VDE251.

fm Page 243 Monday, September 17, 2001 3:36 PM

Veterinary Dermatology 2001, 12, 243 253

Blackwell Science, Ltd

Sebaceous adenitis in the Akita: clinical observations,

histopathology and heredity
IRIS M. REICHLER,* BEAT HAUSER, IRENE SCHILLER, ROBERT W. DUNSTAN,
KELLY M. CREDILLE, HEINRICH BINDER,* TONI GLAUS and SUSI ARNOLD*
Departments of *Reproduction, Pathology and Internal Medicine, Faculty of Veterinary Medicine, University
of Zurich, Switzerland Department of Veterinary Pathobiology, Texas A & M University, College Station,
Texas, USA
(Received 17 September 1999; accepted 14 July 2000)

Abstract Ninety-seven pure-bred Akitas were examined clinically and histologically for sebaceous adenitis. The
diagnosis was established histologically in 23 Akitas by demonstrating an inflammatory reaction targeted against
the sebaceous glands or a reduction in the number of glands. The clinical course of sebaceous adenitis in the Akita
was similar to that seen in other breeds. The first skin lesions occurred mainly on the dorsal midline and ears.
Compared with the Poodle, the age at first onset of the disease was more variable and the hair loss affected mainly
the undercoat. The progression of sebaceous gland destruction varied between dogs and was not seen in all cases.
Because bud-like sebaceous gland proliferation could be identified, it seems that regeneration of the sebaceous
glands may occur. An autosomal recessive inheritance appears to be possible. Apart from a genetic background,
immune-mediated factors possibly influence the onset and course of sebaceous adenitis.
Keywords: Akita, mode of inheritance, regeneration of sebaceous glands, sebaceous adenitis.

INTRODUCTION
Sebaceous adenitis is a specific, primary inflammatory
reaction that is targeted against the sebaceous glands,
and typically leads to their complete destruction.13
Sebaceous adenitis has been described in humans,4,5
cats6,7 and dogs.3,8,9 Decreased production of sebaceous
lipids, particularly wax diesters and cholesteryl esters,
is associated with destruction of the sebaceous glands
in dogs.10 In long-haired breeds, such as the Standard
Poodle or Akita, skin lesions, accompanied by hair loss,
begin on the dorsal midline and head, and may progress
ventrally to the trunk.8,11,12 Short-haired breeds, such
as Vizslas, tend to develop multifocal, often coalescing,
alopecic patches or nodular lesions without marked
hyperkeratosis.13 15
Sebaceous adenitis has been described in 55 canine
breeds and also in mongrels (Credille and Dunstan,
1998, personal communication).1,3,9,11,1420 Although
only single cases are described in most breeds, there
seems to be a true breed predisposition in Standard
Poodles and Akitas (Credille and Dunstan, 1998,
personal communication).11,15 The clinical course, histopathology and mode of inheritance of sebaceous
adenitis are best characterized in the Standard Poodle.
An autosomal recessive mode of inheritance3,21 with a
variable expression is suspected but not proven (Credille
Correspondence: I. M. Reichler, Department of Reproduction,
Faculty of Veterinary Medicine, University of Zurich, Winterthurerstr.
260, CH-8057 Zurich, Switzerland. Tel.: +1635 8266, fax: +1635 8904,
Email: reichler@vetgeb.unizh.ch
2001 Blackwell Science Ltd

and Dunstan, 1998, personal communication). Although

the Akita is quite commonly affected, to date, the disease
has not been studied thoroughly in this breed.
The aim of this investigation was to characterize
the clinical and histopathological appearance and the
mode of inheritance of sebaceous adenitis in the Akita.

MATERIALS AND METHODS

Animals
A total of 97 pure-bred Akitas, 45 males and 52 females,
was examined for the presence of sebaceous adenitis.
Seventy of these were examined at breeder meetings.
The remaining 27 animals with skin problems were
either presented to the Veterinary Teaching Hospital of
Zurich (n = 6) or to collaborating private practitioners
(n = 21). The ages of all dogs ranged from 7 months to
11 years, with an average of 3.7 years. The history, clinical findings and pedigrees of all dogs were recorded.
Visible skin lesions were classified as discrete, if, at
examination, no changes in the fur were visible, but
when the hair was parted skin lesions could be recognized. If at a quick glance, from a short distance, hair
or skin changes were recognized, they were classified
as moderate skin lesions (Fig. 1), and if hair or skin
changes were recognizable from a greater distance, they
were classified as severe skin lesions (Fig. 2).
Skin biopsies
Three biopsies (6 mm in diameter) were taken along
the dorsal midline, from the neck, the back and the base
243

VDE251.fm Page 244 Monday, September 17, 2001 3:36 PM

244

I. M. Reichler et al.

Figure 1. Akita with sebaceous adenitis

showing moderate skin lesions.

Figure 2. Akita with sebaceous adenitis

showing severe skin lesions.

of the tail from each of 88 dogs. These were processed

for histopathology using routine methods. In the
remaining nine dogs, which were presented to private
practitioners, the biopsy sites were taken at random
along the dorsal midline.
Histopathological examination
Histological sections of the biopsies were stained with
haematoxylin and eosin and examined by four pathologists (BH, IS, BD, KC). Sebaceous adenitis was
diagnosed if an inflammatory reaction targeting the
sebaceous glands was found or if the glands were reduced
in number or were absent. There were three degrees of
sebaceous adenitis.
Degree 1: a normal number of sebaceous glands
associated with an inflammatory reaction (Fig. 3).
Degree 2: a reduced number of sebaceous glands,
with or without an inflammatory reaction (Fig. 4).
Degree 3: an absence of sebaceous glands, with or
without an inflammatory reaction (Fig. 5).
A reduced number or the absence of sebaceous glands
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243 253

(Degree 2 or 3) were verified by cutting and examining

serial sections in these areas.
A follow-up of the progression of the disease, with
clinical and histological examination of biopsies from
the same sites, was possible in 10 dogs. One dog (17) had
additional skin samples taken 2 years after initial diagnosis at necropsy. One dog (13), examined for the first
time at a breeders meeting, was clinically and histologically completely normal. One year later, the dog was
presented because of a skin problem and sebaceous
adenitis was diagnosed.
Dogs with skin diseases other than sebaceous adenitis
were not included in this study.
Extended history
An ancestor tree was established and all dogs with
sebaceous adenitis were identified on it. Additional
information about siblings and parents was obtained.
Animals with reports of typical signs of sebaceous
adenitis were marked on the ancestor tree as potentially affected dogs (Fig. 6). A total of 16 litters with

VDE251.fm Page 245 Monday, September 17, 2001 3:36 PM

Sebaceous adenitis in the Akita

245

Figure 3. A normal number of sebaceous

glands associated with an inflammatory
reaction (H&E) (Degree 1).

Figure 4. A reduced number of sebaceous

glands, with or without an inflammatory
reaction (H&E) (Degree 2).

Figure 5. An absence of sebaceous glands,

with or without an inflammatory reaction
(H&E) (Degree 3).

2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243253

VDE251.fm Page 246 Monday, September 17, 2001 3:36 PM

246

I. M. Reichler et al.

2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243 253

Figure 6. Ancestor tree of Akita families with sebaceous adenitis.

VDE251.fm Page 247 Monday, September 17, 2001 3:36 PM

Sebaceous adenitis in the Akita

247

Table 1. Signalement, history, clinical findings and degree of sebaceous adenitis in biopsies in 23 Akitas

No.

Sex*

1
2
3
4
5
6
7
8
9
10
11
12

M
M
F
M
F
F
MC
F
M
M
M
M

History
age (years)
2
2
7
1
2
7
1
2
5
3
5
3

Dogs with re-examination

13
F
6
14
15
16
17
18
19
20
21
22
23

M
11
re-examination
F
2
re-examination
M
5
re-examination
MC
3
re-examination
F
0.8
re-examination
M
0.6
re-examination
F
2
re-examination
F
2
re-examination
F
1
re-examination
F
1
re-examination

First
lesion

Time since
onset (m)

Ear
Ear
Back
Back
Ear
Diss.
Diss.
Ear
Ear
Tail
Trunk
Ear

3
3
4
5
5
12
13
13
18
21
36
42

Skin lesions at presentation

Affected areas

Type of lesion

Head

Back

Tail

Hair loss

Scaling

+
+

+
+
+
+
+
+
+

+
+
+
+
+
+
+

+
+
+
+

+
+
+
+

+
+
+
+

+
+
+
+
+
+
+
+
+
+
+
+

+
+
+
+
+
+
+
+
+
+
+
+

+
+
+
+
Ear
+
+
+
+

Leg

Crusts
+
+
+
+
+
+
+
+
+

Neither clinical nor histological signs of sebaceous adenitis

Back
4
+
+
+
+
+
+
+
Ear
1
Ear
+
13
+
+
+
+
+
+
Ear
2
Ear
+
+
10
Ear
+
+
+
+
Back
4
+
+
+
+
+
+
+
16
+
+
+
+
+
+
+
Back
4
+
+
+
+
+
35
+
+
+
+
+
Back
4
+
+
+
+
+
+
5
+
+
+
+
+
+
Trunk
8
+
+
+
+
+
+
9
+
+
+
+
+
+
Head
8
+
+
+
+
+
+
42
+
+
Diss.
1
+
+
+
+
+
12
Neither clinical nor histological signs of sebaceous adenitis
Ear
12
Ear
+
+
24
Ear
+
+
Head
48
+
+
+
+
+
+
+
60
+
+
+
+
+
+
+

Clinic

Sebaceous
glands**

2
3
3
2
3
3
3
1
3
3
3
3

Degree 2
Degree 3
Degree 3
Degree 3
Degree 2
Degree 3
Degree 3
Degree 3
Degree 3
Degree 3
Degree 3
Degree 2

2
2
3
1
2
3
3
2
2
3
3
3
3
3
1
1

Degree 3
Degree 1
Degree 2
Degree 3
Degree 3
Degree 3
Degree 3
Degree 2
Degree 3
Degree 2
Degree 3
Degree 2
Degree 2
Degree 2
Degree 2
Degree 1

1
1
3
3

Degree 1
Degree 1
Degree 2
Degree 3

*Sex at disease onset, M = male, F = female, C = neutered. Age at disease onset. Localization of first skin lesion, which was recognized by the
owner. Time from first skin lesion to histological signs, m = months. Macroscopic grading of dermatological abnormalities: 1 = discrete;
2 = moderate; 3 = severe. **Degree of sebaceous adenitis as determined in Materials and methods. Diss. = disseminated.

family information was available for analysis of the

mode of inheritance.
Statistics
The possible interdependence of the duration of the
disease and the degree of gland destruction was analysed
using analysis of variance () after logarithmic
transformation of the duration of the disease. Only the
results of the first examination were included in the
analysis. The mode of inheritance of sebaceous adenitis
was verified using the a priori method with correction
of the Mendelian expectation for truncate binomial
distribution assuming incomplete ascertainment.22

RESULTS
Sebaceous adenitis was confirmed histologically in 23 dogs.
In 16 cases, the initial skin lesions were observed during
the first 3 years of life; seven dogs were aged 5 years or
older (Table 1). Sixteen of the 23 owners of affected dogs

reported that illness, glucocorticoid or progestagen treatment, general anaesthesia, heat, moulting, neutering or
environmental changes preceded the onset of the disease.
In 20 cases, the first skin lesion was localized hair
loss with scaling, often appearing on the ears (n = 9) or
back (n = 6). Similar initial lesions, but in a multifocal
pattern, were reported in only three cases (Table 1).
At the time of diagnosis, the skin lesions had been
present for a period of 148 months (mean 11.8 months)
(Table 1). Loss of tufts of hair, with follicular casting of
hair shafts (Fig. 7) and scaly skin involving mainly the
head, back and tail were the predominant clinical signs
(Table 1). Most owners reported a complete loss of the
undercoat with minimal re-growth, but with only a
focal and transient loss of cover hair. Over half the
animals (16 of 23) showed markedly crusty patches in
affected areas. In four cases, the ears were affected
exclusively. The skin of the pinna and the external ear
canals was dry, erythematous and scaly. One dog (21)
had a thin coat as the only clinical sign. According to
the history, in this dog, generalized hair loss had
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243253

VDE251.fm Page 248 Monday, September 17, 2001 3:36 PM

248

I. M. Reichler et al.

Figure 7. Loss of hair tuft with follicular

casting of hair shafts.
Table 2. Correlation between duration of the disease at first consultation and skin lesions (n = 23)
Skin lesions:
level of
clinical signs
Discrete
Moderate
Severe

Duration
of the
disease

Ln time
Least squares
means

4
5
14

4.2
3.0
10.7

1.44
1.10
2.37

Probability of significant difference

Discrete

Moderate

Severe

0.6021
0.0995

0.6021

0.0186

0.0995
0.0186*

Duration of the disease (months). Duration of the disease after logarithmic transformation (Ln time). Least squares means by
one-way analysis of variance (). *Significant.

occurred 1 month before presentation (Table 1). On

re-examination, 1 month to 3 years after the diagnosis
of sebaceous adenitis was established, clinical signs
were unchanged in 6 of 10 dogs (Table 1). Two dogs
which had only dry, scaly skin of the ears at first
examination, presented with disseminated changes on
the whole trunk 8 and 12 months later (14, 15). In two
animals the skin condition had improved (20, 21). One
dog (20), which was first presented with generalized
scaling, focal hair loss and crusty patches on head, neck,
trunk and tail showed only very subtle skin changes
such as dry skin on the ears, neck and vulva and some
scaling on the neck 3 years later. The coat recovered
totally. Another dog (21), which initially suffered from
extensive hair loss and was first presented with a thin
coat, had no clinical signs when re-examined 1 year later.
At the time of presentation those dogs with moderate
clinical signs had been suffering from the disease for a
shorter period than dogs with severe signs (Table 2).
Histopathological findings
Sebaceous glands were completely absent in 12 dogs
(Degree 3), whereas in eight dogs the number of sebaceous glands was reduced (Degree 2). In three dogs an
inflammatory process was targeted against sebaceous
glands that were present in normal numbers ( Degree 1).
In most of the dogs examined, the intensity of the histological changes did not vary significantly between
the regions of the dorsal midline.
The cellular infiltrates at the level of the sebaceous
glands were composed of histiocytes, macrophages,
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243 253

neutrophils, eosinophils, mast cells, plasma cells and

lymphocytes. The intensity of the inflammatory reaction,
as well as the cellular composition of the infiltrates, varied
between individual dogs and between the first and followup examinations. A predominance of lymphocytes
was never observed. In one dog (16) exhibiting complete gland destruction, occasional small groups of
basal cells protruding from the hair follicles into the
surrounding connective tissue were present at the level
of the destroyed sebaceous glands (Fig. 8). A similar
feature was observed in a dog with a reduced number
of sebaceous glands (20); one small, bud-like group of
basal cells attached to a hair follicle developed a slightly
foamy cytoplasm towards the centre, and there were
occasional small sebaceous glands attached firmly to
the hair follicle epithelium that lacked secretory ducts
in serial sections (Fig. 9). These features were interpreted
as early stages of sebaceous gland regeneration.
Additional skin changes were seen in many patients
with sebaceous adenitis. These were hyperkeratosis of
the epidermis and/or hair follicle epithelium (16 dogs),
folliculitis, perivascular infiltration with neutrophils,
eosinophils and plasma cells (five dogs) or mast cells
(nine dogs) and perifollicular fibrosis at the level of the
isthmus (one dog).
Histological findings on re-examination
Ten dogs were biopsied 134 months after the initial
diagnosis. Persistent sebaceous adenitis could be confirmed in nine animals ( Table 1), while one dog (21) was
histologically normal. The nine dogs were divided into

VDE251.fm Page 249 Monday, September 17, 2001 3:36 PM

Sebaceous adenitis in the Akita

249

Figure 8. Group of basal cells protruding

from the hair follicle into the surrounding
connective tissue at the level of the destroyed
sebaceous glands (H&E).

Figure 9. Occasional small sebaceous

glands connected intensely with the hair
follicle epithelium but lacking secretory
ducts in serial sections (H&E).

three groups based on the severity of the histological

changes at the time of the first examination.
1 No reduction of the number of glands (Degree 1:
two dogs). At re-examination, the sebaceous glands
had partially disappeared in one dog (14), whereas
the histological picture had not changed in the
other (22).
2 Reduced number of glands (Degree 2: five dogs).
Four of these animals still had a poor hair coat
at the time of re-examination. Histologically, the
sebaceous glands had disappeared in the routine
biopsy sites in three animals (17, 18, 23), whereas
the picture had not changed in one dog (19). In
one of these animals (17), the second examination was performed at necropsy: sebaceous glands
were absent on the eye lids (except the Meibomian
glands which were intact), pinnae, mandibular
area, neck, back and scrotum, and the destruction
was advanced, with intense lymphocytic infiltration,
in the skin of the tail and croup. The sebaceous

glands of the nasal bridge revealed only minimal

inflammatory changes and those of the toes and
the perianal area were intact. The last case of
this group (20), which initially had signs of sebaceous gland regeneration (Fig. 9), had normal
numbers of sebaceous glands in two of three skin
biopsies. Only in the neck biopsy were the glands
still inflamed. The clinical skin condition had
returned to normal, except for a minimal degree
of scaling.
3 No sebaceous glands present (Degree 3: dogs 15,
16). At the time of re-examination, the histological
picture had not changed. There were still scattered
leukocytic infiltrates within the areas of the lost
glands. The clinical condition of the skin was either
unchanged or had worsened.
No significant relationship could be shown between
the duration of the disease and the degree of sebaceous
gland destruction (Table 3), although the duration of the
disease tended to appear longer in dogs with destroyed
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243253

VDE251.fm Page 250 Monday, September 17, 2001 3:36 PM

250
Degree of
sebaceous
adenitis
Degree 1
Degree 2
Degree 3

I. M. Reichler et al.

Duration
of the
disease

Ln time
Least squares
means

3
8
12

2.3
8.7
7.8

0.83
2.16
2.06

Probability sebaceous adenitis

Degree 1

Degree 2

Degree 3

0.0713
0.0792

0.0713

0.8365

0.0792
0.8365

Table 3. Correlation between the duration

of the disease at first consultation and the
degree of sebaceous adenitis (n = 23)

Duration of disease (months). Duration of the disease after logarithmic transformation (Ln
time). Least squares means by one-way analysis of variance ().

Table 4. Cross-tabulation of the level of clinical signs and degree of

sebaceous adenitis (n = 23)
Clinical
signs
Discrete
Moderate
Severe
Total

Sebaceous adenitis
Degree 1

Degree 2

Degree 3

Total

2
1
0
3

0
2
6
8

2
2
8
12

4
5
14
23

glands than those only with glandular inflammation.

The clinical condition depended upon the destruction
of some or all of the sebaceous glands. Dogs with this
condition exhibited remarkably more severe signs
than dogs with only inflamed, but not destroyed,
glands (Table 4). Owing to insufficient cell counts, statistical verification was not feasible and is therefore not
included.
Genetics
Most dogs examined were closely related and had
common ancestors within six or fewer generations.
Sporadic cases of sebaceous adenitis occurred in nearly
all examined lines. Twenty-three dogs with sebaceous
adenitis came from 16 litters with a total of 82 puppies
(Fig. 6). The number of affected dogs (23) was not significantly different from the expected incidence (31.7)
under the hypothesis of an autosomal recessive mode
of inheritance (Table 5).

DISCUSSION
As suggested in the literature, the Akita is a breed
with a high predisposition for sebaceous adenitis.9,13,15
It tends to appear most frequently in young adult to
middle-aged dogs. Similar findings have been reported
in the Poodle.11 However, in contrast to the Poodle, there
seems to be a larger proportion of Akitas, 30% in the
present study vs. 10% of Poodles,3 developing the first
clinical signs at the age of 5 years or older.
In 10 cases, the first skin lesions occurred along the
dorsal midline, similar to that described in Poodles.11
In nine of 23 dogs the initial skin lesions were on the ears.
Otitis externa may be the only initial sign of sebaceous
adenitis (White, 1998, personal communication). In
one dog the visible skin lesions were still limited to the
ears 24 months later, whereas in the other nine dogs the
disease spread to other parts of the body over the observation period. Initially, disseminated skin changes were
seen by the owners in only three cases.
Twenty Akitas with sebaceous adenitis were initially
presented to the veterinarian with localized or disseminated hair loss and yellowbrown, greasy keratosebaceous debris. In general, the first skin lesions were
presented as small areas of scaling and alopecia, which
over time could be found over the entire body. This
pattern has been described as the generalized form of
sebaceous adenitis in the Akita.9 In principle, the same
pattern is seen in short-haired dogs such as Vizsla,

Table 5. Verification of the distribution of affected puppies in 16 litters with correction of the Mendelian expectation (autosomal recessive
inheritance) for incomplete ascertainment (q = frequency of affected puppies)
Size*
s

Frequency
fs

Total puppies
s fs

Affected puppies
r

Expected /litter
s qr

Expected total
s fs q r

Parents normal (q = 0.25)

3
4
5
6
7
Total

1
2
5
1
2
11

3
8
25
6
14
56

1
3
7
2
2
15

1.297
1.463
1.639
1.825
2.020

1.297
2.926
8.195
1.825
4.040
18.283

2
1
1
1
5

8
5
6
7
26

3
2
2
1
8

2.132
2.580
3.048
3.528

4.264
2.580
3.048
3.528
13.420

Father affected (q = 0.5)

4
5
6
7
Total

Parents normal or father affected

Number of litters
Total puppies
16
82

Affected puppies
23

Expected
31.703

2 = 2.72; x 2 (1; 0.05) = 3.84 not significant. *s = litter size. fs = frequency of litter with size s.
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243 253

VDE251.fm Page 251 Monday, September 17, 2001 3:36 PM

Sebaceous adenitis in the Akita

Boxer and Pinscher. In these breeds the skin changes
are described as annular lesions.9,13,14,18 In agreement
with the literature,9 most Akitas initially showed a
thin coat due to loss of the undercoat. At the time of
presentation they had additional lesions such as
papules, pustules and matted hair, which are secondary
lesions typical for sebaceous adenitis in long-haired
breeds.1,9
During the course of the disease there was re-growth
of the cover hair, but (except for two dogs) there was no
obvious re-growth of the undercoat, in particular over
the dorsal midline. Similar findings have been seen in
the Poodle.23
The skin condition did not deteriorate consistently
in all Akitas, in fact, in some cases it improved over
time. Apart from skin changes, the dogs were healthy
and alert. This is in contrast to previous reports of
sebaceous adenitis in Akitas, which describe some dogs
with systemic signs such as fever, malaise and weight
loss.8,9
Dogs suffering from sebaceous adenitis go through
an early, fully developed and late phase,3 during which
there are variations in the histological appearance of
the skin lesions. In the early phase, discrete inflammatory infiltrates are present at the isthmus. The fully
developed phase is characterized by a strong inflammatory reaction targeted against the sebaceous gland.
After the sebaceous gland is destroyed, the disease
progresses to the late stage. The inflammatory reaction
decreases and perifollicular fibrosis occurs.9,11 This disease pattern has been described in the Poodle and was
also seen in the affected Akitas.
In contrast to the Poodle, it was often not possible to
distinguish clearly between the second and last phase of
sebaceous adenitis in Akita skin biopsies. There was no
correlation between the degree of destruction and the
inflammatory reaction targeted against the glands. Even
months after the complete destruction of the sebaceous
gland there was still an inflammatory reaction present.
The progression of sebaceous gland destruction was
individually very variable. In one case the glands were
destroyed completely 2 months after the onset of the
disease, whereas in another case some glands were still
present 48 months after the onset of sebaceous adenitis.
Possibly, this individual temporal variation is not due
to a different progression of gland destruction, but
rather to an individual ability to regenerate glands. This
assumption is supported by one dog which initially had
a considerable reduction of sebaceous glands in all skin
biopsies, on re-examination in one biopsy there was
only one hair follicle with the absence of a sebaceous
gland and the dog had almost completely recovered from
his severe skin lesions. Also, the identification of a budlike proliferation of as yet undifferentiated cells in this
dog, and one other, could be signs of possible glandular
regeneration, as these cells may serve as stem cells for
sebaceous glands.24
The pathogenesis of sebaceous adenitis is not fully
understood. Different possible mechanisms have been
described.

251

1 A primary structural defect in sebaceous glands

or ducts, that results in the leakage of sebum and
subsequent development of a foreign body inflammatory response.3
2 An immune-mediated or autoimmune reaction
targeted against the sebaceous gland.1,3,9
3 A defect of keratinization leading to obstruction
of the sebaceous duct and to subsequent inflammation of the gland.
4 An abnormality of the lipid metabolism affecting
the keratinization and the production of sebum.11
The histological features of the three biopsies taken
in the dorsal midline were similar in each individual
dog. In only one dog was it possible to take many additional skin biopsies from different sites. In this dog, histopathological examination showed intact sebaceous
glands as well as all different degrees of destruction and
or inflammation targeted against the sebaceous glands.
This interesting finding does not allow any conclusion
to be drawn on the pathogenic mechanism. The results
of a recent immunohistochemical study of dogs with
sebaceous adenitis revealed a marked infiltration and
activation of dendritic antigen-presenting cells and
T cells, which suggests an immune-mediated pathogenesis. Cell-mediated damage is more likely to occur
because no circulating autoantibodies were detected.25
It can be assumed that in highly predisposed breeds,
such as the Standard Poodle and the Akita, a genetic
basis is present. An extensive study has only been performed in the Poodle, the results of which were suggestive of an autosomal recessive inheritance.3 Equally,
the frequency of affected Akitas does not differ significantly from expectation, assuming autosomal recessive inheritance, as shown by the a priori method with
correction for truncate binomial distribution under
incomplete ascertainment.
Pedigree analysis in the Akita, checking the possible
genealogic pathway of the defective gene, did not yield
further evidence to confirm or reject the assumed mode
of inheritance. Even if a single gene defect is responsible for sebaceous adenitis, other factors are likely to be
involved in the onset and course of the disease. Otherwise there is no explanation for the large age range, from
7 months to 11 years, during which the disease can occur.
Stressful situations, such as preceding diseases or
surgery, may be triggering events, which is in agreement with the history of numerous affected Akitas. The
history of one Akita is especially remarkable, as it was
initially completely sound. A short time later, after treatment with glucocorticoids, the dog developed sebaceous
adenitis. A similar history is reported in a cat that was
treated with immune-suppressive drugs before the onset
of sebaceous adenitis.6
Even if sebaceous adenitis were to be confirmed as
an autosomal recessive inherited disease, it would be
rather difficult to work out a suitable breeding management. The most simple recommendation of not breeding with homozygote animals would fail due to the
possible late onset of the disease. For the same reason
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243253

VDE251.fm Page 252 Monday, September 17, 2001 3:36 PM

252

I. M. Reichler et al.

restricted admission for breeding with progeny analysis

would also fail. The exclusion from breeding of affected
families would narrow the genetic base tremendously, as
sporadic cases of sebaceous adenitis are seen in virtually
all breeding lines of Akita. At present there is no possibility of identifying carriers or homozygote animals
before they become affected. Most likely, sebaceous
adenitis in the Akita can only be eliminated by a suitable
genetic test that requires either the identification of the
genetic defect or the availability of a suitable marker.

ACKNOWLEDGEMENTS
Thanks to Madeleine Hubler, Adrian Fairburn,
Dagmar Meisl and Pierre Arnold.

REFERENCES
1. Scott, D.W. Granulomatous sebaceous adenitis in dogs.
Journal of the American Animal Hospital Association
1986; 22: 631 4.
2. Stewart, L.J. Newly reported skin disease syndromes
in the dog. Veterinary Clinics of North America, Small
Animal Practice 1990; 20: 1603 13.
3. Dunstan, R.W., Hargis, A.M. The diagnosis of sebaceous
adenitis in standard poodle dogs. In: Kirk, R.W., ed. Current Veterinary Therapy XII. Philadelphia: W.B. Saunders,
1995: 619 22.
4. Renfro, L., Kopf, A.W., Guttermann, A. et al. Neutrophilic sebaceous adenitis. Archives of Dermatology 1993;
129: 910 11.
5. Martins, C., Tellechea, O., Mariano, A. etal. Sebaceous
adenitis. Journal of the American Academy of Dermatology
1997; 36 (5): 845 6.
6. Scott, D.W. Adnite sbace pyogranulomateuse strile
chez un chat. Point Vtrinaire 1989; 21 (120): 10711.
7. Wendlberger, U. Sebadenitis bei einer Katze. Kleintierpraxis 1999; 44: 235 312.
8. Rosser, E.J. Sebaceous adenitis. In: Kirk, R.W., ed. Current
Veterinary Therapy XI. Philadelphia: W.B. Saunders, 1992:
534 6.
9. Scott, D.W. Sterile granulomatous sebaceous adenitis in
dogs and cats. The Veterinary Annual 1993; 33: 23643.
10. Burton, D.E., Bailey, D.L., Jeromin, A.M. et al. Quantitative determination of canine sebaceous lipids by thin
layer chromatography. Journal of Planar Chromatography
1995; 5: 179 83.

11. Rosser, E.J., Dunstan, R.W., Breen, P.T. et al. Sebaceous

adenitis with hyperkeratosis in the standard poodle: a
discussion of 10 cases. Journal of the American Animal
Hospital Association 1987; 23: 3415.
12. Scarff, D.H., Whitbread, T.J. Sebaceous adenitis in the
standard poodle. Veterinary Record 1993; 133: 100.
13. Muller, G.H., Kirk, R.W., Scott, D.W. Small Animal Dermatology. Philadelphia. W.B. Saunders, 1989: 5557.
14. Stewart, L.J., White, S.D., Carpenter, J.L. Isotretinoin
in the treatment of sebaceous adenitis in two vizslas.
Journal of the American Animal Hospital Association
1991; 27: 6570.
15. White, S.D., Rosychuk, R.A.W., Scott, K.V. et al. Sebaceous
adenitis in dogs and results of treatment with isotretinoin
and etretinate: 30 cases (1990 1994). Journal of the American Veterinary Medical Association, 1995; 207: 197200.
16. Guagure, E., Alhaidari, Z., Magnol, J.P. Adnit
sbace granulomateuse propos de trois cas. Pratique
Mdicale et Chirougical de lAnimal de Compagnie 1990;
25: 16975.
17. Marshall, C., Williams, J. Re-establishment of hair growth,
skin pliability and apparent resistance to bacterial infection after dosing fish oil in a dog with sebaceous adenitis.
Advances in Veterinary Dermatology 1990; 1: 446.
18. Carothers, M.A., Kwochka, K.W., Rojko, J.L. Cyclosporineresponsive granulomatous sebaceous adenitis in a dog.
Journal of the American Veterinary Medical Association
1991; 198: 16458.
19. McAllister, M.M. Adenohypophysitis associated with
sebaceous gland atrophy in a dog. Veterinary Pathology
1991; 28: 3401.
20. Koutinas, A.F., Tontes, D. Granulomatous sebaceous
adenitis in the dog. EATION E. KTHN. ETAIPEIIA
1994; 45: 5966.
21. Scarff, D.H. Sebaceous adenitis in the standard poodle.
Veterinary Record 1994; 135: 264.
22. Wiesner, E., Willer, S. Genetische Beratung in der Tierrztlichen Praxis. Stuttgart: Gustav Fischer-Verlag, 1993.
23. Dunstan, R.W., Credille, K.M. Why do some standard
poodles with sebaceous adenitis get better? Genodermatosis
Research Foundation Newsletter 1997; Spring/Summer:
17.
24. Lavker, M., Miller, S., Wilson, C. et al. Hair follicle stem
cells: their location, role in hair cycle, and involvement in
skin tumor formation. Journal of Investigative Dermatology 1993; 101 (Suppl. 1): 1626.
25. Rybnicek, J., Affolter, V.K., Moore, P.F. Sebaceous adenitis:
an immunohistological examination. In: Kwochka, K.W.,
Willemse, T., von Tscharner, C., eds. Advances in Veterinary
Dermatology. Oxford: Butterworth Heinemann, 1996:
53940.

Rsum Quatre-vingt dix-sept Akitas de race pure ont subi un examen clinique et histopathologique pour
rechercher une adnite sbace. Le diagnostic a t ralis par lhistopathologie chez 23 Akitas, avec mise en
vidence dune raction inflammatoire dirige contre les glandes sbaces ou une diminution du nombre de
glandes sbaces. Lvolution clinique de ladnite sbace chez lAkita est identique celle rapporte dans
dautres races. Les premires lsions cutanes apparaissent principalement sur la ligne du dos et les oreilles. A la
diffrence du Caniche, lge dapparition des lsions est plus variable chez lAkita, et la chute pilaire est plus
limite au sous-poil. La destruction des glandes sbaces a volu de faon variable, en fonction des animaux, et
tait parfois absente. Lobservation de prolifrations en bourgeons au niveau des glandes sbaces laisse penser
quune rgnration de ces glandes est possible. Un mode de transmission autosomal rcessif semble tre possible.
En plus des facteurs gntiques, il semble que des facteurs immunologiques puissent influencer lapparition
et lvolution de ladnite sbace. [Reichler, I. M., Hauser, B., Schiller, I., Dunstan, R. W., Credille, K. M.,
Binder, H., Glaus, T., Arnold S. Sebaceous adenitis in the Akita: clinical observations, histopathology and heredity.
2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243 253

VDE251.fm Page 253 Monday, September 17, 2001 3:36 PM

Sebaceous adenitis in the Akita

253

(Adnite sbace chez lAkita: observations cliniques, histopathologiques et gntiques.) Veterinary Dermatology
12: 243 253.]
Resumen Se examinaron clnica e histopatolgicamente noventa y siete Akitas de raza pura para la deteccin
de adenitis sebcea. El diagnstico pudo establecerse histolgicamente en 23 Akitas demostrando una reaccin
inflamatoria dirigida a las gndulas sebceas o una reduccin en el nmero de glndulas. El curso clnico de la
adenitis sebcea en el Akita fue similar al observado en otras razas. Las primeras lesiones cutneas se produjeron
en la lnea media dorsal y en las orejas. Comparado con el Caniche, la edad de la primera presentacin de la
enfermedad fue ms variable y la prdida de pelo afect principalmente el pelo secundario. La progresin de la
destruccin de glndulas sebceas vari segn el perro y no se vio en todos los casos. La observacin de proyecciones iniciales de glndulas sebceas sugiere que puede producirse regeneracin de stas. Parece posible que se trate
de una forma hereditaria autosmica recesiva. Aparte de la base gentica, factores inmunomediados podran
influir en el inicio y evolucin de la adenitis sebcea. [Reichler, I. M., Hauser, B., Schiller, I., Dunstan, R. W.,
Credille, K. M., Binder, H., Glaus, T., Arnold S. Sebaceous adenitis in the Akita: clinical observations, histopathology
and heredity. (Adenitis sebcea en el Akita: observaciones clnicas, histopatologa y heredabilidad.) Veterinary
Dermatology 12: 243 253.]
Zusammenfassung Siebenundneunzig reinrassige Akitas wurden klinisch und histologisch auf Sebadenitis
berprft. Die Diagnose wurde bei 23 Akitas durch Nachweis einer gegen die Talgdrsen gerichteten Entzndungsreaktion oder eine Reduzierung der Drsenanzahl histologisch gestellt. Der klinische Verlauf der Sebadenitis beim Akita war dem bei anderen Rassen hnlich. Die ersten Lsionen erschienen hauptschlich auf dem
Rcken und an den Ohren. Verglichen mit Pudeln war das Alter, in dem die Krankhiet zuerst auftrat, variabler
und der Haarverlust betraf hauptschlich die Unterwolle. Die Progression der Talgdrsenzerstrung variierte
von Hund zu Hund und wurde nicht bei allen Fllen gesehen. Da keim-hnliche Talgdrsenproliferation identifiziert wurde, scheint eine Regeneration der Talgdrsen mglich. Ein autosomal-rezessiver Erbgang scheint
mglich. Neben dem genetischen Faktor knnen immun-bedingte Faktoren mglicherweise das Auftreten und
den Verlauf der Sebadenitis beeinflussen. [Reichler, I. M., Hauser, B., Schiller, I., Dunstan, R. W., Credille, K. M.,
Binder, H., Glaus, T., Arnold S. Sebaceous adenitis in the Akita: clinical observations, histopathology and heredity.
(Sebadenitis beim Akita: Klinik, Histopathologie und Erbgang.) Veterinary Dermatology 12: 243253.]

2001 Blackwell Science Ltd, Veterinary Dermatology, 12, 243253