Veterinary Dermatology 2004, 15, 381 388

Pemphigus foliaceus in the horse: a retrospective study of 20 cases

Blackwell Publishing, Ltd.

SOPHIE I. J. VANDENABEELE*, STEPHEN D. WHITE, VERENA K. AFFOLTER,

PHILIP H. KASS and PETER J. IHRKE
*Veterinary Medical Teaching Hospital, Department of Medicine and Epidemiology, Department of
Pathology, Microbiology and Immunology, Department of Population Health and Reproduction, School of
Veterinary Medicine, University of California, Davis, CA 95616, USA
(Received 3 December 2003; accepted 14 June 2004)

Abstract Twenty horses with pemphigus foliaceus were seen over a period of 15 years in a veterinary medical
teaching hospital. Breeds seen were seven quarterhorses, five thoroughbreds, three cross-bred horses, two Arabians
and one of each of the following: standardbred, Tennessee walker and warmblood. There was no breed, age or
sex predisposition. Nine were mares, ten were geldings and one was a stallion. Ages ranged from 2.5 months to
25 years, with a mean of 8.6 years. Sixteen (80%) of the pemphigus foliaceus horses first exhibited signs between
September and February. There was a statistically significant more common occurrence of pemphigus foliaceus
during those months. Signs in the four other horses were first noted in March, May or June. Three of those horses
were < 13 months of age. Oedema (14 / 20) and crusts (13/20) were the most common lesions. Pain was present in
9/20 horses, pruritus in 7/20 and pyrexia in 7/20. Follow-up was available for 13 horses. Five of these horses were
euthanased. In three horses the reason for euthanasia was laminitis secondary to treatment. Four horses remained
lesion-free after medication was discontinued. Two horses required maintenance medication and are doing well at
the time of writing.
Keywords: dexamethasone, equine pemphigus foliaceus, horse, laminitis, seasonality, September to February.

IN TRO D U CT I ON
Pemphigus foliaceus (PF) is a rare autoimmune skin
disease recognized in humans, dogs, cats, goats, llamas
and horses.15 The term pemphigus is derived from the
Greek word for blister. As scaling and crusting are the
most prominent features of this disease, foliaceus,
meaning leaf-like, was added.6,7 PF is an intraepidermal vesiculo-pustular disease in animals. It is characterized immunologically by the presence of antibodies
against cell-adhesion proteins (desmosomal proteins)
on the surface of the keratinocytes leading to a loss of
intercellular cohesion (acantholysis). More specifically,
the desmosomal protein desmoglein 1 (dsg 1) is the
major PF antigen found in people and dogs.8,9 The typical histopathology of PF demonstrates acantholysis,
i.e. epidermal cell detachment in the subcorneal or
granular layer resulting in intraepidermal clefts. Acantholytic keratinocytes can also be seen on the histopathology and cytology of other suppurative dermatoses.
However, when acantholytic keratinocytes are seen in
large numbers or in clusters (rafts) they are strongly
suggestive of PF.4
PF is the most common autoimmune skin disease in
horses. It was first described in this species in 1981.10
The first retrospective study was published in 1987 and

Correspondence: S. I. J. Vandenabeele Veterinary Medical Teaching

Hospital School of Veterinary Medicine University of California,
Davis, CA 95616, USA. E-mail: s.vandenabeele@ugent.be
2004 European Society of Veterinary Dermatology

included nine horses.11 Subsequently, there have been

no large series of cases published. The objective of
this article was to retrospectively examine data from
20 cases of equine PF.

M AT E R IA L S A N D M E T H O D S
Case material
The database of the Veterinary Medical Teaching
Hospital (VMTH), University of California, Davis was
searched for cases of equine PF seen by the Dermatology Service between January 1987 and December 2002.
Originally the database listed 30 horses with a diagnosis
of PF. Cases were excluded because of the lack of the
original biopsy specimens or conclusive histopathology.
Thus, only 20 cases were included in this survey. The
20 horses had histopathological findings diagnostic for
PF combined with compatible history, clinical findings
and response to therapy. The horses had always lived in
Northern California.

Clinical data
Clinical data were collected and summarized from the
database at the VMTH. The data were derived from
the medical records and included each horses signalment, history, physical examination, treatment, outcome and the biopsy results. Signalment was evaluated
for evidence of breed, sex or age predilections and the
clinical course was reviewed. Information was also
gathered regarding clinical outcome.
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Results of complete blood cell counts and serum

chemistry profiles were reviewed when available. Followup information was obtained by reviewing the records
and calling the owners and referring veterinarians.

Histopathology
Multiple skin biopsy specimens of each horse were
examined. Skin biopsies were fixed in 10% neutral
buffered formalin and stained with haematoxylin and
eosin (H&E) for routine morphological evaluation.
Specimens from all 20 horses were also evaluated using
periodic acid Schiff (PAS) stains in order to evaluate
for the presence of dermatophytes.

Statistic analysis
Data regarding breed, age and month of onset of
clinical signs of the horses with PF were compared with
the general VMTH equine population. The chi-squared
test of association with a significance level of P < 0.05
was used to evaluate possible equine breed predispositions, age predispositions and seasonality of onset of
clinical signs.

R E SU LTS
Clinical data
Twenty horses with PF seen between 1987 and 2002
were included in the study. The breed, age and sex of
each animal are listed in Table 1. Seventeen pure-bred
horses and three cross-bred horses were seen. Quarterhorses were the most common breed (n = 7). Thoroughbreds and Arabians were the only other breeds with
more than one horse per breed. The chi-squared test
did not reveal a predisposition (P = 0.89) for any
breed. Nine horses were mares and eleven were males
(ten geldings and one stallion).

Age of onset ranged from 2.5 months to 25 years,

with a mean of 8.6 years and a median of 12.6 years.
Five horses (25%) were less than 2 years of age when
they first exhibited clinical signs. There was no age predisposition (P = 0.61) for the development of PF.
Sixteen (80%) of the PF horses included in this study
first exhibited clinical signs between September and
February. Horses seen at the University of California,
Davis have a significant higher risk (P = 0.0006) of
developing clinical signs of PF during those months.
Interestingly, the 10 other horses that were diagnosed
with PF but excluded from the study because of lack of
the original biopsy specimens or conclusive histopathology all developed clinical signs between September and February. Three of the four horses that
did not develop PF within this 6-month period were
younger than 2 years old. One of these horses had a
history of developing PF lesions after treatment with
trimethoprim-sulfa (TMS) drugs.
Skin lesions were similar in most horses. Crusts were
the most common and predominating lesions noted,
although they were not always the first clinical sign of
PF. Seven horses had generalized crusting, three had
crusts on the head and extremities and three had crusts
on the ventrum and extremities (Figs 13). Fourteen of
the 20 horses had ventral oedema. Often the sheath
and distal extremities were most severely affected. In
seven horses, ventral oedema was the first clinical sign
noted. Pustules, vesicles or bullae were not seen in any
of the horses. Oral ulcerations were not reported. Nine
of the horses had evidence of pain. The most severely
affected horses were reluctant to move. Seven horses
were pruritic. Pyrexia was noted in seven horses.
A complete blood cell count was performed in 16
horses and a biochemical profile was obtained from 10.
Neutrophilia (range 8.614.7 109/L; normal 2.36.8
109/L) was found in four horses. Eight horses had a

Table 1. Signalment, seasonal onset, treatment and outcome for the 20 horses with pemphigus foliaceus
Case

Breed

Age

Sex

Onset

Treatment

Outcome

1
2

Arabian
Thoroughbred

20 y
3m

Gelding
Stallion

June
June

Maintenance medication
Remission no medication

Thoroughbred

2.5 m

Mare

May

4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20

Tenessee Walker
Quarterhorse
Quarterhorse
Crossbred
Thoroughbred
Quarterhorse
Thoroughbred
Quarterhorse
Quarterhorse
Quarterhorse
Arabian
Thoroughbred
Standardbred
Quarterhorse
Warmblood
Crossbred
Crossbred

1y
2y
3.5 y
14 y
18 y
3y
12 y
16 y
5y
11 y
5.5 m
11 y
4y
25 y
6y
18 y
5y

Mare
Mare
Mare
Gelding
Gelding
Gelding
Gelding
Gelding
Gelding
Mare
Mare
Mare
Mare
Gelding
Gelding
Gelding
Mare

March
September
September
September
September
October
October
October
November
November
December
December
January
February
February
February
February

Prednisolone
Aurothioglucose weekly and
dexamethasone
Aurothioglucose weekly and
dexamethasone
Dexamethasone
Dexamethasone
Dexamethasone
Prednisone
Azathioprine and prednisolone
Dexamethasone
Prednisolone
Prednisone
Dexamethasone
Prednisone
Dexamethasone
Dexamethasone
Dexamethasone
Dexamethasone
Prednisolone
Dexamethasone
Dexamethasone

2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 381 388

Lost to follow up
Lost to follow up
Euthanasia (laminitis)
Euthanasia (laminitis)
Maintenance medication
Remission no medication
Remission no medication
Euthanasia
Lost to follow up
Remission no medication
Sold
Lost to follow up
Sold
Euthanasia (laminitis)
Lost to follow up
Lost to follow up
Euthanasia
Lost to follow up

Pemphigus foliaceus in the horse

383

Figure 4. Horse 2, cytology of a peeled crust reveals numerous

neutrophils and some acantholytic cells. Diff Quik stain.
Bar = 80 m.

Figure 1. Horse 20, generalized crusting.

Cytology and histopathology

Records indicated that when cytology was performed
acantholytic cells were found (Fig. 4). The most consistent and prominent findings in all biopsies were
large, serocellular crusts, indicating an intraepidermal
pustular disease. Often these serocellular crusts were
layered and expanded over multiple hair follicle openings. The crusts contained numerous nondegenerative
neutrophils and individual as well as rafts of acantholytic keratinocytes (Figs 5 and 6). Subcorneal and/or
intraepidermal pustules and vesicles with intralesional
acantholytic keratinocytes (often in rafts) were found
in only five horses (Figs 6 and 7).
The majority of cases presented with a mild mixed
superficial perivascular dermatitis (17/20). In one of
two cases of tissue eosinophilia the infiltrate extended
into the mid-dermal vascular plexus surrounding the
adnexae. Eosinophil blood counts were unavailable for
these two horses.
A reactive vascular component consisting of endothelial swelling and hyaline degeneration of the vessels

Figure 2. Horse 20, close up from the crusts.

Figure 3. Horse 2, lesions on the face.

low haematocrit (range 0.2170.292 L/L; normal 0.30

0.46 L/L). Eight horses had hyperfibrinogenaemia (range
57 g/L; normal < 4 g/L) and two had a hyperglobulinaemia (range 5262 g/L; normal < 47 g/L). A hypoalbuminaemia (range 2022 g/L; normal > 23 g/L) was
present in three horses. Eosinophilia (3.06 109/L;
normal 0.02.00 109/L) was present in one horse.

Figure 5. Horse 7, close up of the serocellular crust with neutrophils

and acantholytic cells. H&E. Bar = 100 m.

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SIJ Vandenabeele et al.

Figure 6. Horse 2, equine epidermis; intraepidermal pustule

crossing multiple hair follicles with neutrophils and clusters of
acantholytic cells (rafts). H&E. Bar = 1000 m.

Figure 7. Horse 2, close up of Fig. 6. Equine epidermis;

intraepidermal pustule with neutrophils and clusters of acantholytic
cells (rafts). H&E. Bar = 100 m.

was found in three horses indicating the presence of a

vasculopathy (Fig. 8). Dermatophytes were not found
on any of the PAS-stained biopsy sections.

Treatment and clinical follow-up

The treatment and clinical follow-up for each horse is
listed in Table 1.
Eleven horses were administered dexamethasone orally
at immunosuppressive induction doses of 0.050.1 mg/
kg per day (2040 mg per horse). Three horses were
treated with oral prednisone at 12 mg/kg. Two of the
three horses treated with prednisone did not respond
when treated with the prednisone, but did respond to a
comparable dose of prednisolone or dexamethasone.
Three horses were treated with oral prednisolone at
12 mg/kg (200400 mg per horse). Two horses were
treated weekly with aurothioglucose (injectable gold
salts) 1 mg/kg with concurrent daily dexamethasone
administration. One horse was treated with both daily

Figure 8. Horse 8, reactive vessels consisting of endothelial swelling

and hyaline degeneration of the vessels. H&E. Bar = 100 m.

oral prednisolone and azathioprine at 1 mg/kg. Once

the lesions were in remission (1014 days of treatment)
the treatment regimen was changed to an alternate-day
dosing of the glucocorticosteroid. Doses were further
tapered and discontinued when possible.
Follow-up was available for 13 horses. Five of these
were euthanased (horses 5, 6, 10, 16, 19). In three the
reason for euthanasia was the development of acute
laminitis following initiation of treatment with dexamethasone. For horse 10 the reason for euthanasia was
the need for high doses of daily prednisolone in order
to control the PF. The exact reason for euthanasia in
the fifth horse was unknown. Two horses were sold
once the PF was in remission and subsequently lost to
clinical follow-up. Four horses remained lesion free
after medication was discontinued. They had received
medications for 312 months. These horses have been
in remission for 13 years. Horse 12 developed clinical
signs compatible with PF 2 years after treatment was
stopped. The lesions were first noted in January and
consisted of crusts on the head and legs. A biopsy was
not obtained to conclusively diagnose PF but the
lesions responded to immunosuppressive doses of
dexamethasone. The horse went into remission and the
dexamethasone treatment was tapered over a period
of 2 months and discontinued. Laminitis did develop
during the dexamethasone treatment and was successfully managed. At the time of writing, the horse is still
lesion free. Two horses (1, 7) are doing well with maintenance medications (prednisolone at 0.51 mg/kg EOD).
Follow-up was available for two of the five horses
younger than 2 years of age. One horse was euthanased
because of the development of laminitis, the other
horse is still in remission without medications.

D ISC U S S IO N
Although PF is the most common autoimmune skin
disease observed in horses it is still rare.4,12 Previous

2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 381 388

Pemphigus foliaceus in the horse

studies of equine PF have found a breed predilection
for Appaloosas.11 In contrast, no breed predisposition
was found in this study. Although more quarterhorses
were seen in comparison with any other breed, none of
the horse breeds were at elevated risk when compared
with the hospital equine population. Equine PF can
develop at any age. The age of the horses in this
report ranged from a few months to 25 years. The lack
of an age predisposition is in accordance with a
previous study,11 but in contrast with the common
belief that PF in horses has a bi-modal age distribution, seen more commonly in either young or very old
horses.12
PF is an exfoliative skin disease. The most consistent
and prominent lesions observed in horses with PF are
crusts.4,12 The earliest sign, however, may be oedema,
especially oedema of the distal extremities and ventral
abdomen, as seen in seven horses in this study. Ventral
oedema associated with PF in adult horses has been
attributed to hypoproteinaemia, although laboratory
evidence of such has often been absent.13 This correlates with our findings that of the horses with ventral
oedema only three had evidence of hypoproteinaemia.
The exact pathophysiological mechanism of the oedema
is unknown.13
Haematological and serum chemistry profile changes
were predominantly seen in the more severe cases of
PF, although the severity of the disease may also have
caused the owners to be more likely to agree to have
laboratory tests performed. Changes included anaemia,
leukocytosis, neutrophilia and hyperglobulinaemia.
The vast majority of the horses (16/20) in this study
first exhibited clinical signs between the months of
September and February. To the authors knowledge,
this is the first time that seasonality has been reported.
The importance and consistency of this finding will
need to be confirmed in larger, multicentre studies.
One hypothesis is exposure to insect bites such as
Simuliidae (black fly). Horses may have been bitten by
the black flies in the summer and fall and consequently
developed an antibody response that cross-reacted with
epidermal antigens such as dsg 1 and consequently
produced disease. Interestingly, equine PF has been
reported in a group of horses that had Culicoides
hypersensitivity for 13 years.4
In humans, an endemic form of PF called fogo selvagem (Portuguese: wild fire) has been correlated with
exposure to black fly bites.1417 The pathogenesis of
fogo selvagem has been proposed as an initial period of
sensitization (possibly mediated by antigenic mimicry
between the environmental antigen and desmoglein 1)
and subsequent progression to clinical expression of the
disease. A small subset of sensitized individuals shows
a marked increase in serum levels of antibodies against
dsg 1.18 A period between sensitization and onset of
clinical PF might explain why the seasonal prevalence
of equine PF in our study occurred a few months after
the season (summer) in which horses have the greatest
exposure to insects, especially Culicoides spp. and
black flies.

385

Another possible hypothesis for seasonality of

disease onset could be the administration of a specific
drug such as an anthelmentic, within this timeframe.
However, association between drug administration
and disease onset could not be determined in this
retrospective study.
Four horses developed PF outside the autumnwinter
season. Only one of these was older than 2 years (horse
1). In horse 2, the TMS could potentially be linked to
the onset of the PF, as TMS was administered just
prior to the development of skin lesions. In people,
drugs containing a thiol group or a sulfur molecule are
considered to have a greater risk of triggering PF.19,20 It
is thought that the drugs and their metabolites can
bind to the cell membrane as haptens causing inadequate cellcell adhesion or changing the conformation
of the cell-surface antigens and thus leading to antibody production and acantholysis.21 Administration
of TMS has been linked to cases of PF in dogs.22 24 The
TMS in this horse was administered to treat a Rhodococcus equi infection. Stress and systemic disease have
been suggested as underlying causes for the development of PF4,12 and could have been contributing
factors in this horse.
The typical histopathology of PF includes acantholysis (epidermal detachment) in the subcorneal or
granular layer of the epidermis resulting in clefts.4,12
The exact pathomechanism is unknown.4,13 In this
study, the most consistent histopathological finding of
equine PF was large layered crusts, spanning several
hair follicles. The crusts consisted of mostly nondegenerative neutrophils and acantholytic cells. These findings are consistent with histopathological changes
observed in cats and dogs.2,25 Vesiculopustules or microabscesses with acantholysis in subcorneal, intraepidermal or follicular locations are highly suggestive of PF,
but were present in only 20% of our cases. This contrasts with canine PF where intraepidermal intact
pustules can often be observed.2,25 The lack of intact
pustules can be a diagnostic challenge with the diagnosis of PF relying on the presence of the acantholytic
cells in crusts4,12 emphasizing the importance of not
surgically preparing the skin prior to biopsy. Two
horses in this study had marked perivascular and follicular eosinophilic infiltrates. The predominance of
eosinophils in the inflammatory infiltrate has been
reported in about one third of horses with PF.11 Similar
infiltrates have been noted in early lesions of some cases
of human PF.26,27 Three horses had histopathological
vaculopathy. Clinically, these horses had exfoliative
dermatitis. This probably represents an inflammatory
state that affects the entire integument, in which there
is an uncontrolled feedback loop between the dermis
and the epidermis.
The epidermis then may produce significantly
elevated amounts of circulating vascular endothelial
growth factor/vascular permeability factor resulting
in dermal vascular proliferation, increased vascular
permeability and subsequent vessel wall degeneration
consistent with a vasculopathy.29

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SIJ Vandenabeele et al.

In all 20 horses fungal infection was unlikely, as PAS

staining did not reveal fungal elements of any sample.
Infections with Trichophyton equinum have been reported
to cause a generalized, papular, pustular, crusting,
exfoliative dermatitis histologically resembling equine
PF.30 These cases of Trichophyton equinum infection
also contained acantholytic cells, presumably caused
by the proteolytic enzymes of these dermatophyte
strains.30
Treatment of equine PF requires high doses of glucocorticoids with or without other immunomodulatory drugs to induce remission. The most commonly
administered drugs for initial treatment of PF are high
doses of glucocorticosteroids.4,12 Seventeen horses were
treated with glucocorticosteroids only. Two of three
horses treated with prednisone did not respond, but
did respond to a comparable dose of prednisolone or
dexamethasone. It has been reported that horses that
do not respond to prednisone, usually respond to
orally administered prednisolone or dexamethasone.4
Possible reasons why horses do not respond as well to
oral prednisone are poor absorption, rapid excretion,
failure of hepatic conversion to prednisolone or a combination of all of the above factors.31 In one study of
horses with chronic obstructive pulmonary disease it
was found that neither prednisone nor prednisolone
could be detected in the blood of the horses that were
administered oral prednisone.32
Equine PF may be a severe disease and it is not
uncommon that horses have to be euthanased because
of the disease itself or medical problems developing
subsequent to treatment. Five of 20 horses in this
report were euthanased; three because of the development of progressive laminitis (founder). Laminitis
secondary to glucocorticosteroid administration is
well documented.33 It is believed that the corticosteroids alter the blood flow in the horses hooves, causing
hypoxia in the lamina. Alternatively, corticosteroids
may have a direct effect on epidermal cell metabolism.34 Only free glucocorticoid is metabolically active.
There is a specific corticosteroid-binding globulin with
a relatively low binding capacity. When large doses of
glucocorticoids are administered, this globulins binding capacity is exceeded and albumin becomes the
binding protein. Animals with a low serum albumin
level have a lower capacity for binding, and unbound
glucocorticoid becomes freely available, increasing toxicity.31 In our study, two of the three horses that were
treated with dexamethasone and subsequently developed laminitis had a low serum albumin level. The
albumin level of the third horse was not measured. Initiation of treatment for PF with prednisolone and not
dexamethasone in patients with a low serum albumin
may be indicated.
In horses that do not respond to glucocorticosteroid
administration, or when glucocorticosteroid side effects
are too severe, steroid-sparing drugs may be added.4,35
Horse 8 was treated with prednisolone and azothiaprine
and the disease went into remission. The drugs were
slowly tapered and discontinued, and the horse has

not relapsed. In humans and rodents azathioprine is

metabolized in the liver (and possibly other organs)
by thiopurine methyltransferase (TPMT) an enzyme
detectable in human lysed red blood cells (RBC).36,37
When the TPMT RBC enzyme level was measured in
dogs, cats and horses, it was found that the level was
highest in dogs, lower in cats and lowest in horses.38 Low
activity of RBC TPMT in people has clinically been
correlated with an increased risk of myelosuppression
with azathioprine administration.36,37 The lack of clinical or haematological side effects of azathioprine in
horses has three possible explanations. The horse may
have poor oral absorption of the drug, metabolism of
the drug is non-TPMT dependent or the TPMT activity
in the liver is higher than the TPMT activity in the
RBC resulting in adequate metabolism of the drug and
thus lower toxicity in the horse. Other equine autoimmune diseases have been treated with azathioprine.4
The lack of side effects observed thus far may indicate that this drug may be an option to treat equine
PF.
Another option is chrysotherapy. Horse 3 was treated
with weekly injections of gold salts, combined with
dexamethasone. When the horse went into remission,
the aurothioglucose became unavailable. Injections
were therefore discontinued and the dexamethasone
slowly tapered. The horse is still in remission without
medication. Gold compounds are capable of modulating several phases of the immune response, but the
exact mechanism is unknown. The treatment takes up
to 16 weeks before beneficial effects may be seen, so
typically glucocorticosteroids are added until the
lag-phase has passed. Side effects have not been reported
in horses.39
In general it is believed that younger horses may
respond better to treatment and may eventually stay in
remission once treatment is withdrawn.4,12 In our
study, follow-up was available for two young horses,
one 3-month-old foal that responded well to therapy
and was weaned off of all drugs successfully and one 2year-old horse that was euthanased due to the development of laminitis. Unfortunately no follow-up was
available for the three other horses of 1 years of age or
younger so we are unable to comment on age-related
prognosis of equine PF.
In this study, the survival rate was 46% and the
disease severe. A guarded prognosis should therefore
be given for equine PF. The survival rate may be higher
if development of laminitis is avoided, possibly by
treating with prednisolone rather than dexamethasone,
especially if a low serum albumin is present, and/or by
using steroid sparing drugs to lower the glucocorticoid
dosage.

AC K N OW L E D G E M E N T S
The authors wish to thank Dr Hilde DeCock for her
assistance in taking the histopathology pictures and all
her help with digitizing of the images.

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Pemphigus foliaceus in the horse

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Rsum Vingt chevaux souffrant de pemphigus foliac ont t vus sur une priode de 15 ans dans un centre hospitalier universitaire vtrinaire. Les races reprsentes taient: 7 Quarterhorses, 5 Thoroughbreds, 3 croiss, 2
Arabes et un Standardbred, un Tennessee Walker et un Warmblood. Aucune prdisposition de race, dge ou de
sexe na t observe. Il sagissait de neuf juments, dix mles castrs et un talon. Lge variait entre 2.5 mois et
25 ans, avec une moyenne de 8.6 ans. Seize (80%) des animaux ont prsent des signes cliniques initialement entre
septembre et fvrier. Lapparition de lsions dans cette priode tait statistiquement significative. Pour les quatre
autres chevaux, les symptmes sont apparus en mars, mai ou juin. Trois chevaux taient gs de moins de 13 mois.
Les lsions les plus frquentes taient un oedme (14/20) et des crotes (13/20). Une douleur a t rapporte chez
9/20 chevaux, un prurit dans 7/20 cas et une hyperthermie dans 7/20 cas. Un suivi tait disponible pour 13 chevaux.
Cinq animaux ont t euthanasis. Dans trois cas, leuthanasie a t conscutive une fourbure secondaire au
traitement. Quatre chevaux nont plus prsent de lsion aprs discontinuation du traitement. Dans deux cas, le
traitement a d tre pousuivi; ces animaux sont toujours bien contrls au moment de la rdaction de cet article.
Resumen Se visitaron veinte caballos con pnfigo foliceo durante un perodo de 15 aos en un hospital veterinario universitario. Las razas fueron: 7 Cuarto de Milla (Quarterhorses), 5 Purarazas, 3 cruzados, 2 rabes y uno
de cada una de las siguientes: Standard, Tennessee Walker y Warmblood. No exista una predisposicin de raza,
edad o sexo. Nueve fueron hembras, diez machos castrados y uno macho entero. Las edades se encontraban entre
2.5 meses y 25 aos, con una media de 8,6 aos. Diecisis (80%) de los caballos con PF mostraron los primeros
sntomas entre septiembre y febrero. Se produca una incidencia significativamente mayor de PF durante estos
meses. En los cuatro caballos restantes se presentaron los primeros sntomas en marzo, mayo o junio. Tres de
aquellos caballos tenan < 13 meses de edad. Las lesiones ms frecuentes fueron edema (14/20) y costras (13/20).
9/20 caballos mostraban dolor, 7/20 prurito y 7/20 pirexia. Se pudo realizar un seguimiento en 13 caballos. Cinco
de estos caballos fueron eutanasiados. En tres caballos la razn de la eutanasia fue la laminitis secundaria al
tratamiento. Cuatro caballos permanecieron sin lesiones despus de terminar la medicacin. Fue necesario mantener la medicacin en dos caballos y se encontraban en buen estado en el momento de escribir este artculo.
Zusammenfassung Einundzwanzig Pferde mit Pemphigus foliaceus wurden in einem veterinrmedizinischem
Lehrhospital ber eine Periode von 15 Jahren untersucht. Betroffene Rassen waren: 7 Quarterhorses, 5 Vollblter,
3 Kreuzungen, 2 Araber und jeweils eines der folgenden Rassen: Standardbred, Tennessee Walker und Warmblut.
Es gab keine Rasse, Alters- oder Geschlechtsprdisposition. Neun waren Stuten, zehn Wallach und eines war
Hengst. Das Alter rangierte von 2,5 Monaten bis 25 Jahren, mit einem Durchschnitt von 8,6 Jahren. Sechszehn
(80%) der PF Pferde zeigten zwischen September und Februar erste Anzeichen. Es gab ein statistisch signifikant
hufigeres Auftreten von PF whrend dieser Monate.Bei den vier anderen Pferden wurden erste Anzeichen im
Mrz, Mai oder Juni beobachtet. Drei dieser Pferde waren unter dreizehn Monate alt. dem (14/20) und Krusten
(13/20) waren die hufigsten Lsionen. Schmerz war bei 9/20, Juckreiz bei 7/20 und Fieber bei 7/20 vorhanden.
Katamnese war bei 13 Tieren vorhanden. Fnf dieser Pferde wurden euthanasiert. Bei drei Pferden war der
Grund fr die Euthanasie Laminitis aufgrund der Behandlung. Vier Pferde blieben frei von Lsionen nachdem
die Medikation beendet wurde. Zwei Pferde bentigten Erhaltungsmedikation und waren bei gutem Allgemeinbefinden zum Zeitpunkt der Niederschrift dieses Berichtes.

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