Veterinary Dermatology 2005, 16, 269275

Case report

Blackwell Publishing, Ltd.

Zinc-responsive dermatosis in goats suggestive of hereditary

malabsorption: two field cases
REINHILD KRAMETTER-FROETSCHER, SIMONE HAUSER and
WALTER BAUMGARTNER
Clinic for Ruminants, Clinical Department for Farm Animals and Herd Management, Veterinary University of
Vienna, 1210 Vienna, Austria
(Received 9 September 2004; accepted 27 April 2005)

Abstract Two cases of zinc deficiency in dairy goats from different flocks and not associated with a zinc-deficient
diet are described. Hard, dry, hyperkeratotic skin, hair loss and pruritus especially prominent on the back, legs,
udder, face and ears were the most common clinical signs. Skin biopsy findings revealed a mixture of orthokeratotic and parakeratotic hyperkeratosis. On initial examination, serum zinc concentrations were low in both goats
(461 g L1 and 521 g L1, respectively). Although mild skin lesions persisted during the early stages of zinc supplementation, skin lesions completely resolved after prolonged oral zinc supplementation. Withdrawal of zinc
supplementation resulted in re-appearance of lesions in both animals. Case 2 gave birth to two kids, one of which
showed mild skin lesions at 8 months of age together with a low serum zinc concentration (434 g L1), suggestive
of hereditary zinc malabsorption. The other kid remained free of skin lesions and had a serum zinc concentration
(530 g L1) within the normal range. On the basis of historical and clinical findings, the cases presented here
more closely resemble Syndrome 1 hereditary zinc deficiency as seen in Nordic dog breeds rather than other zinc
deficiency conditions seen in other species. It is suggested that zinc deficiency in these goats was due to hereditary
malabsorption of dietary zinc. This is the first descriptive study of this condition in goats. Life-long zinc supplementation may be necessary in such patients.

IN TRO D U CT ION
Naturally occurring cases of zinc-responsive dermatosis in goats are rarely described. Field reports of zinc
deficiency in goats induced by feeding zinc-deficient
diets have been described by Nelson1 in pygmy goats,
by Reuter2 in Angora goats and by Schulze3 in Turkish
Angora goats. Caprine experimental zinc deficiency
has also been described.4,5 Limited stores of readily
available zinc in the body necessitate a daily supply
of zinc in the diet. A minimum of 0.70.8 mg zinc per
kilogram bodyweight is generally indicated.6 Zinc
absorption depends on feed composition, high calcium
and marginal zinc (40 mg/kg) in the ration may contribute to relative zinc deficiency in goats. This might
explain zinc deficiency in nonlactating does or male
goats kept on a high calcium lactating goat ration.
Most natural diets will supply sufficient zinc.
Brief reports in the literature have only alluded to the
possibility of a genetic predisposition to decreased zinc
absorption in sheep and goats. The implication is that,
when identified, such animals may require life-long
Correspondence: R. Krametter-Froetscher, Clinic for Ruminants,
Clinical Department for Farm Animals and Herd Management,
Veterinary University of Vienna, 1210 Vienna, Austria. E-mail:
reinhild.krametter@vu-wien.ac.at
2005 European Society of Veterinary Dermatology

zinc therapy.7,8 Hereditary zinc deficiency has, however,

been documented in Angus calves,9 Friesian calves,10
shorthorn beef calves11 and in a Simmental calf.12
Inherited parakeratosis in calves is known to result
from an impairment of zinc transport across the intestinal mucosa.911
Clinical manifestations of dietary zinc deficiency
in goats are alopecia, focal erythema, hard dry skin,
rough hair coat and erosions and fissures on the feet.
Hair loss and thick, dry, scaly skin is especially prominent on the head, neck, scrotum and hind limbs. Cutaneous lesions typically surround the ears, eyes, nose
and mouth. Crusting of the skin is prominent. Other
clinical signs include small testicles, horny overgrowth
of the dental pad and reduced feed consumption. Pruritus is not evident in all cases.1,6,1315 Clinical signs,
skin biopsies indicating hyperkeratosis, decreased concentrations of zinc in the hair and serum, and response
to zinc supplementation is diagnostic. The diagnosis of
zinc-responsive dermatosis solely on the basis of laboratory tests is not conclusive. Reuter1 documented a
case where goats affected with parakeratosis had similar plasma zinc concentrations to those of unaffected
goats grazing on a neighbouring farm.
The aim of these two case reports is to describe
zinc deficiency in goats not attributable to dietary
deficiency.
269

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R Krametter-Froetscher, S Hauser and W Baumgartner

Figure 3. Hind limbs of a goat with zinc-responsive dermatosis,

case 1. Note erosions and bleeding fissures on the hind limbs.

Figure 1. Mouth and nose of a goat with zinc-responsive

dermatosis, case 1. Note thick, crusted lesions encircling the
nose and the mouth.

Figure 4. Hind limbs of case 1, 12 weeks after oral zinc

supplementation therapy. The erosions and bleeding fissures
have completely disappeared.

Figure 2. Ear of a goat with zinc-responsive dermatosis, case 1.

Note thick scaly lesions on the left ear.

C ASE REPO RT S
Case 1
A 2-year-old, female, cross-bred lactating goat was
presented with a 2-month history of crusted lesions
around the ears, mouth and on the feet. The owners
first recognized the skin lesions during pregnancy. The
goat originated from a flock of 200 dairy goats of purebred Saanen and German improved white goats. This
goat was the only affected animal in the herd and all
animals received the same ration. On physical exami-

nation,16 the goat appeared to be in good general health.

Dermatological examination revealed a dull, rough
hair coat with loss of hair and hard, dry, hyperkeratotic
skin encircling the eyes, nose and mouth (Fig. 1). The
udder and ears (Fig. 2) had thick, crusted lesions and
erosions and bleeding fissures were on the legs (Fig. 3).
Small scabs were present in many areas. Mucous
membranes were not affected, but pruritus was evident.
Differential diagnoses included ectoparasite infestation,
dermatophytosis, pyoderma, allergy and zinc-responsive
dermatosis.
Multiple skin scrapings were negative for the presence of ectoparasites. A large amount of hair, plucked
by grasping the hair shafts close to the skin surface,
and scrapings from the margins of the lesions, were
collected from the head, ears, limbs and udder, and
submitted for fungal culture. Prior to collection of
the samples the areas were gently cleaned with a 70%
alcohol-impregnated gauze and allowed to dry before
sampling. Samples were labelled by anatomical location
and transported for fungal culture in separate envelopes.
Specimens were inoculated onto Sabouraud dextrose
agar (SDA, Oxoid, Basingstoke, England) containing

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 269275

Zinc-responsive dermatosis in goats

271

Figure 7. Face of case 2, 5 weeks after treatment. Notice crusts have

completely disappeared from the face. Only mild crusts were seen
inside the left ear.

Figure 5. Caprine zinc-responsive dermatosis, case 1. Skin biopsy

showing massive orthokeratotic hyperkeratosis with epidermal
hyperplasia and dermal perivascular mixed inflammatory infiltrate.
Note the hyperkeratotic spike (black arrow). H&E, 100.

Figure 6. Face of a goat with zinc-responsive dermatosis, case 2.

Note crusts encircling the ears, nose and mouth.

antibiotics [Cycloheximide (Sigma, Vienna, Austria)

500 mg L1; Chloramphenicol (Sigma) 50 mg L1] and
additionally onto dermatophyte test medium including Cycloheximide (DTM, Becton Dickinson, Sparks,
USA), together with antibiotics [Gentamicin sulphate
(Sigma) 100 mg L1; Chlortetracycline HCl (Sigma)
100 mg L1]. A sample of Microsporum canis was used as
a positive control to confirm the suitability of the culture
technique. Cultures were incubated at 30 C for 4 weeks

and examined daily for fungal growth. For identification

purposes, fungal cultures were microscopically examined
for conidiation using lactophenol cotton blue stain.
The sample derived from the udder proved positive for
Trichophyton, but this was not specified further.
Skin biopsies were obtained with 8-mm biopsy
punches under local anaesthesia. The hair overlying
biopsy sites was carefully trimmed with scissors, but
not surgically prepared. Two skin biopsies were taken
from the centre of lesions on the forelimbs, hind limbs,
udder and head and from nonlesional skin on the back.
One sample was taken from the margin of lesions on
forelimbs, hind limbs, udder and head. Excess blood
was removed and biopsies were fixed on cardboard in
10% buffered formalin. Histopathological examination
revealed moderate irregular epidermal hyperplasia,
pronounced parakeratotic and orthokeratotic hyperkeratosis and a moderately intense inflammatory
cell infiltrate (lymphocytes, plasma cells, occasional
eosinophils and some neutrophils) in the underlying
dermis with some cells extending into the overlying
epidermis. Dermatophytes were not visible with H&E
or Grocott-staining.
Routine haematology and blood biochemistry results
were normal. Serum zinc concentrations were measured
by atomic absorption spectroscopy using blood drawn
from the jugular vein into a special purpose trace elementfree tube. Serum zinc concentration was low (461 g L1;
normal range = 569628 g L1). Laboratory analysis
revealed that the diet fed to the goat contained 55 mg
zinc per kilogram dry matter (DM). This was within
the cited recommended level of dietary zinc for production goat diets at 4575 mg zinc per kilogram DM.8
Calcium and trace elements such as iron and copper in
the ration were within normal ranges.
Dermatological signs, fungal culture, serum zinc
concentration and histopathological lesions were
suggestive of a zinc-responsive dermatosis with a
Trichophyton infection confined to the udder.
After hospitalization the goat received 50 mg of zinc
oxide supplementation daily (equivalent to 40 mg

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R Krametter-Froetscher, S Hauser and W Baumgartner

elemental zinc) but the diet remained unchanged. An

antimicrobial spray (Terramycin Aerosol Spray, Pfizer
Corporation, Vienna, Austria) was used for local treatment of the erosive skin lesions on the legs once daily
for 1 week. The fungal infestation was treated topically
with a 0.2% solution of enilconazole (Imaverol, JanssenCilag Pharma, Vienna, Austria) four times in association with Bovilis Ringvac (Intervet, Vienna, Austria), a
vaccine against Trichophyton verrucosum. Re-examination
of hair samples 1 month later revealed that they were
negative for dermatophytes. However, the goat did not
show complete clinical improvement during the first
month of zinc therapy. Improvement was only recognized on the udder previously showing scales, hair loss
and mild redness. These lesions may have been caused
by the Trichophyton infection. The milk production of
the animal was between 1.5 and 2 kg daily following
the beginning of hospitalization. One month after
admission the goat was dried off with a dry off infusion.
Marked clinical improvement was seen after 10 weeks
of zinc supplementation. Approximately 12 weeks of
zinc oxide supplementation was required for the skin
and hair to return to normal (Fig. 4). At this point the
serum zinc concentration was within the normal range
(612 g L1; normal range = 569628 g L1). The
goat was kept at the clinic for further observation and
fed with a normal dietary concentration of zinc and
other minerals. After 7 weeks without zinc oxide treatment the goat again showed pruritus and after 8 weeks
moderate crusted lesions encircling the ears, eyes, nose
and mouth were recognized. Clinical signs became
more pronounced and patches of thick, dry, scaly skin
were also found over the dorsal areas of the neck,
thorax and lumbar regions. Serum zinc concentration
dropped to 476 g L1 and skin biopsies revealed
marked orthokeratotic hyperkeratosis, minimal focal
parakeratotic hyperkeratosis, irregular epidermal hyperplasia and mild inflammation (lymphocytes, neutrophils
and eosinophils) around superficial dermal blood
vessels (Fig. 5). The goat showed only minimal improvement after re-introduction of 50 mg zinc oxide daily
supplements and no additional benefit after 100 mg of
zinc oxide daily. Substitution of daily oral zinc oxide
with 1 g zinc sulphate (equivalent to 227 mg elemental
zinc) revealed a good response after 2 months of treatment and resolved all clinical signs of the dermatosis.
As with zinc oxide, mild lesions also re-appeared intermittently with zinc sulphate supplementation but
usually resolved after 1 to 3 weeks. No further lesions
have been recognized over the last 4 months.

profiles. Dermatological examination revealed alopecia

and thick-crusted pruritic lesions around the ears, eyes,
nose and mouth (Fig. 6). The hair coat was rough and
dry with small patches of hair loss and scaly skin on
the dorsum, udder and perianal region. Differential
diagnoses were as for case 1 and similar samples were
obtained. Microscopic examination of skin scrapings
was negative for ectoparasites and hair samples and
skin scrapings from head, dorsum, udder and perianal
region were negative for dermatophytes on culture.
Serum zinc concentrations were decreased (521 g L1)
from the normal range (569628 g L1). Skin biopsies
from affected areas revealed orthokeratotic and parakeratotic hyperkeratosis and mild inflammation of the
superficial dermis.
A provisional diagnosis of zinc-responsive dermatosis was made. The goat was dried off and treated
orally with 50 mg of zinc oxide daily. Five weeks after
the initiation of zinc oxide treatment, only mild crusts
inside the left ear remained (Fig. 7). Resolution of the
condition was complete after 6 weeks of treatment. At
this point serum zinc concentrations were within the
normal range (622 g L1). Twenty-three days later the
goat had a normal parturition and produced two physically normal female kids. About 2 months after parturition skin lesions recurred in the periorbital area and
on the ventral mandible. Two weeks later alopecia was
most extensive on the head, neck, flanks, udder and
lower portion of the limbs. Zinc oxide supplementation
was repeated for several weeks, first with a dose of
50 mg orally daily and later with 200 mg orally, daily.
No clinical improvement was recognized and the treatment was changed to zinc sulphate (1 g orally daily;
equivalent to 227 mg elemental zinc). As in case 1 the
goat showed a good clinical response to the zinc
sulphate treatment. Mild lesions, however, also reappeared intermittently during zinc supplementation,
but usually resolved within 2 to 3 weeks on the same
dose. No further skin lesions have re-appeared over the
past 4 months of oral zinc sulphate supplementation.
At the age of 8 months one kid showed mild crusted
lesions around the eyes and on the ear. Her serum zinc
concentration was lower (434 g L1) than the normal
range. To date, after 15 months, the lesions have
persisted without zinc therapy. The other kid remains
free of skin lesions and has a normal serum zinc
concentration (530 g L1).

Case 2

Zinc-deficient diets or high levels of dietary components

that bind zinc and prevent absorption and utilization
can cause zinc-responsive dermatosis. Alternatively, in
some species, a hereditary zinc deficiency has been
described. Only a few field cases of zinc-responsive
dermatosis caused by nutritional imbalances have been
documented in small ruminants.13,17,18 Alopecia, wool
eating, general malaise, depression, crusting fissured
skin, skin covered with crusted scales, stiff gait and

A 2-year-old, German improved, white, pregnant,

lactating goat was admitted with skin lesions that primarily affected the head. The problem began with scales
around the eyes at the end of the first pregnancy. As in
case 1 this animal was the only affected goat of the herd
that was fed the same ration. General physical examination was unremarkable. No abnormalities were found
on standard haematological and serum biochemical

D IS C U S S IO N

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Zinc-responsive dermatosis in goats

arching of the back were documented in small ruminants in field cases. Several cases of experimentally
produced zinc deficiency in goats have been
described.4,5,19,20 Zinc-deficient diets fed to ram lambs
and sexually mature male goats caused impaired
testicular growth, no libido and complete cessation of
spermatogenesis.19,20 Miller4 documented dull rough
hair, loss of hair and hyperkeratinized skin in male
growing goats experimentally fed a low zinc diet,
especially on the rear legs, neck and head, around the
mouth, on the scrotum and erosions and fissures on the
feet. Inflammation of the mouth with ulcers, horny
overgrowth of dental pads, shrunken scaly scrotal skin
and very small testicles as well as listlessness and weakness were also recognized. Similar skin lesions have
been described by Neathery5 in sexually mature goats
experimentally fed with a zinc-deficient diet. Gnashing
of the teeth, gingivitis, conjunctivitis, horn changes,
abnormal hooves, cracked nostrils and small testicles
were also described by Neathery.5 In contrast to the
cases described by Miller 4 and Neathery 5 the cases
documented here did not reveal affected mucous membranes, abnormal hooves horn changes, or cracked
nostrils. Moreover, the goats described here were constantly bright and alert and decreased feed intake was
not seen. Miller4 reported that zinc deficiency caused
by an impaired diet greatly weakened the animals.
Accordingly, these animals often die from nonspecific
conditions. However, we did not recognize any convincing signs of generalized immunodeficiency in the
cases described.
Skin lesions previously described in goats suffering
from zinc deficiency caused by a deliberate or accidental
zinc-deficient diet were similar in many respects to
those seen in our cases.15 Although zinc analysis of the
feed can provide tentative support to a diagnosis of a
zinc-responsive dermatosis, its value is limited by
sampling technique whereby the diet tested must be
representative of the patients intake within the herd,
and the amount quantified must be assumed to be
assimilated by the animal. Furthermore, when only an
isolated animal within a herd shows clinical signs consistent with a zinc-responsive dermatosis, it is less likely
to reflect a zinc deficiency in the herds diet.
In dogs, zinc-responsive dermatosis caused by nutritional imbalances is called Syndrome 2. Usually
Syndrome 2 is diagnosed in young, rapidly growing
puppies. However, it can also occur in adults undergoing
the stress of pregnancy, lactation or illness. As in dogs,
dietary zinc deficiency in sheep is usually confined to
lambs, while adults are least affected.18 An inherited skin
disorder has been described in several calf breeds1012
and appears when calves are between 4 and 6 weeks
old. The characteristic signs of this condition include
scaly, crusty lesions on the skin, formation of scaly
debris over the body, poor appetite, salivation and
alopecia. However, calves suffering from hereditary zinc
deficiency usually die of secondary infections despite
treatment, due to immunodeficiency. The lesions
resolve after administration of a zinc supplement, but

273

withdrawal of the zinc results in recurrence of clinical

signs.
Jezyk21 described a similar lethal syndrome involving growth retardation and skin disease in bull terrier
pups. Family studies showed that affected calves and
bull terriers inherit the condition as an autosomal
recessive trait. The condition in dogs and calves is
similar in many respects to acrodermatitis enteropathica
in human infants, which is characterized by the development of alopecia, periorificial dermatitis and diarrhoea.
A separate hereditary zinc deficiency in dogs, called
Syndrome 1, has also been described. Syndrome 1 is
a genetic defect affecting Siberian huskies, Alaskan
malamutes and other arctic breeds that results in
diminished intestinal zinc absorption. In contrast to
lethal acrodermatitis in bull terriers and hereditary
zinc deficiency in calves, Syndrome 1 usually occurs in
animals older than 6 months. Fifty-nine per cent of
such dogs develop cutaneous lesions when they are older
than 2 years. 22 Although skin lesions usually occur
during puberty, oestrus, stress, pregnancy or concurrent
disease may precipitate the dermatosis.23 Cutaneous
lesions in Syndrome 1 include focal erythema,
alopecia, scaling, and crusting that primarily develop on
the head. Scales and crusts typically encircle the eyes,
ears, nose and mouth. Cutaneous lesions may also be
seen on the footpads, perianal region, and pressure
points of the limbs. White20 diagnosed pruritus in 40% of
examined dogs with zinc-responsive dermatosis. In contrast to the cases reported here, pruritus was not evident
in the cases documented by Nelson1 in small ruminants.
The two cases reported here are similar in many
respects to Syndrome 1 in Nordic dog breeds. In both
goats, skin lesions were first recognized during pregnancy; skin lesions typically encircled the eyes, ears,
nose and mouth, but also the genital areas and extremities, and in particular the pressure points. Pruritus was
diagnosed in both goats. Despite skin lesions, the
animals were in good general health. The goats responded
to oral zinc supplementation with complete remission
of signs. Skin lesions recurred in both cases if zinc
supplements were discontinued. Therefore, both goats
may require zinc supplementation indefinitely.
The goats were examined over several weeks by
different individuals before they were integrated into
the goat herd of the clinic. As a result of handling and
subordination within the new herd it is conceivable
that the animals were stressed during this time, and reappearance of isolated mild skin lesions during early
zinc therapy could have been consequential to this
stress. Skin lesions have not re-appeared in either animal
over the last 4 months of continuous zinc therapy.
Relapsing skin lesions may also occur in dogs on longterm constant-dose zinc supplementation in connection
with concurrent diseases.23 In contrast to hereditary zinc
deficiency in calves and bull terriers, case 2 described
here showed no signs of immune deficiency. In case 1 it
cannot be ruled out that zinc deficiency facilitated the
Trichophyton infection secondary to immunodeficiency.
However, the Trichophyton infection was localized

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R Krametter-Froetscher, S Hauser and W Baumgartner

and not substantially responsible for the dermatosis

observed, as it could not be isolated from all skin
lesions. In this respect the remaining lesions were
probably due to zinc deficiency. Additionally, the
time-course of the dermatosis, i.e. resolution after
zinc-supplementation and re-appearance after zinc
supplementation withdrawal, is strongly suggestive of
zinc-responsive dermatosis.
In calves, parakeratotic hyperkeratosis is the
primary histopathological finding.11 Orthokeratotic
hyperkeratosis has also been described in dogs in addition to the most common histological finding of parakeratotic hyperkeratosis.21,24 In experimentally induced
zinc deficiency in sheep, parakeratotic hyperkeratosis
is a prominent histological finding. However, in some
field cases, histopathology of the skin revealed predominantly orthokeratotic hyperkeratosis accompanied sometimes by parakeratotic hyperkeratosis.1,18
This finding is consistent with the cases described here
whereby, histologically, hyperkeratosis was predominantly of the orthokeratotic type.
Traditionally inorganic zinc sources are used to
treat zinc deficiency in sheep and goats.6 According to
Wedekind25 zinc oxide is commonly used as a dietary
supplement. A number of bioavailability comparison
studies of zinc oxide and zinc sulphate are reported
in the literature in cattle and sheep, but not in goats.
Experimental studies documented in sheep, swine and
chicks have shown that zinc sulphate had a higher bioavailability than zinc oxide.2628 In contrast to Rojas,28
Sandoval29 documented no significant differences in
the bioavailability of zinc from inorganic sources for
sheep. While zinc oxide has also been the treatment of
choice at our clinic for zinc deficiency in ruminants, the
presented patients failed to respond to further supplementation after interruption of zinc oxide treatment.
Consequently treatment was continued with a higher
dose of zinc sulphate, which has proven effective by
other investigators. 7,8,13 Such treatment also proved
efficacious in the presented patients.
In conclusion, zinc-responsive dermatosis was
diagnosed in these two goats on the basis of history,
cutaneous signs, histopathological features, serum zinc
concentration, and the response to zinc administration. As cutaneous lesions re-appeared in the face of
normal dietary concentrations of zinc and interfering
minerals, we propose that the disease is associated with
hereditary impairment of zinc absorption from the
gastrointestinal tract. To our knowledge this is the first
detailed case description of zinc deficiency secondary
to intestinal tract malabsorption in goats, and a hereditary component to the condition cannot be ruled out.

ACKN OWLEDGE ME NT S
The authors would like to thank Dr Klemens Alton for
the photomicrograph and Dr Joachim Spergser for
technical assistance. I wish to thank Cameron McCulloch, PhD, for help with the manuscript.

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Rsum Deux cas de dficit en zinc chez des chvres de diffrents troupeaux, non associes un dficit en zinc
alimentaire sont rapports. Des lsions cutanes sches, hyperkratosiques, associes une chute de poils et un
prurit, particulirement marqu sur le dos, les membres, les mamelles, la face et les pavillons auriculaires taient
nots. Les biopsies ont montr une hyperkratose orthokratosique et parakratosique. Les taux de zinc srique
taient faibles chez les deux animaux (461 g/l et 521 g/l respectivement). Bien que des lsions cutanes
minimes aient persist au dbut de la supplmentation en zinc, les lsions ont totalement disparu aprs une
supplmentation prolonge. Larrt de la supplmentation sest accompagn dans les deux cas dune rechute des
lsions cutanes. Le cas 2 a eu deux petits, un desquels a prsent lge de 8 mois des lsions cutanes modres
avec des taux faibles de zinc (434 g/l), ce qui est vocateur dune malabsorption hrditaire du zinc. Lautre petit
avait un taux de zinc dans les normes (530 g/l) sans lsion cutane. Sur la base des donnes anamnestiques et
cliniques, les cas prsents ici ressemblent plus la dermatose amliore par le zinc de type I dcrite chez les chiens
nordiques quaux autres dficits en zinc rencontrs dans dautres espces. Il est suggr que le dficit en zinc
observ chez ces chvres est li une malabsorption hrditaire du zinc. Il sagit de la premire description de
cette maladie chez la chvre. Une supplmentation vie en zinc peut tre ncessaire chez ces patients.
Resumen A continuacin describimos dos casos de deficiencia en zinc en cabras lecheras de diferentes rebaos,
no asociados a una dieta deficiente en zinc. Los signos clnicos ms caractersticos observados fueron piel seca,
endurecida y con hiperqueratosis, prdida de pelo y prurito, especialmente en el dorso, extremidades, ubre, cara
y orejas. Mediante biopsia de piel observamos una mezcla de hiperqueratosis ortoquerattica y paraquerattica.
En el examen inicial, la concentracin de zinc en el suero sanguneo era baja en ambas cabras (461 g/l y 521 g/
l, respectivamente). Aunque algunas lesiones leves persistieron durante los estadios tempranos del tratamiento
con suplemento de zinc, stas desaparecieron completamente tras una administracin ms prolongada. En ambas
cabras las lesiones reaparecieron tras suspender el suplemento de zinc. El caso nmero 2 pari dos cabritos, uno
de los cuales present lesiones leves a los ocho meses de edad, a la vez que tena una concentracin baja de zinc
en el suero sanguneo (434 g/l), indicativo de una malabsorcin hereditaria de zinc. El segundo cabrito no present lesiones y tena una concentracin normal de zinc en suero (530 g/l). Basados en los hallazgos e historia
clnica, los casos que presentamos tienen mayor semejanza con el Sndrome de Deficiencia Hereditaria en Zinc
de Tipo I, tal y como se observa en perros de raza Nrdica, en lugar de otras deficiencias en zinc observadas en
diferentes especies. Por lo tanto, sugerimos que la deficiencia en zinc en estas dos cabras fue debida a malabsorcin
hereditaria. Este es el primer estudio descriptivo de esta condicin en cabras. Pacientes con este sndrome
requeriran suplemento de zinc de por vida.
Zusammenfassung Zwei Flle von Zinkmangel bei Milchziegen von verschiedenen Herden, der nicht im
Zusammenhang stand mit einer Zink-Mangelernhrung, wird beschrieben. Die hufigsten klinischen
Vernderungen waren harte, trockene, hyperkeratotische Haut, Haarausfall und Juckreiz, welche vor allem am
Rcken, Extremitten, Euter, Gesicht und Ohren auffllig waren. Die Analyse von Hautbiopsien ergab eine
Mischung aus orthokeratotischer und parakeratotischer Hyperkeratose. Bei der Erstuntersuchung waren
die Zink Konzentrationen im Serum bei beiden Ziegen niedrig (461 g/l bzw. 521 g/l). Obwohl leichte
Hautvernderungen whrend der Anfangsphasen der Zinkergnzung bestehen blieben, verschwanden diese zur
Gnze nach prolongiertem oralen Zinkzusatz. Das Absetzen der Zinkergnzung fhrte zur Wiederkehr der
Hautlsionen bei beiden Tieren. Fall 2 gebar zwei Zicklein, von denen eines im Alter von acht Monaten leichte
Hautvernderungen zusammen mit einer niedrigen Zink-Konzentration im Serum (434 g/l) zeigte, was auf eine
erbliche Zink Malabsorption hinwies. Das andere Zicklein blieb ohne Hautvernderungen und hatte eine Serum
Zink-Konzentration im Normalbereich (530 g/l). Basierend auf Anamnese und klinischen Befunden sind die
hier prsentierten Flle dem Syndrom I des hereditren Zinkmangels, die man bei nordischen Hunderassen sieht
hnlicher, als anderen Zinkmangel-Krankheiten von anderen Spezies. Es wird nahegelegt, dass der Zinkmangel
bei diesen Ziegen wegen einer erblichen Malabsorption von Zink aus der Nahrung vorlag. Es handelt sich hierbei
um die erste deskriptive Studie dieser Krankheit bei Ziegen. Bei diesen Patienten kann eine lebenslange
Zinkergnzung notwendig sein.
2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 269275