198 DISC

Veterinary Dermatology 2000, 11, 261270

Anti-isthmus autoimmunity in a novel feline acquired

alopecia resembling pseudopelade of humans*
THIERRY OLIVRY,{ HELEN T. POWER,{ JENNIFER C. WOO,} PETER F. MOORE} and
DESMOND J. TOBIN}
{Department of Clinical Sciences, North Carolina State University College of Veterinary Medicine, Raleigh,
NC 27606, USA and Department of Dermatology, University of North Carolina School of Medicine, Chapel
Hill, NC 26515, USA
{Dermatology for Animals, Campbell, CA 95008, USA
}Department of Pathology, Microbiology and Immunology, University of California School of Veterinary
Medicine, Davis, CA 27606, USA
}Department of Biomedical Sciences, University of Bradford, Bradford BD7 1DP, UK
(Received 5 January 1999; accepted 21 July 1999)

Abstract Pseudopelade is a primary scarring (cicatricial) alopecia of humans characterized by lymphocyterich inammation centred around the hair follicle isthmus. Lymphocyte folliculotropism is associated with
isthmus apoptosis and, ultimately, follicular destruction and dermal brosis. In a cat, an acquired alopecia
was diagnosed as pseudopelade based on the following criteria: (i) an adult-onset, patchy to diuse
nonpruritic hair loss; (ii) an early folliculo-destructive phase in which lymphocytes and dendritic cells
accumulated in and around the follicular isthmus; and (iii) a late stage in which the lower segments of hair
follicles underwent atrophy and were replaced by brosing tracts. Additionally, immunological investigations
characterized the cytotoxic phenotype of isthmotropic lymphocytes and demonstrated the presence of
circulating IgG autoantibodies specic for multiple follicular antigens. Altogether, the results of the present
study suggest an immune-mediated pathogenesis for this case of feline pseudopelade, similarly to that causing
alopecia areata in humans and other mammalian species.
Keywords: alopecia areata, antifollicular autoantibodies, autoimmunity, cat, cicatricial alopecia, pseudopelade.

INTRODUCTION
In humans, the generic terminology `cicatricial
alopecia' (syn: scarring alopecia) applies to various
acquired dermatoses in which hair loss occurs
subsequent to stem cell failure.1 Stem cell inadequacy
most commonly follows the destruction of mid hair
follicles by inammatory cells.1 Any follicular infection, trauma, neoplasia, congenital/hereditary defects
or autoimmune process that causes follicular destruction therefore can result in cicatricial alopecia.1,2
Primary scarring alopecia is a subgroup of cicatricial
alopecia in which pilosebaceous units, but not the
associated reticular dermis, are specically targeted
by inammatory cells.1 Pseudopelade (PP) is a
primary scarring alopecia characterized in humans
by grossly noninammatory and usually permanent
patchy baldness. First reported in 1885 by the
*Part of this study was presented at the 3rd World Congress of
Veterinary Dermatology (1996) as follows: Power, H.T., Olivry, T.,
Woo, J., Moore, P.F. Novel feline alopecia areata-like dermatosis:
cytotoxic T-lymphocytes target the follicular isthmus (abst. 9.29).
Correspondence and request for reprints: Dr Thierry Olivry,
Department of Clinical Sciences, North Carolina State University,
College of Veterinary Medicine, 4700 Hillsborough Street, Raleigh,
NC 27606, USA, Tel.: (919) 5136276, Fax: (919) 513 6336
# 2000 Blackwell Science Ltd

Parisian dermatologist L. Brocq, the denomination

pseudopelade was coined because of the clinical
resemblance to alopecia areata (pelade in French).3,4
The cutaneous histopathology of human PP is
variable, depending upon lesional stage. In early PP,
mononuclear cells, mainly lymphocytes, surround and
invade the follicle isthmus region and cause follicular
destruction.1,2,5,6 As opposed to that seen in alopecia
areata, the inammatory inltrate of PP spares the
lower segments of the follicles.5 In the late phase of
PP, brous cords occupy the space left by disappearing follicles.5,6 Naked hair shafts sometimes are seen
in vertically orientated foreign body granulomas.1
The aetiology of PP remains presently uncharacterized. Its pathogenesis, nevertheless, is suspected to
involve a cytotoxic T-lymphocyte-mediated destructive
inammation directed against the follicular isthmus.1
This study characterizes the clinical features, skin
histopathology and immunological abnormalities in a
cat with a novel acquired cicatricial alopecia resembling PP of humans. In this patient, cytotoxic
T-lymphocytes invaded the follicular isthmus resulting in its destruction. This follicle `vandalism' was
followed by furunculosis and a granulomatous
response. Circulating autoantibodies, directed against
a variety of follicular proteins, were detected concurrent to the active disease process.
261

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METHODS
Specimens
Punch biopsy of lesional skin and serum were
obtained from a 6-year-old male castrated domestic
longhaired cat with acquired alopecia (clinical
description see below). The samples were bisected,
one half of each specimen was placed in neutral
buered formalin and processed for routine histopathology. The second half was deposited in Optimal
Cutting Temperature medium (OCT Tissue Tek,
Baxter Diagnostics Inc., McGaw Park, Illinois), and
plunged in isopentane cooled to its freezing point in
liquid nitrogen. These specimens were stored at
770 8C until processed for immunostaining.
Immunophenotyping of cutaneous mononuclear cells
Sections of frozen skin biopsy specimens were cut in a
cryostat and immunostained using a three-step
streptavidin method.7,8 The phenotype of skininltrating mononuclear cells was characterized with
a panel of monoclonal antibodies specic for feline
leukocyte antigens (Table 1).9,10 All of the latter
monoclonal antibodies were generated at the University of California Davis (JCW, PFM). Additionally, antibodies directed against the cytoplasmic
domain of animal and human T-and B-cell receptor
accessory proteins (CD3e and CD79a, respectively)
were utilized as previously described.11,12
Detection of tissue-bound autoantibodies
Skin-xed IgG autoantibodies were detected by direct
immunouorescence (IF) testing of paran-embedded skin sections using uorescein-labelled goat
antifeline IgG antibodies (Cappel, Organon Technika
Corp, West Chester, PA) as reported previously.13
Antigen retrieval was performed with trypsin proteolysis (Sigma, St Louis, MO) 0.1% for 45 min at 37 8C.
To decrease the autouorescence of the background,
all sections were counterstained with Evans' Blue
(Sigma, St Louis, MO) and 4' 6 diamidino-2phenylindole (DAPI) (Vector laboratories, Burlingame, CA). Normal feline lip was used as a negative
control. The positive controls were skin lesions from
a cat aected with bullous pemphigoid (BP).

Table 1. Panel of antibodies specic for leukocyte antigens

Cell Type

Antigen

Clone/
Catalogue #

Dendritic cells

MHC II
CD1a
CD3e

42.3
FE1.5F4
A0452

T-lymphocytes

CD5
CD4
CD8a
CD8b
CD79a

FE1.1B11
FE1.7B12
FE1.10E9
FE5.4D2
HM57

B-lymphocytes

Source
P.F. Moore
P.F. Moore
Dako, Carpinteria,
CA
P.F. Moore
P.F. Moore
P.F. Moore
P.F. Moore
Dako, Carpinteria,
CA

# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 261270

Detection of circulating autoantibodies

Initial screening of circulating IgG autoantibodies
was performed with an indirect IF method using
normal feline, canine and equine haired skin substrates and serial dilutions of the patient's serum. The
extinction titre of hair follicle-specic antibodies was
determined using uorescein-labelled antifeline IgG
antiserum.13 Pooled sera from 5 normal cats was used
for negative controls. Serum from a cat with
mucinous degenerative mural folliculitis (MDMF),
a disease in which lymphocyte folliculotropism also is
abundant, was utilized as an additional negative
control. Finally, the serum from a cat with BP served
as the positive control. All control sera were tested at
1 : 100 dilution.
Identication of antigens targeted by circulating
autoantibodies
Six M urea extracts of plucked human anagen hair
follicles (15 mg/lane) were separated, under reducing
conditions, by sodium dodecyl sulphate 8% polyacrylamide gel electrophoresis and electroblotted
onto polyvinylidene diuoride microporous membranes (Imobilon, Millipore, Bedford, MA). The
membranes were blocked with 2% nonfat milk in
phosphate buered saline (pH 7.4) for 2 h. The
individual feline sera (1 : 100 dilution) were incubated
for 12 h at 4 8C in blocking buer. The membranes
were overlaid with peroxidase-conjugated goat antifeline IgG antibodies (Organon Teknica, West Chester,
PA) and developed with 4-chloro-naphtol.14 The
negative control consisted of the serum of the cat
with MDMF also tested in IF studies.
RESULTS
Clinical summary
Generalized, nonpruritic, noninammatory hair loss
progressed during a 18-month period in this patient.
The alopecia was located initially on the rear legs and
abdomen and extended inexorably to the anks, tail
and nally the face (Figs 1, 2). There were no
remaining hair shafts in contrast to the stubby pelage
seen in self-induced alopecia. The border between
haired and alopecic regions was discrete without
blending of aected to nonaected areas. Onychorrhexis of the rear claws was observed (Fig. 3) whilst
the front claws had been removed surgically prior to
disease onset. Where hair was still present on the
dorsum, ne scaling was evident and the skin felt oily
to the touch.
Repeated coat-brushing dermatophyte cultures
and skin scrapings remained negative at all times.
Complete blood cell counts, serum chemistry panels,
thyroxin serum levels and retroviral (FeLV and FIV)
testing yielded unremarkable results.
Treatment was attempted, at various times, with
repositol methylprednisolone acetate, prednisone at
immunosuppressive dose (2 mg kg71 every 12 h),

198 DISC
Feline pseudopelade

263

Figure 1. Alopecia is evident on the

legs, abdomen, anks and legs.

Figure 2. Clinically noninamed facial

alopecia resembles that observed in
alopecia areata.

cyproheptadine and cephalexin without noticeable

hair regrowth. After one year, cyclosporin A was
prescribed because of the suspected autoimmune
pathogenesis of the hair loss (Neoral, Novartis, East
Hanover, NJ; 5 mg kg71, given orally, twice daily).
Weekly cyclosporin 12-h blood trough levels were
performed and the dosage of the medication was
adjusted to achieve cyclosporinemias of 350500 mg
mL71. After one month of treatment, remarkable
hair regrowth was evident, and the dosage of
cyclosporin A was reduced to 2 mg kg71 twice daily.
Despite repeated adjustments of cyclosporin A
dosages, adequate trough levels could not be established and the cat became increasingly dicult to
treat. Hair loss recommenced therefore after 3
months of cyclosporin therapy. This cat shortly
thereafter developed a distinctive circular patch of

spontaneous alopecia in the remaining haired area of

the dorsum. This new lesion was diagnosed as
Microsporum canis dermatophytosis. The owners
requested cyclosporin A discontinuation and declined
further immunomodulating therapy. The dermatophyte infection was treated successfully with oral
itraconazole. During the following year, the nonpruritic and noninammatory hair loss progressed
from a patchy to total hair loss.
Cutaneous histopathology
Histopathological examination of skin biopsy specimens, collected at 3 dierent times during 3 months,
yielded identical results. Biopsies of active lesions
exhibited severe follicular inammation in and
around the follicular isthmus but sparing the hair
bulbs and adnexae (Figs 4, 5). Inammatory cells
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T. Olivry et al.

Figure 3. Noninammatory alopecia

and onychorrhexis can be seen on the
hind feet.

Figure 4. Early folliculocentric inammation is rich in mononuclear cells. Lymphocyte-associated apoptosis of isthmus keratinocyte is evident. Note that the hair bulb and lower follicle remain
unaected. Hematoxylin and eosin; original magnication 666.

# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 261270

Figure 5. Full-blown follicular inammation is characterized by

mid-follicle destruction and ejection of naked hair shafts to the
perifollicular dermis. Haematoxylin and eosin; original magnication 650.

198 DISC
Feline pseudopelade
consisted initially of lymphocytes, histiocytic/dendritic cells, mast cells, and rare neutrophils, eosinophils
and plasma cells. Isthmus inammation was associated with apoptosis of keratinocytes and led to
follicular rupture. Dermal release of naked hair shafts
triggered a foreign body granulomatous response
with giant cells and melanophages (Fig. 6).
Biopsies from areas where the hair had been absent
for the longest time did not exhibit noticeable
inammation. In such areas, the follicular groups
had undergone atrophy of lowest and middle segments leaving infundibula and sebaceous glands
unaected. Healing of the inferior section of follicles
was followed by vertically orientated broblast hyperplasia, brosis and rare foreign body macrophages
(Fig. 7). Examination of all biopsies with fungal stains
(Gomori's methenamine silver and periodic acid of
Schi) did not demonstrate any organisms.

265

cells (* 25%). Folliculotropic (i.e. mural) lymphocytes expressed primarily CD8 a and b chains,
markers of cytotoxic phenotype (Figs 8, 9). In
contrast, perifollicular T-cells expressed the CD4
glycoprotein categorizing them as helper T-lymphocytes. Occasional perifollicular dendritic cells expressed low levels of CD4, signifying an activated
state. Mature B-lymphocytes, expressing CD79a,
were remarkably rare in the lesions examined. Most,
if not all, inammatory cells expressed class II major
histocompatibility complex (MHC II) molecules.
Follicular keratinocytes, conversely, had not upregulated MHC II heterodimers.
In older lesions, the inammation was markedly
reduced or absent. There was hyperplasia of dendritic
CD1a+ and MHC II+ epithelial Langerhans' cells
indicative of a previously activated status.

Immunophenotyping of cutaneous mononuclear cells

Skin-inltrating mononuclear cells were characterized by means of indirect immunohistochemical
staining using a panel of monoclonal antibodies
specic for leukocyte antigens. In actively inamed
lesions, perifollicular cells consisted predominantly of
CD3+, CD5+ T-lymphocytes (* 75% of the cells)
and CD1a-expressing dendritic antigen-presenting

Detection of tissue-bound autoantibodies

Direct IF testing of paran-embedded sections yielded
variable results depending upon the inammatory
stage of the biopsies. Active lesions, characterized by
current follicular destruction, exhibited weak IgG
deposition interspersed between collagen bundles
around the mid-follicle region. However, IgG deposits
were not detected in older lesions, i.e. those exemplied
by vertically orientated brous tracts. In no biopsies

Figure 6. Giant cell formation is triggered by follicular destruction.

Haematoxylin and eosin; original magnication 6100.

Figure 7. Fibrous tracts, melanophages and rare giant cells occupy

the site of previously destroyed lower hair follicles. Haematoxylin
and eosin; original magnication 633.
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T. Olivry et al.

Figure 8. CD8a+ T-lymphocytes target the follicular isthmus.

Immunohistochemistry, FE1.10E9 monoclonal antibody, AEC
chromogen and haematoxylin counterstain; original magnication
625.

Figure 9. Detail of Fig. 8 Lymphocyte folliculotropism is

associated with follicular destruction. Immunohistochemistry,
FE1.10E9 monoclonal antibody, AEC chromogen and
haematoxylin counterstain; original magnication 680.

were follicular-specic autoantibodies detected. There

was no IgG deposition in the normal feline skin
(negative control) whilst immunostaining of the skin of
the cat with BP demonstrated basement membranexed IgG autoantibodies (positive control).15

hair follicles. IgG antibodies to hair follicles were

detected in the serum of this cat, but not in that of the
control individual. Autoantibodies of highest titre
were directed against a 200220 kDa antigen doublet
with a migration pattern similar to trichohyalin14 and
against proteins of molecular weight 142 kDa, 105
kDa and 4065 kDa cluster (most likely hair keratins)
(Fig. 11). Autoantibodies specic for other minor
antigens were also detected with a fainter intensity.

Detection of circulating autoantibodies

Indirect IF testing, performed using homo- and
hetero-specic haired substrates, yielded similar
results. In this patient, a high titre (1 : 500) of IgG
autoantibodies, specic for the lower hair follicle
region, was detected. These autoantibodies targeted
the matrical precortex, lower hair cortex and inner
root sheath (Fig. 10). Autoantibodies were not
observed using the normal feline pooled sera or the
serum from the cat with MDMF. The serum from a
cat with BP exhibited circulating IgG against the
epidermal basement membrane, a nding expected in
this autoimmune blistering skin disease.15
Identication of antigens targeted by circulating
autoantibodies
Serum obtained from the present patient and a control cat with MDMF were tested by immunoblotting
against 6 M urea extracts of plucked human anagen
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 261270

DISCUSSION
The present study provides evidence for the existence
of a novel feline autoimmune alopecia that exhibits
resemblance to pseudopelade (PP) in humans.1
Similarly to its human counterpart, feline PP is
characterized by: (i) an adult-onset patchy to diuse
alopecia; (ii) an early inammatory phase in which Tlymphocytes and dendritic antigen-presenting cells
accumulate in and around the follicular isthmus and
cause its destruction; and (iii) a late stage in which the
hair follicles undergo atrophy and are replaced by
brosing tracts. Our report additionally documents
the cytotoxic phenotype of isthmotropic lymphocytes

198 DISC
Feline pseudopelade

267

Figure 11. Circulating IgG autoantibodies recognize multiple

follicular antigens including presumably trichohyalin (200 kDa)
and hair keratins (4065 kDa cluster). Immunoblotting; human
anagen hair follicle extract; (A) patient's serum (B) serum from a
cat with mucinous degenerative mural folliculitis.
Figure 10. Circulating IgG autoantibodies target the matrical
precortex, the lower hair cortex and the inner root sheath. Indirect
immunouorescence, normal equine haired skin substrate; original
magnication 620.

and demonstrates the presence of circulating IgG

autoantibodies specic for follicular antigens. These
results are supportive of an autoimmune aetiology for
this case of feline PP, similarly to that demonstrated
in humans and animals suering from alopecia areata
(AA) (reviewed in 16).
In humans, clinical lesions of PP consist of
irregularly dened and conuent patches of smooth
and soft alopecia, mild perifollicular erythema and
moderate skin atrophy.1,2,17 Scaling is either mild or
absent.1 The alopecic patches commonly originate and
terminate on the scalp, however, extensive lesions can
be seen more rarely.1 In most human cases of PP, the
evolution of baldness is chronic and slowly progressive, but a fulminant form also has been described.1,17
Our cat's lesions were extensive from the onset and
progressed more rapidly than during PP in humans.
The facial alopecic patches, which developed late in
the course of this cat's disease, dramatically resembled AA lesions seen in nonhuman mammalian
species.8,16,18 The pattern of hair loss on the lower
body, however, was reminiscent of that seen in feline
self-induced alopecia. In this case, nevertheless,
pruritus was absent and broken-o hair shafts were

not seen. A remarkable feature, in the present cat,

was the presence of onychorrhexis of rear claws,
suggesting important damage to the claw matrix.
The lesions of PP in humans do not respond very
well to immune-modulating drugs, presumably because of stem cell destruction. Transient hair growth
followed cyclosporin therapy in this cat, however.
Cyclosporin had to be discontinued because of our
inability to maintain adequate drug blood trough
levels, increasing diculty in administering treatment
to this cat, and development of clinical dermatophytosis. Even though it could be argued that dermatophytosis could have been present from the onset of
the dermatosis and possibly could have lead to the
folliculocentric immune response, we do not favour
this hypothesis as 3 coat-brushing dermatophyte
cultures and fungal histopathological stains always
failed to reveal infective organisms.
In this cat, skin biopsies of alopecic patches
showed microscopical lesions that resemble those of
human PP. In humans and this feline patient, early
lesions exhibit mononuclear cells inltrating the
follicular isthmus and the dermis at the mid-follicle
region.1,2,5,6 Adjoining isthmus keratinocytes show
microscopic features characteristic of apoptosis,
indicative of synchronized programmed cell death.19
During the course of PP, inammation typically
spares the hair bulb, as opposed to human and
animal AA.16 In humans and this cat with PP,
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biopsies of ageing lesions reveal brous tracts at the

location of previously destroyed follicles.1,5,6
Whereas sebaceous glands reportedly are hypoplastic
or absent in chronic lesions of human PP,1,5,6 these
adnexae were unaected by the inammatory process
in biopsies from lesions of dierent stages in the
present patient. The reasons for this dierence in
sebaceous gland targeting between this case and
human patients with PP remains unknown at the
moment. In this cat, focally severe granulomatous
inammation seemed to occur in response to
follicular destruction and hair shaft dermal ejection.
This type of granulomatous inammation, however,
is a rare feature of PP in humans.1,2,5,6
In this case of feline PP, immunological investigations support an autoimmune pathogenesis targeting
follicular antigens at the isthmus region. A predominance of cytotoxic T-lymphocytes in the follicular
sheath and a mixture of helper T-lymphocytes and
dendritic antigen-presenting cells in the perifollicular
dermis were demonstrated using an immunohistochemical method. This duality of perifollicular cells is
similar to that reported in humans with PP.20
Whereas low-grade IgG deposition was observed in
the perifollicular dermis of active lesions of our cat,
follicular-specic autoantibody deposition was not
seen. Similarly, direct IF examination of skin biopsies
of human PP lesions does not demonstrate follicular
IgG deposits.1,2,17 Indirect IF testing revealed, however, that the present patient's serum exhibited a very
high titre of circulating IgG autoantibodies specic
for lower hair follicle structures. Immunoblotting
studies conrmed that the autoimmune reaction was
directed against multiple follicular antigens presumably including trichohyalin (* 200 kDa), hair
keratins (4060 kDa cluster) as well as some other
unidentied proteins. Whilst it could be hypothesized
that the observed antifollicular humoral immune
response occurred because of the exposure of cryptic
antigenic epitopes secondary to follicular destruction,
several lines of evidence counter this. Firstly, indirect
IF and immunoblotting studies performed using the
serum of a cat with MDMF did not reveal follicularspecic autoantibodies, in spite of the prominent
lymphocyte folliculotropism and keratinocyte mucinous vacuolation of that disease. Secondly, in dogs
with demodicosis, circulating antifollicular autoantibodies are not detected via immunoblotting,14 even
though histopathological examination of skin biopsy
specimens reveals a basal cell destructive interface
mural folliculitis.21 Finally, there is preliminary
evidence that antifollicular antibodies that target
trichohyalin and/or hair keratins might be pathogenic.18 Indeed, we recently demonstrated that IgG
autoantibodies, puried from the serum of a horse
with AA, were able to alter hair growth in one
experiment of passive transfer into murine skin.18
The present histopathological and immunological
studies, along with those performed in dogs with a
similar condition,22 provide evidence for the existence
# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 261270

of an isthmotropic autoimmune alopecia analogous,

if not homologous, to PP in humans. The relationship
of this cat's dermatosis and the acquired `linear
alopecia' of horses is unknown. Equine `linear
alopecia' has been characterized, histologically, as a
lymphocytic mural folliculitis present in the lower
hair follicles and sparing the bulbs.23 Unfortunately,
the lack of detailed published reports of the
histopathological lesions of equine `linear alopecia'
prevents the determination whether or not this
dermatosis of horses is similar to PP in humans,
dogs and this cat.
In conclusion, PP needs to be added to the expanding group of animal immune-mediated disorders
resulting in hair loss such as AA and demodicosis.16,21 Future studies on the immunopathology of
PP and AA in dogs and cats may provide insights on
the triggering factors of the follicle-specic immune
reaction as well as information regarding immunemodulating therapeutic strategies.
ACKNOWLEDGEMENTS
The authors are indebted to Dr Thelma Lee Gross for
performance of the initial histopathology and for her
invaluable contribution in the evaluation of skin
biopsies of cats with mural folliculitis. Additionally,
we would like to acknowledge the participation of the
Dermatology Service at the University of California,
Davis for freezing and shipping some of the specimens.
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mural folliculitis resembling pseudopelade in humans.
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dermatoses. Veterinary Clinics of North America
Equine Practice 1995; 11: 10510.

Resume La pseudopelade est une alopecie cicatricielle de l'homme, caracterisee par une inammation
lymphocytaire centree sur l'isthme folliculaire. Le folliculotropisme des lymphocytes est associe a une
apoptose des cellules de l'isthme et, dans la phase nale, a une destruction folliculaire et a une brose
dermique. Un cas d'alopecie chez un chat a ete diagnostique comme une pseudopelade sur les criteres suivants:
(i) une chute de poils en taches ou diuse, non prurigineuse et non inammatoire (ii) une phase initiale de
destruction du follicule pileux, dans laquelle les lymphocytes et les cellules dendritiques etaient accumulees
dans et autour de l'isthme folliculaire; et (iii) un stade tardif pour lequel les segments profonds des follicules
pileux etaient atrophies et remplaces par des trajets breux. En outre, des etudes immunologiques ont permis
de montrer un phenotype cytotoxique pour les lymphocytes isthmotropiques et la presence d'autoanticorps de
type IgG circulants, speciques de nombreux antigenes folliculaires. Les resultats de cette etude suggerent une
pathogenie immunologique pour ce cas de pseudopelade feline, comme il a ete propose pour l'alopecia areata
chez l'homme et dans d'autres especes de mammiferes. [Olivry, T., Power, H. T., Woo, J. C., Moore, P. F. et
Tobin, D. J. Anti-isthmus autoimmunity in a novel feline acquired alopecia resembling pseudopelade of
humans. (Autoimmunite dirigee contre l'isthme dans une nouvelle alopecie feline acquise ressemblant a la
pseudopelade chez l'homme.) Veterinary Dermatology 2000; 11: 261270.]
Resumen La Pseudopelade es una alopecia cicatricial primaria de humanos caracterizada por una
inamacion rica en linfocitos centrada alrededor del istmo folicular. El folliculotropismo linfoc tico se
asocia con la apoptosis en el istmo y, en unltima instancia, con la destruccion folicular y la brosis dermica.
En un gato, se diagnostico una alopecia adquirida como pseudopelade basada en los criterios siguientes: (i)
aparicion a edad adulta, perdida de pelo no-inamatoria, no-prur tica, multifocal a difusa; (ii) fase destructiva
temprana del fol culo en la que los linfocitos y las celulas dendr ticas se acumulaban en el interior y alrededor
del istmo folicular; y (iii) fase tard a en la que los segmentos inferiores de los fol culos se atroaban y se
sustitu an por septos brosos. Ademas, las investigaciones immunologicas se caracterizaban por linfocitos
istmotropicos de fenotipo citotoxico y demostraron la presencia de anticuerpos IgG circulantes espec cos
para multiples ant genos foliculares. En conjunto, los resultados del estudio sugieren una patogenesis
inmunomediada para este caso de pseudopelade felina, parecida a la que causa alopecia areata en humanos y
en otras especies de mam feros. [Olivry, T., Power, H. T., Woo, J. C., Moore, P. F. e Tobin, D. J. Anti-isthmus
autoimmunity in a novel feline acquired alopecia resembling pseudopelade of humans. (Autoinmunidad antiistmo en una nueva alopecia adquirida felina parecida a la pseudopelade de humanos.) Veterinary
Dermatology 2000; 11: 261270.]

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198 DISC
270

T. Olivry et al.
Zusammenfassung Pseudopelade ist eine primare, vernarbende (cicatrixe) Alopezie des Menschen, die durch
eine um den Isthmus des Haarfollikels angeordnete, lymphozytenreiche Entzundungsreaktion charakterisiert
ist. Lymphozytarer follikularer Tropismus ist assoziiert mit Apoptose des Isthmus und schluendlich der
Zerstorung des Follikels sowie dermaler Fibrose. Bei einer Katze wurde eine erworbene Alopezie anhand
folgender Kriterien als Pseudopelade diagnostiziert: (i) ein achiger bis diuser, nicht juckender, nicht
entzundlicher Haarverlust mit Beginn im adulten Alter; (ii) eine fruhe follikeldestruktive Phase, in der
Lymphozyten und dendritische Zellen sich in und um den follikularen Isthmus ansammeln; und (iii) ein spates
Stadium, in dem die tieferen Segmente der Haarfollikel atrophisch wurden und durch brosierende Strange
ersetzt wurden. Zusatzlich charakterisierten immunologische Untersuchungen den zytotoxischen Phanotyp
der isthmotropischen Lymphozyten und demonstrierten die Anwesenheit zirkulierender IgG Autoantikorper
spezisch fur multiple follikulare Antigene. Zusammengenommen deuten die Ergebnisse der vorliegenden
Studie auf eine immunvermittelte Pathogenese fur diesen Fall feliner Pseudopelade hin, ahnlich der Alopecia
areata beim Menschen und anderen Saugetierarten. [Olivry, T., Power, H. T., Woo, J. C., Moore, P. F. und
Tobin, D. J. Anti-isthmus autoimmunity in a novel feline acquired alopecia resembling pseudopelade of
humans. (Anti-Isthmus Autoimmunitat in einer neuartigen, erworbenen felinen Alopezie, die der
Pseudopelade des Menschen ahnelt.) Veterinary Dermatology 2000; 11: 261270.]

# 2000 Blackwell Science Ltd, Veterinary Dermatology, 11, 261270