Page 952 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

904 SECTION | XIV Poisonous Plants

VetBooks.ir Toxicity TAXUS BACCATA L. (TAXACEAE FAMILY)
The toxic parts are the seeds, flowers, and leaves. Young
Common Name: Yew
plants are more toxic than older plants. These plants con-
tain hepatotoxic pyrrolizidine alkaloids including: jaco- The yew (Taxus baccata) has been noted as the most poi-
bine, jacidine, jaconine, and retrorsine. Retrorsine is the sonous plant in all of Europe. The yew is a tree or shrub
most widely distributed pryrrolizidine alkaloids. of the family Taxaceae that will accommodate all types
Not all animal species are equally susceptible, since of soils and grows in shade and sun. It is planted in parks,
some species can activate, detoxify and eliminate pyrroli- gardens, and cemeteries, especially for ornamental fences.
zidine alkaloids. While cattle and horses are quite suscep- Other yew species are also toxic; T. cuspidala (Japanese
tible, needing, e.g., a dry-mass intake of Senecio jacobea yew) and T. canadensis (Canada yew) are widely planted
of only about 5% of their BW to be lethal, sheep and in gardens. Poisoning occurs in animals located in pas-
goats are more resistant, requiring intakes of several hun- tures, woods, or gardens or as a result of careless disposal
dred percent of their BWs (Cheeke and Shull, 1985). of yew clippings or leaves. All parts of the tree are poi-
Susceptibility is influenced by species-specific metabo- sonous, and all species of animals are susceptible. The
lism, age, sex and other temporary factors (i.e., biochemi- leaves are harmful at all stages of plant growth, and dry-
cal, physiological, and nutritional status). Young animals ing and storage do not lessen their toxicity. The sexes are
are generally more susceptible to pyrrolizidine alkaloids separate, and the pistillate plants bear bright scarlet fruit
than aged animals (Colegate and Molyneux, 2008). in the fall. The red flesh covers a hard seed, and although
the flesh is not poisonous, the seed is extremely poison-
ous. The sap of the tree contains volatile oils that are irri-
Clinical Presentation tants, and the leaves contain the alkaloid taxine (taxine A
and taxine B) and ephedrine and cyanide (hydrocyanic
Seneciosis is an acute and chronic hepatic insufficiency
acid). Taxine is found in all parts of the tree except the
caused by the ingestion of plants containing senecio.
fleshy red part of the berry. These compounds are capable
Poisoning occurs when the fresh plant is ingested (in pas-
of causing hypotension, bradycardia, and depressed myo-
tures) or when it contaminates hay or silage (Vos et al.,
cardial contractility and conduction delay, similar to digi-
2002). All animals can be affected, but cattle and horses
talis poisoning (Alexander et al., 1946).
are especially sensitive.
Poisoning can present after a latent period of weeks to
months. The clinical picture is characterized by a syn- Toxicity
drome of photosensitization, jaundice and CNS derange-
Chewing seeds has proven fatal to animals and humans.
ment. Clinical signs are extremely diverse and include
The foliage is even more toxic, and it is this that proves
anorexia, weight loss, poor hair coat, constipation, mild
so poisonous to cattle, sheep, goats, pigs and horses.
jaundice of the mucosa, reduction in vision followed by
There are probably more problems with children eating
blindness, ataxia with trembling, weakness, and drowsi-
these berries than any other, except possibly pokeweed.
ness. Generally, poisoning results in liver failure, jaun-
Chewing these seeds and then swallowing can cause seri-
dice, and death. The lesions are characterized
ous poisoning. The relatively greater resistance of rumi-
by enlargement and congestion of the liver, hepatitis
nants is probably due to the dilution of the ingested
(a cirrhotic form) with ascites, nephritis, and edema of the
material by the rumen contents. This effect may also
abomasum (Lorgue et al., 1996). Dose-dependent swelling
account for the individual variation in susceptibility of
of hepatocytes is the first cellular indication of pyrrolizi-
different animals and for the delay, sometimes seen in
dine alkaloid intoxication. Acute intoxication often pro-
cattle, before clinical signs of yew poisoning become
duces pan-lobular hepatocellular necrosis accompanied by
apparent (Humphreys, 1988).
hemorrhage and minimal inflammation. Serum biochemi-
cal changes include massive elevations in AST, SDH,
ALK and GGT activities with increased amounts of bili- Clinical Presentation
rubin and bile acids (Colegate and Molyneux, 2008).
The conditions of poisoning are by consumption of leafy
Most outbreaks occur in animals on pasture, but can
branches or lying in situ (fall) in the soil after harvest or a
occur in housed animals, fed hay contaminated by the
thunderstorm. The most common feature of yew poison-
foliage or seeds. In horses, photosensitization may
ing is sudden death (1 48 h depending of the amount
develop following plant ingestion. Pyrrolizidine alkaloids
ingested). The clinical signs observed are nervousness,
can be passed into the milk of lactating animals (Goeger
trembling, ataxia, dyspnea, and collapse (Barbier, 2005).
et al., 1982).
Bradycardia progressing to cardiac standstill and death