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Veterinary Dermatology 2002, 13, 253260

Case report

Blackwell Science, Ltd

Follicular dysplasia in five Weimaraners

Follicular dysplasia in Weimaraners

CATHERINE LAFFORT-DASSOT,* LUC BECO and DIDIER NOEL CARLOTTI*


*Cabinet de dermatologie vtrinaire, Hliopolis B3, avenue de magudas, F-33700 Bordeaux Mrignac, France
Clinique vtrinaire, 104 Avenue Reine Astrid, B-4900 Spa, Belgium
(Received 30 July 2001; accepted 7 May 2002)

Abstract This study evaluated the clinical and histopathological features and results of light and electron
scanning microscopy assessments of follicular dysplasia in five Weimar Pointers. The data were compared with
those obtained in three normal Weimaraners. In our study, this dermatosis affected young adults that showed
progressive alopecia of the trunk (head and limbs were spared) associated with recurrent folliculitis/furunculosis.
Exclusion of other dermatoses and the presence of histopathological lesions and hair shafts abnormalities seen
in light and/or scanning electron microscopy similar to colour dilution alopecia led to the diagnosis of follicular
dysplasia. The lesions we observed are the same as those described previously in colour dilution alopecia, but
they were less pronounced in all our samples.
Keywords: colour dilution alopecia, follicular dysplasia, Weimaraners.

INTRODUCTION
The follicular dysplasias make up a group of recently
discovered, partially understood and controversial
genodermatoses. The term, dysplasia, is itself now in
disrepute as it can have many different meanings.
In veterinary dermatology, it defines a collection of
conditions of the hair follicle, which have a strong
hereditary basis but are not congenital; abnormal hair
follicle development leads to structural abnormalities
and alopecia.1 The bounds of this group are quite
vague and vary with different authors but in essence it
can be divided as follows:
colour-linked follicular dysplasias;
noncolour-linked, cyclical follicular dysplasias;
noncolour-linked, noncyclical follicular dysplasias.
Colour-linked follicular dysplasias
These are the best known and are linked to coat colour.
They include colour dilution alopecia and black hair
follicular dysplasia, which some authors consider to
be clinically identical.24 Colour dilution alopecia has
been reported in colour dilute individuals of many breeds:
Doberman,2,410 Yorkshire Terrier,2,8,1115 Miniature
Pinscher,2,7 Great Dane,4,5,8 Whippet,4,5,8 Italian
Greyhound,2,8,16 Saluki,8,12 Chow-chow,5,8 Smooth-haired
Dachshund,4,5,8 Wire-haired Dachshund,3 Silky Terrier,17
Boston Terrier,18 Newfoundland,18 Bernese Mountain Dog,18,19 Shetland Sheepdog,18,19 Schipperke,18,19
Correspondence: Catherine Laffort-Dassot, Cabinet de dermatologie
vtrinaire, Hliopolis B3, avenue de Magudas, F-33700 Bordeaux
Mrignac, France.
2002 Blackwell Science Ltd

Chihuahua,2,7 Poodle,2,6,8 Irish Setter4,5,8 and crossbreed.20 Black hair follicular dysplasia has been
reported in young bicoloured or tricoloured animals of
the following breeds: Dachshund,6 Papillon,6 Saluki,21,22
Bearded Collie,23 Cavalier King Charles Spaniel,24
Border Collie,24,25 Beagle,18,19 Basset Hound,18,19 Cocker
Spaniel,2 Pointer,2 Gordon Setter,2 Schipperke18 and
cross-breed.26,27
Diagnosis of these two conditions is based on a
combination of clinical signs, hair microscopy and
skin histopathology. Clinical signs consist of alopecia or
progressive hypotrichosis in a young animal of predisposed colour and breed. Tan areas are spared in colour
dilution alopecia and only black areas are affected
in black hair follicular dysplasia.18,19,28 Hair examination shows numerous large melanin clumps in the
cortex and medulla of hairs from the affected area and
defects and fractures of the hair cuticle.3,9,21,29,30 The
histopathological features are epidermal and follicular
orthokeratotic hyperkeratosis, dystrophy of hair follicles
and shafts, free melanin deposits at every level of the
hair follicle and shaft, numerous perifollicular, and in
particular peribulbar, melanophages and pigmentary
incontinence.2,8,9,19,21,29,31
The genetic basis of colour dilution alopecia and
its autosomal recessive mode of transmission has been
demonstrated in a family of wire-haired Dachshunds3
and is strongly suspected in other breeds. Analysis
of the pedigree of a family of dogs with black hair
follicular dysplasia has also suggested an autosomal
recessive mode of inheritance.32 The fact that both
colour dilution alopecia and black hair follicular
dysplasia have the same mode of inheritance is another
253

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C. Laffort-Dassot et al.

reason to suggest that the two conditions are very


similar. Most authors agree that the pathophysiology
of colour dilution alopecia involves problems of both
melanogenesis and hair follicle function.8,33 A more
recent theory suggests that dogs with colour dilution
alopecia have disordered calcium ion conduction.15
Calcium ions and protein kinase C, which they activate,
play a major part in the keratinization process.15
Noncolour-linked, cyclical follicular dysplasias
Recurrent flank alopecia is a seasonal, localized,
noncolour-linked follicular dysplasia. It has been reported
in 30 breeds, affecting young dogs of either sex.3437
Clinically, it involves alopecia, usually bilaterally
symmetrical, in the thoracolumbar region. Hair usually
regrows some months later, duller in colour and drier
in texture than before. Breed and individual variations
may occur in the frequency and extent of recurrence.38
Histopathological examination of skin biopsies taken
during the alopecic phase demonstrate lesions which
are particularly suggestive of recurrent flank alopecia:
follicular atrophy with marked infundibular hyperkeratosis spreading to secondary follicles (witchs foot
or medusa).
The precise aetiology of recurrent flank alopecia is
still unknown although a breed and sometimes familial
incidence suggest a genetic basis.36,37 In addition, seasonal recurrence and reverse seasonality in the southern
hemisphere suggest that photoperiod, mediated by two
photodependent hormones, melatonin and prolactin,
is involved in the pathogenesis of this dermatosis.34
Noncolour-linked, noncyclical follicular dysplasias
Other follicular dysplasias have been reported in certain
breeds. Knowledge of these is even more scanty than
for the follicular dysplasias described above. They
produce an alteration in coat, and alopecia in the growing puppy or young adult. The following conditions
are found in this group: follicular dysplasia of nordic
breeds of dog (alopecia X), follicular dysplasia of the
Portuguese Water Dog and other curly coated dogs, and
follicular dysplasia of the black or brown Doberman.
So-called follicular dysplasia of nordic breeds of dog
is associated with loss of primary hairs from the trunk
and areas of friction. Secondary hairs change colour
and consistency: the coat becomes dry and reddish.39,40
In the Irish Water Spaniel, Portuguese Water Dog
and Curly Coated Retriever, alopecia affects the trunk,
cranial limbs and periocular region of young adults.41,42
In the black or brown Doberman, alopecia starts between
the age of 2 and 4 years and affects the dorsolumbar
region and flanks.10 In the Pont Audemer Spaniel,
alopecia is restricted to brown-haired areas of the
trunk and ears.43
Diagnosis of these three conditions is based on
history, clinical examination, excluding other causes of
similarly presenting alopecia (mainly endocrinopathies),
and in particular on histopathological examination
of skin biopsies. Epidermal, and especially follicular,
orthokeratotic hyperkeratosis, dysplastic hair shafts
2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 253 260

and follicles, and pigmentary incontinence around


deep sections of hair follicles are revealed. It would
appear that flame follicles are merely a particular
histopathological characteristic of Nordic breeds and
not specifically of follicular dysplasia reported in these
breeds.38 However, apoptosis of keratinocytes in the
external and internal root sheaths and vacuolation of
hair matrix cells are part of the key to the histopathological diagnosis of follicular dysplasia of curly coated
breeds.19,41
We present the results of a prospective study, carried
out on five Weimaraners with a follicular dysplasia.
Data from three normal dogs of the same breed are
included for comparison.

MATERIALS AND METHODS


Inclusion and exclusion criteria
Dogs recruited were adult Weimaraners with a several
year history of diffuse truncal alopecia, scaling and
recurrent pyoderma. Exclusion criteria were evidence
of other dermatoses, including demodicosis and endocrinopathies. Skin scrapings were performed on every
dog to look for evidence of pathogenic agents. Blood
analysis, consisting of at least a haematological profile, assessment of serum glucose, cholesterol, alkaline
phosphatase and total thyroxine, was conducted.
Laboratory diagnosis of hypothyroidism was based on
serum total thyroxine concentrations. Sexual hormone
imbalance was evaluated in a male Weimaraner (case
4) by dosage of serum testosterone before and after
stimulation with HCG. If results of endocrine screening
assays were equivocal, and the dog did not respond to
specific treatment (e.g. neutering, sodium levothyroxine
or testosterone), it was included in the study.
Diagnostic tests
Skin biopsies were taken after local anaesthesia with
a 6-mm biopsy punch from the affected areas (trunk)
and if possible (with owner consent), from normal
areas (head). They were fixed in 10% formol saline,
mounted in paraffin blocks, sectioned into 4 m slices
and stained with haematoxylin, eosin and safran
(HES). Normal and dysplastic follicles (twisted, thin,
irregular outline, containing abnormal hair shafts with
melanin aggregates) were counted at high power (400)
in a single vertical section through of each sample.
Hairs were collected from the affected region (trunk)
and a normal region (head). They were mounted
between a glass slide and coverslip in chloral lactophenol
for examination under the light microscope. For each
sample, the number of melanin aggregates in 10 hairs
was assessed by examining 3 low power fields (100)
per hair. Reading was done blind. Results were recorded
as follows: 050 aggregates per field of view, 50100
aggregates per field of view, > 100 aggregates per field
of view.
Other hairs were fixed on an aluminium plate with
a piece of double-sided adhesive tape (Cellophane)

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Follicular dysplasia in Weimaraners

255

and coated in gold in a sputtering apparatus (Balzer


Union). These samples were then examined with a
scanning electron microscope (Philips 501). The presence
of cuticular defects on each of 10 hairs was recorded
as follows: no cuticular defects, presence of bulges
and/or craters, presence of numerous craters.
Control dogs
Diagnostic tests were performed in three Weimaraners
of normal appearance, with the consent of their owners.
Skin biopsies were performed, stained and examined
in the same way as for the other animals. Hair samples
were also taken and examined using light and electron
microscopy.

Figure 1. Bilaterally symmetrical hypotrichosis in a Weimaraner


with follicular dysplasia (case 1).

RESULTS
Clinical aspects and preliminary tests
One entire female, three entire males and one castrated
male animals were studied (Table 1). The age at onset
of signs varied between 1 and 3 years (average 2.2 years).
As the condition developed, lesions underwent phases
of exacerbation and remission. In all cases, alopecia
involved the back (from the back of the neck to the
base of the tail), thorax (lateral and ventral sides),
flanks and abdomen. In dog 1, it spread to the sternum
and in dog 4, it also affected the tail. Head and limbs
were always spared.
Lesions were consistent in the five cases and consisted of diffuse bilaterally symmetrical partial alopecia
(hypotrichosis, Fig. 1), hairs dry and harsh to the touch,
a moderate degree of fine scaling, and numerous
hypomelanotic macules notably on the flanks and
abdomen (Fig. 2). Rarely, some hyperpigmented
macules and hairs were present (Fig. 3). In dogs 3 and
4, numerous comedones, papules and pustules were
present. Cytological examination of pustular contents
revealed lots of neutrophils phagocytosing cocci,
suggesting a bacterial folliculitis. In all cases, the owners
reported recurrent bouts of folliculitis/furunculosis,
controlled with various antibiotic treatments. There
was no pruritus even when pyoderma was present.
Skin scrapings did not demonstrate any evidence
of pathogenic agents. The results of haematology,
biochemistry and endocrine profiles were within the

Figure 2. Hypotrichosis and hypomelanotic


Weimaraner with follicular dysplasia (case 5).

macules

in

Figure 3. Hyperpigmented hair in a Weimaraner with follicular


dysplasia (case 4).

Table 1. Clinical presentation of the five reported cases


Number

Age
(years)

Sex

Age of
onset (years)

10

MN

Summary of clinical signs

Ineffective prior therapy

Diffuse truncal alopecia


Recurrent pyoderma
Diffuse truncal alopecia
Recurrent pyoderma
Diffuse truncal alopecia
Recurrent pyoderma
Diffuse truncal alopecia
Recurrent pyoderma
Diffuse truncal alopecia
Recurrent pyoderma

T4

T4
Testosterone
Castration

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C. Laffort-Dassot et al.

reference limits except for dogs 1 and 3, for which the


level of basal thyroxine was low (respectively 7.2 nmol/L
and 11 nmol/L), and dog 4, for which the level of
testosterone, before and after stimulation with HCG,
was low.
In these three cases, hormone supplementation was
instituted. Dogs 1 and 3 received thyroid hormones
(sodium levothyroxine, 0.02 mg/kg twice daily for over
3 months,18) and dog 4 received testosterone (testosterone undecanoate, 1 mg/kg every 48 h, for 3 months,18)
without improvement. Dog 5 was castrated, although
endocrine assays were within normal limits, but no
improvement in the dermatosis was seen. These results
are summarized in Table 1.
Histopathology of skin biopsies

Figure 4. Skin biopsy from an affected area of a Weimaraner with


follicular dysplasia: there is orthokeratotic hyperkeratosis, epidermal
hyperpigmentation and keratin plug formation in the infundibula
(case 3, 100).

Samples taken from three normal Weimaraners Melanocytes containing large melanosomes were present in
the epidermis. Hair follicles were in anagen phase.
Few or no keratin plugs, or free intrafollicular melanin
deposits, were present. On average, 20% of follicles
were dysplastic, in that they were distorted in their
shape or outer contour. Other epidermal adnexae
were normally represented. No dermal melanophages
were seen.
Samples taken from normal area (head) of affected
Weimaraners (two of five dogs) Biopsies from normal
areas (head) were taken in only two dogs. Owners of
three dogs refused to have biopsies taken from this
region. The epidermis and dermis were close to normal,
as described above. Some follicular sections showed very
mild changes consisting of a few, small melanin deposits
in the hair shafts and slight orthokeratotic hyperkeratosis.
Fifty per cent of hair follicles were dysplastic.
Samples taken from affected area (all five dogs) The epidermis was of normal thickness. Slight hyperplasia and
orthokeratotic hyperkeratosis were sometimes seen.
Basal melanocytes were engorged with melanin and
there were a lot more numerous than those seen in
the three normal Weimaraners (Fig. 4). The majority of
the hair follicles had an abnormal aspect (Fig. 5). On
average, 72% were dysplastic, with marked orthokeratotic
hyperkeratosis and keratin plug formation. Voluminous
melanin clumps were present within hair keratin.
Sebaceous and sweat glands were normally represented
in dogs 3 and 4, but were sometimes sparse in dog 5.
Very large keratin plugs were seen in dog 5. The dermis
was usually not inflamed. A few melanophages were
seen around the periphery of the hair follicles. A
pyogranulomatous inflammatory infiltrate was present
in the perifollicular region in dogs 3 and 4, indicating a
folliculitis/furunculosis.
Hair examination using light microscopy
Hairs taken from three normal Weimaraners These hairs
contained melanin aggregates in the cortex and
2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 253 260

Figure 5. Hair follicle bulb from a Weimaraner with follicular


dysplasia. Note the voluminous melanin clumps (case 3, 200).

medulla. The density of these aggregates was moderate


(90% of the fields examined during the trichogram
contained fewer than 100 clumps of melanin) and their
distribution was even. The distribution of melanin
clumps in the 90 fields examined is shown in Table 2.
No cuticular lesions were seen.
Hairs taken from normal area of affected Weimaraners
(three of five dogs) These were taken from only three
of five dogs because of the wishes of the owners. Hairs
showed similar characteristics as described for the
healthy dogs (Table 2).
Hairs taken from alopecic region (five dogs) These hairs
contained melanin aggregates in the cortex and
Table 2. Light microscopy percentage of fields examined containing
different numbers of clumps in three normal Weimaraners (i.e. 90
fields), normal area of three affected Weimaraners (i.e. 90 fields),
alopecic region of five affected Weimaraners (i.e. 150 fields)
Number of
clumps per field

Healthy
dogs

Affected dogs
Normal area

Alopecic
region

0 50
51100
> 100

57% (51)
33% (30)
10% (9)

43% (39)
50% (45)
7% (6)

21% (32)
37% (55)
42% (63)

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Follicular dysplasia in Weimaraners

Figure 6. Hair shaft from a Weimaraner with follicular dysplasia.


Note the melanin aggregates and the irregular outline of the hair
shaft (case 1, 200).

257

Figure 7. Scanning electron microscopy of two hair shafts from a


Weimaraner with follicular dysplasia. Note the cuticular deformities
and craters (case 4, 250).

Table 3. Scanning electron microscopy type of lesions and


frequency in the hairs examined in three normal Weimaraners (i.e.
30 hairs), normal area of three affected Weimaraners (i.e. 30 hairs),
alopecic region of five affected Weimaraners (i.e. 50 hairs)
Cuticular
lesions

Healthy
dogs

Affected dogs
Normal area

Alopecic
region

None
Bulges, craters
Numerous craters

100% (30)
0
0

50% (15)
50% (15)
0

50% (25)
0
50% (25)

medulla. As well as being larger than in normal dogs,


the melanin clumps were more numerous (Table 2), and
variably distributed along the whole length of the hair
shaft. Some parts of the hairs resembled hair from the
normal dogs. In other regions, melanin aggregates
were seen in both cortex and medulla. Concentrations
of these were associated with a defect in the hair that
became sinuous and progressively wider (Fig. 6).
Cuticular lesions (fractures, craters) were also seen in
the regions of these melanin aggregates.

Figure 8. Scanning electron microscopy of a hair shaft from a


Weimaraner with follicular dysplasia note the crater (case 5, 1900).

Hair examination using scanning electron microscopy


No cuticular abnormalities were seen in any of the hairs
taken from the normal Weimaraners (Table 3). Holes
and numerous bulges were seen sporadically in the
cuticle of hairs from clinically normal areas of affected
dogs, whereas hairs from affected areas regularly
contained craters and defects in the cuticle (Figs 79).

DISCUSSION
In each of the five cases presented in this study, the
history and clinical picture were very similar: age of
onset of lesions was between 1 and 3 years and initial
presentation was a diffuse truncal hypotrichosis which
worsened progressively. Apart from the head and limbs,
the dogs became practically hairless. All dogs had
episodes of folliculitis/furunculosis that responded well
to antibiotics.
The differential diagnosis included endocrinopathy,
in particular hypothyroidism and hyperadrenocorticism

Figure 9. Scanning electron microscopy of a hair shaft from a


Weimaraner with follicular dysplasia. Close-up view of the crater of
the dog illustrated in Figure 8 (case 5, 8000).

(diffuse truncal alopecia, recurrent pyoderma). However,


none of these dogs had any systemic or biochemical
signs despite the chronicity of lesions. In the absence of
clinical response to thyroid hormone supplementation,
the two low basal T4 results may be explained by the
concomitant presence of chronic pyoderma (euthyroid
sick syndrome). Excluding hypothyroidism with a
TSH stimulation test would have been useful but as pure,
good quality TSH was unavailable, we did not carry
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C. Laffort-Dassot et al.

out this test. Although assay of endogenous TSH may


assist in the assessment of thyroidal status, it was not
assayed because spurious values may be found.44 Lack
of response to treatment with T4 (sodium levothyroxine, 0.02 mg/kg twice daily for over 3 months,18) made
a diagnosis of hypothyroidism unlikely, although post
pill serum T4 concentrations were not monitored to
be sure that this recommended dose was appropriate in
these dogs.
Truncal alopecia without systemic signs was
suggestive of other endocrinopathies such as adult
hyposomatotropism and reproductive hormone
imbalances. One of the dogs in our study had low
levels of testosterone before and after stimulation with
HCG. However, testosterone supplementation failed
either to improve the alopecia or prevent recurrence
of pyoderma. A reproductive hormone imbalance was
therefore reasonably excluded in this case.
Histopathology can suggest, or even confirm, the
endocrine nature of alopecia. This procedure is essential
in Weimaraners, because the coat colour of these
dogs leads to suspicion of colour dilution alopecia,
the diagnosis of which is primarily histopathological.
Histopathological abnormalities common to the
two disorders are epidermal and follicular orthokeratotic
hyperkeratosis with keratin plug formation, follicular
atrophy, and the predominance of telogen hair follicles.
Moderate sebaceous gland atrophy, seen in the samples
from dog 5, can occur in chronic follicular dysplasia
associated with cessation of all follicular activity,
and frequently in endocrinopathy.18,33 The diagnosis was
based on the presence of large numbers of dysplastic
hair follicles in the affected dogs. In follicular dysplasia,
hair follicles and hairs are abnormally shaped
(twisted).33 In a retrospective study of skin biopsies
from 72 dogs with follicular dysplasia and 102 dogs
with endocrinopathy, Rothstein also showed that the
presence of abnormal melanin clumps in dysplastic
hair shafts was characteristic of follicular dysplasia.31
Both dystrophic hair follicles and melanin clumping
in dysplastic hair shafts were found in biopsies taken
in our study from alopecic areas of affected dogs. They
were found much more frequently than in samples
taken from normal skin of affected dogs or from
normal dogs.
It is important to note that the pigmentary abnormalities in the alopecic areas of these Weimaraners
were much less pronounced than those encountered
in colour dilution alopecia in other breeds such as
the Doberman or Dachshund. Qualitatively, lesions
resembled those seen in colour dilution alopecia but
quantitatively, abnormalities were much less marked.
Equally, cuticular lesions seen under the electron
microscope were typical of colour dilution alopecia
but were far less common than those seen in seven
Dachshunds with colour dilution alopecia.3
Light microscopy revealed hair lesions somewhat
different to those of colour dilution alopecia. Cuticular
craters and hair shaft defects, seen in moderate
numbers with the electron microscopy, were found.
2002 Blackwell Science Ltd, Veterinary Dermatology, 13, 253 260

However, the large melanin aggregates, which using


light microscopy, can be used to distinguish a normal
dog with a dilute colour from a dog with colour dilution
alopecia, were extremely rare. Compared with hairs
from normal dogs or hairs taken from a normal region,
variations in size of melanin clumps were not appreciable.
However, in hairs taken from alopecic areas, there were
regions where these clumps much more concentrated.
Typically, they were more numerous in affected hairs
than normal hairs.
The quantitative variations observed could be
explained to some degree, by the pale colour (and
therefore the small amount of melanin) in the Weimaraner.
In a study of colour dilution alopecia in the Dachshund
by Beco et al.3 the number of craters seen using electron
microscopy varied greatly between individuals of the
same colour and also between individuals of different
coat colour (wild boar or blue and tan). The samples
showed individual variation in the lesions seen.
The other possible theory is that in the Weimaraner,
there might exist a noncolour-linked follicular dysplasia. The relatively mild pigmentary abnormalities,
compared with those in colour dilution alopecia, have
actually been reported in follicular dysplasia of the
Portuguese Water Dog19 and follicular dysplasia of brown
and black Dobermans.10 There has been no electron
microscope study of hairs from dogs with noncolourlinked follicular dysplasia. It is reasonable to question
therefore whether these hairs have cuticular lesions
and if so, to what extent. Hairs from dystrophic hair
follicles may also be abnormal. Severity may be correlated with histopathological lesions and therefore
less marked than in colour dilution alopecia. It would
be interesting to carry out this procedure to confirm the
likely absence of craters in dogs with an endocrinopathy,
as the hair follicles of these dogs are simply atrophic.
The animals were not treated, apart from regular
application of keratolytic shampoos and antibiotics for
episodes of pyoderma. However, animals were prevented
from breeding as a precautionary measure.
Given the current state of knowledge, it is usually
possible to distinguish between an endocrinopathy and
follicular dysplasia in its broad sense. However, in the
Weimaraner, colour dilution alopecia cannot easily be
distinguished from noncolour-linked follicular dysplasia.
We therefore propose to retain for now, the term
follicular dysplasia of the Weimaraner. This discussion
is summarized in Table 4.

CONCLUSION
Follicular dysplasia of the Weimaraner is a skin condition of young adults. It manifests clinically as diffuse,
nonpruritic, truncal alopecia and recurrent pyoderma.
Diagnosis is based on history and clinical signs,
microscopic and ultramicroscopic hair lesions, and
compatible histopathology. Endocrinopathy should be
considered in the differential diagnosis. There is
currently no known treatment. Studies investigating

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Follicular dysplasia in Weimaraners

259

Table 4. Study of the different diagnostic parameters for the three differentials

Skin lesion
Abnormal serum hormone levels
Associated nondermatological signs
No response to specific hormonal supplementation
Orthokeratotic hyperkeratosis
Follicular hyperkeratosis
Hair follicles in telogen
Sebaceous gland atrophy
Pigmentary abnormalities
Melanin clumps in hair keratin
Numerous dysplastic hair follicles
Craters/cuticular defects
Familial

Endocrinopathy

Colour dilution
alopecia and
black hair
follicular dysplasia

Other follicular
dysplasias
(noncolour
linked)

Follicular
dysplasia of
the Weimaraner Skin

++
++
++

++
++
++
++

+/

++
+/

++
++
++
++

++
++
++
++
++

+
+/

++
++
++
++

+
+
++
?
++

++
+/

++
++
++
++
+/
+
+
++
+
?

++, Strongly suggestive; +, slightly suggestive; ?, uncertain; , strongly against; , slightly against; +/, occasionally present.

the existence of familial inheritance, and possibly


determining the genetic mode of transmission, would
be useful.

ACKNOWLEDGEMENTS
The authors would like to thank Dr Morard for
microscopical slides, Mr Charlier for the electron
microscopy and Drs Mathet, Ximenes and Boulet for
their assistance. C. Laffort-Dassot would also like to
thank Pfizer, Schering-Plough, Sepval, Vetoquinol and
Virbac for their support during her ECVD residency
program.

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467 9.
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alopecia in seven Dachshunds. A clinical study and the
hereditary, microscopical and ultrastructural aspect of
the disease. Veterinary Dermatology 1995; 7: 917.
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6. ONeil, C. Hereditary disease in the dog and cat.
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Veterinarian 1981; 3: 791 800.
7. Langebaeck, R. Variation in hair coat and skin texture
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Rsum Cette tude a valu les aspects cliniques, histopathologiques et ultrastructuraux de cinq cas de
dysplasie folliculaire chez des Braque de Weimar. Ces donnes ont t compares avec celles obtenues chez trois
Braque de Weimar sains. Dans notre tude, la dermatose atteignait des adultes jeunes, avec une alopcie progressive du tronc pargnant la tte et les extrmits, associe des pisodes rcidivants de folliculite et de furonculose.
Le diagnostic de dysplasie folliculaire a t fait en excluant les autres hypothses diagnostiques, au vu des images
histopathologiques et des lsions en microscopie optique et lectronique, semblables celles observes dans les
alopcies des robes dilues. Les lesions observes ici sont les mmes que celles dcrites en cas dalopcie des robes
dilues, mais elles taient moins prononces dans tous les prlvements examins.
Resumen Este estudio evaluaba las caractersticas clnicas e histopatolgicas y los resultados del examen con
microscopa ptica y electrnica de barrido, de la displasia folicular de cinco pointers Weimar. Estos datos compararon con los obtenidos en tres Weimaraners normales. En nuestro estudio, esta dermatosis afectaba adultos
jvenes que mostraban una alopecia progresiva del tronco (cabeza y extremidades no se encontraban afectadas)
asociadas a una foliculitis/furunculosis recidivante. La exclusin de otras dermatosis y la presencia de lesiones
histopatolgicas y de anomalas en el pelo observadas en microscopa pica o electrnica de barrido similares a la
alopecia de color diluido, llev a un diagnstico de displasia folicular. Las lesiones observadas son iguales a las
descritas previamente en la alopecia de color diluido, pero eran menos pronunciadas en todas nuestras muestras.
Zusammenfassung Diese Studie befasste sich mit den klinischen und histopathologischen Merkmalen und den
Ergebnissen licht- und elektronenmikroskopischer Untersuchung follikulrer Dysplasien bei fnf Weimaraner
Vorstehhunden. Diese Daten wurden mit denjenigen dreier normaler Weimaraner verglichen. In unserer Studie
betraf diese Dermatose junge erwachsene Hunde, die eine fortschreitende Alopezie des Krperstammes (Kopf
und Extremitten blieben ausgespart) mit rezidivierender Follikulitis/Furunkulose zeigten. Die Diagnose einer
follikulren Dysplasie wurde anhand des Ausschlusses anderer Dermatosen und des licht- und/oder elektronenmikroskopischen Nachweises von histopathologischen Vernderungen und Haarschaftanomalien hnlich denen
der Farbverdnnungsalopezie gestellt. Die Befunde waren mit denen der Farbverdnnngsalopezie identisch,
jedoch in allen Proben weniger markant.
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