225 DISC

Veterinary Dermatology 2000, 11, 191203

Alopecia in the horse an overview

Abstract Dr Stannard explains dierent forms of alopecia in the horse with emphasis on the hair follicle and
its function in the production of hairs. Both normal and abnormal patterns of hair growth and shedding in the
horse are reviewed. Overviews of several specic hair follicle abnormalities, both inammatory and
noninammatory, are discussed in detail with their clinical relevance. Some of the clinical entities covered in
this section (linear alopecia and alopecia areata) are caused by immunological attack against normal
structures and could have been placed in Immunologic diseases. However, because the clinical presentation for
these entities is alopecia, Dr Stannard chose to include them in his notes on alopecia. Other inclusions in this
section include cutaneous bacterial infections (e.g. pastern folliculitis and dermatophilosis) as well as fungal
infections of the hair (dermatophytosis).
Keywords: Alopecia areata, dermatophilosis, dermatophytosis, linear alopecia, pastern folliculitis, telogen euvium.

ALOPECIA
General considerations
1 Alopecia refers to an absolute decrease in the
number of hairs per given area of body surface or
hairs that are shorter than normal even though their
number is within normal limits.
2 Alopecia may be congenital or acquired.
a. Congenital alopecia is referred to as hypotrichosis and is usually an inherited defect.
i. This appears to be an extremely rare disorder
in the horse.
ii. Of greatest concern to the horse owners and
veterinarians are the acquired forms of alopecia.
b. Prognostically, acquired alopecia is divided into
cicatricial and noncicatricial types.
Aetiology and pathogenesis of alopecias
1 In noncicatricial alopecia, future hair growth will
occur if the causative factors are eliminated or
corrected. Noncicatricial alopecia can be caused by:
a. Trauma (pruritus/self-trauma)
b. Altered hair follicle function
c. Hair follicle dystrophies
d. Defects in the hair shafts
e. Inammation of the hair follicle (folliculitis and
furunculosis)
f. Infections of the hair shaft with or without an
associated folliculitis.
3 Trauma in the form of pruritus is the most
common cause of alopecia in the horse. Examples
of pruritic diseases characterized by alopecia
include oxyuriasis, culicoides hypersensitivity and
pediculosis.
4 Basic to our understanding of alopecia is a brief
discussion of normal hair follicle function.
a. A follicle does not produce hair constantly.
b. It goes through an anagen or growing phase in
which hair is produced.
c. After a brief transition phase (catagen), the
# 2000 Blackwell Science Ltd

follicle reverts to the telogen or resting phase in

which hair growth ceases.
d. After a period of time the follicle reverts back to
the anagen phase and a new hair is formed.
e. As the new hair emerges the old hair is lost.
5 Horses have two distinct patterns of hair growth.
a. The growth of the body hairs are periodically
synchronized resulting in seasonal shedding.
b. The growth of the long hairs of the mane and
tail remains asynchronous, analogous to human
scalp hair. Thus these hairs do not undergo
periodic shedding.
6 The most important alterations in hair follicle
function that results in alopecia are the euviums.
7 Hair follicle dystrophies have only recently been
recognized. Although their pathogenesis is not known,
heredity probably plays a role in most. Colour-linked
dystrophy of the body hairs of the Appaloosa horse
is one example. The syndrome formerly named
idiopathic dystrophy of the mane and tail (also known
as mane and tail seborrhoea see Diseases of
cornication) represents a form of alopecia areata.
8 Sterile folliculitis is an increasingly recognized
cause of alopecia.
a. The classic example is alopecia areata.
b. This is thought to be a cell-mediated autoimmune disease with damage to the hair bulb.
9 Bacterial and fungal infections of the hair follicle
and/or hair shaft are important causes of equine
alopecia.
a. The most common bacterial infection is dermatophilosis.
b. Folliculitis and furunculosis due to Staphylococcus spp1 and Corynebacterium pseudotuberculosis are uncommon (see Editors' comments at the
end of aetiology of alopecia).
c. Dermatophytosis is the fungal folliculitis of
importance.
10 The only parasitic infestations of the follicle that
result in alopecia, Demodex equi and Pelodera
strongyloides, are extremely rare. Symmetrical
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A. A. Stannard

atrophy of hair follicles secondary to endocrine

disorders, which is a common cause of alopecia in
dogs, is extremely rare or nonexistent in the horse.
11 Cicatricial alopecia is characterized by permanent
destruction of the hair follicles and regrowth of hair
will not occur.
a. The most common causes include physical,
chemical or thermal injury, severe furunculosis,
neoplasia, and certain inammatory diseases such
as cutaneous onchocerciasis.
Editors comments
Dr Stannard's more recent thoughts on the incidence
and signicance of pyodermas had recently changed
as he asked Dr Stephen White to specically address
antibiotic responsive skin disease in the horse at the
Third World Congress of Veterinary Dermatology.
(Personal communication: Dr Stephen White, UC
Davis, USA, 1999) During the equine workshop at
Edinburgh, it was agreed that although staphylococcal skin infections are probably uncommon in the
horse, there may be various presentations and they
should be given stronger consideration in the
dierential of various equine dermatoses.2
Clinical signs
1 Alopecias in the horse may be focal or generalized,
inammatory or noninammatory.
2 Telogen euvium, when recognized in the horse,
occurs in two distinct types:
a. Telogen euvium refers to the shedding of
normal telogen (club) hairs from a large number
of follicles that have entered the telogen phase of
the hair cycle in a relatively synchronous fashion
(Figs 1, 2 and 3). The euvium occurs when new
hairs are produced during the next anagen cycle
dislodging the club hairs. Normal seasonal shedding
of the body hairs can be viewed as a `physiological
telogen euvium'.
b. When a telogen euvium occurs at an abnormal
time of the year (mid-summer, mid-winter) or in an
area that normally does not undergo synchronous
shedding (mane and tail), it is considered abnormal.
While the cause of this is often unknown, stressors
(such as starvation) and febrile diseases, can precipitate the phenomenon. In this type of euvium,
there is a signicant lag period (one to several months)
between the causative event and the hair loss.
3 Anagen euvium (deuxion) results when some
factor inhibits synthesis in the hair bulb during
anagen phase resulting in a defective portion of the
hair shaft which subsequently breaks o.
a. This phenomenon is most commonly associated
with severe stress and certain chemical compounds
(e.g. antimitotic agents). In contrast to telogen
euvium, anagen euvium is characterized by a
very short lag period (few days to weeks) between
the causative event and the hair loss.
4 Several types of inammatory alopecias occur in
the horse and the diagnosis is based on rule-outs by
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 191203

Figure 1. Telogen euvium after pneumonia in a horse (Case

material: University of California, Davis).

Figure 2. Telogen euvium. Close-up of horse from Fig. 1 and

clumps of hair which are easily epilated (Case material: University
of California, Davis).

Figure 3. Telogen euvium. Horse with widespread alopecia over

rump and back (Case material: Stannard).

cytology, culture and, in some cases, a lack of

response to treatment. Clinical ndings are described
with each entity.
5 Cicatricial and noncicatricial alopecias occur from
a broad variety of aetiologies and it is not always
possible to predict the outcome of an alopecia.

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Alopecia in the horse

193

Histological ndings
1 Biopsies of telogen euvium are misleading as they
will demonstrate most follicles in the active growing
(anagen) phase (Fig. 4).
2 Histological ndings of alopecias with infections
and inammation are covered below.
Diagnosis
1 Microscopic examination of plucked hairs in
telogen euvium reveals nonpigmented `club' or
telogen roots.
2 Microscopic examination of plucked hairs in
anagen deuxion reveals fragmented hair shafts and
the absence of a root.
3 The diagnosis and management of specic inammatory and infectious alopecias are discussed later in
the section.

Figure 4. Telogen euvium. By the time the biopsy is taken, the

skin is essentially normal, with follicles in the anagen phase.
(H & E. Magnication614.)

Clinical management
The clinical approach to alopecia in the horse is to
identify the cause and, if it is something which may
benet from pharmaceutical treatment, then therapy
may resolve the clinical signs.
LINEAR ALOPECIA (LINEAR
KERATOSIS)
General considerations
1 This disease has a classic clinical and histological
presentation.
2 Although it occurs in a wide variety of breeds,
Quarter horses appear to be predisposed.3
Aetiology and pathogenesis
1 This entity is thought to be caused by an
immunological attack on the follicular wall, the cause
of which is unknown, but in which T lymphocytes are
most probably involved.
2 The folliculitis does not appear to be associated
with an aetiologic agent.
3 Particularly baing is the gross linear conguration of the lesions. They do not follow vessels or
nerves/dermatomes.
4 The vertical orientation might suggest some external
factor that `dripped' down the skin surface causing the
lesion. To date this has not been documented.
Clinical features
1 The lesions consist of one or more vertically
orientated linear areas of alopecia with varying
degrees of scaling or crusting (Figs 5 and 6).
2 The lesions are usually 210 mm wide and vary in
length from a few centimetres to over a metre.
3 Common sites are the neck and lateral aspects of
the thorax.
4 The lesions are usually asymptomatic (i.e. no
pruritus, etc.).
5 The clinical presentation and temporal development is usually unknown or gradual.

Figure 5. Linear alopecia. Linear hyperkeratosis and alopecia on

the trunk of a Quarter horse (Case material: Stannard).

Histological ndings
1 The primary lesion is an inltrative lymphocytic
mural folliculitis with subsequent damage to the wall
(Figs 7 and 8). Subtle to severe oedema of the
follicular walls can be present.
2 In lesions which are presumed to be older (or more
well-developed), epithelioid cells and giant cells can
be seen inltrating the outer root sheath of aected
follicles (Fig. 9).
3 The end stage of the process may result in complete
follicular destruction (Fig. 10) and permanent nonreversible alopecia.
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A. A. Stannard

Figure 8. Linear alopecia. The lesion is mural folliculitis.

Lymphocytes inltrate into the outer root sheath of an aected
follicle. There is no luminal exudate. (H & E. Magnication6156.)

Figure 6. Linear alopecia. Alopecia and crusting of the hair in a

linear conguration (Case material: Stannard).

Figure 9. Linear alopecia. Aected follicles may contain dystrophic

hair shafts. Note the multinucleate giant cell (arrow) within the
outer root sheath. (H & E. Magnication6226.)

Figure 10. Linear alopecia. The follicles may be obliterated by the

granulomatous mural folliculitis. (H & E. Magnication6129.)

Figure 7. Linear alopecia. Low power photomicrograph to

illustrates the follicular targeting. (H & E. Magnication637.)
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 191203

4 Sebaceous glands may be aected, apparently

destroyed by the same inammatory process.
5 In some, but not all cases, there may be signicant
surface epidermal lesions, suggestive of erythema
multiforme (Fig. 11). These are represented by epidermal necrosis (single cell) and lymphocytic satellitosis
with variable parakeratosis. Other epidermal lesions

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Alopecia in the horse

195

ALOPECIA AREATA
General considerations
1 Alopecia areata is an autoimmune skin disease.
2 Currently it is considered to be a rare disease,
however, with increased awareness by both clinicians
and pathologists, its recognition will surely increase.
3 Too few cases have been documented to determine
if any breed or sex predilection exists.
4 Little information is available about alopecia
areata in animals and much of what we know is
extrapolated from the human literature. From the
human disease; species dierences, clinical manifestations, prognosis, histopathology, response to treatment, etc. are likely.
Aetiology and pathogenesis
1 A major factor in the pathogenesis of alopecia
areata is damage to the growing hair mediated by T
lymphocytes, presumably specic for antigens of the
hair matrix and root sheath epithelium, which cause
damage to the epithelium (see additional Editors'
comments).
2 In humans, hereditary factors have clearly been
implicated in the severity and susceptibility of
individuals to this condition.4
Figure 11. Linear alopecia. In some lesions scattered necrotic
keratinocytes (arrow) are reminiscent of lesions of erythema
multiforme. (H & E. Magnication6296.)

include diuse spongiosis and exocytosis.

6 Varying degrees of perivascular eosinophilic inltration also may be present.
Diagnosis
1 The clinical presentation is usually diagnostic. A
major dierential diagnosis is linear epidermal nevus.
In this condition, the skin surface is very hyperkeratotic and has a `rough appearance'.
2 Although alopecia and scaling are two hallmarks
of dermatophytosis, the linear conguration of the
lesions should easily dierentiate the two conditions.
3 Linear alopecia must be dierentiated from linear
trauma (scratches, whip marks, etc.).
4 Biopsies are usually diagnostic. However, it should
be emphasized that the changes may be subtle and,
unless the pathologist is familiar with this type of
process, they may be overlooked.
Clinical management
1 The lesions are persistent with no tendency for
spontaneous regression. The owner should be made
aware that with our present knowledge of the disease,
therapy can help but cannot cure.
2 Corticosteroid therapy (either topically or systemically) may slow the progression of the lesion
temporarily; rarely resolution may be achieved.
3 Any of the keratolytic shampoos can be used on a
regular basis (every 34 days) if there is a signicant
degree of scaling/crusting.

Clinical features
1 In the horse, the disease presents as diuse thinning
of the mane and/or tail, or as one or more
circumscribed areas of complete or nearly complete,
alopecia (Figs 12, 13 and 14). The onset may be
insidious or rapid.
2 The aected areas may coalesce to produce extensive regions. Usually there is no clinical evidence of
inammation and the disease is nonpruritic. However,
some clinical cases with compatible typical histopathologic ndings will have crusts and may exhibit
histological ndings suggesting pruritus or pain.
3 Human patients with alopecia areata may also
have associated nail changes.4 Thus, defective hoof
growth may theoretically occur in horses with the
disease.
4 Depigmentation is seen in a small percentage of
human cases.4 Some examples of spotted leukotrichia
in the horse are also associated with hair loss in the
aected areas. These may actually represent a variant
of alopecia areata.
5 The clinical course of the disease is extremely
variable. Periods of spontaneous remission may
occur or one area may regress while another is
developing. This erratic behaviour makes judging the
eectiveness of treatment very dicult.
6 The prognosis for complete and permanent
remission is guarded to poor. In humans it is felt
that the earlier in life the disease occurs the poorer
the prognosis.
Diagnosis
1 Alopecia areata should be considered in the
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A. A. Stannard

Figure 12. Alopecia areata.

Horse with coalescing focal
areas of alopecia of the trunk
(Case material: Stannard).

Figure 13. Alopecia areata. Noninammatory alopecia of the head

of same horse as in Fig. 12 (Case material: Stannard).

Figure 14. Alopecia areata. Total alopecia of the tail (Case

material: Ontario Veterinary College).

dierential diagnosis of any patchy, nonpruritic, apparently noninammatory alopecia involving the body.
2 Denitive diagnosis requires histological conrmation. Multiple biopsies need to be collected from these

patients, as lesions with pathognomonic lymphocytic

bulbitis can be sparse. Biopsies from newly developed
areas of alopecia are more likely to be helpful than
those from older lesions.

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225 DISC
Alopecia in the horse

197

3 It is likely that some cases diagnosed as mane and

tail hair follicle dystrophy are actually alopecia
areata. This could occur when dystrophic hairs are
present but the classic histopathologic lesions of
alopecia areata are not found in the biopsies.
Histological ndings
1 The two major histological features of alopecia
areata are the presence of `miniature' hair follicles
and a lymphocytic bulbitis (Fig. 15). Early in the
disease most of the diminutive hair follicles are in
early anagen phase while later in the disease most
follicles are in telogen phase.
2 The lymphocytic bulbitis involves anagen follicles
and is best found in recently developed areas of
alopecia. The degree of inammation varies markedly
from follicle to follicle (Fig. 16). The lymphocytes
surround the lower half of the follicle and often
invade the matrix of the bulb and the outer root
sheath (Figs 17 and 18). The bulbitis may be very
dicult to demonstrate.
3 Follicles in the anagen phase may exhibit defective
keratinization of the hairs resulting in hair shafts
containing nucleated cells and staining abnormally.
Follicles in the telogen phase usually contain either
no hair or a small, dystrophic hair (Fig. 19).
4 In chronic lesions, inammation may be minimal
to nonexistent. Thus, biopsies from such areas may
only exhibit small telogen follicles lacking hair shafts.

Figure 15. Alopecia areata. Low power view showing focal

inammatory lesions targeting anagen hair bulbs in an active
lesion of alopecia areata. Such lesions are rare. (H & E.
Magnication654.)

Clinical management
1 While a variety of topical and systemic therapies
have been tried in humans, corticosteroids appear to
be the most eective and reliable. They may be
utilized topically, intralesionally or systemically.
2 In horses, treatment of a limited number of cases
with systemic corticosteroids has produced minimal
response. As long-term immunosuppressive doses
appear required, it is questionable if such therapy is
justied for a `cosmetic' problem in light of the less
than satisfactory results.
Editors' comments
Regarding the histological diagnosis of alopecia
areata It cannot be overstressed that it is dicult,
and sometimes impossible, to nd the classic, `swarm
of bees' lymphocytic bulbitis lesion in alopecia areata
biopsies. Clues indicating that the pathologist should
cut further sections from the tissue block or request
additional biopsies include: (i) evidence of matricial
damage, indicated by one or more apoptotic cells,
sometimes with an adjacent inltrating lymphocyte;
(ii) the presence of malacic hair shafts in some
follicular ostia, indicating previous damage to the
generative hair matrix cells and (iii) a subtle increase
in peribulbar brous tissue. The editors are less
impressed by `miniaturization' of the anagen follicles
as an indicator lesion although in chronic cases there
may be a preponderance of telogen follicles and these
may be somewhat atrophic.

Figure 16. Alopecia areata. Even in active lesions, hair follicle

involvement is sporadic. Note the normal follicle adjacent to the
aected one. (H & E. Magnication6126.)

Regarding the pathomechanisms of alopecia areata

Several pathogenetic mechanisms have been proposed
to explain the lesions of alopecia areata, including
cytotoxic damage by T-lymphocytes reacting to
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A. A. Stannard

Figure 17. Alopecia areata. Small lymphocytes inltrate around a

miniaturized anagen bulb. (H & E. Magnication6111.)

Figure 19. Alopecia areata. The presence of dystrophic hair shafts

in follicular ostia may be the only lesion seen, particularly in
chronic cases. (H & E. Magnication6146.)

Figure 18. Alopecia areata. Small lymphocytes may also inltrate

into the bulb, the so-called `swarm of bees' lesion. There may be
associated hydropic degeneration and single cell necrosis of matrix
cells. (H & E. Magnication6226.)

follicular antigens. Intrabulbar lymphocytes are more

frequently identied as CD8+ (cytotoxic) than CD4+
(helper) cells. Recently, attention has been focused on
the role of autoantibodies. In equine alopecia areata,
autoantibodies specic for a variety of hair follicle
antigens, especially trichohyalin, have been detected.5
Whether or not these are pathogenic, or simply
represent epiphenomena, remains to be proven.
DERMATOPHYTOSIS
General considerations
1 Dermatophytosis refers to a supercial infection of
keratinized tissues by fungi belonging to the dermatophyte group.
2 The disease is world-wide in distribution and is
most common in geographical regions with warm,
humid climates.
3 Young horses are more frequently infected than
adults; however, there does not appear to be any sex
or breed predilection.
4 Although dermatophytosis is an infectious disease,
the degree of contagion is quite variable. In some
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 191203

instances there is limited spread to other horses on

the premises while, in other situations, the disease
occurs as an explosive outbreak.
5 The disease is overdiagnosed. This is the result of
erroneously incriminating dermatophytes as the
cause of all dermatoses characterized by scaling,
crusting and/or alopecia. Dermatophytes are only
one cause of such changes.
Aetiology and pathogenesis
1 Microsporum spp. and Trichophyton spp. are the
two genera involved in the aetiology of almost all
cases of equine dermatophytosis. Trichophyton equinum is the most common isolate followed by M.
equinum, M. gypseum and T. mentagrophytes. Past
reports of M. canis as the cause of equine dermatophytosis were probably caused by M. equinum.
2 Dermatophytes produce disease by several dierent mechanisms. First, the invasion of the hair shaft
with fungal elements weakens it and facilitates
breakage. Second, the fungi elaborate substances
that can act either as irritants or as allergens.
3 The transmission of dermatophytes is usually by
direct contact with an infected host. However,
fomites, such as contaminated tack, play an important role in many cases.6
4 Compared to the ease of transmission of dermatophytosis from small animals to people, transmission
to equine owners is less common.

225 DISC
Alopecia in the horse
Clinical features
1 The lesions are usually focal or multifocal (Fig. 20).
Only on rare occasions are lesions generalized.
2 Initially, the lesions may be urticaria-like. Early
urticarial-like lesions of dermatophytosis will not pit
on pressure like hives.
3 The typical lesions are characterized by relatively
sharply demarcated areas of scaling, crusting and
alopecia. Due to the normally pigmented skin of the
horse, erythema is usually not recognized.
4 Multiple lesions of varying size and stage of
development are commonly observed.
5 Pruritus is variable but rarely severe and most
horses are nonpruritic.
6 Suppuration may occur under the scab or crust
and, if present, is more probable with M. gypseum
han with T. mentagrophytes.

199

Figure 20. Dermatophytosis. Focal lesion of dermatophytosis on

head (Case material: Stannard).

Histological ndings
1 Lesions target the follicles resulting in either
supercial luminal folliculitis or inltrative mural
folliculitis with follicular wall oedema (Fig. 21).
2 Dermatophytes can be found in the follicular
lumen (Fig. 22) but more often they are noted only
in the stratum corneum or in the crust.
Diagnosis
1 `Diagnosis' is made frequently on the basis of the
medical history and clinical ndings. However, a
denitive diagnosis requires the visualization of
fungal elements (i.e. biopsy, trichogram) or their
isolation in culture.
a. Specialized media for dermatophyte cultures are
widely available and directions should be followed
closely.
b. The skin should be cleaned rst with mild
detergent or alcohol and rinsed with water to
decrease the collection of saprophytes.
c. The hairs should be plucked from the periphery
of a new lesion, if possible.
d. The keys to diagnosis are daily observation of
the media and microscopic identication of the
suspect fungal colonies.
e. This is especially critical in chronic cases and
those in which there is a group of aected horses.
Clinical management
1 It must be stressed that dermatophytosis is a
spontaneously regressing disease in otherwise healthy
horses. This usually requires 2 to 3 months.
2 Most information on treatment is based on
anecdotal clinical observation. Recent work in
other species (especially the cat) indicates that
many of the recommended topical treatments are
probably ineective. 7
Editors' comments
Although Dr Stannard considered that there was no
proven therapy for dermatophytosis in the horse, in
Europe and Canada where enilconazole (Imaverol,

Figure 21. Dermatophytosis. Supercial pustular folliculitis in a

biopsy. A dermatophyte infected hair (arrow) is present in ostium.
(H & E. Magnication645.)

Figure 22. Dermatophytosis. A higher magnication of an infected

hair. The hypae do not stain in H & E sections but are silhouetted
against the keratin. (H & E. Magnication6111.)

Jansen) is available there is widespread use of this

topical treatment in the horse. There are also
anecdotal reports of success with intravenous 20%
NaI (250 mL 500 kg71 horse every 7 days, 12
times; contraindicated in pregnant mares as it may
cause abortion, and the anecdotal use of griseofulvin's ecacy in horses at a dose of 100 mg kg71
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A. A. Stannard

daily for 7 days. (Personal communication, Dr

Stephen White, UC-Davis, USA, 1999.)
DERMATOPHILOSIS
(Streptothricosis, Rain scald, Rain rot)8
General considerations
1 Dermatophilosis is a relatively common disease
that aects horses throughout the world.
Aetiology and pathogenesis
1 The aetiologic agent is a Gram positive, branching
actinomycete, Dermatophilus congolensis.
2 Chronically aected animals (carrier animals) are
believed to be the primary source of infection.
3 These horses are at risk of infection when their
skin becomes macerated from chronic moisture
resulting in the release of zoospores, the infective
stage of the organism.
4 Mechanical transmission of the organism occurs by
both biting and nonbiting ies as well as ticks.
5 Normal healthy skin is quite impervious to
infection with D. congolensis.
6 Some predisposing factor that results in decreased
resistance of the skin is necessary for infection to
occur, prolonged wetting of the skin by rain being
one of the most important.
Clinical features
1 The disease can be seen at any time of the year when
chronic moisture and wetting of the skin can occur.
2 The dorsal surfaces of the animal are aected
primarily (Figs 23 and 24).
3 Occasionally the lesions involve the lower extremities when animals are kept in damp environments
or exposed to dew.
4 In the early stages of the disease, the lesions can be
felt better than they can be seen. Thick crusts can be
palpated under the hair coat.
5 When these crusts are manually removed, the hair
comes with the crust (Fig. 25). The undersurface of
the crusts is usually concave with the roots of the
hairs protruding.
6 The underlying skin surface may appear relatively
normal, erythematous, or sometimes eroded. Suppuration of the underlying skin is not common.
Histological ndings
1 The characteristic microscopic feature is a stratied
or layered crust.
2 It is made up of alternating bands of parakeratotic
and/or orthokeratotic keratin and dense accumulations of degenerating inammatory cells (Fig. 26).
3 The layering reects the cyclic activity of the
organism and is an excellent example of horizontal
stratication.
4 Large numbers of organisms are present within the
crust (Fig. 27).
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 191203

Figure 23. Dermatophilosis over rump and back of adult horse.

Note areas where rain would likely keep area dampened. (Case
material: Ontario Veterinary College).

Figure 24. Dermatophilosis. Close up of matted crusts on rump of

horse in Fig. 23 (Case material: Ontario Veterinary College).

Figure 25. Dermatophilosis. Removal of a dermatophilus crust with

hairs protruding and erythematous skin beneath (Case material:
University of California, Davis).

5 Other changes include a suppurative luminal

folliculitis and a mixed perivascular inltrate.

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201

7 For more generalized disease dermatophytosis,

pemphigus foliaceus and generalized granulomatous
disease are the important dierential diagnoses.
8 In some environments the clinical condition in the
horse is called `dry dermatophilosis' and these horses
present with alopecia and dorsal scaling with an
absence of any moist exudates or heavy crusting. This
may be a clinical presentation over the rump of
groups of horses with recurrent disease.

Figure 26. Dermatophilosis. Horizontally laminated scale-crust is

typical of dermatophilosis lesions. (H & E. Magnication627.)

Clinical management
1 Although most cases of dermatophilosis will
spontaneously regress with the advent of dry weather,
certain measures are benecial.
2 Aected animals should be protected from further
exposure to rainfall or chronic wetness.
3 Grooming to remove the crusts should be encouraged. This is very painful and horse may need
sedation for the actual removal.
4 In severe cases, systemic antibiotic therapy such as
penicillin or trimethoprim-sulphonamide is utilized.9
PASTERN FOLLICULITIS

Figure 27. Dermatophilosis. Large numbers of lamentous,

transversely and longitudinally divided bacteria are found in the
surface crust. (H & E. Magnication6384.)

Diagnosis
1 The clinical features of dermatophilosis are fairly
characteristic.
2 For a denitive diagnosis, a portion of the crust
should be minced and mixed with a few drops of
water on a glass slide, air dried, heat xed, gramstained and examined microscopically. Touch preparations of the soaked under-surface of a new crust
can also be useful to identify the organism.
3 D. congolensis is a branching, Gram positive
organism and is seen under oil immersion. The
laments can usually be seen dividing both transversely and longitudinally into thick bundles of coccoid
forms (Fig. 28).
4 Occasionally, it is necessary to culture the organism if the direct microscopic examination is either
negative or questionable.
5 When taking biopsies, one should select a crusted
lesion and ask that the crust be sectioned and
embedded, even if it lifts o of the biopsy in the xative.
6 Dermatophilosis involving the lower extremities
must be dierentiated from contact dermatitis,
contact photosensitization, atypical dermatophytosis, pastern folliculitis and pastern leukocytoclastic
vasculitis.

General considerations
1 This is an uncommon bacterial skin disease of
horses.
2 The incidence of other manifestations of pyoderma
in the horse is unknown.
3 There appears to be no breed, sex or age
predilection.
Aetiology and pathogenesis
1 The causative agent is Staphylococcus spp.
2 The pathogensis and underlying trigger are unknown.
Clinical features
1 The lesions are usually limited to the posterior
aspect of the pastern and fetlock regions (Fig. 29).
2 One or more limbs may be involved.
3 The initial lesions consist of papules. Pustules are
uncommon.
4 If left untreated, the lesions coalesce and may
produce large areas of ulceration and suppuration.
5 The disease is not associated with systemic signs
and the general health of the animal is unaected.
Diagnosis
1 The clinical features of the disease are reasonably
characteristic. Biopsies are needed rarely.
2 Pustule contents, if available, may be obtained for
gram-stained smears for cytological conrmation,
bacterial culture and antibiotic sensitivity testing.
3 If any papular or crusted lesions are present,
dermatophytosis should also be considered.
4 Pastern folliculitis should be considered in the
dierential diagnosis of diseases lumped under the
term `Grease Heel'.
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225 DISC
202

A. A. Stannard

Figure 28. Dermatophilosis. Cytology preparation of minced crust

(Case material: Ontario Veterinary College).

Clinical management
1 It may be necessary to heavily sedate or anaesthetize the animal for the initial treatment, since the
lesions can be quite painful.
2 The aected area(s) should be clipped and washed
well with a mild antibacterial shampoo or cleansing
shampoo.
3 An appropriate antimicrobial ointment is then
applied twice a day.
4 Systemic antibiotic therapy, such as penicillin, is
rarely, if ever, indicated
REFERENCES
1. Biberstein, E.L., Jang, S.S., Hirsch, D.C. Species
distribution of coagulase-positive staphylococci in
animals. Journal of Clinical Microbiology 1984; 19:
6105.
2. White, S., Rosenkrantz, W.S. Workshop report 7.12:
Advances in equine dermatology In: Kwochka, K.W.,
Willemse, T., Von Tscharner, C. eds. Advances in
Veterinary Dermatology. Vol. 3. Oxford: Butterworth
Heinemann, 1998: 40913.
3. Fadok, V.A. Update on four unusual equine
dermatoses. Veterinary Clinics of North America:
Equine Practice 1995; 11(1): 10510.

Figure 29. Pastern folliculitis on the posterior aspect of the pastern

(Case material: Stannard).

4. Olsen, E.A. Hair disorders. In: Freedberg, I.M., Eisen,

A.Z., Wol, K., Austen, K.F., Goldsmith, L.A., Katz.
S.I., Fitzpatrick, T. B.eds. In: Fitzpatrick's
Dermatology in General Medicine 5th edn, Vol. 1.
New York: McGraw-Hill, 1999: 7379.
5. Tobin, D.J., Alhaidari, Z., Olivry, T. Equine alopecia
areata autoantibodies target multiple hair follicle
antigens and may alter hair growth. A preliminary
study. Experimental Dermatology 1998; 7: 28997.
6. Moriello, K.A., DeBoer, D.J., Semrad, S.D. Diseases
of the Skin. In: Reed, S.M. & Bayly, W.M. Equine
Internal Medicine. Philadelphia: W.B. Saunders, 1998:
pp 51357.
7. Scott, D.W. Large Animal Dermatology. Philadelphia:
W.B. Saunders, 1988: pp 12067.
8. Pascoe, R.R.R., Knottenbelt, D.C. Manual of Equine
Dermatology. Oxford: W.B. Saunders, 1999: pp 1026.
9. Logas, D.B., Barbet, J.L. Inammatory, Infectious,
and Immune Disease. In: Colahan, P.T., Merritt, A.M.,
Moore, J.N., Mayhew, I. G.eds. Equine Medicine and
Surgery. 5th edn, St. Louis: Mosby, 1999: 191027.

Zusammenfassung Dr Stannard erklart unterschiedliche Formen der Alopezie beim Pferd mit Schwerpunkt
auf Haarfollikel und ihrer Funktion in der Produktion der Haare. Normale und anormale Muster des
Haarwachstums und Haarverlusts beim Pferd werden beschrieben. Spezische entzundliche und
nichtentzundliche Erkrankungen der Haarfollikel werden im Detail mit ihrer klinischen Bedeutung
abgehandelt. Einige der klinischen Syndrome, die in diesem Kapitel behandelt werden (lineare Alopezie
und Alopezia areata) werden durch eine immunologische Reaktion gegen normale Strukturen verursacht und
hatten im ersten Teil abgehandelt werden konnen. Da jedoch die klinische Symptomatik durch Alopezie
gekennzeichnet ist, beschloss Dr Stannard, sie in seine Anmerkungen uber Alopezie mit einzuschlieen.
Andere Erkrankungen in diesem Kapitel sind bakterielle Hautinfektionen (z.Bsp. Fesselekzem und
Dermatophilose) sowie Pilzinfektionen (Dermatophytose). [Stannard A. A. Alopecia in the horse an
overview. (Alopezie beim Pferd eine Ubersicht.) Veterinary Dermatology 2000; 11: 191203.]

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225 DISC
Alopecia in the horse

203

Resume Le Dr Stannard explique les dierents formes d'alopecie chez le cheval, en insistant sur le follicule
pileux et son fonctionnement pour la synthese de poils. Les mecanismes normaux et les anomalies de la
croissance pilaire et des mues sont abordes. Certaines maladies speciques du follicule pileux, inammatoires
ou non, sont etudiees en detail notamment sur un plan clinique. Certaines des entites decrites dans ce chapitre
(alopecie lineaire et alopecia areata) sont dues a une attaque immunologique contre des structures normales
du follicule et auraient pu etre decrites dans le chapitre I. Cependant, comme la presentation clinique de ces
maladies se manifeste sous la forme d'une alopecie, le Dr Stannard a choisi de les inclure dans ce chapitre. Les
autres entites envisagees dans ce chapitre sont les infections bacteriennes cutanees (eg folliculite des paturons
et dermatophilose) et les infections fongiques (dermatophytoses). [Stannard A. A. Alopecia in the horse an
overview. (Un apercu des alopecies equines.) Veterinary Dermatology 2000; 11: 191203.]

Resumen El Dr Stannard explica diferentes formas de alopecia en el caballo con enfasis en el fol culo piloso y
en su funcion en la produccion del pelo. Se revisan tanto los patrones normales como anormales del
crecimiento del pelo y su muda en el caballo. Se discuten en detalle, incluyendo su importancia cl nica,
diferentes anormalidades del fol culo piloso, tanto inamatorias como no-inamatorias. Algunas de las
entidades cl nicas que abarca esta seccion (alopecia linear y alopecia areata) son causadas por un ataque
inmunologico contra estructuras normales y podr an haberse incluido en la Seccion I. Sin embargo, ya que la
presentacion cl nica de estas entidades es la alopecia, el Dr Stannard eligio incluirlas en sus notas en la
alopecia. Otras inclusiones en esta seccion incluyen las infecciones cutaneas bacterianas (p.ej. foliculitis de la
cuartilla y la dermatolosis) as como las infecciones fungicas del pelo (dermatotosis). [Stannard A. A.
Alopecia in the horse an overview. (Alopecia en el caballo una revision.) Veterinary Dermatology 2000;
11: 191203.]

# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 191203