Veterinary Dermatology 2004, 15, 188 193

Case report

Blackwell Publishing, Ltd.

Suspected wood poisoning caused by Simarouba amara (marup/

caixeta) shavings in two dogs with erosive stomatitis and dermatitis
JAN DECLERCQ
Department of Medicine and Clinical Biology of Small Animals, Ghent University,
Faculty of Veterinary Medicine, Salisburylaan 133, B-9820 Merelbeke, Belgium
(Received 29 May 2003; accepted 23 October 2003)

Abstract Two male Labrador retrievers developed bleeding erosions/ulcerations involving the oral mucosa,
mucocutaneous junctions of the lips, nose, prepuce and anus, ulcerated nodules on the chin, and crusting lesions
on the elbows, hocks and scrotum. One of the dogs was anorexic and depressed, had haematological abnormalities consistent with damage to the liver and signs of neurological disease. As these dogs had recently been exposed
to bedding containing Simarouba amara shavings and because of the striking similarities of clinical signs to those
described for horses, a probable diagnosis of wood poisoning was made. This assumption was supported by the
clinical course as healing of skin lesions occurred when the dogs were no longer exposed to the bedding.
Keywords: dog, erosive dermatitis, Simarouba, stomatitis, wood poisoning.

I NTRO D U CTI ON
Simarouba amara, commonly referred to as marup
or caixeta, is a tropical hardwood tree in the Simaroubaceae family from South America. Its wood is
imported and used internationally by furniture and
moulding manufacturers. The leaves and bark of Simarouba have a long history of use as a natural medicine
in the tropics and the indigenous peoples still use
Simarouba as a remedy for malaria and dysentery.1,2
In 1998, a disease outbreak among stabled horses
was reported in Argentina.3 Affected animals presented with erosive lesions in the oral cavity, on the
tongue, and around the nose, lips, anus and external
genitals. Other signs were oedema and jaundice. Biochemical analysis showed hyperbilirubinemia and a
rise in liver enzymes. Deaths had occurred during the
outbreak. As virological, bacteriological and mycological studies eliminated the possibility of a transmitted
infectious disease, the focus of the diagnosis was on a
possible toxic cause. Exposure to wood shavings from
Simarouba amara used for bedding stalls of affected
horses was strongly associated with the outbreak, and
clinical signs in horses were successfully reproduced in
experimental trials. Horses with marup bedding and
fed on alfalfa hay spread on the shavings developed
a similar disease to that observed in natural cases,
whereas horses with a wheat bedding remained healthy.
Correspondence: Jan Declercq, Department of Medicine and
Clinical Biology of Small Animals, Ghent University, Faculty of
Veterinary Medicine, Salisburylaan 133, B-9820 Merelbeke, Belgium.
E-mail: jan.declercq.vet@skynet.be
188

In 2000, a disease condition in horses caused by

exposure to wood shavings of Simarouba amara was
also recognized in Japan.4 Horses developed erosive
lesions in the oral cavity, around the nose, lips and anus,
and on the tongue within 48 h. A few horses showed
depression and pyrexia, and some died. Hyperbilirubinemia and a rise in hepatic enzymes were detected in
blood samples. Fatty degeneration of the liver, necrosis
of hepatic cells, and degeneration and necrosis of
urinary tubules were observed in samples obtained
at necropsy. The cause of the toxicity was proved by
ingestion tests. Horses fed pelleted feed mixed with
caixeta wood shavings developed erosive stomatitis
and dermatitis, anorexia and depression within 48 h
post exposure. One horse had an attack of tonic convulsion and another developed lack of co-ordination.
Outbreaks of erosive stomatitis in a group of horses
associated with marup bedding has also been
reported in Canada5,6 and the USA.7,8
This report describes an erosive stomatitis and dermatitis in two dogs from Belgium that were in contact
with wood shavings of Simarouba amara (marup).

C A SE R E P O RT
Case history
Two male Labrador dogs, a 10-year-old (dog 1) and an
8-year-old (dog 2), were used as guard dogs at a furniture manufacturing enterprise. Both dogs lived outdoors and during the day were confined to a fenced
area with access to a kennel with a layer of wood shavings for bedding. At night the dogs were allowed to
2004 European Society of Veterinary Dermatology

Suspected wood poisoning caused by Simarouba amara

roam freely within the factory. The animals were fed
dry commercial dog food which was supplied in feeding bowls attached to the wall. Water given to the dogs
was supplied from the mains. The dogs had not been
off the property before the onset of disease.

189

11). Analysis of a urine sample obtained by catheterization revealed 2+ bilirubin, no casts or cells and a
specific gravity of 1.037. Both dogs were referred on the
13th day for unusual and progressive skin disease.

Clinical findings at referral

Initial clinical findings
Dog 1 was examined in the kennel by the referring
veterinarian (day 1) because of anorexia and depression, signs which had been noticed by the owner 2 days
previously. On physical examination, the dog had
a rectal temperature of 39.3 C, was depressed and
showed increased salivation. The oral mucosal surface
appeared normal but wood shavings were adhered
to the perioral saliva. Hindlimb paresis was also
observed. The animal was hospitalized for further evaluation. Results of a standard haematological and
serum biochemical profile revealed a normal red blood
cell count and an increased white blood cell count, with
an increased immature neutrophil count. There were
increased serum concentrations of aspartate aminotransferase (AST), alanine aminotransferase (ALT)
and alkaline phosphatase (ALP) and low levels of
albumin and total protein (Table 1 day 1). Treatment
with intravenous fluids and clindamycin at a dose of
5.5 mg kg1 twice daily was initiated.
On day 2 the dog was still anorectic and facial erosions became evident. The margins of the lips, the buccal mucosa of the upper lip and the commisures of the
mouth were the most severely affected sites. Ulcerated
nodules were present on the chin and oral examination
revealed erosions on the tongue and hard palate.
On the same day dog 2 was admitted for a dermatitis
that affected the lips. The dog was apparently healthy
and had a good appetite. Physical examination
revealed a similar but less severe skin disease to dog 1
with erosions and erosive nodules on the lips and in the
oral cavity. No abnormalities were found on routine
laboratory analysis. Daily clindamycin was administered to prevent secondary infection of the lesions.
At this point the diagnosis focused on possible caustic or toxic causes. As there was no known exposure to
other possible chemical substances, preservatives to
protect wood against termites and rot were implicated
as causal agents, and on day 4 the wood shavings were
removed from the dogs bedding. Over the next 7 days
the lesions on the lips of dog 1 progressed to severe
ulcerations with a haemorrhagic discharge, and new
lesions developed around the nose and scrotum.
Except for progressive skin lesions, dog 2 remained in
good health. Dog 1, with the more severe clinical presentation, had an improved appetite for 2 days and then
became anorectic again. A second blood sample was
obtained from dog 1 on day 11 by the referring veterinarian and urinalysis was performed. The blood analysis was incomplete and revealed a decreased red blood
cell count, packed cell volume and haemoglobin
concentration; leucocytosis with neutrophilia and left
shift; and decreased serum levels of albumin and total
protein. Urea and creatinine were normal (Table 1, day

On physical examination dog 1 was depressed and

appeared underweight. Dog 2 was alert and in good
body condition. Dog 1 had a rectal temperature of
38.8 C, showed wasting of facial muscles and had
moderate paresis in the hind limbs. The patellar
reflexes were hyporeflexive but there were no abnormalities in proprioceptive perception. Both dogs had a
similar skin condition, mainly confined to the perioral
and nasal area, but the lesions were more severe and
extensive in dog 1. The skin condition of dog 2 was
improved and some of the lesions were resolving. The
cutaneous lesions were nonpruritic and not painful
upon palpation. Erosions/ulcerations with a sanguinous discharge were observed on the labial margins of
the upper lips and commisures of the mouth (Figs 1
and 7). Ulcerated nodules were distributed on both
sides of the chin (Fig. 1). Erosions were present at and
in the nasal cavity and the nasal planum was dry and
fissured (Fig. 2). Examination of the oral cavity

Figure 1. Dog 1. Lips and chin of a Labrador retriever with suspected

Simarouba poisoning on day 13. Photograph illustrating the
predominant involvement of the marginal buccal mucosa and
commisures of the mouth. Notice the presence of ulcerated nodules
on the chin.

Figure 2. Dog 1. Dryness and fissuring of the nasal planum, and

mucocutaneous and mucosal erosion/ulceration of the nose on day 13.

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J Declercq

Figure 3. Dog 1. Oral cavity in a Labrador retriever with suspected

Simarouba poisoning on day 13. Erosions/ulcerations are present on
the tongue, hard palate, along the buccal mucosa of the upper lip
margins and on the glossopalatine folds.

Figure 5. Dog 1. Lateral hock of a Labrador retriever with

Simarouba poisoning on day 13. Notice the presence of two
circumscribed crusted lesions.

Figure 6. Dog 1. Scrotum of a Labrador retriever with Simarouba

poisoning on day 13. Thick adherent crusting and fissuring.

Figure 4. Dog 1. Anus of a Labrador retriever with Simarouba

poisoning on day 13. Note minor erosions mainly of the lower
portion of the anus.

revealed ulcerations affecting the buccal mucosa along

the upper lip margins and on the glossopalatine folds,
the hard palate and the dorsal and ventral lingual surfaces (Fig. 3). Minor erosions were found on the mucocutaneous junctions of the prepuce and anus (Fig. 4).
The dogs had crusting lesions involving the elbows,

Figure 7. Dog 2. Facial lesions in a Labrador with Simarouba

poisoning on day 13. Note less severe clinical presentation and
regressing lesions on the lips (erosion/ulceration) and nose
(residual depigmentation).

hocks and scrotum (Figs 5 and 6). Erythema and oedematous swelling of the ears were noticed only in dog 1.
Wedge biopsies from lesional skin of the upper lip and
chin were obtained from dog 1 for histopathological
examination. Microscopic evaluation revealed nondiagnostic ulcerative dermatitis. Signs of oesophageal

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Suspected wood poisoning caused by Simarouba amara

Table 1. Laboratory results from dog 1
RBC
Haemoglobin
PCV
WBC
Neutrophil count
Band neutrophil count
Platelets
Urea
Creatinine
Total protein
Albumin
AST
ALT
ALP

191

Day 1

Day 11

Day 19

Reference ranges

6.37
9.7
44.3
15.7
12.07
1.09
NA
3.5
47.74
48
23.4
88
526
140

5.29
8
35.4
18.7
15.42
0.9
NA
5.0
42.43
35
13.8
NA
NA
NA

3.76
5.8
24.3
9.7
9.30
0.0
71
5.5
38.01
44
NA
NA
NA
NA

5.5 7.5 1012 L1

8.5 12 mmol L1
4254%
8.0 12.0 109 L1
3.211.8 109 L1
0.0 0.30 109 L1
200 400 109 L1
2.0 6.7 mmol L1
50 + 1/ kg BW umol L1
58 75 g L1
28 38 g L1
15 30 U L1
25 55 U L1
10 50 U L1

Abbreviations: RBC, red blood cell count; PCV, packed cell volume; WBC, white blood cell
count; AST, aspartate aminotransferase; ALT, alanine aminotransferase; ALP, alkaline
phosphatase; BW, body weight; NA, not available.

discomfort such as exaggerated swallowing and extension of the head and neck were not present, but facilities for endoscopic examination were not available.
The appearance of similar clinical signs in the two
dogs at the same time suggested that they were commonly exposed to a caustic or toxic agent. A thorough
history revealed recent changes in the bedding provided for the dogs. Four days before the onset of health
problems, beech-wood shavings mixed with shavings of
a recent imported tropical wood called marup were
introduced for bedding. Exposure to preservatives in
the wood, especially to arsenic preservatives, was initially suspected. Samples of hair, nails, urine and wood
shavings were submitted for analysis and determination of arsenic concentrations, but these were normal
in all samples. As marup wood had been implicated as
a causative toxic agent in poisoning incidents in horses
and because of the striking similarities between the
toxic effects produced in horses and the findings in the
recently exposed dogs of this report, a probable diagnosis of marup wood poisoning was made. Supportive antibiotic therapy was continued.

Outcome
Telephone communication with the referring veterinarian on the 23rd day revealed that the skin and oral
lesions in both dogs had resolved. A third but incomplete blood analysis of dog 1 on day 19 showed more
pronounced anaemia, a leucocyte count within the
normal range, thrombocytopaenia and hypoproteinaemia (Table 1, day 19). Because of the progressive hind
limb paresis and results of the latest blood analysis, a
decision was made to have dog 1 euthanized. Necropsy
was not performed.

D ISCU SSION
Wood poisoning appears to be a rare condition and has
been reported in horses when bedded on wood shavings containing either Juglans nigra911 (black walnut)

or Simarouba amara (marup/caixeta).38 No references of Simarouba poisoning in the dog were found
during a search of the available literature.
The history, clinical signs and clinical course in the
reported dogs were compatible with a diagnosis of
Simarouba poisoning. The history of a similar clinical
condition in two dogs housed together and recently
exposed to shavings from Simarouba amara supported
that probability. Toxicity could occur when these confined dogs chewed and consumed shavings out of boredom. The onset of signs on the 4th and 6th day of
exposure, respectively, was consistent with the historical findings of provocative exposure testing in horses.3,4
The distribution pattern of the lesions in the dogs
was striking and almost identical to that observed
in horses with Simarouba poisoning. The distribution
on the body was symmetrical and involved the oral
mucosae (buccal mucosa, tongue, hard palate), mucocutaneous junctions (lips, nasal, prepuce and anus),
pressure points (elbows and hocks), nasal planum,
scrotum and, in one dog, the lateral aspect of the pinnae. The most severe lesions were noticed on contact
sites where these dogs could have chewed on wood
shavings (lips, commisures of the mouth, buccal
mucosa and around the nose, with involvement of the
nasal planum and point of the chin). This finding suggests that contact is a factor strongly associated with
the development of lesions. The presence of lesions on
other mucosal contact sites (preputial, anal) would
suggest that moistening is another determinant in
causing dermatitis by dissolving the causal chemical
substance. In provocative studies in horses, wetting was
an observed causal factor as the risk of developing the
disease increased by a factor of 5 if the shavings had
been wetted.7 The morphology of the lesions was
similar to those observed in horse cases. The stomatitis
and dermatitis was characterized by bleeding erosions/
ulcerations, ulcerated nodules, crusting, dryness and
fissuring of the nasal planum and, in one dog, erythema
and oedema of the pinnae. Finally, the self-limiting
course of the condition after removal of the bedding

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J Declercq

was consistent with a cause-and-effect relationship. In

the reported horses, remission of symptoms occurred
within 5 to 7 days and in two animals after more than
30 days.3 In the two dogs reported here, cutaneous
lesions were regressing by day 13 in dog 2 and had
resolved in both dogs on day 23.
The only way to confirm suspected cases of Simarouba amara poisoning is to reproduce the disease by
provocative exposure, which was considered unacceptable for obvious ethical reasons.
Little information is available about the toxicity of
Simarouba amara and the causative toxin has not been
identified. Simarouba may produce systemic toxicity
and clinical signs reported in horses include liver
necrosis, a rise in hepatic enzymes and, less commonly,
neurological signs (lack of co-ordination in one horse;
tonic convulsion in another horse).4 Abnormalities
in hepatic biochemistry and indications of possible
neurological disease were recognized in dog 1. The
initial blood analysis demonstrated increased serum
concentrations of ALT and ALP. Unfortunately, as
subsequent serum biochemical analyses were incomplete, it was not possible to determine whether hepatic
enzyme activities normalized or progressed. The cause
of progressive hindlimb paresis in dog 1 was not determined and could have been either a toxic effect or an
unrelated finding.
Dermatitis associated with exposure to an arsenic
compound has been described in a dog.12 As the
reported lesions included severe ulceration and necrosis of the mucocutaneous junction of the upper lips and
because arsenic chemicals are commonly used wood
preservatives, a tentative diagnosis of arsenic poisoning was made at the time of initial admission. However,
arsenic poisoning was excluded by documenting normal amounts of arsenic in samples of hair, nails, urine
and wood shavings. In retrospect, arsenic poisoning
was unlikely as the use of arsenic wood preservatives is
strictly regulated. Chromated copper arsenate (CCA)
is the approved compound for use and CCA-preserved
wood poses no health risks.13
On the basis of the findings in this report, dog
owners using wood shavings for bedding should be
informed regarding the potential for toxic reactions. To
avoid similar problems, it is advisable to ask which tree
(wood) species are included in the shavings before
using the product. Wood poisoning must be considered
in the differential diagnosis of stomatitis, ulcerative
mucocutaneous disorders, scrotal dermatitis and disorders affecting the planum nasale.

AC K N OW L E D G E M E N T S
The author would like to thank Dr Ann Kuhweide,
for referring and management of the cases, and Dr
G Manigot, for sharing information based on experience
of an outbreak of erosive stomatitis in horses in Argentina. He is also very grateful to Dr Kris Baert and
Dr Siska Croubels, Department of Toxicology, Ghent
University, for performing the toxicological examination and for valuable advice.

REFERENCES
1. Boot P, Creemers J, Dubelaar JM et al. Soemaroepa. In:
Hout Vademecum. Almere: Stichting Centrum Hout,
2001: 338.
2. Bont F, Barr P, Pinguet P et al. Simarouba amara
extract increases human skin keratinocyte differentiation. Journal of Ethnopharmacology 1996; 53: 6574.
3. Barrandeguy M. Outbreak of erosive stomatitis in
Argentina. Equine Disease Quarterly 1999; 7: 3.
4. Matsumura T. Simarouba poisoning in horses Japan.
Equine Disease Quarterly 2002; 10: 2.
5. Wright B. Horse Disease Surveillance Report, Fall 1999.
Newsletter of the Ontario Ministry of Agriculture and
Food 1999; 7: 23.
6. Lewis R. Equine erosive dermatitis revisited. Animal
Health Centre Newsletter. Diagnostic Diary 1999: 9: 2.
7. Campagnolo ER, Trock SC, Hungerford LL et al.
Outbreak of vesicular dermatitis among horses at a Midwestern horse show. Journal of the American Veterinary
Medical Association 1995; 207: 21113.
8. Kim LM, Morley PS, McCluskey BJ et al. Oral vesicular
lesions in horses without evidence of vesicular stomatitis
virus infection. Journal of the American Veterinary Medical Association 2000; 216: 1399404.
9. True RG, Lowe JE, Heissen J et al. Black walnut shavings as a cause of acute laminitis. Proceedings of the 24th
Annual Convention of the American Association of
Equine Practitioners. St Louis, USA, 1978: 51113.
10. Galey FD, Twardock AR, Goetz TE et al. Gamma
scintigraphic analysis of the distribution of perfusion of
blood in the equine foot during black walnut (Juglans
nigra)-induced laminitis. American Journal of Veterinary Research 1990; 51: 68895.
11. Eaton SA, Allen D, Eades SC et al. Digital Starling
forces and hemodynamics during early laminitis induced
by an aqueous extract of black walnut (Juglans nigra) in
horses. American Journal of Veterinary Research 1995;
56: 133844.
12. Evinger JV, Blakemore JC. Dermatitis in a dog associated
with exposure to an arsenic compound. Journal of the
American Veterinary Medical Association 1984; 184: 12812.
13. Hall AH. Chronic arsenic poisoning. Toxicology Letters
2002; 128: 6972.

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Suspected wood poisoning caused by Simarouba amara

193

Rsum Deux Labrador Retrievers mles ont prsent des rosions/ulcrations accompagnes dhmorragie,
localises la muqueuse orale, les jonctions cutanomuqueuses (lvres, truffe, prpuce, anus) et des nodules
ulcrs sur le menton, et des lsions croteuses sur les coudes, les hanches et le scrotum. Un des chiens tait anorexique et abattu, avec des anomalies hmatologiques compatibles avec une atteinte hpatique et des signes neurologiques. Comme ces chiens avaient t exposs rcemment des sols recouverts de copeaux de Simarouba
amara et cause de la similitude des lsions celles rapportes chez les chevaux, un diagnostic dintoxication a
t pos. Ceci a t confirm par lvolution clinique, les lsions ayant disparu aprs lviction des copeaux de
lenvironnement.
Resumen Dos machos de Labrador Retriever desarrollaron erosiones/ulceraciones sangrantes, implicando la
mucosa oral, las uniones mucocutneas de los labios, plano nasal, prepucio, ano, ndulos ulcerados en la barbilla,
y lesiones costrosas en los codos, corvejones y escroto. Uno de los perros era anorxico y se encontraba abatido,
presentaba alteraciones hematolgicas compatibles con dao heptico y sntomas de enfermedad nerviosa.
Puesto que estos animales haban sido expuestos a un lecho que contena virutas de Simarouba amara y debido
a las notables similitudes de los sntomas clnicos con los que se describen en el caballo, se realiz un diagnstico
presuntivo de intoxicacin por madera. Esta suposicin fue ms tarde apoyada tambin por la evolucin clnica
ya que las heridas cutneas curaron cuando ces la exposicin de los perros al lecho.
Zusammenfassung Zwei mnnliche Labrador Retriever entwickelten blutende Erosionen/Ulcerationen im
Bereich der Mundschleimhaut, der muko-kutanen bergnge an Lippen, Nase, Prputium, Anus, ulzerierende
Knoten am Kinn und krustige Lsionen an den Ellbgen, Sprunggelenken und am Skrotum. Einer der beiden
Hunde war anorektisch und niedergeschlagen, hatte hmatologische Vernderungen wie bei einem Leberschaden
und Anzeichen einer neurologischen Erkrankung. Da diese Hunde krzlich mit einer Simarouba amaraSgemehl enthaltenden Schlafunterlage Kontakt hatten und aufgrund der offensichtlichen hnlichkeiten mit den
bei Pferden beschriebenen klinischen Anzeichen, wurde die mutmaliche Diagnose Holzvergiftung gestellt. Diese
Vermutung wurde durch den klinischen Verlauf bestrkt, bei dem Heilung der Hautlsionen eintrat, als die
Hunde nicht mehr der Schlafunterlage ausgesetzt waren.

2004 European Society of Veterinary Dermatology, Veterinary Dermatology, 15, 188193