Journal of Veterinary Diagnostic

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Diagnosis of Taxus (Yew) Poisoning in a Horse

Asheesh K. Tiwary, Birgit Puschner, Hailu Kinde and Elizabeth R. Tor
J VET Diagn Invest 2005 17: 252
DOI: 10.1177/104063870501700307

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252 Brief Communications

J Vet Diagn Invest 17:252–255 (2005)

Diagnosis of Taxus (Yew) poisoning in a horse

Asheesh K. Tiwary1, Birgit Puschner, Hailu Kinde, Elizabeth R. Tor

Abstract. A 2-year-old bay Thoroughbred colt was found dead overnight in its stall without a known history
of any illness, existing disease, or toxicant exposure. No information on the clinical signs before this animal’s
death was reported. A full necropsy was performed the next morning and revealed a mild to moderate degree
of endocardial hemorrhages in both ventricles. Microscopic examination of the heart showed an acute mild
mutifocal necrosis of papillary muscles and ventricles. The stomach content contained approximately 2% Taxus
alkaloids as determined by gas chromatography/mass spectrometry. In the past, diagnosis of Taxus poisoning
has been mainly based on history of exposure and the presence of plant parts in the gastrointestinal tract.
Pathological lesions associated with Taxus poisoning have not been published for horses. Therefore, this is the
first report of cardiac lesions in a horse after lethal exposure to Taxus. On the basis of these findings, it is
suggested that Taxus exposure needs to be considered in the differential diagnosis of horses that die suddenly
or have cardiac lesions suggestive of Taxus exposure, even if intact plant parts are not identified in the stomach
by the naked eye.
Key words: Animal; gas chromatography; heart; horse; mass spectrometry; plant; poisoning; Taxus; toxi-
cosis.

Taxus (yew) are popular ornamental shrubs that are
known to contain toxic alkaloids (taxines) and irritant oils.
When ingested, these plants are well known to cause sudden
death in a wide variety of animals and humans.20 Death is
considered to be an outcome of the cardiotoxic effects of
the taxines. Pathological lesions in animals associated with
Taxus poisoning are few and nonspecific. Among the studied
livestock species, horses are suspected to be most susceptible
to toxicosis, but pathological lesions have not been reported
previously.
In October 2003, a 2-year-old bay Thoroughbred colt was
found dead in its stall with no known history of any previous
disease or exposure to toxins. Gross necropsy examination
revealed ecchymoses on the endocardial wall of the ventric-
ular chambers and papillary muscles. Microscopic exami-
nation of the heart sections revealed an acute multifocal con-
traction band necrosis of the ventricular wall and the papil-
lary muscles (Fig. 1). In other sections of the myocardium,
there were occasional neutrophilic and lymphocytic infil-
trates in the interstitium. The liver was marked by rare peri-
portal neutrophilic infiltrates. The lung had areas of atelec-
tasis and showed marked congestion. The epithelial mucosa
of the small and large intestines showed a moderate degree
of autolysis and marked congestion of the capillaries in the
submucosa. The spleen, brain, kidney, and adrenals were
unremarkable. The lesions in the heart suggested exposure
to a cardiotoxin.
On the basis of the cardiac lesions, the stomach content
From the California Animal Health and Food Safety Laboratory
System, University of California–Davis, Davis, CA 95616 (Pus-
chner, Tiwary, Tor), and the California Animal Health and Food
Safety Laboratory System, San Bernadino, CA 92408 (Kinde).
1 Corresponding Author: Asheesh Tiwary, California Animal
Health and Food Safety Laboratory System, Toxicology Laboratory,
University of California, West Health Science Drive, Davis, CA
95616.
was analyzed for oleandrin and strophanthidin glycosides
present in the cardiotoxic plants oleander (Nerium oleander)
and summer pheasant’s eye (Adonis aestivalis), respectively.
Both plants have been reported to cause sudden deaths
among livestock in California.5,6,21 However, neither olean-
drin nor strophanthidin was detected by liquid chromatog-
raphy/mass spectrometry (LC/MS). In addition, the stomach
content was analyzed for cardiotoxins that included gitoxin,
digitoxin, gitoxigenin, and grayanotoxins I and III, using a
2-dimensional thin-layer chromatographic method,8 but none
of these cardiotoxins were detected. The stomach content
also tested negative for the alkaloids—anabasine, atropine,
coniine, deltaline, nicotine, scopolamine, and sparteine—us-
ing gas chromatography/mass spectrometry (GC/MS).9 The
brain contained a normal cholinesterase activity for horses.
The liver contained nontoxic concentrations of lead, arsenic,
zinc, copper, iron, mercury, cadmium, and manganese and
had a normal selenium concentration.
After the negative results for the cardiotoxic glycosides
and alkaloids, the stomach content was analyzed and found
positive for Taxus alkaloids using a modified GC/MS meth-
od.9 In brief, 5 g of the stomach content was extracted with
100 ml of 5% ethanol in ethyl acetatea (vol/vol) after the
addition of 1 ml, 10 N sodium hydroxide,a and 50 g sodium
sulfate.a A 40-ml aliquot was extracted with a total volume
of 15 ml of 0.5 N hydrochloric acid, after the addition of
100 ml hexane.a The aqueous extract was sparged with a
stream of nitrogen, and the pH increased to greater than 10,
using 10 N sodium hydroxide. The extract was then ad-
sorbed on a polymeric C18 SPE column.b The Taxus alka-
loids were eluted with 2 ml of ethyl acetate. The extract
was evaporated to dryness and derivatized with
bis(trimethylsilyl)trifluoroacetamide.c This extract was qual-
itatively analyzed using GC/MS and a 12 m 3 0.2 mm 3
0.33 mm HP-1 capillary column.d Three major chromato-
graphic peaks with retention times (Rt) of 17.1, 17.2, and
17.7 minutes were present in the extract of the Taxus bac-

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 Brief Communications
Figure 1. Equine heart. Taxus poisoning with acute contraction band necrosis of myocardium. HE. Bar 5 10 mm.
cata reference plant. The largest peak eluted at 17.2 minutes
and generated a mass spectrum with m/z 492 (relative inten-
sity 100), 420 (10), and 265 (10). A similar peak with iden-
tical Rt and spectrum was present in the stomach content of
the horse. The concentration of Taxus alkaloids in the stom-
ach content was estimated to be 2% on the basis of com-
parison of the peak area of the alkaloid eluting at 17.2 min-
utes with the peak area of the control matrix spiked with 1%
T. baccata at the same Rt. The chromatographic peaks at
17.1 and 17.7 minutes with mass spectra of m/z 420 (100),
212 (10), and 73 (25) and m/z 490 (20), 400 (40), 310 (10),
282 (100), and 73 (80), respectively, were also used to con-
firm the presence of Taxus alkaloids in the stomach content.
The match quality of these spectra was 93% and 98%, re-
spectively, when compared with the spectra identified in the
extract of T. baccata.
Feed microscopy was performed on the stomach content
to identify toxic plant parts. Plant materials from English (T.
baccata), Japanese (T. cuspidata), and Pacific/Western yew
(T. brevifolia) were obtained as reference materials for mi-
croscopic identification. The plant parts in the stomach con-
tent of the horse most closely resembled the Pacific/Western
yew with respect to the stomatal patterns, although the cel-
lular pattern was slightly different and was suggestive of a
hybrid or another species. English yew and Japanese yew
are the commonly encountered species in California and
North America.7 Interestingly, they are also more toxic than
the other known Taxus species. Reports of poisoning in an-
imals after exposure to Pacific/Western yew could not be
found in the literature.
On the basis of the pathological, toxicological, and mi-
croscopic findings and elimination of other possible causes
of sudden death, a diagnosis of Taxus poisoning was estab-
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253
lished. Taxaceae or ‘‘yew’’ family comprises 6–10 evergreen
tree or shrub species.4 They have alternate, stiff, flattened,
1–3 cm, needle-like, dark green leaves attached to the fibrous
stem.19 With the exception of the 1–2-cm-long fleshy red
fruit (aril) surrounding the hard brown seed, all plant parts
are poisonous throughout the year, whether fresh or dried.
The older, darker leaves are more toxic than the new ones.10
The foliage has significantly higher levels of taxines in win-
ter, than during other seasons.
Taxine alkaloids are relatively abundant in English and
Japanese yew and low in Pacific yew. Taxines are formed
from nitrogen-free polyhydroxylic diterpenes, esterified with
b-dimethylamino-b-phenylpropionic acid and acetic acid.20
The major alkaloids are represented by taxines A and B. The
taxines cause an increase in cytoplasmic calcium by inter-
fering with both the calcium and the sodium ion channel
conductance across the myocardial cells. This results in the
depression of cardiac depolarization, causing bradycardia,
arrhythmias, and diastolic cardiac arrest that are not influ-
enced by the autonomic nervous system. Taxine B induces
inotropic effects leading to an increased A–V conduction
time, widened QRS duration, and an absence of the P
wave.2,18,20 Taxine A has a milder effect. Therefore, taxines
do not act as cardiac glycosides; rather they act as a de-
pressant of the conduction system of the heart.1 Taxines are
rapidly absorbed, metabolized, conjugated in liver, and elim-
inated as conjugated benzoic acid (hippuric acid) by the kid-
neys. Herbivores have the ability to convert large quantities
of benzoic acid to hippuric acid and may have a greater
ability to eliminate taxines.7 In addition, yews also contain
nitriles (cyanogenic glycoside esters), ephedrine, and irritant
oils that are likely to be responsible for the colic and diarrhea
reported in animals exhibiting a subacute clinical syndrome.
254 Brief Communications

Figure 2. a, Stomach content from the horse that died of Taxus poisoning. No identifiable material resembling any part of the intact
plant was visible to the naked eye. b, Taxus baccata plant with characteristic 2–3-cm-long needle-like leaves. Bar 5 2.5 cm. c, Stomach
content from a cow that died of T. baccata poisoning. Intact plant parts/leaves (see top left corner) are often readily identified in rumen
contents, leading to a confirmatory diagnosis of exposure.

Clinical signs of Taxus poisoning in horses include inco-
ordination, nervousness, difficulty in breathing, bradycardia,
diarrhea, and convulsions, but sudden death is often all that
is seen. In an experimental study, 0.1% body weight of green
T. cuspidata foliage was administered to Shetland ponies.13
One hour after the exposure, the ponies were pawing the
ground as if hungry. In addition, the animals showed a de-
creased lip and tail tone, weak pulse, ataxia, trembling of
legs, and a respiratory grunt. On forced movement, the po-
nies collapsed, became recumbent, and developed short con-
vulsions. Death followed 15 minutes after the onset of clin-
ical signs. No remarkable gross or histological findings were
observed on necropsy; however, the heart was not examined.
In another study, horses that died from exposure to Japanese
yew had congested and edematous mucosa of the stomach
and the small intestine.10 However, these gastrointestinal (GI)
tract lesions are not consistent because of the acute nature
of the poisoning. Death in most animals occurs within a
couple of hours to a few days after toxic-dose exposure but
usually minutes after the onset of clinical signs.1,19 Sudden
death may be the only sign in some cases. Death is consid-
ered to be because of cardiac arrhythmias, together with car-
diovascular collapse or respiratory failure (or both). Many
of the discussed adverse clinical signs may be because of
secondary anoxia.7
Horses are more succeptible to Taxus poisoning than cat-
tle, sheep, goats, pigs, dogs, and fowl.20 Ingestion of 0.5%
body weight of yew leaves may be lethal to an adult cow,
whereas 0.05% body weight ingestion could kill a horse.19
Reported minimum lethal dose for yew leaves are as follows:
200–400 mg/kg body weight for horses (0.02–0.04%); 100–
200 g of T. baccata have been reported to be toxic to horses
and sheep; 500 g in cattle; 75 g in pigs; and 30 g in dogs
and fowl.15 Poisonings have also been reported in humans,
deer, goats, burros, alpacas, llamas, rabbits, rats, and mice.7
Starvation, boredom, pica, feed contamination, and plant
trimmings increase the risk of consumption of this otherwise
relatively unpalatable plant. Malicious poisoning should also
be considered.
Association between pathognomonic/cardiac lesions and
Taxus poisoning in horses have not been reported in the
literature. In some cases, GI tract inflammation has been
observed probably because of the irritant nature of the es-
sential oils that are present in Taxus species. In cattle, myo-
cardial hemorrhages and mild focal nonsuppurative intersti-
tial myocarditis have been reported after the ingestion of T.
cuspidata.1 Superficial hemorrhagic areas on the right ven-
tricular myocardium and the right atrium have also been re-
ported in cattle poisoned with T. baccata.16 The diagnosis is
usually based on a history of Taxus exposure or presence of
the Taxus plant in the surrounding area where the animal
was located, along with the evidence of its presence in the
stomach. In ruminants, presence of intact plant parts can
often be achieved by the naked eye. However, stomach con-
tents of horses are more difficult to assess because of more
extensive mastication and digestion processes (Fig. 2).
Therefore, confirmatory analyses may be required to estab-
lish a diagnosis of Taxus poisoning in horses. In the past,
taxine alkaloids have been identified using thin-layer chro-
matography and GC/MS techniques.12,20 More recently, LC/
MS has been applied to identify taxines in biological spec-
imens.3,11,14 Identification of taxine alkaloids in specimens
collected from an animal with suspect exposure provides a
definitive diagnosis.
Potential differential diagnoses for Taxus poisoning in-
clude vitamin E or selenium deficiency (or both), ionophore
toxicosis, metal toxicity/deficiency, or exposure to cardio-
toxic plants such as oleander (N. oleander), foxglove (Dig-
italis purpurea), lily of the valley (Convallaria majalis),
milk weed (Asclepias spp.), false hellebore (Veratrum cali-
fornicum), rhododendrons and azaleas (Rhododendron spp.),
and summer pheasant’s eye (A. aestivalis). Most cardiotoxic

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 Brief Communications
plants take more time, up to 12 hours, to manifest the clinical
signs. Unlike Taxus, most of the above-listed cardiotoxic
plants also result in GI irritation.
Treatment of animals that have developed clinical signs
of Taxus poisoning is nonspecific and directed toward de-
contamination and the stabilization of cardiovascular func-
tion. Activated charcoal and magnesium sulfate at 2 g/kg
body weight should be given through a stomach tube. Fluid
therapy and other supportive measures are also recommend-
ed to support the cardiovascular system. In humans having
ingested Taxus extract, atropine and lidocaine have been ef-
fective for a short time to control arrhythmias. However,
atropine may prolong the retention of toxic plant material in
the GI tract and its use has to be carefully evaluated. Nor-
epinephrine has also been used successfully. Sodium bicar-
bonate was reported to be of benefit in a human case but
did not prove to be beneficial in pigs infused with extract of
Taxus media.17
It is imperative to consider Taxus poisoning when evalu-
ating horses that die acutely or have cardiac lesions, even if
there is no history of exposure or no grossly identifiable
toxic plant material in the stomach content. The development
of cardiac lesions may be dependent on the dose, the dura-
tion of clinical signs, and the time until death occurs. At
lower doses, or exposure to less toxic species, the chances
of developing and detecting postmortem cardiac lesions
could be greater. Taxus species are commonly planted
around fairgrounds, arenas, and barns, and horse and live-
stock owners should be advised of their toxic potential. Spe-
cies other than the well-established Japanese and English
varieties should also be considered as a potential threat to
animals.
Acknowledgements. We thank Dr. John Reagor for the mi-
croscopic examination of the stomach content and plant ma-
terials, and Marcia Booth for providing plant reference ma-
terials. We thank the Toxicology staff of the California An-
imal Health and Food Safety Laboratory System for their
assistance with the analysis. We acknowledge Dr. William
Bell for his help and timely assistance in providing the di-
agnostic specimens.
Sources and manufacturers
a. Fisher Scientific, Pittsburg, PA.
b. Transgenomic, Omaha, NE.
c. Pierce, Rockford, IL.
d. Agilent, Palo Alto, CA.
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