Veterinary Dermatology 2006, 17, 63 69

Case report

Blackwell Publishing Ltd

Generalized alopecic and cystic dermatosis in a cat: a counterpart

to the hairless mouse phenotype or a unique congenital dermatosis?
ARIANE E. NEUBER*, ADRI H. M. VAN DEN BROEK*, SUSAN M. RHIND, PETER B.
HILL* and KEITH L. THODAY*
*The University of Edinburgh, Dermatology Unit, Division of Veterinary Clinical Studies
Veterinary Pathology Unit, The Royal (Dick) School of Veterinary Studies, The Hospital for Small Animals,
Easter Bush Veterinary Centre, Roslin, Midlothian EH25 9RG, Scotland, UK
(Received 28 September 2004; accepted 17 October 2005)

Abstract A 2-year-old, male neutered, domestic semi-long-haired cat was presented with a 1.5-year history of
progressive, initially nonpruritic alopecia and malodorous greasy exudate affecting the distal extremities, trunk
and neck but sparing the head and tail. The extensive alopecia and seborrhoea were associated with severe thickening of the skin and fold formation on the dorsal head and distal extremities as well as the lateral thorax and
abdomen. The hair was easily epilated, numerous milia were seen on the ventral abdomen and the caudal and
lateral thighs, and mild paronychia was present. Histopathological examination of skin biopsies revealed marked
cystic dilation of hair follicles and sebaceous glands with follicular hypoplasia, infundibular hyperkeratosis and
variable associated inflammation. Systemic glucocorticoid therapy in combination with topical washes with
chlorhexidine and miconazole resulted in a marked improvement and some hair regrowth, but the cat was
subsequently lost to follow-up. The dermatosis resembles a number of conditions in other species, but it is not
clear whether it is a counterpart to the hairless mutant mouse or is a unique dermatosis.

CASE H ISTORY
An approximately 2-year-old, male neutered, domestic
semi-long-haired cat weighing 3 kg was presented to
the Dermatology Unit of the Royal (Dick) School of
Veterinary Studies, The University of Edinburgh, with
a 1.5-year history of progressive, initially nonpruritic
alopecia and malodorous greasy exudate affecting the
distal extremities, trunk and neck but sparing the head
and tail.
At approximately 6 months of age, when it was
adopted as a stray by the present owner, a veterinary
surgeon, the cat was noted to lack undercoat. At 9
months of age, alopecia and excessive skin fold formation began to develop on the distal extremities of all
four limbs. The alopecia resolved without therapy, but
recurred 3 months later expanding proximally to
involve the abdomen and lateral thorax. Concurrently,
patches of hyperpigmentation and a malodorous,
greasy exudate were also seen. A combination of 2%
chlorhexidine and 2% miconazole (Malaseb, Leo
Animal Health, Princes Risborough, UK) baths once
weekly and oral cephalexin (Rilexine, Virbac Bury,
St Edmonds, UK) at a dosage of 25 mg kg1 twice daily
led to only slight improvement, and treatment was
Correspondence: Keith L. Thoday, The University of Edinburgh,
Dermatology Unit, Division of Veterinary Clinical Studies. E-mail:
k.l.thoday@ed.ac.uk

stopped after 3 weeks. The condition continued to

progress.
When the cat was approximately 16 months old, hair
pluckings taken from the edge of an alopecic area and
a single skin biopsy, taken from an alopecic area on
a distal foreleg, were submitted to separate commercial
laboratories for fungal culture and histopathological
examination, respectively. Trichophyton mentagrophytes
was isolated, but no associated cutaneous histopathological changes were described. Subsequently, the cat
received a total body clip and was treated with Malaseb
baths as before and oral griseofulvin (Fulcin, Zeneca,
Wilmslow, UK) at a dosage of 20 mg kg1 once daily,
both for 4 weeks. Hair regrew in the previously normal
areas but not in the previously alopecic areas. Follow-up
fungal cultures were not carried out when treatment
was stopped.
At approximately 20 months of age, the condition
began to progress to affect the ventral neck. Griseofulvin
and Malaseb therapy, as mentioned previously, were
reinstituted, but stopped after 4 weeks when a malodorous greasy exudate, together with comedones and
pustules, were noted. Cephalexin was administered
for 2 weeks as before, but did not alter the appearance
of the pustules. Blood was collected for standard haematological and biochemical examinations and feline
leukaemia virus (FeLV) and feline immunodeficiency
virus (FIV) status. Mild lymphoepenia was the only
abnormality reported.

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AE Neuber et al.
Table 1. Results of haematological and biochemical examinations

Figure 1. The cat at first referral. Note the extent of the alopecia.

Haematology test

Units

Reference range

Red blood cells

PCV
Haemoglobin
MCV
MCHC
White blood cells
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Platelets

6.29 1012 L1
0.283 L/L
9.4 g dL1
45.0 f L1
33.2%
8.5 109 L1
5.1 109 L1
0.0 109 L1
2.55 109 L1
0.68 109 L1
0.17 109 L1
0.0 109 L1

5.500 10.000
0.24 0.45
8.000 14.000
39.000 55.000
30.0 36.0
7.000 20.000
2.500 12.800
1.500 7.000
0.070 0.850
0.000 1.000
0.000 0.200
300.000 600.000

Biochemistry test

Units

Reference range

Total protein
Albumin
Globulin
Bile acids
Alanine aminotransferase
Alkaline phosphatase
(AMP)
Bilirubin
Glucose
Creatinine
Urea
Chloride
Calcium
Inorganic phosphate
Sodium
Potassium

62.0 g L1
28.8 g L1
33.2 g L1
0.5 mol L1
61.0 IU L1
9.0 IU L1
1.4 mol L1
12.2 mmol L1
123.0 mol L1
7.4 mm L1
116.0 mmol L1
2.33 mmol L1
1.720 mmol L1
147.0 mmol L1
4.6 mmol L1

69.00 79.00
28.00 39.00
23.00 50.00
0.00 7.00
6.00 83.00
10.00 100.00
0.00 6.80
3.30 5.00
40.00 177.00
2.80 9.80
117.00 140.00
2.100 2.900
1.400 2.500
145.00 156.00
4.00 5.00

MCHC, mean corpuscular haemoglobin concentration; MCV, mean

corpuscular volume; PCV, packed cell volume; AMP, 2-amino-2methyl-1-propanol buffer.
Abnormal results are indicated in bold.
Figure 2. Close-up of the left forelimb at first referral, showing
severe alopecia and skin fold formation.

On referral, the cat was said to be overgrooming.

The results of general physical examination were unremarkable. Dermatological examination revealed
extensive alopecia affecting all four limbs, the trunk
and the dorsal head (Figs 1 and 2). This was associated
with a malodorous greasy exudate and severe thickening of the skin, with fold formation on the dorsal head
and distal limbs as well as on the lateral thorax and
abdomen (Figs 1 and 2). The hair was easily epilated.
The previously reported pustules were found to be
numerous retention cysts of sebaceous glands (milia),
which were present over the ventral abdomen and the
caudal and lateral thighs. Brown, waxy material was
tightly adherent within all claw folds.
Differential diagnoses for the initially nonpruritic,
grossly noninflammatory alopecia included dermatophytosis, demodicosis, a congenital disorder of the
adnexae, follicular dysplasia, mural folliculitis, a previously undescribed congenital ectodermal or adnexal
disorder, sebaceous adenitis, cretinism and cutaneous
lymphoma. Secondary bacterial pyoderma and
Malassezia dermatitis were considered for the pruritus
and paronychia that had developed subsequently.
Multiple deep skin scrapings were negative for
Demodex mites. A trichogram revealed normal hair

shafts with greater than 90% telogen hairs and some

anagen hairs. Material collected from the whole
body by the MacKenzie brush technique subsequently
proved negative for dermatophytes on fungal culture.
Tape strips from the stratum corneum of the feet
collected for cytological examination revealed keratinocytes, but no bacteria or Malassezia yeasts. Cytological examination from a dry scraping of the proximal
aspect of a claw surface revealed numerous cocci, some
rods and numerous yeast organisms. Blood was collected
for standard haematological and biochemical examinations (Table 1) and revealed a total lymphopenia,
monocytosis, an absence of platelets, mild hypoproteinaemia and hyperglycaemia, the latter attributed to
stress during collection of the sample.
Numerous skin biopsies were collected from alopecic
areas on the dorsal neck, the trunk, the dorsum, the
distal right hind and a milium on the caudal abdomen,
and submitted for histopathological examination. They
revealed mild orthokeratotic hyperkeratosis of the
surface epidermis with follicular infundibular hyperkeratosis (Figs 3 and 4). Most follicles were cystic with
the remainder being hypoplastic and superficial; very
occasional deeper anagen-phase follicles were identified. The superficial to mid-dermis was characterized
by sebaceous gland dilatation forming large cystic
structures with sebaceous gland tissue incorporated

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Alopecic and cystic dermatosis in a cat

65

Figure 3. Skin biopsy showing large cystic structures in the mid-dermis.

Haematoxylin and eosin stain (H&E); original magnification
40.

Figure 5. Skin biopsy showing apparent connection of the cystic

areas to sebaceous glands. H & E; higher magnification from
Figure 4, original magnification 600.

Figure 4. Skin biopsy showing apparent connection of the cystic

areas to sebaceous glands. H & E; original magnification 40.

Figure 6. Whole-body view 8 weeks after initial referral, showing the

progression of the alopecia.

in the wall of some of the cysts (Fig. 5). In the deeper

dermis, marked cystic dilatation of both the hair follicles
and the sweat glands was seen. The sections contained
no evidence of fungal or bacterial infection. In some
sections, there was very mild associated inflammation
dominated by macrophages and giant cells but with
smaller numbers of neutrophils in the surrounding
dermis. The provisional diagnosis was cystic dilatation
of the sebaceous glands, but because of the unusual
features, histological material and clinical images were
sent to a clinical veterinary dermatologist with a special
interest in dermatopathology (DWS), a medical clinical
dermatologist with a special interest in dermatopathology
(GMK) and a specialist on human sebaceous glands
(RNP). Two considered the clinical and histopathological
features of this case to be unique, whereas one (RNP)
felt that the animal showed many similarities to the
hairless mouse model.
With the fungal culture and the histopathological
examination pending, twice-weekly baths with Malaseb
shampoo were begun to reduce the number of the
bacteria causing the bacterial overgrowth and to

reduce possible further environmental contamination

with fungal spores in case the fungal culture revealed
a persistent T. mentagrophytes infection. The owner was
advised to pay particular attention to the claw folds.
Subsequently, the histopathological findings as well
as treatment options were discussed with the owner.
Retinoids were identified as the drugs most likely to have
an effect on the condition, but were declined by the owner.
Re-evaluation at 8 weeks revealed more pronounced
alopecia (Fig. 6) and more slack, folded skin (Fig. 7)
in addition to the features noted during the first consultation. There were more areas of hyperpigmentation,
especially circular patches on the dorsum with a zebralike configuration on the hind legs (Fig. 8) together
with dorsal scaling and associated erythema. On the
left lateral thigh, some palpable, apparently cystic lesions
containing sebaceous-type material were found. The
owner reported that the cat stopped over-grooming
immediately after each bath, but began again as soon
as the greasy exudate had reached a certain degree.
The results of cytological examination from the claw
folds were unchanged.

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AE Neuber et al.

Figure 9. Close-up of the area of hair regrowth on the dorsal neck 8

weeks after beginning prednisolone therapy.

Figure 7. Frontal view of the thorax and forelimbs 8 weeks after

initial referral. There is extreme skin fold formation and complete
alopecia.

Figure 10. The cat 12 weeks after beginning prednisolone therapy.

Some hair regrowth is now present on most of areas of the body.

Figure 8. Hyperpigmentation on the hind limbs in a zebra-like

configuration: 8 weeks after initial referral.

Prednisolone at a dose of 2 mg kg1 once daily was

initiated for its anti-inflammatory properties and for its
potential to cause pilosebaceous atrophy in some species.
Malaseb shampoo bathing was continued once weekly.

After 4 weeks of prednisolone therapy, dermatological examination revealed a reduction in greasiness and
odour and a complete resolution of the over-grooming
behaviour. Cytological examination of material from
the claw folds was unchanged. To determine whether
the clinical improvement on glucocorticoid therapy
was reflected histologically, repeat skin biopsies were
taken. These had pronounced cyst development similar
to those seen in the initial series. Additionally, in one
sample taken from the palpable cystic lesions on the
left lateral thigh, there was pyogranulomatous inflammation associated with rupture of one of the cysts and
release of contents. This inflammation extended from
the mid-dermis to the subcutis.
Prednisolone therapy was continued as previously,
and the owner was advised to continue cleaning the
claw folds.
After a further 4 weeks, some hair regrowth was
noted on the dorsal neck. Dermatological examination

2006 The Authors. Journal compilation 2006 European Society of Veterinary Dermatology

Alopecic and cystic dermatosis in a cat

was similar to before, with some hair regrowth on the
dorsal neck (Fig. 9).
After 12 weeks on prednisolone therapy, the cat was
re-evaluated. Dermatological examination revealed
sparse hair growth and a reduction in the size of the
skin folds (Fig. 10). Multiple papules and nodules were
evident on the dorsum, which, according to the owner,
occasionally ruptured to release a sebaceous-type
material. The hyperpigmentation, which had previously formed a zebra pattern, now more diffusely
affected the trunk and extremities. Paronychia, with a
brown-black discharge in the claw folds, was still
present. Cytology from the claw folds continued to
reveal numerous cocci and occasional rods and yeasts.
The owner was instructed to reduce the daily
prednisolone dosage by 0.5 mg kg1 once a month.
Four weeks later, the cat was reported to be receiving
1.5 mg kg1 orally daily and was progressing satisfactorily,
but was subsequently lost to follow-up.

D ISCU SSION
To the authors knowledge, this condition is unique,
not having been previously reported in any species,
including humans. Similarities were found to a number
of conditions described in humans or mice, but none
was identical, either clinically or histopathologically,
to the disease described in this case report.
The condition in this cat most closely resembles that
in the hairless mutant mouse. Mice with the hairless
mutation1 develop a syndrome characterized by loss of
hair after growth of the first pelage, rudimentary mammary gland development, abnormal growth of the nails
and a high incidence of thymic lymphoma. The skin of
these mutants is characterized by the formation of pilary
cysts, dilated sebaceous gland ducts, granulomatous
inflammation in the dermis associated with rupture of
hair follicles and generalized acanthosis and orthokeratotic hyperkeratosis. In the first 14 days of life, these mice
develop a normal pelage and subsequently lose the coat
in a cephalocaudal pattern to remain entirely naked.1
It has been shown that in these mice, loss of function
of the hairless (h) gene causes dysregulation of catagen
as a result of premature apoptosis of the proximal
hair bulb and destruction of normal hair follicle
architecture.1
Numerous other hairless variants of mice have been
described, e.g. the rhino mutation, which is an allele to
the hairless gene and is a more severe manifestation of
this mutation and the Yurlovo (hrrhY) mice, which are
characterized by complete hair loss during the first 3 to
5 weeks after birth, as well as extensive skin thickening
and folding caused by formation of cystic structures in
the dermis.1
The cystic changes identified in this cat were clearly
associated with both hair follicles and sebaceous glands.
However, it was not possible to determine from which
tissue the cysts emanated. Additionally, in this case,
the hair loss began on the limbs and then spread

67

to the trunk, whereas the normal pattern of hair loss

in the hairless mutant mouse is in a cephalocaudal
pattern.2 The normal pattern of hair loss in mice and
cats is, however, very different;3,4 hence, this difference
in shedding pattern may not be significant. One further
notable feature in this case was the sparse hair
regrowth following therapy, suggesting that not all
follicles were affected or destroyed, and was supported
by the occasional observation of deeper anagen follicles
in the biopsies.
Steatocystoma multiplex is an uncommon autosomal
dominant disorder of humans resulting from a keratin
17 defect and involves the pilosebaceous unit, causing
the formation of cystic sebaceous glands.5 The condition
is frequently associated with vellus hair cysts or pachyonychia congenital type 2 and may be a heterogeneous
group of genotypes with similar phenotypic and clinical
presentations. On histological examination, the cysts
found macroscopically are located in the mid-dermis.
The cyst lining is a crenulated or wavy, homogeneous,
eosinophilic horny layer collapsed around thin cystic
spaces. The spaces hold varying amounts of keratin,
vellus hairs and sebum esters. The walls are formed
from several layers of epithelial cells, and embedded
flattened lobules of sebaceous glands are among the
epithelial cells. There are invaginations resembling rudimentary hair follicles emptying into the cysts. The cyst
units are attached to the overlying normal epidermis
by a thin strand of undifferentiated epithelial cells. The
histopathological features of the skin biopsies of the cat
described in this case report differed in that the cysts
appeared round, did not have a folded cyst wall and
had no eosinophilic horny layer.
Cutis laxa (CL) is a rare, inherited or acquired,
connective tissue disorder in which the skin becomes
inelastic and hangs loosely in folds.6,7 The precise cause
is unknown, but it may be because of abnormal elastin
metabolism, resulting in markedly reduced dermal elastin content. The clinical presentation and the mode of
inheritance show considerable heterogeneity. Autosomal
dominant, autosomal recessive and X-linked recessive
patterns have been noted in inherited forms. Histopathological analysis of the skin reveals alterations in the
quantity or the morphology of elastin, in which fragmentation or a loss of elastic fibres is present. Additionally,
evidence of abnormal cross-linking of elastin exists
in some patients. Clinically, the excessive folds noted in
the cat described in this case report appear very similar,
but the histopathological changes found in skin biopsies obtained from this cat were not consistent with the
changes described for CL.
The cats physical features resemble human granulomatous slack skin, a form of cutaneous lymphoma.8
It is characterized by circumscribed areas of pendulous,
lax skin containing clonal infiltrates of helper T cells,
which infiltrate the epidermis in a manner similar to
that in mycosis fungoides. These attract a granulomatous
component that mediates massive dermal elastolysis.
The disease has an indolent but relentless course. Hodgkins
disease develops in some cases.9 The histopathological

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AE Neuber et al.

features of granulomatous slack skin do not resemble

the findings of the cat described in this report in any way,
and any similarities are merely physical.
The cystic structures in the dermis in this case comprised both cystic follicles, sebaceous glands and ducts.
Occasional anagen-phase follicles were identified, as were
hypoplastic follicles. The palpable nodules that appeared
initially on the flanks and later in other locations on
the body were deep pyogranulomatous dermatitis and
panniculitis reactions consistent with release of cyst
contents into the surrounding tissue, provoking a
foreign body reaction. Whether the paronychia represents a separate entity or has a similar pathogenesis
as the sebaceous gland condition remains unclear.
Certainly, nail/claw changes have been described in
several of the diseases described previously, and a
connection appears possible in this case. Although the
finding of bacterial and yeast overgrowths was persistent,
these did not seem to affect the cat.
Glucocorticoids were chosen as an initial therapy for
their anti-inflammatory properties and their potential
to cause atrophy of sebaceous glands. Shampoo therapy
consisting of a 2% chlorhexidine and 2% miconazole
shampoo was used to remove the greasy exudate and to
control the bacterial and yeast overgrowth that particularly affected the claw folds. Oral antibiotic therapy
was not deemed necessary because of the lack of evidence
of bacterial pyoderma (no cytological evidence of inflammatory cells was found at any time) and because of the
body location (claw fold) in which the bacteria were
found. Other treatment discussed with the owners was
isotretinoin for its effect on inducing sebaceous gland
atrophy.
Retinoids have been described as a treatment for
SM10 with the therapeutic response most likely reflecting
their anti-inflammatory effects.11 As prednisolone had
a beneficial effect on the cats condition, the owner,
declined retinoid use. The examination of further skin
biopsies when the cat showed good hair regrowth on
glucocorticoid therapy would have been very interesting,
but the cat was lost to follow-up.
In conclusion, this report describes a congenital
condition in a cat, which has no direct counterpart in
any species. Given the current lack of knowledge of the
development of hair follicles and sebaceous glands in
felines, it is impossible to decide whether the dermatosis
is a feline equivalent to the hairless mouse phenotype
or is truly a unique dermatosis.

AC K N OW L E D G E M E N T S
The authors thank veterinary surgeons W. Balmain
and A. Blyth for referring the case. They are particularly
grateful to colleagues Dr D. W. Scott, College of Veterinary
Medicine, Cornell University, New York, USA, Dr G.
M. Kavanagh, Department of Clinical Sciences and
Community Health, The University of Edinburgh,
Edinburgh, Scotland, and Dr R. M. Porter, Cancer
Research UK Cell Structure Research Laboratory,
University of Dundee, Scotland, for their valued opinions
about the clinical images and the histological sections.

REFERENCES
1. Panteleyev AA, Paus R, Ahmad W et al. Molecular and
functional aspects of the hairless (hr) gene in laboratory
rodents and humans. Experimental Dermatology 1998;
7: 24967.
2. Chase HB, Rauch R, Smith VW. Critical stages of hair
development and pigmentation in the mouse. Physiological
Zoology 1951; 24: 18.
3. Takashima I, Kauragishi I. Comparative Study of Hair
Growth in Mammals, with Special Reference to Hair
Grouping and Hair Cycle, and Hair Growth in the Juvenile
Stumptailed Macqaque. Baltimore: Park Press, 1976.
4. Lavker RM, Bertolino AP, Freedburg IM et al. Biology
of hair follicles. In: Freedburg IM, Eisen LA, Eisen AZ
et al. eds. Dermatology in General Medicine, 5th edn.
New York: McGraw-Hill, 1999: 23044.
5. Covello SP, Smith FJ, Sillevis Smitt JH et al. Keratin 17
mutations cause either steatocystoma multiplex or pachyonychia congenita type 2. British Journal of Dermatology
1998; 139: 47580.
6. Reed WB, Horowitz RE, Beighton P. Acquired cutis laxa.
Primary generalized elastolysis. Archives of Dermatology
1971; 103: 6619.
7. Fitzsimmons JS, Gilbert G. Variable clinical presentations
of cutis laxa. Clinical Genetics 1985; 28: 28495.
8. Schot JDL. Granulomatous slack skin. British Journal
of Dermatology 1989; 120: 807.
9. Noto G, Pravata G, Arico M. Granulomatous slack skin:
a report of a case associated with Hodgkins disease and
a review of the literature. British Journal of Dermatology
1994; 131: 2759.
10. Moritz DL, Silverman RA. Steatocystoma multiplex
treated with isotretinoin: a delayed response. Cutis 1988;
42: 4379.
11. Lonnie L, Cole A. Steatocystoma multiplex. Archives of
Dermatology 1976; 112: 14379.

Rsum Un chat europen mle castrg de 2 ans a t prsent pour une alopcie non prurigineuse et un exudat
des extrmits distales, du tronc et du cou, pargnant la tte et la queue, voluant depuis un an et demi. Lalopcie
extensive et la sborrhe taient associes un paississement svre de la peau, et la formation de plus
sur la tte et les extrmits distales ainsi que sur les faces latrales du thorax et de labdomen. Les poils taient
facilement pils, de nombreux milia taient nots sur labdomen et sur les cuisses et une paronychie modre
tait observe. Lexamen histopathologique a montr une dilatation kystique des follicules pileux et des glandes
sbaces avec une hypoplasie folliculaire, une hyeprkratose infundibulaire et une inflammation variable. Un
traitement systmique avec des glucocorticoides et des bains de chlorhexidine et de miconazole ont permis une
amlioration marque et une repousse pilaire, mais le chat a t perdu de vue. La maladie ressemble des maladies
dcrites dans dautres espces, mais il nest pas clair sil sagit dun modle de la souris mutante sans poil ou dune
maladie nouvelle.
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Alopecic and cystic dermatosis in a cat

69

Resumen Un gato castrado de dos aos de edad, de pelo semilargo se present con una historia clnica de 1.5
aos con alopecia sin prurito y con exudado graso y maloliente afectando la parte distal de las extremidades,
el tronco y el cuello, pero sin afectar la cabeza ni la cola. La extensa alopecia y la seborrea se asociaron con
engrosamiento de la piel y la formacin de pliegues en la parte dorsal de la cabeza y la parte distal de las extremidades, as como en los laterales del trax y en el abdomen. El pelo se depilaba fcilmente, y numerosos quistes
de queratina (millium) se observaron en el vientre, y en la parte lateral y caudal de los muslos, as como ligera
paroniquia. El examen histopatolgico de las biopsias de piel desvel una marcada dilatacin qustica de los
folculos pilosos y de las glndulas sebceas, acompaado de hipoplasia de los folculos, hiperqueratosis infundibular e inflamacin de variada intensidad. El tratamiento sistmico con glucocorticoides en combinacin con
baos tpicos con clorexidina y miconazol result en una marcada mejora y algo de crecimiento del pelo, pero
lamentablemente no se obtuvo ms seguimiento clnico. Esta condicin parece tener semejanza con otras condiciones descritas en diferentes especies, pero no esta claro si representa el mismo proceso que el ratn mutante
sin pelo o si es una dermatosis de caractersticas nicas.
Zusammenfassung Ein 2-Jahre alter, kastrierter, halblanghaariger Hauskater wurde mit einer eineinhalbjhrigen
Anamnese eines progressiven, ursprnglich nicht juckenden Haarausfalls und mit belriechendem schmierigen
Exudat vorgestellt, welches sich an den distalen Extremitten, am Rumpf und Hals befand, jedoch nicht am Kopf
und Schwanz. Die ausgedehnte Alopezie und Seborrhoe traten zusammen mit starker Hautverdickung und
Faltenformation dorsal am Kopf und distal an den Extremitten, sowie am lateralen Thorax und Abdomen auf.
Die Haare konnten leicht ausgezupft werden, zahlreiche Milia (Hautgrie) waren am ventralen Abdomen sowie
an den kaudalen und lateralen Oberschenkeln zu sehen und milde Paronychia war vorhanden. Die histopathologische Untersuchung der Hautbiopsien zeigte eine deutliche zystische Dilatation der Haarfollikel und Talgdrsen
mit follikulrer Hypoplasie, infundibulrer Hyperkeratose und einem unterschiedlichen Ausma an Entzndung.
Systemische Glukokortikoidtherapie kombiniert mit topischen Chlorhexidin und Miconazol Waschungen
resultierte in einer markanten Verbesserung und etwas Nachwachsen der Haare, aber die Katze wurde in der
Folge fr eine Nachuntersuchung aus den Augen verloren. Dieser Zustand hnelt zahlreichen Zustnden bei
anderen Spezies, aber es ist unklar, ob es sich um das Pendant zur haarlosen Mausmutante handelt oder um eine
einzigartige Dermatose.

2006 The Authors. Journal compilation 2006 European Society of Veterinary Dermatology