Veterinary Dermatology 2005, 16, 125130

Case report

Blackwell Publishing, Ltd.

Hereditary equine regional dermal asthenia in three related Quarter

horses in Brazil
ALEXANDRE S. BORGES*, LISSANDRO G. CONCEIO, ANA L. G. ALVES,
VICIANY E. FABRIS and MARCELO A. PESSOA
*Universidade Estadual Paulista, Faculdade de Medicina Veterinria e Zootecnia, Unesp, Botucatu, SP, Brazil
Universidade Federal de Viosa, Viosa, MG, Brazil
Universidade Estadual Paulista, Faculdade de Medicina Veterinria e Zootecnia, Unesp, Botucatu, SP, Brazil
Universidade Estadual Paulista, Faculdade de Medicina, Unesp, Botucatu, SP, Brazil
Rua Antonio Molina 2068, Bauru, SP, Brazil
(Received 6 May 2004; accepted 23 September 2004)

Abstract Hereditary equine regional dermal asthenia belongs to a group of inherited, congenital connective
tissue dysplasias usually described as hyperelastosis cutis, cutaneous asthenia, dermatosparaxis, or EhlersDanloslike syndrome. This report presents the clinical and histological features of three related Quarter horses affected
with regional dermal asthenia. These horses had bilateral asymmetric lesions of the trunk and lumbar regions,
where the skin was hyperextensible. Handling of the skin elicited a painful response and superficial trauma led
to skin wounds. The skin was thinner than normal in the affected areas, with thickened borders and harder fibrotic
masses (pseudotumours). The histopathological findings included thinner and smaller collagen fibrils, and a loose
arrangement of collagen fibres in the middle, adventitial and deep dermis. Massons trichrome and Calleja stains
did not reveal any abnormality of collagen and elastic fibres. Electron microscopy showed no abnormalities. As
in human patients, pseudotumour histopathological findings included fibroplasia and neovascularization. The
pedigree chart of these animals supports an autosomal recessive type of inheritance, which has been suggested
by other studies. This is the first report of this disease in Brazil. Its clinical and histological features resemble those
described in horses affected with this condition in the United States.

IN TRO D U CT ION
Cutaneous asthenia is a group of inherited, congenital
dysplasias of the connective tissue. These dysplasias
are characterized by loose, hyperextensible, abnormally fragile skin, which is easily torn by minor
trauma.1 Cutaneous asthenia has been described in a
number of different species, including cattle, horses,
sheep, dogs, pigs and cats.14 In human patients, this
condition is known as EhlersDanlos syndrome
(EDS). This is the most prevalent heritable disorder of
connective tissue, and it includes several subclassifications.5 In veterinary medicine, the characterization of
this disease is difficult; therefore, this connective tissue
dysplasia has been referred to as cutaneous asthenia,
dermatosparaxis, EhlersDanlos-like syndrome or,
most commonly, hyperelastosis cutis.
In equine clinical practice this skin abnormality is
infrequently diagnosed. There are a few case reports
characterizing its clinical features and histological
findings. The first report described two Quarter horses
with multiple, fragile, hyperextensible skin areas in
Correspondence: A. S. Borges, Universidade Estadual Paulista,
Faculdade de Medicina Veterinria e Zootecnia, Unesp, Botucatu,
SP, Brazil, 18618000. E-mail: asb62@cornell.edu
2005 European Society of Veterinary Dermatology

the thoracic region.6 In another report a 6-year-old

Thoroughbred gelding was described with skin sores
in the saddle and shoulder areas. Healing was characterized by atrophic scars; the skin was elastic and took
several minutes to assume its original shape after being
stretched or pulled outwards. Histopathology showed
thinning of the dermis and irregularities in size, shape
and staining affinity of collagen fibres.7 A third report
described a 2-year-old Arabian cross filly with large
areas of hyperextensible fragile skin, interspersed with
areas of normal skin. The affected skin tore easily and
contained reduced amounts of dermal collagen. The
collagen fibres were fragmented and disorganized,
and many fibres had abnormal red-stained centres in
trichrome-stained sections. Collagen fibres with foci of
degeneration have been observed using electron microscopy. The fibrils within these fibres were fragmented,
loosely packed and widely separated by granular material.8 This condition has also been described in two
Quarter horses that developed frequent skin wounds.9
The deep dermal layer of the lumbar region was
thinner in the affected horses, and contained bundles
of more loosely packed collagen fibres. Recently, a
Quarter horse with zonal dermal separation has been
described.10 In the United States 50 Quarter horses and
their crosses have been studied. The name hereditary
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AS Borges et al.

Figure 1. Pedigree chart showing the relationship of animals

included in this study. Solid symbols represent affected animals.
Grey symbol represents an affected animal without clinical
examination and biopsy.

equine regional dermal asthenia has been suggested

for the condition found in these Quarter horses,11
which is considered an autosomal recessive connective
tissue disorder.1113 No abnormalities were described
apart from those in the skin.
This study describes the clinical and histopathological aspects of the first reported cases of hereditary
equine regional dermal asthenia in Brazil.

C ASE REPO RT S
Three Quarter horses were referred to the Faculdade
de Medicina Veterinria e Zootecnia, Unesp, Botucatu, Brazil for evaluation of skin lesions. The horses
belonged to the same farm located in Sao Paulo,
Brazil, and were otherwise healthy. Figure 1 is a pedigree
chart showing these patients.
Horse 1, a 4-year-old, chestnut mare, was presented
with a history of recurrent skin wounds in the saddle
area for the past 2 years. Two skin lacerations had
developed on the dorsum after riding, and had been
replaced by an extensive thickened scar. Physical examination revealed several depressed plaques in the thoracic region and lumbar areas. The skin in the affected
areas appeared fragile and thinner than normal; it was
loosely attached to the subcutaneous tissue and easily
raised when pinched together (slack skin). A pachymeter or cutimeter (pair of jaws with a scale in tenths
of a mm, connected to a spring; Hauptner, n. 33865,
Metzingen, Germany) was used to measure skin thickness. The measurements revealed a threefold difference
between the affected and nonaffected skin in the
contralateral side. Some skin plaques showed raised,
thicker edges and the skin was painful when manipulated. During exercise, depressed plaques did not sweat
like the rest of the body. Occasionally, the edges
contained hard, tumour-like masses. Throughout the
2 years, minor skin trauma had induced wounds with
hypertrophic scars and pronounced folding. At first,
the ulcerative wounds were in the saddle area. The
slack skin was evident in the thoracic region, hip joint
and dorsal portion of caudal-lumbar areas. Skin areas
that were thin and hyperextensive were surrounded by
clinically normal skin. Lesions were bilateral without
evident symmetry.

Horse 2 was a 2.5-year-old mare, half-sister of the

first horse with the same sire. She had bilateral scars on
the dorsum and hyperextensibility of the skin in the
neck and thoracic and caudal-lumbar areas. Affected
areas were thinner than other areas. The horse also had
a large ulcerated wound on the hip joint due to trauma
suffered 30 days previously.
Horse 3 was a 2-year-old stallion, full brother of the
first horse. He had scars on the dorsum, thorax and hip
joint areas. The skin of the neck showed hyperextensibility and was thinner than the normal areas. The horse
also had ulcers on the anterior aspect of the right
thoracic leg due to trauma suffered 7 days earlier. This
lesion took a long time to heal. Dorsal lesions were less
evident than in the first animal, probably because this
animal had not been ridden. However, the number and
size of hyperextensible areas in this horse and his full
sister were similar.
The three horses had areas of thin and hyperextensible skin surrounded by visibly normal skin. All had
skin thickening at the edges of ulcers. None had any
joint hypermotility and there were no clinical abnormalities apart from the skin changes (Figs 2 and 3).
Complete blood count and biochemical profile
(BUN, creatinine, AST, alkaline phosphatase, GGT,
total protein, albumin, globulin, glucose and CPK)
revealed no abnormalities.

Histopathological findings
Skin biopsies were taken from the lateral neck, dorsal
and abdominal area of each horse. Visibly normal skin
of the affected horses was also sampled. Similar skin
biopsies were obtained from the same areas of a control horse of the same age and breed. Biopsies were
attached to cardboard, fixed in 10% neutral buffered
formalin, routinely processed, embedded in paraffin
wax, and stained with haematoxylin and eosin (H&E),
Massons trichrome and Calleja stain for elastin fibres.
The most remarkable histopathological findings
were the thin and small collagen fibrils, which created
a loose arrangement of collagen fibres within the deep
dermis (Figs 4 and 5). Occasionally, the collagen fibre
arrangement was loose and the fibres were thin in the
superficial and periadnexal dermis (Figs 6 and 7).
In some areas, focal haemorrhage, increased vascularization and a few haemosiderin-laden macrophages
were noted. In some sections the deep dermis of the visibly normal skin showed reduced denseness when compared to normal control horses. The collagen fibres of
all affected horses, including visibly unaffected skin,
were paler on the H&E stain than the collagen from
control normal horses. Subcutaneous fat was not
present in any biopsy samples. The Calleja special stain
did not reveal any abnormality of elastic fibres. Some
collagen bundles of the middle and deep dermis stained
red with Massons trichrome, as did some skin sections
of the normal control horses. Neither the epidermis
nor the adnexal epithelium showed any histopathological change. The pseudotumour histopathological
findings included fibroplasia and neovascularization,

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Hereditary equine regional dermal asthenia

127

Figure 2. Affected animal with fragile skin that was easily raised
when pinched (slack skin). In the affected areas, the skin was loosely
attached to the subcutaneous tissue. These areas were surrounded by
clinically normal skin and by scar tissue.

Figures 4 5. Normal (4) and affected skin (5). Note the paler,
thinner and loose arrangement of the collagen fibres in the affected
skin compared to the same area of a normal horse. H&E.
Bar = 50 m.

Figure 3. Ulcerated wound with hypertrophic scar and pronounced

folded skin. Skin thickening at the edge of the lesion is also visible.

usually arranged at right angles to each other (mature

granulation tissue).
Elastic fibres appeared to be reduced in number and
size, with focal fibre fragmentation in the pseudotumour lesions. However, more elastic fibres were present
in the mature granulation tissue than in the deep dermis of the normal control horse. No significant abnormalities were observed by electron microscopy.

D ISCU SSION
The clinical description of affected horses presented in
this study is similar to the condition that has been
described in 50 affected animals in different areas of
the United States. 11 In the patients described here,
the skin of affected areas was easily stretched when
pinched and shaped into a fold that gradually flattened
Figures 6 7. Normal (6) and affected skin (7). The peri adnexal
dermis of the affected skin shows thinner and paler collagen fibres.
Note the increased intercollagen clear spaces. Normal skin biopsies
were taken from the same areas of a normal horse of same age and
breed. H&E. Bar = 50 m.
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AS Borges et al.

out as the skin returned to its normal position. In

addition, affected areas were easily injured, resulting
in marked scars surrounded by thickened skin, and
discomfort was observed when the hyperextensible skin
was handled.6,7,911 The affected animals were cutting
horses, as described by other authors, but no cases have
been described in Brazil.13
All hyperextensible areas felt thinner and this was
confirmed by pachymeter measurement of skin thickness. Although we did not evaluate the morphometry
of histological sections, we noticed that the deep dermis was decreased in thickness. The loose collagen in
this area may have flattened during compression, possibly causing the reduction in skin thickness of the
affected horses. The deep dermal collagen of clinically
normal skin of the affected animals was looser, when
compared to normal control horse skin. These findings
are similar to previously reported cases in which skin
sections of animals presenting hyperelastosis cutis
showed an average thickness of the deep dermis that
was less than half the average of the thickness in control animals.9
Under light microscopy, we noticed abnormalities in
distribution, orientation and density of collagen fibres
within the deep dermis, as well as staining differences
of collagen fibres, similar to that described in other
affected horses.6,7,9 Nevertheless, the collagen abnormality in the superficial dermis observed in two of the
our cases has only been reported by one other author.8
Other reports referred to abnormalities restricted to
the deep dermis. The presence of thin and disorganized
collagen fibres at the periadnexal dermis has not been
described in any other study. Staining abnormalities
with H&E were also found in our study, similar to
those previously described.6,7
A dermal splitting zone was also observed in our
samples. Unlike other reports10 we believe that dermal
splitting is a useful artefact because of collagen fragility, which may occur depending on the severity of the
collagen abnormality and amount of traction suffered
during sample processing. Therefore, punch biopsies
may not yield adequate samples for the characterization of hyperelastosis cutis, as suggested before.10 In
contrast to previous reports, no collagen abnormalities
were observed by electron microscopy.8
Skin thickening was present around hyperextensible
areas, without visible lesions. Similar pseudotumours
have been described in humans affected by Ehler
Danlos syndrome and the histological features are
similar to those found in these animals.5,14 Pseudotumour pathogenesis is not well understood. The most
accepted hypothesis is the development of granulation
tissue in response to haemorrhages caused by traumatic injury, i.e. tissue repair following haematoma. In
human patients, pseudotumours are known to occur
in areas previously exposed to trauma (e.g. knees).
Although the lesions from the horses presented in this
study were not found exactly in areas subject to pressure, they may have resulted from saddle movement or
trauma during exercise.

Dermatosparaxia, cutaneous asthenia, EhlersDanlos

syndrome, cutis hyperelastica, dermal or collagen dysplasia, and hyperelastosis cutis are the most common
terms used to describe skin hyperextensibility in many
species.13,15 These conditions show distinct histopathological and ultrastructural changes. Abnormalities in
elastic fibres, as previously described,9,11 were not seen
in the horses described here. A focal decrease in the
number of elastic fibres was observed only in the pseudotumours. The hyperextensibility of the skin is caused
by collagen abnormality, not by elastic fibre abnormality.
Hyperelastosis cutis therefore seems to be an inappropriate term to describe this condition in horses. The most
appropriate name for the histological abnormalities
present would be cutaneous asthenia, as suggested
previously.11 We choose not to use the human term
EhlerDanlos-like because this syndrome includes
abnormalities in other tissues not found in these horses.
In 1986, the International Nosology of Heritable
Disorders of Connective Tissue redefined EDS into
subtypes IVIII & X. The molecular defects in some of
these subgroups are known. Based on clinical information, we conclude that the most similar subtypes to the
horses studied here are I, II and VIIc. Subtype VIIc,
also named dermatosparaxis, has been described and
well characterized in cattle.16
There are similarities between the clinical presentation
of type II EhlersDanlos syndrome and the abnormalities described in horses, except for the joint involvement described in human patients. In types I and II of
EhlerDanlos syndrome, electron microscopy reveals
gross abnormalities of fibril shape and size, suggesting
a defect in fibrillogenesis.5 Mutation of genes COL5A1
and COL5A2, which may be involved in type V collagen
fibrils, have been shown.5,1719 In addition, other reports
describe possible abnormalities in types I, II and III
collagen.20 Nevertheless, types I and II in human patients
are inherited as an autosomal dominant trait,2123
unlike the syndrome in horses, which is inherited as a
recessive trait.11,13 Generally, dominant abnormalities
are linked to mutations in collagen structural genes,
while recessive traits are linked to mutations in genes
responsible for collagen-processing enzymes. In type
VIIc EhlerDanlos (dermatosparaxis), for instance,
there is decreased activity of procollagen N proteinase.
And in type VI EDS there are signs of mutation in
lysil hydroxylase genes.24 Nevertheless, both conditions
have clinical and histological features different from
those shown by the horses of our study, suggesting that
a dissimilar mechanism may be involved in the horse.

R E FE R E N C E S
1. Scott DW. Congenital and hereditary diseases. In:
Scott DW ed. Large Animal Dermatology. Philadelphia:
W.B. Saunders, 1988: 33457.
2. Patterson DF, Minor RR. Hereditary fragility and
hyperextensibility of the skin of cats. A defect in collagen
fibrillogenesis. Laboratory Investigation 1977; 37: 1709.

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3. Anderson JH, Brown RE. Cutaneous asthenia in a dog.
Journal of the American Veterinary Medical Association
1978; 173: 7423.
4. Kawaguchi T, Fukazawa H, Naito Y et al. Dermal
dysplasia characterized by collagen disorder-related
skin fragility in a cow. American Journal of Veterinary
Research 1988; 49: 965 71.
5. Burrows NP. The molecular genetics of the Ehler
Danlos syndrome. Clinical and Experimental Dermatology 1999; 24: 99 106.
6. Lerner DJ, Mccracken MD. Hyperelastosis cutis in 2
horses. Journal of Equine Medicine and Surgery 1978; 2:
350 2.
7. Solomons B. Equine cutis hyperelastica. Equine Veterinary Journal of 1984; 16: 5412.
8. Gunson DE, Halliwell RE, Minor RR. Dermal collagen
degradation and phagocytosis. Occurrence in horse with
hyperextensible fragile skin. Archives of Dermatology
1984; 120: 599 604.
9. Hardy HH, Fisher KRS, Vrablic OE et al. An inherited
connective disease in the horse. Laboratory Investigation
1988; 59: 253 62.
10. Brouts SH, Rashmir-Raven AM, Black SS. Zonal dermal separation: a distinctive histopathological lesion
associated with hyperelastosis cutis in a quarter horse.
Veterinary Dermatology 2001; 12: 219 24.
11. White SD, Affolter V, Bannasch DM et al. Hereditary
equine regional dermal asthenia (hyperelastosis cutis) in
50 horses: clinical, histological, ultrastructural and
immunohistological findings. Veterinary Dermatology
2004; 15: 20717.
12. Pascoe RR, Kottenbelt DC. Manual of Equine Dermatology. Philadelphia: W.B. Saunders, 1999.
13. Von Tscharner C, Kunkle G, Yager J eds. Stannards
illustrated equine dermatology notes Congenital
diseases: epitheliogenesis imperfecta, epitheliogenesis
bullosa and hyperelastosis cutis. Veterinary Dermatology
2000; 11: 21115.
14. Wenstrup RJ. Heritable disorders of connective tissue with
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Minor RR, Lein DH, Patterson DF et al. Defects in collagen fibrillogenesis causing hyperextensible, fragile skin
in dogs. Journal of the American Veterinary Medicine
Association 1983; 182: 1428.
Nusgens BV, Verellen-Dumoulin CH, Hermanns-L T
et al. Evidence for a relationship between Ehlers-Danlos
type VIIC in humans and bovine dermatosparaxis.
Nature Genetics 1992; 1: 2147.
Loughlin L, Irven C, Hardwick LJ et al. Linkage of the
gene that encodes the alpha 1 chain of type V collagen
(COL5A1) to type II EhlersDanlos syndrome (EDS II).
Human Molecular Genetics 1995; 4: 164951.
Burrows NP, Nicholls AC, Yates JWE et al. The gene
encoding collagen alpha 1(V) (COL5A1) is linked to
mixed EhlersDanlos syndrome type I/II. Journal of
Investigative Dermatology 1996; 106: 12736.
Schwarze U, Atkinson M, Hoffman GG et al. Null alleles of the COL5A1 gene of type V collagen are a cause of
the classical forms of EhlersDanlos syndrome (types I
and II). American Journal of Human Genetics 2000; 66:
175765.
De Paepe A, Nicholls A, Narcisi P et al. EhlersDanlos
syndrome type I: a clinical and ultrastructural study of a
family with reduced amounts of collagen type III. British
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Wenstrup RJ, Florer JB, Willing MC et al. COL5A1
haploinsufficiency is a common molecular mechanism
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Rsum Lasthnie dermique rgionale hrditaire appartient un groupe de dysplasies du tissu conjonctif,
gntiques, congnitales, gnralement dcrits sous les termes dhyperelastosis cutis, dasthnie cutane, de dermatosparaxie, ou de syndrome dEhlers-Danlos. Cet article rapporte les donnes cliniques et histopathologiques
de trois Quarter Horse affects par cette maladie. Les chevaux prsentaient des lsions bilatrales asymtriques,
localises sur le tronc et la rgion lombaire, o la peau taut hyperextensible. La manipulation de la peau provoquait une raction douloureuse et les traumatismes superficiels des plaies. Dans les zones atteintes, la peau tait
plus fine que la normale, avec des bords paissis et des masses fibreuses dures (pseudotumeurs). Lexamen histopathologique a montr des fibrilles de collagne petites et fines, et des fibres de collagne anormales dans les
dermes moyens, annexiels et profond. La coloration de Masson et celle de Calleja na pas montr danomalie des
fibres de collagne et dlastine. La microscopie lectronique na pas montr danomalie. Comme chez lhomme,
lexamen histopathologique des pseudotumeurs a montr une fibroplasie et une novascularisation. Lanalyse du
pedigree de ces animaux est en faveur dun mode de transmission autosomique rcessif, comme dj suggr par
dautres tudes. Il sagit de la premire description de cette maladie au Brsil. Les donnes cliniques et histopathologiques ressemblent celles dcrites chez les chevaux prsentant cette affection aux Etats-Unis.
Resumen La astenia drmica regional hereditaria pertenece a un grupo de displasias congnitas, hereditarias,
de tejido conjuntivo, normalmente descritas como hiperelastosis cutis, astenia cutnea, dermatosparaxis, o
sndrome pseudo-Ehlers-Danlos. Este artculo presenta las caractersticas clnicas e histolgicas de tres Quarter
Horses relacionados, afectados por una astenia drmica regional. Estos caballos tenan unas lesiones simtricas
bilaterales en el tronco y regiones lumbares, dnde la piel era hiperextensible. La manipulacin de la piel generaba
una respuesta de dolor y el traumatismo superficial causaba heridas cutneas. En las reas afectadas, la piel era
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AS Borges et al.
ms delgada de lo normal, con mrgenes engrosados y masas fibrticas ms duras (pseudotumores). Los hallazgos histopatolgicos incluan fibras de colgeno ms delgadas y pequeas, y una disposicin laxa de las fibras
de colgeno en la dermis media, profunda y adventicia. Las tinciones tricrmica de Masson y de Calleja no revelaron ninguna anormalidad de las fibras de colgeno y fibras elsticas. La microscopa electrnica no mostr
anormalidades. Como en los pacientes humanos, los hallazgos histopatolgicos del pseudotumor incluan fibroplasia y neovascularizacin. El pedigr de estos animales apoya una forma de herencia autosmica recesiva, que
ha sido sugerida en otros estudios. ste es el primer estudio de esta enfermedad en Brasil. Sus caractersticas clnicas e histolgicas se parecen a las descritas en caballos afectados por esta enfermedad en los Estados Unidos.

Zusammenfassung Die heriditre equine regionale dermale Asthenie gehrt zu einer Gruppe von vererblichen, congenitalen Bindewebsdysplasien, die normalerweise als Cutis hyperelastica, cutane Asthenie, Dermatosparaxis oder Ehlers-Danlos-Syndrom bezeichnet werden. Dieser Bericht prsentiert die klinischen und
histologischen Eigenschaften von 3 miteinander verwandten Quarter Horses, die mit regionaler dermaler
Asthenie befallen waren. Diese Pferde hatten bilateral asymmetrische Lsionen im Bereich des Rumpfes und der
Lumbarregionen, in denen die Haut hyperextensibel war. Die Berhrung der Haut lste eine schmerzhafte Reaktion aus und oberflchliches Trauma fhrte zu Hautwunden. In befallenen Bereichen war die Haut dnner als
normal, mit verdickten Rndern und verhrteten fibrotischen Massen (Pseudotumoren). Die histopathologischen Befunde umfassten dnnere und kleinere Kollagenfasern und eine lockere Anordnung der Kollagenfasern in der mittleren, adventitialen und tiefen Dermis. Masson-Trichrome- oder Calleja-Frbung zeigten keine
Anormalitt der kollagenen oder elastischen Fasern. Elektronenmikroskopie zeigte keine Anormalitt. Wie auch
bei humanen Patienten waren Fibroplasie und Neovaskularisierung histopathologische Befunde in den Pseudotumoren. Die Ahnentafel dieser Tiere gibt Hinweise auf einen autosomal rezessiven Erbgang, was in anderen Studien schon vermutet wurde. Dieses ist der erste Bericht ber diese Krankheit in Brasilien. Ihre klinischen und
histologischen Eigenschaften hneln denen, die bei Pferden mit dieser Erkrankung in den Vereinigten Staaten
beschrieben wurden.

2005 European Society of Veterinary Dermatology, Veterinary Dermatology, 16, 125130