reaction is

222 DISC
Immunologic diseases

Figure 4. Urticaria. In the late phase of an urticarial reaction,

oedema is inapparent. (H & E. Magnication6163).

165

Figure 5. Urticaria. The inammatory reaction is typically eosinophilic

and lymphocytic, depending on the duration of the lesions. Some
lesions are not inammatory. (H & E. Magnication6176).

indicated by the development of a line of urticaria at

the site of the pressure line within 15 min.
7 Cold induced urticaria can be diagnosed by
placing an ice cube on the skin for several minutes
and watching for the development of urticaria within
15 min.
8 Specic evaluation for atopic disease involves
intradermal skin testing and/or serum tests for
antigen-specic IgE (RAST or ELISA). This is
usually done only if there is a negative drug history,
a duration of greater than 8 weeks and all other
causes are ruled out. At this time serum IgE testing in
the horse should be interpreted with caution as the
cross reactivity with IgG has not been thoroughly
evaluated.1
9 Food allergies are evaluated by elimination diets
and subsequent challenge with suspected feed or
feed additive.
10 Urticarial lesions can often precede more classical
pemphigus foliaceus and thus this disease may be
considered amongst the dierentials.
Clinical management
1 The initial few episodes of urticaria are usually
treated with short courses of systemic corticosteroids.
2 Recurrent urticaria warrants a diagnostic evaluation. Presumably all known drugs/chemicals have
been discontinued or eliminated. Food elimination is
pursued rst. A complete feed change is instituted,
e.g. if on oat hay, then alfalfa hay is used or vice
versa. Only one food item is used (no grain, etc.). If
there is no improvement within three weeks, then
another feed change is done for an additional three
weeks. After two complete feed changes, each lasting
three weeks, food allergy can probably be eliminated
as the cause of the urticaria.
3 Urticaria lasting eight weeks or longer is classied
as `chronic urticaria'. The next diagnostic step
involves testing for atopic disease using intradermal
skin testing and/or in vitro serum testing for antigen
specic IgE. Depending on the results of these tests,
hyposensitization therapy may be indicated.2
4 Long-term medical management of persistent

Figure 6. Urticaria. Vesicular lesions occur in so-called `oozing'

urticaria. (H & E. Magnication6241).

urticaria involves the administration of corticosteroids and/or antihistamines.

a. Oral administration of prednisone or prednisolone at the lowest possible dose on alternate days is
the method of choice.
b. The antihistamine of choice is oral hydroxyzine
hydrochloride.2 It is a teratogen and it cannot be
used in pregnant mares. Initially, it is given at a
dose of 600 mg horse71 orally thrice daily.
Remission should be noted within 3 or 4 days.
The dose is then gradually reduced to the
minimum maintenance dose needed to keep the
horse symptom free. First the interval is decreased
to twice daily and then the individual doses are
reduced. The only major adverse eects are either
slight sedation, or on occasion, hyperactivity.
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A. A. Stannard

CULICOIDES HYPERSENSITIVITY
(Queensland itch, sweet itch, kasen, dhobie itch)
General considerations
1 This is a commonly encountered skin disease of
horses throughout the world and is known by a wide
variety of names.
2 The disease is allergic in nature and its occurrence
is sporadic, i.e. usually only one animal in a group
will be aected.
3 The disease is rare or nonexistent in horses under
one year of age. The initial age of onset usually
occurs between 2 and 4 years of age.
4 There is evidence of a hereditary predisposition to
develop hypersensitivity.
5 There is no apparent sex predilection.
Aetiology and pathogenesis
1 In years past, Culicoides hypersensitivity (CHS)
erroneously was associated with an infection with the
larid nematode, Onchocerca cervicalis.
2 The CHS results from the development of a
hypersensitivity to the bites of several dierent
Culicoides spp. (biting midges, `no-see-ums'). Culicoides are tiny winged insects usually less than 2 mm
in length. They breed in standing water and have a
limited ight range (12 km). Only the female
Culicoides feeds, usually during the early evening
and early morning hours. Culicoides are most active
during hot, humid and still environmental conditions.
3 Horses can become hypersensitive to other insects
such as Simulium spp., stable ies, mosquitoes
and others.
Clinical signs
1 Initially the disease is seasonal and often rst
appears in the spring, worsens in the summer and
nally regresses in fall. This is dependent on the
geographical location and climate conditions.
2 The disease is recurrent and with each succeeding
year the clinical signs tend to become more severe and
prolonged. The disease eventually may be present
year round, especially in temperate climates.
3 Two major patterns of disease distribution occur.
One is a dorsal pattern primarily aecting the mane
and tail region (Fig. 7). The other involves the ventral
body surface. Additional patterns of distribution
have been documented.3 Dierent species of Culicoides are responsible for each pattern.
4 The dorsal lesions occur at the base of the tail,
rump, back, withers, crest, poll and ears.
5 The ventral lesions usually involve the entire
ventral midline. Other than location, the clinical
features are identical to the dorsal disease.
6 Pruritus and self-trauma are the rst clinical signs
observed.
7 The primary lesions are small papules. In most
cases these are obliterated as a result of the intense
pruritus and self-trauma.
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 163178

8 In early cases there is only partial alopecia. In

chronic cases there is widespread alopecia, lichenication and excoriation.
9 Rugae or folds develop on the withers, neck and
tail head (Fig. 8).
10 Severely aected horses may exhibit weight loss as
a result of the constant irritation.
Histological ndings
1 Biopsies reveal a perivascular eosinophilic and
lymphocytic dermatitis (Figs 9 and 10).
2 There may also be an eosinophilic vasculitis in some
cases (Fig. 11). There may be focal areas of epidermal
damage (necrosis, spongiosis, exocytosis) that probably
are a result of the bites. Intraepidermal vesicopustules
may be present at the site of past insect feeding.
3 In chronic cases brosis may be marked.
4 The histological changes, although suggestive,
are not diagnostic. Biopsies are only useful to
support the clinical diagnosis and possibly to rule
out other diseases.
Diagnosis
1 In most cases a diagnosis can be made based upon
the history and clinical signs.
2 Intradermal skin testing with aqueous whole insect
antigens has been shown to demonstrate hypersensitivity to suspect insects. These antigens are not
available commercially worldwide at this time.
3 Most aected horses have a peripheral eosinophilia.
4 In years past, the major dierential diagnosis was
cutaneous onchocerciasis. Onchocerciasis is uncommon today and there are many dierentiating
features:
a. Age at onset. Culicoides hypersensitivity usually
develops before a horse is 4 years of age.
Onchocerciasis usually occurs in mature horses.
b. Seasonality. Culicoides hypersensitivity is seasonal. Onchocerciasis may or may not be seasonal.
c. Pruritus. Culicoides hypersensitivity is very
pruritic in all cases. Onchocerciasis may or may
not be pruritic. Even when pruritic it is usually less
so than Culicoides hypersensitivity.
d. Depigmentation. This is not a feature of
Culicoides hypersensitivity. It may be a feature of
cutaneous onchocerciasis.
e. Tail involvement. This should be present in most
cases of a dorsal Culicoides hypersensitivity while it
is rarely seen in cutaneous onchocerciasis. Remember, in Oxyuris equi infestation only the base of the
tail is aected and the rest of the body is unaected.
Clinical management
1 The two goals in treating this disease are to prevent
the Culicoides bites and to reduce the hypersensitivity
reaction.
2 It should be kept in mind that Culicoides sp.
primarily feed during the early evening and morning
hours. Thus, eorts at insect control should be geared
toward those times.

222 DISC
Immunologic diseases

Figure 7. Culicoides hypersensitivity. Crusted traumatized lesions

over rump and broken hairs of tailhead (Case material: University
of Florida).

Figure 8. Culicoides hypersensitivity. Folds, alopecia and

lichenication from chronic self-trauma on neck. (Case material:
Baird, Ontario Veterinary College).

Figure 9. Culicoides hypersensitivity. A low power view showing

supercial and deep perivascular dermatitis with lymphocytic foci.
(H & E. Magnication614.6).

167

Figure 10. Culicoides hypersensitivity. The inammatory cell inltrate

is lymphocytic and eosinophilic. (H & E. Magnication655).

Figure 11. Culicoides hypersensitivity. Eosinophilic vasculitis may

be seen in Culicoides-induced lesions. (H & E. Magnication697).

3 Aected animals should be stabled from dusk to

midmorning. Outside openings of the stall should be
screened. This needs to be very ne mesh. Culicoides
can pass through regular window screens and
mosquito netting. The eectiveness of regular
window screen may be improved by periodic
`painting' with an insecticide with good residual
activity such as permethrin.
4 As Culicoides spp. are `weak iers', the use of box
fans in front of nonscreened openings creating a wind
stream away from the stall is benecial. Ceiling fans
may also be of benet.
5 Topical insecticides and repellents are important in
the management scheme. Pyrethrins with synergists
and synthetic pyrethroids are utilized. Two percent
permethrin applied in the late afternoon may act as
an eective repellent in some areas.
6 The drugs of choice to reduce the inammation
and the pruritus are the corticosteroids. Antihistamines appear to be of little value.
7 Covering a horse with a blanket may provide some
protection once the disease is under control.
8 The better the insect control the lower the dose of
corticosteroids required. Except in very mild climates,
it is usually possible to stop medication during the
winter months.
9 In the future it may be possible to utilize
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A. A. Stannard

`immunological therapy' (i.e. hyposensitization or

desensitization). Immunotherapy eorts to date have
been unsuccessful.4
10 Due to the probable inherited predisposition with
this disease, owners of aected animals should be
encouraged to remove aected animals from breeding
programmes.
ERYTHEMA MULTIFORME
General considerations
1 Erythema multiforme (EM) is a well described
disease. It occurs in humans, dogs, cats and has been
recognized in the horse.5,6
2 Currently, erythema multiforme is considered a
rare equine skin disease. However, with increased
recognition, the spectrum of clinical lesions will be
better understood and we may nd it to be more
common than currently believed.
3 There is no known breed, sex or age predilection.
Aetiology and pathogenesis
1 It is likely that most, if not all, forms of erythema
multiforme share similar pathogenesis, even though
aetiological triggers may dier.
2 Erythema multiforme is viewed as a `symptom
complex' that is secondary to a variety of preceding
or concurrent diseases or factors.
3 The most common identied, underlying causes
include:
a. Drugs (`environmental chemicals')
b. Infections: viral (especially herpes), fungal, bacterial
c. Neoplasia (especially lymphoreticular neoplasms).
4 In the broadest sense, EM is considered immunemediated.
5 Even with a careful medical history and an
extensive clinical and laboratory evaluation, many
cases of EM are still classied as idiopathic.
Clinical signs
1 Erythema multiforme is an acute and sometimes
recurrent dermatosis. The severity ranges from
very mild to severe. The lesions tend to have a
symmetrical distribution.
2 The potential involvement of mucous membranes
must be stressed.
3 The clinical appearance of the disease encompasses
a wide spectrum as the name multiforme suggests
(Figs 12 and 13).
4 The primary lesions of erythema multiforme are
macules, vesicles or bulla.
5 Since vesicles are very short-lived in horses, the
vesicular form of erythema multiforme may
present as focal or multifocal erosions, ulcerations
and crusts.
Histological ndings
1 The major epidermal changes include:
a. Single necrotic keratinocytes throughout all
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 163178

layers of the epidermis (Fig. 14). The lesion may

also involve the adnexal epithelium.
b. Lymphocytic exocytosis and satellitosis.
c. Vacuolar alteration of the basal cell layer and/or
the basement membrane zone.
d. Marked parakeratotic scale and crust (Fig. 15).
2 The major dermal changes include:
a. Oedema of the supercial dermis
b. Extravasated erythrocytes in the supercial dermis
c. Supercial perivascular lymphohistiocytic inltrate.
3 If vesiculation occurs it is subepidermal in location.
It may occur due to basement membrane zone
vacuolar degeneration and/or severe supercial
dermal oedema.
4 Necrosis of the keratinocytes may be very extensive
and involve most of the epidermis. Thus the
pathological changes may mimic toxic epidermal
necrolysis (TEN). Some believe that TEN is a severe
variant of erythema multiforme.7
Diagnosis
1 Erythema multiforme should be considered in the
dierential diagnosis of cases of: oral erosions and
ulcerations, mucocutaneous lesions, cutaneous vesicles/bullae, erosive or supercial ulcerative lesions
and erythematous macules. Serpiginous urticaria and
hyperaesthetic leukotrichia may be variants of EM.
2 A careful medical history should be obtained in
cases with emphasis on drug history and prior or
concurrent systemic diseases.
3 Denitive diagnosis is made by histological examination of biopsy material. Early, but well-developed
lesions without secondary changes should be submitted. When in doubt, submit numerous representative samples.
4 There are no specic laboratory ndings in
erythema multiforme. In cases with precipitating
systemic disease, changes in the haemogram, serum
chemistry panel, etc. should be expected, reecting
the location and the severity of the visceral lesions.
Clinical management
1 There is no specic therapy.
2 Mild cases resolve spontaneously in a few weeks or
months.
3 In severe cases, systemic corticosteroids may be
required for symptomatic relief.
DRUG ERUPTIONS
General considerations
1 Drug eruption describes an adverse reaction to a
drug involving the skin.
2 Drug eruptions may be idiosyncratic and can occur
on rst exposure to the drug.
3 The term `drug' is used in a very broad context, i.e.
any chemical compound that gains access to the skin
by any route (ingestion, injection, inhalation, topical
absorption, etc.).

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Immunologic diseases

Figure 12. Erythema multiforme. Note serpiginous raised clinical

lesions of horse with erythema multiforme (Case material: Stannard).

Figure 13. Erythema multiforme lesions with appearance of hives

(Case material: Stannard).

4 Although any chemical compound potentially

can cause a drug eruption, certain classes of
compounds are more often involved than another.
These include:
a. Antibacterial agents (especially penicillin and
the sulphonamides)
b. Phenothiazine-based tranquillizers
c. Nonsteroidal anti-inammatory agents and
antipyretics
d. Diuretics
e. Local anaesthetic agents
f. Anticonvulsants.
5 The true frequency of drug eruptions to specic
agents is unknown in the horse.
Aetiology and pathogenesis
1 Most drug eruptions are believed immunological
in aetiology although the mechanisms are poorly
understood.
Clinical signs
1 A drug eruption can mimic any naturally occurring
skin disease. Therefore, drug eruption has to be
included in the dierential diagnosis of nearly all skin
diseases (Fig. 16).
2 Certain clinical features raise suspicion of a

169

Figure 14. Erythema multiforme. Single cell necrosis of

keratinocytes (arrow), lymphocytic exocytosis and satellitosis are
typical of erythema multiforme. (H & E. Magnication6129).

Figure 15. Erythema multiforme. On low power, the most obvious

lesion is the marked parakeratotic scale-crust. (H & E.
Magnication663).

Figure 16. Drug eruption. Hive eruptions from penicillin (Case

material: Stannard).

possible drug eruption. These include:

a. Urticaria or angioedema
b. Diuse erythema (erythroderma)
c. Bilateral symmetry of lesions
d. Papular eruptions
e. Intense pruritus
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A. A. Stannard

f. Sharply demarcated erosions and ulcerations

(vasculitis)
g. Vesicular and bullous eruptions
h. Photosensitization
i. Noninammatory acquired alopecia.
3 It is important to note that the eruption may occur
after the rst administration of the drug or it may
occur after years of use.
4 The onset of the eruption usually occurs within 24
48 h after the most recent administration but, on
occasion, it may occur up to two weeks later.
5 Following cessation of drug exposure, the course of
the eruption may be short-lived (i.e. 148 h) or it may
be very long (4 than 6 months).
Histological ndings
1 Drug eruptions may manifest with a variety of
histological patterns. The more commonly recognized
resemble erythema multiforme, urticaria or interface
dermatitis. Interface dermatitis is a common pattern
of inammation associated with drug eruptions (Figs
17 and 18).
Diagnosis
1 Unless drug eruptions are constantly being considered in the dierential diagnosis of skin disease
they will be missed.
2 Drug eruptions usually are only tentatively
diagnosed based on: (a) clinical features as outlined
above; (b) the medical history and (c) ruling out
other possibilities. A denitive diagnosis is rare
because provocative challenge may be life threatening to the horse.
3 Histopathological changes may be compatible, but
are rarely diagnostic.
Clinical management
1 All medications are stopped in a suspected case. In
the case of `life-saving' medications, an attempt
should be made to change to a chemically unrelated
compound with a similar pharmacological eect.
2 Corticosteroids may provide some relief but in
many cases relief is only minimal. In fact, the lack of
response to corticosteroids in a disease that should
respond is one indication that the clinician is dealing
with a drug eruption.
3 Future exposures to the implicated compound and
chemically related compounds should be carefully
avoided.
SYSTEMIC GRANULOMATOUS DISEASE
(Generalized granulomatous disease, `Equine sarcoidosis')
General considerations
1 Systemic granulomatous disease (SGD) is a recently
recognized disease of horses usually characterized by
skin lesions as well as widespread internal involvement.
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 163178

2 The disease is rare and there is no known sex or

breed predilection.
Aetiology and pathogenesis
1 The aetiology of systemic granulomatous disease is
unknown; it is probably multifactorial. The pathogenesis of systemic granulomatous disease is presumed to be an abnormal host response to some
antigen or antigens similar to that proposed for
human sarcoidosis.
2 In aetiological investigations cultures for aerobic,
anaerobic, and acid-fast bacteria as well as for fungi
have been negative. Special stains on tissue sections
and laboratory animal inoculation with tissue suspensions from aected horses have failed to reveal
any aetiological agent.
3 Polarization of tissue sections and transmission
electron microscopic examination have also failed to
reveal an agent or any crystalline structures such as
silicon that could account for the induction of a
granulomatous response.
4 `Hairy vetch' (Vincia villosa) has been reported to
produce a similar generalized granulomatous disease
in horses and cattle.8 Not all of the horses with
systemic granulomatous disease seen by Dr Stannard
have had an exposure to the plant. To date, it is not
known if all cases of systemic granulomatous disease
are related to hairy vetch, if there are two diseases
that are indistinguishable, or if hairy vetch is simply
one of many possible antigens inducing this syndrome in predisposed horses.
Clinical signs
1 The onset of clinical signs may be insidious or
explosive.
2 The skin lesions take two forms, the more common
being scaling and crusting associated with varying
degrees of alopecia (Figs 19, 20 and 21). The scaling
and crusting may be focal, multifocal, or generalized
in distribution. Rarely, the skin lesions are nodules or
large tumour-like masses. Both types of skin lesions
may coexist.
3 In addition to the skin lesions, virtually all cases
of systemic granulomatous disease have had internal organ involvement. In order of decreasing
frequency the lungs, lymph nodes, liver, gastrointestinal tract, spleen, kidney, bones, and central
nervous system have been involved. Aside from
weight loss and decreased appetite, a persistent lowgrade fever may be seen. The lungs are the most
common organ, excluding the skin, to be involved.
Clinical signs of lung involvement include exercise
intolerance, increased resting respiratory rate, and/
or mild dyspnoea.
4 Although lymph node involvement has been
seen histologically, peripheral lymphadenopathy is
rarely seen.
5 Liver and gastrointestinal lesions may cause
diarrhoea or icterus. Kidney and spleen lesions are
generally not associated with obvious clinical signs.

222 DISC
Immunologic diseases

171

Figure 17. Drug eruption. Low power showing a mild interface

dermatitis this is an inammatory pattern often associated with
drug reactions. (H & E. Magnication631).

Figure 19. Systemic granulomatous disease. Alopecia and scaling of

horse with chronic granulomatous disease (Case material:
Stannard).

Figure 18. Drug eruption. Single necrotic keratinocytes are typical

of EM-like drug reactions. (H & E. Magnication6180).

Figure 20. Systemic granulomatous disease. Alopecia on head of

horse from Fig. 19 (Case material: Stannard).

6 Bone involvement in one horse was associated with

lameness.
7 The clinical course varies from a chronic, progressive disease to a spontaneously regressing one. The
equine disease may be a more severe disease than
human sarcoidosis.
Histological ndings
1 Regardless of the organ involved, the major
histological change is the presence of variably sized
aggregates of epithelioid cells and multinucleated
giant cells (sarcoidal granulomas).
2 In the skin, the granulomas tend to be located in
the supercial and perifollicular dermis (Fig. 22).
3 The granulomas are not discrete (Fig. 23). Note the
multinucleate giant cells (Fig. 24).
4 Neutrophils, lymphocytes and plasma cells are
present in small numbers.
Diagnosis
1 Laboratory ndings. A complete blood count
may reveal leukocytosis, increased brinogen and
hyperglobulinemia. In severe cases, a mild anaemia
may be seen. Liver and kidney function tests may
be abnormal.

Figure 21. Systemic granulomatous disease. Extensive scaling of the

neck of horse in Fig. 19 (Case material: Stannard).

2 A diagnosis of systemic granulomatous disease is

conrmed by demonstrating the typical granulomatous changes histologically and eliminating other
causes of a granulomatous response. Systemic granulomatous disease is truly a `diagnosis of exclusion'.
3 Skin and peripheral lymph node biopsies are of
greatest value. Percutaneous needle biopsies of lung
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A. A. Stannard

Figure 22. Systemic granulomatous disease. Poorly delineated

granulomas in the supercial dermis. (H & E. Magnication681).

Figure 24. Systemic granulomatous disease. Multinucleate giant

cells and epithelioid macrophages. (H & E. Magnication6170).

dominated granulomatous lesions that typify the

sarcoidosis-like disease described by Stannard.9,10
The granulomatous components of the eosinophilic
disease are restricted to foreign-body type reactions
around foci of collagenolysis.
PEMPHIGUS FOLIACEUS

Figure 23. Systemic granulomatous disease. Higher magnication

of typical dermal granuloma. (H & E. Magnication6113).

or liver or both may also be helpful. In horses with

lung involvement, thoracic radiographs reveal a
widespread interstitial inltrate.
4 The major dermatological dierential diagnosis
include dermatophytosis, dermatophilosis and pemphigus foliaceus.
Clinical management
1 Because of the relatively small number of horses
studied and the variability of clinical course, response
to therapy has not been well documented. The
parenteral administration of corticosteroids is probably the treatment of choice. Once initiated, corticosteroid therapy should probably be continued for
several months.
Editorial comments
Regarding the relationship of chronic granulomatous
disease and chronic eosinophilic enteritis, Pascoe and
Knottenbelt suggest grouping chronic eosinophilic
enteritis together with chronic granulomatous disease.6 The two disorders certainly have very similar
clinical manifestations, but the histological lesions are
very dierent. Cutaneous and internal lesions described by Nimmo-Wilkie are eosinophilic and
lymphocytic with no indication of macrophage# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 163178

General considerations
1 Pemphigus foliaceus (PF) is the most common
autoimmune skin disease of the horse.
2 There is no sex predilection.
3 Age at onset is very important for prognosis. The
majority of cases occur in mature horses, usually 5
years of age or older. A small number of cases occur
in horses 1 year of age or younger. The disease in
these younger horses tends to be less severe than in
older horses, responds better to treatment, and may
spontaneously regress.
4 There is no known geographical distribution or
seasonality associated with disease occurrence.
Aetiology and pathogenesis
1 The pathogenesis of pemphigus foliaceus involves an
abnormal immune response. Based on the presence of
xed and circulating antibodies directed against desmosomal antigens of stratied squamous epithelium,
this disease has been further classied autoimmune.
2 Hereditary factors predispose horses to PF.
3 In many cases of PF, there appears to be a
triggering event that precedes the development of
clinical disease. The administration of certain drugs,
as well as a variety of systemic diseases and/or other
stressful situations have been noted.
4 An occasional `cluster' of cases is seen in
unrelated horses. This may indicate possible infectious or environmental factor(s) in the pathogenesis
of some cases.
Clinical signs
1 The areas that are most commonly aected
include the head (Figs 25 and 26) and the lower

222 DISC
Immunologic diseases

173

Figure 25. Pemphigus foliaceus. Crusts, papules and scale on head

of a young horse; note small brown crusts (Case material:
University of Florida).

Figure 27. Pemphigus foliaceus. Same horse as in Fig. 26 (Case

material: Ontario Veterinary College).

Figure 26. Pemphigus foliaceus. Scaling and crusting of the head.

(Case material: Ontario Veterinary College).

Figure 28. Pemphigus foliaceus. Close up of scaling lesions of same

horse as in Fig. 26 (Case material: Ontario Veterinary College).

extremities (Fig. 27). In severe cases, the entire body

may be aected. Involvement of the coronary bands
may be the only site of involvement or part of a
generalized distribution.
2 The classic, but rarely seen, primary lesion in PF is
a vesicle or pustule. Usually, the earliest lesions visible
clinically are crusted papules and this is the case with
horses. These are best seen in lightly or nonhaired
skin adjacent to mucocutaneous junctions, e.g. the
nostrils, lids or lips. Lesions rapidly coalesce to form
multifocal or diuse areas of crusting (Fig. 28).

Transient, persistent or recurrent urticaria may be the

initial clinical sign and can occur weeks before lesions
are seen.
3 Oedema of the extremities, especially the hind limbs,
and the ventral abdominal region are commonly noted.
It should be stressed that the oedema may be out of
proportion to the degree of surface changes and may
occur without any overlying surface changes.
4 Although equine PF frequently involves the
mucocutaneous junctions, mucous membrane involvement is extremely rare.
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A. A. Stannard

5 In severe cases of PF, systemic signs such as fever,

depression, decreased appetite, etc. may be seen.
Internal organs are not involved.
6 Pruritus is variable, ranging from nonexistent to
extreme. Pain may be much more noticeable than
pruritus.
Histological ndings
1 The primary pathological nding is a subcorneal
and/or intraepidermal vesicopustule associated with a
marked acantholysis (Fig. 29). The acantholytic cells
often detach in `rafts' and may remain attached to the
roof of the pustule, so-called `cling-ons' (Fig. 30). The
vesicopustules are quite fragile and usually rupture
before they reach a clinically recognizable size (Fig. 31).
2 The disease appears to be characterized by waves
of acantholytic activity. Large numbers of microscopic pustules form. These quickly rupture leading
to surface crusting (Fig. 32). This is followed by a
period of relative inactivity followed by another wave
of acantholysis. More often than not, skin biopsies
are taken during these periods of relative inactivity
providing a diagnostic challenge. The only remaining
clue to the diagnosis of PF is the presence of large
numbers of acantholytic keratinocytes embedded in
the serocellular/keratinous surface crusts (Fig. 33).
3 The primary inltrating cell in the vesicopustules is
the neutrophil. Occasionally eosinophils will be
present in large numbers.
4 The upper dermis contains a mixed perivascular
inltrate. The degree of dermal inltration is mild in
comparison to the degree of epidermal changes.
Diagnosis
1 Pemphigus foliaceus must be considered in the
dierential diagnosis of all skin diseases characterized
by scaling and crusting. The major dierential
diagnoses include dermatophytosis, dermatophilosis,
systemic granulomatous disease, and primary or
idiopathic disorders of keratinization (i.e. `seborrhoea')
2 Histological examination of skin biopsies should
rule out systemic granulomatous disease.
3 The location of lesions, limb and/or ventral midline
oedema, and the possible presence of small pustules
favour a clinical suspicion.
4 If intact pustules are seen clinically, an impression
smear may be a useful test. The roof of the pustule is
gently removed and the exudate collected with a
scalpel blade or by a direct impression smear. This is
smeared on a glass slide, xed, stained and examined
microscopically. A diagnostic preparation contains
large numbers of acantholytic keratinocytes, especially in rafts. This is compatible, but not diagnostic,
of pemphigus foliaceus.
5 Multiple biopsies (three or four) for conventional
histopathological examination are the most reliable
diagnostic test. The presence of acantholytic keratinocytes in the crusts is one of the most important
diagnostic features of this disease. It is important to
not surgically scrub the biopsy site. Every attempt
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Figure 29. Pemphigus foliaceus. Classical intact acantholytic

pustules are the exception rather than the rule in biopsies of
pemphigus foliaceus. (H & E. Magnication6113).

Figure 30. Pemphigus foliaceus. Acantholytic keratinocytes are

detaching, singly and in rafts to form a prominent subcorneal
pustule. (H & E. Magnication6226).

Figure 31. Pemphigus foliaceus. An early lesion showing

acantholysis and subcorneal clefting. (H & E. Magnication6226).

should be made to keep the crust(s) attached to the

biopsy specimen. If it falls o during the biopsy
procedure, submit it with the skin biopsies in the
formalin along with a request to the pathologist to
please section and examine the crusts for possible
evidence of pemphigus foliaceus.
6 It must be stressed that multiple biopsies for

222 DISC
Immunologic diseases

175

Figure 32. Pemphigus foliaceus. The typical episodic crusted lesion

seen in most biopsies of equine pemphigus foliaceus. (H & E.
Magnication646).

Figure 33. Pemphigus foliaceus. Higher magnication of surface

crust, showing the retained `ghosts' of acantholytic cells. (H & E.
Magnication6105).

conventional histopathology are far more reliable

than immunopathologic testing in the diagnosis of
pemphigus foliaceus.
7 Considering the severity of the disease, the prognosis, and the extensive and expensive therapy
involved, every attempt should be made to make a
denitive diagnosis.

prednisolone. Readers are referred to other references

for more details regarding therapeutic specics.2
3 The dose of dexamethasone is gradually reduced
once new lesions cease to develop. The dosage should
be reduced about 20% per week. If the dosage is
reduced too rapidly, there is a tendency for the
lesions to recur and exhibit a subsequent resistance
to therapy.
4 Once the minimal daily dose required to keep the
disease in remission is determined, an eort should be
made to substitute prednisolone for dexamethasone.
5 As alternative or adjunctive therapy, gold salts
have been used with success in the treatment of PF.
The most widely used gold compound is aurothioglucose, administered intramuscularly. Initially, it is
given once weekly at a dose of 1 mg kg71 bodyweight. It should be stressed that gold compounds
may take approximately 6 weeks to be eective. Thus,
it is usual practice to use corticosteroids to bring
about the initial resolution of the disease process
while concurrently treating with gold. The gold
therapy may allow either the total discontinuation
of corticosteroid therapy or, at least, a decrease in the
dosage of corticosteroids.
6 The use of other chemotherapeutic agents such as
chlorambucil or azathioprine have not been adequately evaluated in either initial or maintenance
therapy in the horse. This is primarily because of the
expense of these drugs.

Clinical management
1 Of major importance is the dierence in prognosis
and response to therapy between cases of pemphigus
foliaceus in young vs. older horses. The disease in
young horses has an excellent response to therapy
and may require no further therapy once it is in
remission, because of this it is worthwhile to treat the
PF in young horses. In contrast, the disease in older
horses has a less favourable prognosis. Even with
successful initial therapy, the disease usually requires
lifelong maintenance therapy. It is important to
ensure that owners understand the need for prolonged and expensive therapy at the outset.
2 Corticosteroids are the treatment of choice. Dexamethasone is the recommended rst choice. The
initial dose of dexamethasone for loading for
immunosuppression is 0.020.1 mg kg71 either by
injection or oral. After the loading dosage, oral
maintenance of 0.010.02 mg kg71 every 4872 h
may be eective. Each horse has to be treated
individually. Some respond better to prednisone or

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A. A. Stannard

PEMPHIGUS VULGARIS AND BULLOUS

PEMPHIGOID
General considerations
1 Due to the clinical similarity of these two diseases,
they are discussed together.
2 Both are rare, immune-mediated vesicular diseases
with autoantibodies against various skin antigens.
3 As there are very small numbers of documented cases,
no age, breed or sex predilection has been determined.
4 A breed predilection may exist considering that
hereditary factors have been implicated in many of
the immune-mediated diseases in humans and other
species of domestic animals.
Aetiology and pathogenesis
1 Autoantibodies against skin antigens are important
in the production of the lesions.
2 In pemphigus vulgaris (PV), the antibodies are
directed against the dermosomal antigens within the
epidermis (similar to that found in PF).
3 In bullous pemphigoid (BP) the antibodies are
directed against components of the epidermaldermal
junction.11
4 In both diseases circulating antibodies may also
be identied.
Clinical signs
1 Although both diseases usually present as erosive
diseases, the primary lesion is a vesicle or bulla.
2 The lesions involve the skin, the mucocutaneous
junctions and the oral mucosa. (Figs 34 and 35).
3 Even when large bullae have ruptured, the nature
of the antecedent lesions can usually be recognized by
the `ap' of mucosa or epidermis at the periphery of
the lesion that represents the prior roof of the bulla.
4 The lesions are nonpruritic, or mildly pruritic at
most.
5 Horses with signicant oral lesions salivate excessively.
Histological ndings
1 In pemphigus vulgaris there are suprabasilar
vesicles resulting from acantholysis.
2 In bullous pemphigoid there are subepidermal
vesicles or bullae.
3 Early lesions of bullous pemphigoid in humans and
other species of domestic animals have subepidermal
accumulations of eosinophils and the same might be
expected in the horse.
Diagnosis
1 PV and BP should be considered in the dierential
diagnosis of all multifocal erosive diseases especially
if the mucocutaneous junctions and/or the oral
mucosa are involved.
2 Two major dierentials include erythema multiforme and other bullous drug eruptions.
3 The diagnostic test of choice is a skin biopsy.
4 The histological changes in pemphigus vulgaris are
nearly pathognomonic.
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5 The biopsy lesions in bullous pemphigoid are

supportive, but not diagnostic, as several diseases
result in similar appearing subepidermal bullae.
6 Skin biopsies for direct antibody testing and serum
for indirect antibody testing can be examined for
xed and for circulating antibodies, respectively (the
reliability of both the direct and indirect tests in the
horse is presently unknown).
Clinical management
1 Based on very few cases, the prognosis in both
diseases appears grave.
2 Response to attempted immunosuppression with
corticosteroids has been extremely poor.
CUTANEOUS LUPUS ERYTHEMATOSUS
General considerations
1 Cutaneous lupus erythematosus is a relatively rare,
poorly dened immune-mediated disease in the horse.
2 Classically, the disease has been subdivided into
two distinct forms: discoid (localized) lupus erythematosus, a benign, primarily cutaneous form of the
disease; and systemic lupus erythematosus with
multiple organ involvement and a poor prognosis.
3 The disease usually occurs in adult horses.
Aetiology and pathogenesis
1 The pathogenesis of lupus erythematosus is multifactorial.
2 There is probably a hereditary predisposition to
disease development.
3 Antibodies (IgG and/or IgM) and complement (C-3)
can be demonstrated at the epidermaldermal
junction.
4 In many cases there appears to be an associated
triggering of the disease by an episode or incident.
These may include, but are not restricted to, excessive
sunlight exposure, extremes in environmental temperature (either hot or cold), a stressful situation,
such as pregnancy, or the administration of certain
drugs.
Clinical signs
1 The most common clinical sign of equine cutaneous lupus erythematosus is depigmentation.
2 The skin surrounding the eyes, lips and nostrils is
most commonly aected (Fig. 36). In addition, the
perianal, perineal and perivulvar regions as well as
the male genitalia maybe involved.
3 The areas of depigmentation are usually sharply
demarcated.
4 The loss of pigment may be rapid or gradual.
5 There may be varying degrees of erythema and
scaling present.
6 Involvement of haired skin usually results in
alopecia.
7 Clinical signs referable to systemic involvement are
rarely seen.

222 DISC
Immunologic diseases

Figure 34. Pemphigus vulgaris. Oral ulcers and bulla (Case

material: Carlson, University of California, Davis).

Figure 35. Bullous pemphigoid. Multiple focal ulcerations on face

at previous site of bullae (Case material: Stannard).

Histological ndings
1 The major microscopic changes in lupus erythematosus are centred on the epidermaldermal junction.
a. Hydropic degeneration of the basal cell layer,
single cell necrosis (Fig. 37).
b. Vacuolar degeneration of the basement membrane zone (this is not a disease specic nding).
c. Thickening of the basement membrane (dicult
to appreciate in the horse as the basement
membrane zone is normally thick).
d. Pigmentary incontinence.
e. The presence of necrotic cells in the basal cell
layers of the epidermis (Civatte bodies).
f. The deposition of `brinoid material' in the
supercial dermis in the region of the basement
membrane zone and around supercial blood vessels.
2 Unfortunately, the two most common and signicant changes in LE in other species are not as
reliable in the horse. First, in most areas of normal
horse skin the basement membrane zone is very thick
and prominent. Thus, trying to evaluate any increased thickness over normal is dicult at best.
Second, hydropic degeneration of the basal cell layer
is encountered in a variety of supercial inammatory processes in the horse and seems to lack the
specicity it has in humans and other species of

177

Figure 36. Cutaneous lupus erythematosus. Depigmentation

around lips and eyes of 4-year-old Arabian mare (Case material:
Stannard).

Figure 37. Cutaneous lupus erythematosus. Interface dermatitis

with scattered single necrotic keratinocytes (arrow). (H & E.
Magnication6173).

domestic animals.
3 Other histological changes may include surface and
follicular hyperkeratosis, a patchy periappendigial
mononuclear cell inltrate, follicular atrophy and
dermal brosis.
Diagnosis
1 Cutaneous lupus must be considered in the
dierential diagnosis of any equine skin disease
characterized by depigmentation, especially those in
mature or aged horses where the pigment loss involves
mucocutaneous junctions. Juvenile Arabian leukoderma can usually be eliminated based on the breed, age
at onset and lack of any erythema. Of greatest
dierential concern is the idiopathic leukoderma of
mature horses that mimics the disease in young
Arabian horses. In these cases any erythema and/or
scaling in the areas of depigmentation would strongly
indicate the possibility of lupus. The absence of
inammation would suggest idiopathic leukoderma.
2 A denitive diagnosis of lupus erythematosus is
based on compatible histopathology, demonstration
of immunoglobulin (IgM and/or IgG) and complement at the basement membrane zone (positive `lupus
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A. A. Stannard

band' test) and in most cases a positive antinuclear

antibody (ANA).
Clinical management
1 In general, aggressive therapy for equine cutaneous
lupus erythematosus is not indicated.
Editors comments
Regarding the diagnosis of `lupus' Dr Tony Stannard
was adamant that `animals be allowed to have their
disease' and this is particularly true of the lupus
group of diseases in which there are likely to be more
dierences than similarities with the heterogeneous
human disorder for which it was named. He has used
the term cutaneous lupus erythematosus for those
equine skin diseases in which the histopathology
exhibits lupus-specic lesions, as dened in a recent
classication scheme for human lupus erythematosus.12 This refers to an interface dermatitis with
prominent lymphocyte mediated keratinocyte cell
death. This lesion is found in both localized and
systemic forms of lupus in humans and in horses.

4.

5.
6.
7.

8.

9.
10.

REFERENCES
1. Foster, A.P., Cunningham, F.M. The pathogenesis and
immunopharmacology of equine hypersensitivity In:
Kwochka, K.W., Willemse, T., von Tscharner, C. eds.
Advances in Veterinary Dermatology, Vol. 3, Oxford:
Butterworth Heinemann. 17789, 1998.
2. Rosenkrantz,
W.S.
Systemic/topical
therapy.
Veterinary Clinics of North America: Equine Practice
1995; 11: 12746.
3. Greiner, E.C., Fadok, V.A., Rabin, E.B. Equine
Culicoides hypersensitivity in Florida: biting midges

11.

12.

aspirated from horses. Medical Veterinary Entomology

1990; 4: 37581.
Barbet, J., Bevier, D., Greiner, E.C. Specic
immunotherapy in the treatment of Culicoides
hypersensitive horses: a double-blind study. Equine
Veterinary Journal 1990; 22: 2325.
Marshall, C. Erythema multiforme in two horses.
Journal of the South African Veterinary Association
1991; 62: 133.
Pascoe, R.R.R., Knottenbelt, D.C. Manual of Equine
Dermatology. London: W.B. Saunders, 1999.
Fritsch, P.O., Elias, P.M. Erythema multiforme and
toxic epidermal necrolysis In: Fitzpatrick, T.B., Eisen,
A.Z., Wol, K., Freedberg, I.M., Austen, K.F. eds.
Dermatology in General Medicine 4th edn. New York:
McGraw-Hill, 1993: 5969.
Anderson, C.A., Divers, T. Systemic granulomatous
inammation in a horse grazing hairy vetch. Journal of
the American Veterinary Medical Association 1983; 183:
56970.
Pass, D.A., Bolton, J.R. Chronic eosinophilic
gastroenteritis in the horse. Veterinary Pathology
1982; 19: 48696.
Nimmo-Wilkie, J.S., Yager, J.A., Nation, P.N., Clark,
E.G., Townsend, H.G.G., Baird, J.D. Chronic
eosinophilic dermatitis: a manifestation of a
multisystemic, eosinophilic, epitheliotropic disease in
ve horses. Veterinary Pathology 1985; 22: 297305.
Olivry, T., Borrillo, A.K.G., Xu, L. et al. Equine
bullous pemphigoid IgG autoantibodies target linear
epitopes in the NC16A ectodomain of collagen XVII
(BP180, BPAG2). Veterinary Immunology and
Immunopathology 2000; 73: 4552.
Sontheimer, R.D. The lexicon of cutaneous lupus
erythematosus A review and personal perspective
on the nomenclature and classication of the cutaneous
manifestations of lupus erythematosus. Lupus 1997; 6:
8495.

Zusammenfassung Ausgewahlte Hautkrankheiten des Pferdes, fur die es Indizien fur eine immunologische
Atiologie gibt, werden hier abgehandelt. Urtikaria, Culicoides-Allergie, Erythema multiforme,
Medikamentenuberreaktionen und progressive Granulomatose werden besprochen. Die autoimmunen
Hautkrankheiten des Pferdes (Pemphigus foliaceus, Pemphigus vulgaris, Bulloses Pemphigoid und kutaner
Lupus erythematodes) werden ebenfalls abgehandelt. Die Symptome und die diagnostischen Befunde dieser
immunologisch bedingten equinen Dermatosen sowie die in der Diagnostik und Therapie auftretenden
Schwierigkeiten werden besprochen. [Stannard, A. A. Immunologic diseases. (Immunologische Erkrankungen.)
Veterinary Dermatology 2000; 11: 163178.]
Resume Ce chapitre decrit certaines dermatoses equines pour lesquelles une etiologie immune est suspectee. Il
s'agit de l'urticaire, de l'hypersensibilite aux Culicoide, de l'erytheme polymorphe, des toxidermies et de la
maladie granulomateuse systemique. Les dermatoses auto-immunes (pemphigus foliace, pemphigus vulgaire,
pemphigoide bulleuse et lupus erythemateux cutane) sont egalement discutees. Les signes cliniques et les
moyens diagnostiques sont evoques, ainsi que la diculte a realiser un diagnostic denitif et a mettre en place
un traitement ecace. [Stannard, A. A. Immunologic diseases. (Dermatoses immunologiques.) Veterinary
Dermatology 2000; 11: 163178.]
Resumen Se discuten en esta seccion enfermedades equinas cutaneas en las que existe una fuerte evidencia de
etiolog a inmunologica. Se incluyen las alteraciones reactivas como la urticaria, la hipersensibilidad a
Culicoides, el eritema multiforme, las erupciones medicamentosas y las enfermedades granulomatosas
sistemicas. Se discuten las enfermedades autoinmunes del caballo con manifestaciones cutaneas (pengo
foliaceo, pengo vulgar, pengoide bulloso y el lupus eritematoso cutaneo). Se denen las caracter sticas
cl nicas y los hallazgos diagnosticos de estas dermatosis equinas inducidas inmunologicamente, y se presentan
las bases para realizar un diagnostico denitivo y un tratamiento de los s ntomas cl nicos. [Stannard, A. A.
Immunologic diseases. (Enfermedades inmunologicas.) Veterinary Dermatology 2000; 11: 163178.]
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