Veterinary Dermatology 2004, 15, 260 265

Case report

Blackwell Publishing, Ltd.

Alopecia areata with lymphocytic mural folliculitis affecting

the isthmus in a thoroughbred mare
SILVIA COLOMBO*, JOHN A. KEEN, DAVID G. BROWNSTEIN, SUSAN M. RHIND,
BRUCE C. MCGORUM and PETER B. HILL*
*Hospital for Small Animals, and Equine Hospital, Division of Veterinary Clinical Studies, and Diagnostic
Clinicopathology Unit, The University of Edinburgh, The Royal (Dick) School of Veterinary Studies, Easter
Bush Veterinary Centre, Roslin, Midlothian, EH25 9RG, UK
(Received 23 August 2003; accepted 27 November 2003)

Abstract A 13-year-old, thoroughbred mare was presented with an 8-year history of multifocal, generalized,
noninflammatory alopecia and a 3-month history of alopecia, erythema and scaling of the white star on the forehead and muzzle. Histopathological examination of biopsy samples from multiple sites on the body (mane, neck,
shoulder, flank and gluteal region) showed a subtle lymphocytic inflammatory infiltrate affecting and surrounding the anagen hair bulbs, consistent with a diagnosis of alopecia areata. The biopsy sample from the star on the
forehead showed atrophic hair follicles with perifollicular and mural mononuclear folliculitis affecting the isthmus. Immunohistochemical staining with a CD3 marker confirmed the T-lymphocytic origin of the inflammatory
infiltrate in all the samples. The concurrent presence of lymphocytic infiltration at the bulbar and isthmic level
of the hair follicles in the same horse is unusual. This finding may represent a variation of the histological appearance of alopecia areata.
Keywords: alopecia areata, horse, lymphocytic isthmic mural folliculitis.

I N TRO D U CTI ON
Alopecia areata (AA) is a nonscarring inflammatory
hair loss observed in humans, dogs, cats, horses, cattle,
primates, poultry, mice and rats.1,2 The pathogenesis is
currently thought to be autoimmune, with production
of autoantibodies targeting various hair follicle antigens
and T lymphocytes infiltrating the follicular bulb on
histopathological examination.1,36
To the authors knowledge, only five cases of AA have
been reported in horses,5,710 one of which was a preliminary study on the autoantibodies produced in this
species.5 The horses in these case reports presented with
alopecia variably affecting the body, mane and tail, and
had characteristic findings of intra- and peri-bulbar
lymphocytes,79 in one case identified by immunohistochemical examination as cytotoxic CD8+ T lymphocytes.7
The aim of this case report is to describe a case of
equine AA, in which unusual clinical and histopathological findings were observed. Besides the previously
reported clinical features, this horse presented clinically with alopecia, erythema, scaling and crusting affecting the white areas on the face. On histopathological
Correspondence: P. B. Hill, Division of Veterinary Clinical Studies,
Royal (Dick) School of Veterinary Studies, University of Edinburgh,
Hospital for Small Animals, Easter Bush Veterinary Centre,
Roslin, Midlothian, EH25 9RG. E-mail: pbhill@ed.ac.uk
260

examination, biopsies from various body sites were

consistent with AA, while the facial lesions showed
mononuclear mural folliculitis affecting the follicular
isthmus. The infiltrating cells were identified as T lymphocytes by immunohistochemical examination in all
the biopsy samples.

C A S E R E P O RT
A 13-year-old, chestnut thoroughbred mare was presented
with an 8-year history of multifocal, generalized, noninflammatory, nonpruritic alopecia. Focal alopecia was
first noticed on the hocks when the horse was 5 years
old, and it gradually progressed to involve the trunk,
neck and hindquarters. The hair loss also involved
the mane and tail. According to the owner, temporary
improvement in the horses coat condition had been
noticed every year during the winter. However, the
partial hair re-growth had invariably been followed by
development of new focal areas of alopecia. Histopathological examination of two biopsy samples taken by
the referring veterinarian approximately 2 years before
referral showed only one atrophic hair bulb with one or
two inflammatory cells in one sample. This was considered mildly suggestive of AA.
Three months before presentation, the alopecia
extended to the white star on the forehead and muzzle
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261

Figure 3. Mane, 13-year-old thoroughbred mare. Partial alopecia.

Figure 1. Thirteen-year-old thoroughbred mare. Multifocal,
noninflammatory, areas of alopecia on the head, neck, shoulders,
chest, abdomen and proximal parts of the limbs. Note the rat tail.

Figure 2. Gluteal region and flank, 13-year-old thoroughbred mare.

Multifocal, noninflammatory areas of alopecia.

and was associated with erythema, scaling and focal

crusting. Various herbal-based creams and pure
petroleum jelly (Vaseline, Lever Faberg, London, UK)
had been applied to these areas, none of which produced
any improvement.
Previous history included bilateral osteoarthritis of
the tarsal joints and bilateral navicular disease, diagnosed 5 years before presentation. The horse had been
in the owners possession for 9 years and was used for
general riding purposes. It was regularly wormed and
vaccinated, kept outside during the day and stabled
overnight. The diet consisted of hay, cereal mix and
alfalfa hay.
General physical examination was unremarkable.
On dermatological examination, there were multifocal,
noninflamed, irregularly shaped, coalescing areas of
alopecia on the neck, shoulders, chest, abdomen and
proximal limbs (Figs 1 and 2). The alopecia affected
the mane (Fig. 3) and tail, which had a rat-tail-like
appearance. The alopecic lesions also involved the
head and the white areas on the face (star on the forehead and muzzle). The nonpigmented areas were

Figure 4. White star on the forehead, approximate size 12 8 cm,

13-year-old thoroughbred mare. Well-demarcated alopecia,
erythema, scaling and focal crusting.

inflamed, with severe erythema, scaling and focal

crusting (Figs 4 and 5). The white area on the left hind
pastern was not affected.
Differential diagnoses for the multifocal noninflammatory alopecia included AA, mane and tail dystrophy, and telogen defluxion. Anagen defluxion,
dermatophytosis and demodicosis were considered
unlikely due to the length of the history. The lesions on
the white areas on the face were consistent with either
sunburn secondary to the hair loss, drug-induced or
contact irritant/hypersensitivity reaction to the topical
products applied by the owner or photo-sensitization
(primary or hepatogenous), although the pastern was
not involved.

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S Colombo et al.

Figure 6. Skin biopsy of the gluteal region, 13-year-old

thoroughbred mare. (a): Lymphocytic inflammatory infiltrate
affecting and surrounding an anagen hair bulb. H&E, bar = 60 m.
(b): Immunohistochemical staining with a CD3 marker for T
lymphocytes (Polyclonal rabbit antihuman CD3, Dako),
confirming the T-lymphocytic origin of the inflammatory infiltrate.
Bar = 60 m.

Figure 5. Muzzle, 13-year-old thoroughbred mare. Alopecia,

erythema and scaling. Note the clear demarcation of the lesions.

The horse was sedated with romifidine (Sedivet,

Boehringer Ingelheim, Bracknell, UK) at 0.04 mg kg1
and butor-phanol (Torbugesic, Fort Dodge Animal
Health, Southampton, UK) at 0.02 mg kg1, both
administered intravenously. Multiple skin scrapings
were negative for demodicosis, and a fungal culture was
negative for dermatophytes. Hair trichograms showed
a normal mixture of anagen and telogen hair bulbs. A
blood sample was taken for haematological examination
and biochemical examination limited to the parameters
assessing the liver function (total proteins, albumin,
globulin, total bilirubin, bile acids, alkaline phosphatase,
gamma-glutamyl transferase and glutamate dehydrogenase). All parameters were within the respective
normal reference ranges. Six skin biopsy samples were
taken from the forehead, mane, neck, shoulder, flank
and gluteal region for histopathological examination
and fixed in 10% buffered formalin solution.
There were similar histopathological changes in skin
biopsies taken from the mane, neck, shoulder, flank
and gluteal region. These consisted of mild lymphocytic infiltrates in and around scattered anagen
hair bulbs, in conjunction with vacuolation of some
hair matrix cells (Fig. 6). The epidermis showed mild
orthokeratotic hyperkeratosis, mild epidermal hyperplasia and occasional blunt rete-ridges. The dermis
showed very mild superficial perivascular dermatitis of
mixed mononuclear cells. The sample taken from the
forehead contained atrophic hair follicles with prominent perifollicular and mural collars of lymphoid cells
in the region of the isthmus (Fig. 7). The sebaceous
glands were absent. The epidermis was mildly parakeratotic, with uneven acanthosis and blunt rete-ridges.
In the deeper layers of the epidermis, there was

Figure 7. Skin biopsy of the white star on the forehead, 13-year-old

thoroughbred mare. (a): Perifollicular and mural mononuclear
folliculitis affecting the isthmus. Note the absence of sebaceous
glands. H&E, bar = 80 m. (b): Immunohistochemical staining with
a CD3 marker for T lymphocytes (Polyclonal rabbit antihuman CD3
Dako) confirming the T-lymphocytic origin of the inflammatory
infiltrate. Bar = 100 m.

intercellular oedema and neutrophilic infiltration. The

superficial dermis showed oedema with mild, mainly
neutrophilic perivascular dermatitis. Immunohistochemical staining of all biopsies with anti-CD3 (Polyclonal rabbit antihuman CD3, Dako, Dako UK Ltd,
Ely, UK) revealed that most lymphoid cells infiltrating
in and around anagen hair bulbs and isthmus were T
cells (Figs 6 and 7).
Once the results of the diagnostic tests were received,
the poor prognosis and lack of a reported effective treatment for AA in horses were discussed with the owner.
However, it was felt that the inflammatory changes on
the horses face required treatment. A topical preparation containing 0.5% fusidic acid and 0.1% betamethasone (Fuciderm carbomer gel, Leo Animal Health
Mekuvej, Denmark) was dispensed, to be applied once
daily on the white areas. It was also recommended that
the horse be kept stabled during the day, to avoid suninduced damage to the white skin areas. During a telephone conversation 1 month post referral, the owner
indicated that the erythema and scaling on the face had
markedly improved, but no hair re-growth had been
observed. The owner was reluctant to continue the
treatment because of the possibility of adverse effects
of glucocorticoids, and the treatment was discontinued.
At the time of writing (9 months since diagnosis), no hair

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Equine alopecia areata

re-growth has occurred, but the erythema, scaling and
crusting affecting the white star on forehead and muzzle
has completely resolved. The horse has been mainly kept
stabled, and a 50 SPF (sun protection factor) sunscreen
has been applied on the face when it was outdoors.

D ISCU SSION
AA is a nonscarring, inflammatory alopecia affecting
approximately 1.7% of the human population and, less
commonly, numerous animal species.1 Autoantibodies
of the immunoglobulin G subclass (IgG) targeting hair
follicle antigens have been identified in humans, dogs,
horses, rats and mice.1,3,5,6 In dogs, the main antigen
is trichohyalin, a 200220 kiloDalton (kDa) protein
expressed mainly in the inner root sheath.6,11 In the
horse, the antigens targeted are heterogeneous and
include trichohyalin and hair keratins of 4060 kDa,5
while in humans and rodents the hair keratins represent the main target.1 The role of autoantibodies has
not been completely elucidated, although they are not
likely to be a result of hair shaft destruction as, in
humans, they can occur before hair loss is evident.1,5
Autoantibodies against hair follicle antigens are not
found in unaffected humans, and IgG from an affected
horse induced hair telogenization and prevented hair
re-growth when injected into normal black mice.1,5
Genetics also play a role and, in rodents, AA seems
to be a polygenic disease with incomplete penetrance
and variable expression.1 In humans it has been associated with some human leukocyte antigens (HLA)
alleles, and it is commonly seen in Downs syndrome
patients.12
Two of the reported equine cases7,8 have been categorized as alopecia universalis, which, in humans, is
the most severe form of AA and implies complete loss
of scalp and body hair. The use of this term may not be
appropriate, as the alopecia in horses is not usually
complete. In this case, the mane and tail were severely
affected, while in the reported cases this finding has
been variably present.5,710 The clinical entity previously known as mane and tail dystrophy is likely to be
a manifestation of AA.4 The main differential diagnoses in this case were anagen and telogen defluxion,
although the 8-year history and lack of association
with a severe systemic disease were not consistent with
these conditions.13
Histopathological examination reveals similar findings in all species. In canine and equine cases, the
pathognomonic lesion is a lymphocytic bulbitis affecting anagen hair follicles, which may be subtle and
difficult to demonstrate in horses.3,4 In this case, the
biopsies taken by the referring veterinarian showed
very mild changes, and a final diagnosis could not be
made, although AA was suspected. Atrophic hair follicles, dystrophic hair shafts and vacuolated or apoptotic matrical cells have also been reported.4,5,79 In
humans and rodents, the histopathological findings are
similar and the severity and type of infiltrate may vary,

263

depending on the biopsy site and duration of the disease.1 All the histopathological findings described were
observed in this case, except the dystrophic hair shafts.
In humans and dogs, the lymphocytes infiltrating
the bulbs are T-cytotoxic cells (CD8+), while around
the affected hair follicles T-helper cells (CD4+) and
dendritic cells predominate.1,3,11 Immunohistochemical
examination in horses showed infiltrating CD8+ T lymphocytes and dendritic cells.7 In the case described
here, immunohistochemical staining identified the
infiltrating cells as T lymphocytes (CD3+), but further
studies were not possible because the relevant antibodies were unavailable.
Unusual histopathological findings were observed in
the forehead biopsy sample. The lymphocytic inflammation targeted the follicular isthmus and sebaceous
glands were absent. In humans and rodents with AA,
the infiltrate may extend to the level of the sebaceous
glands.1 The lack of significant involvement of the
bulbs in the forehead biopsy may be due to the subtleness of the lesions in horses and biopsy sample variability. Primary targeting of the follicular isthmus has
not been reported in AA, while it was the main finding
in a condition in five dogs and one cat described as
resembling pseudopelade of humans.14,15 A further
case of a dermatosis characterized by cytotoxic T lymphocytes targeting the follicular isthmus had been previously reported in a cat and named alopecia-areata
like dermatosis.16 The disease described in these case
reports is characterized by noninflammatory alopecia,
lymphocytic isthmic mural folliculitis, apoptosis of follicular keratinocytes, occasional absence of sebaceous
glands and atrophy and fibrosis of the hair follicles
in chronic stages. The infiltrating T lymphocytes are
CD8+, with perifollicular CD4+ and CD8+ T lymphocytes and dendritic cells. Circulating autoantibodies
against various hair follicles antigens (trichohyalin
and 142, 105 and 4065 kDa proteins) are also found.
The authors concluded that this condition resembles
the human disease known as pseudopelade of Brocq,
but also shares similarities with AA.14,15 Pseudopelade
of Brocq is currently not considered to be a specific
condition, but the end stage of chronic inflammatory
diseases, such as lichen planus pilaris and discoid lupus
erythematosus.17 The disease described as resembling
pseudopelade of humans might therefore represent
the end stage of other chronic diseases or might be a
species variation of AA, as suggested by the findings
observed in this horse.
Lymphocytic mural folliculitis is a reaction pattern
mainly seen in the cat, and it could be an early manifestation of epitheliotropic cutaneous lymphoma, a
histopathological feature of dermatophytosis, food
hypersensitivity/intolerance and adverse drug reaction,
or it could be idiopathic.1820 In this case, the facial
lesions did not progress and a fungal culture for dermatophytosis was negative, while food hypersensitivity
was not investigated. Lymphocytic isthmic mural folliculitis can also occur in cases of granulomatous sebaceous adenitis, a disease which has not been reported in

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S Colombo et al.

the horse. In this disease, the primary targets of the

inflammation are the sebaceous glands, and the inflammatory infiltrate can be lymphohistiocytic to pyogranulomatous.18 Interestingly, the sebaceous glands were
absent in this case in the forehead biopsy sample. A
granulomatous mural folliculitis has been observed in
horses receiving various topical and systemic medicaments.21 This condition is characterized by infiltration
and eventual replacement of follicular epithelium, and
occasionally sebaceous glands, with granulomatous
inflammation.21 A contact irritant/hypersensitivity
reaction could have been present as a complicating
factor, and might explain the inflammatory appearance
of the lesions on this horses face and some of the
histopathological findings (epidermal acanthosis,
intercellular oedema and neutrophilic infiltration,
superficial dermal oedema with mild neutrophilic
inflammation).21,22 The other differential diagnoses for
the facial lesions were sunburn and photosensitization,
but the white pastern was not affected and results of
histopathological and biochemical examinations were
not consistent with these diagnoses.21,22
Spontaneous, temporary hair re-growth has been
described in horses with AA, although the long-term
prognosis is unknown.4,5,8,9 There is no effective treatment for equine patients, and systemic glucocorticoids
produce minimal improvement.4 In humans, response
to topical or systemic glucocorticoids, contact sensitizers,
photodynamic therapy, minoxidil and cyclosporin A
has been observed, although there is no permanent cure.1
In veterinary species, AA is a cosmetic disease and
does not affect the quality of life. The use of immunosuppressive treatments is, therefore, ethically questionable.

ACKN OWLEDGE ME NT S

6.

7.

8.
9.

10.

11.

12.

13.
14.

15.

16.

The authors are very grateful to Dr Keith L. Thoday

for revising the manuscript.

R E FEREN CES
1. McElwee KJ, Boggess D, Olivry T et al. Comparison of
alopecia areata in human and nonhuman mammalian
species. Pathobiology 1998; 66: 90 107.
2. McElwee KJ, Hoffmann R. Alopecia areata animal
models. Clinical and Experimental Dermatology 2002;
27: 410 17.
3. Olivry T, Moore PF, Naydan DK et al. Antifollicular
cell-mediated and humoral immunity in canine alopecia
areata. Veterinary Dermatology 1996; 7: 6779.
4. Stannard AA. Alopecia in the horse an overview. In:
Von Tscharner C, Yager JA, Kunkle G. eds. Stannards
Illustrated Equine Dermatology Notes. Veterinary Dermatology 2000; 11: 191203.
5. Tobin DJ, Alhaidari Z, Olivry T. Equine alopecia areata
autoantibodies target multiple hair follicle antigens and

17.

18.

19.

20.

21.
22.

may alter hair growth. Experimental Dermatology 1998;

7: 28997.
Tobin DJ, Olivry T, Bystryn JC. Anti-trichohyalin antibodies in canine alopecia areata. In: Kwochka KW,
Willemse T, Von Tscharner C. eds. Advances in Veterinary
Dermatology, Vol. 3. Oxford: Butterworth Heinemann,
1998: 35562.
Affolter VK, Cannon AG. Alopecia universalis in a
horse. Proceedings of the 14th AAVD and ACVD Meeting. San Antonio, Texas, 1998: 912.
Middleton DJ, Church S. Alopecia universalis in a horse.
Veterinary Dermatology 1994; 5: 1235.
Schott HC, Petersen A, Dunstan RW et al. Spontaneous
recovery from equine alopecia areata/universalis: case
report and comparison of the disorder in other species.
In: Kwochka KW, Willemse T, Von Tscharner C. eds.
Advances in Veterinary Dermatology, Vol. 3. Oxford:
Butterworth Heinemann, 1998: 469.
Black SS, Rashmir-Raven AM, Williams S. Equine clinical snapshot #4. Compendium on Continuing Education for the Practicing Veterinarian 2001; 23: 758.
Olivry T, Luther PB, Dunston SM et al. Canine alopecia
areata: clinical, pathological and immunological observations (24 cases). Proceedings of the Annual Meeting of
the International Society of Veterinary Dermatopathology. San Francisco, California, 2000.
McDonagh AJG, Tazi-Ahnini R. Epidemiology and
genetics of alopecia areata. Clinical and Experimental
Dermatology 2002; 27: 4059.
Milne EM, Rowland AC. Anagen defluxion in two
horses. Veterinary Dermatology 1993; 3: 13943.
Gross TL, Olivry T, Tobin DJ. Morphologic and immunologic characterization of a canine isthmus mural folliculitis resembling pseudopelade of humans. Veterinary
Dermatology 2000; 11: 1724.
Olivry T, Power HT, Woo JC et al. Anti-isthmus autoimmunity in a novel feline acquired alopecia resembling
pseudopelade of humans. Veterinary Dermatology 2000;
11: 26170.
Power HT, Olivry T, Woo J et al. Novel feline alopecia
areata-like dermatosis: cytotoxic T lymphocytes target
the follicular isthmus. In: Kwochka KW, Willemse T,
Von Tscharner C. eds. Advances in Veterinary Dermatology, Vol. 3. Oxford: Butterworth Heinemann, 1998: 538.
Amato L, Mei S, Massi D et al. Cicatricial alopecia; a
dermatopathologic and immunopathologic study of 33
patients (pseudopelade of Brocq is not a specific clinicopathologic entity). International Journal of Dermatology 2002; 41: 815.
Gross TL, Stannard AA, Yager JA. An anatomical classification of folliculitis. Veterinary Dermatology 1997; 8:
14756.
Declerq J. A case of diet-related lymphocytic mural
folliculitis in a cat. Veterinary Dermatology 2000; 11:
7580.
Scott DW, Miller WH, Griffin CE. Muller and Kirks
Small Animal Dermatology, 6th edn. Philadelphia:
W.B. Saunders, 2001.
Scott DW, Miller WH. Equine Dermatology. Philadelphia: W.B. Saunders, 2003.
Pascoe RRR, Knottenbelt DC. Manual of Equine
Dermatology. London: W.B. Saunders, 1999.

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Rsum Une jument ge de 13 ans, a t prsente pour une alopcie multifocale gnralise, non inflammatoire voluant depuis 8 ans, associe une alopcie, un rythme et un squamosis des balzanes de lencolure et
du chanfrein voluant depuis 3 mois. Lexamen histopathologique de biopsies cutanes multiples (crinire, cou,
paules, flancs) a montr un infiltrat lymphocytaire modr, localis autour des bulbes anagnes, compatible avec
une alopecia areata. La biopsie cutane de la face a montr des follicules pileux atrophiques et des images de
prifolliculite et de folliculite murale mononucle, atteignant listhme. Un marquage immunohistochimique avec
un marqueur CD3 a confirma lorigine lymphocytaire T de linfiltrat inflammatoire sur tous les prlvements.
La prsence concommitante dun infiltrat lymphocytaire du bulbe et de listhme nest pas usuelle. Cette observation
pourrait reprsenter une variante de lapparition histologique de lalopecia areata chez le cheval.
Resumen Una yegua de 13 aos de pura raza (Troroughbred ) presentaba una historia de ocho aos de alopecia
multifocal, generalizada y no inflamatoria, y una historia de tres meses de alopecia, eritema y descamacin de
la estrella blanca de la frente y hocico. El examen histopatolgico de las muestras de biopsia de diferentes reas
corporales (crin, cuello, espalda, flanco y regin gltea) mostraron un infiltrado inflamatorio linfoctico discreto
afectando y rodeando los bulbos pilosos en anagen, compatible con un diagnstico de alopecia areata. La muestra
de biopsia de la estrella de la frente mostr folculos pilosos atrficos con foliculitis mononuclear perifolicular y
mural afectando el istmo. Las tinciones inmunohistoqumicas con un marcador de CD3 confirmaron el origen
en linfocitos T del infiltrado inflamatorio de todas las muestras. La presencia concomitante de la infiltracin
linfoctica a nivel bulbar e stmico de los folculos pilosos en el mismo caballo es inusual. Este hallazgo podra
representar una variante de la presentacin histolgica de la alopecia areata.
Zusammenfassung Eine 13 Jahre alte Vollblut-Stute wurde wegen multifokaler, generalisierter, nicht-inflammatorischer Alopezie seit 8 Jahren und wegen Alopezie, Erythem und Schuppen seit 3 Monaten im Bereich des
weien Sterns auf der Stirn und an der Mauls vorgestellt. Die histopathologische Untersuchung von Biopsien
verschiedener Krperregionen (Mhne, Hals, Schulter, Flanke und Glutealgegend) zeigten ein geringes
lymphozytres inflammatorisches Infiltrat in und um anagene Haarfollikel wie bei Alopecia areata. Die Biopsie
von dem Stern auf der Stirn zeigte atrophische Haarfollikel mit perifollikulrer und muraler mononuklerer
Follikulitis im Bereich des Isthmus. Immunhistochemische Frbung mit einem CD3-Marker besttigte in
allen Proben die T-lymphozytre Herkunft des entzndlichen Infiltrates. Die gleichzeitige Prsenz einer
lymphozytren Infiltration im Bereich von Bulbus und Isthmus des Haarfollikels bei dem gleichen Pferd ist
ungewhnlich. Diese Entdeckung kann eine Variation des histologischen Erscheinungsbildes von Alopecia areata
darstellen.

2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 260265