Page 903 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

858 SECTION | XIV Poisonous Plants

VetBooks.ir (Panter and Keeler, 1989). Coniine predominates in late Canadian geese (Panter et al., 1999a). Poisoning in wild
geese eating small seedlings in early spring was most
growth and is found mainly in the seeds. γ-Coniceine is
recently reported (Panter, personal communication).
seven or eight times more toxic than coniine in mice.
This makes the early growth plant most dangerous in the Human cases of poisoning are frequently reported in the
early spring and the seedlings and regrowth again in the literature, and a case of a child and his father mistakenly
fall. This is also the time when green feed is limited to ingesting the plant has been reported. Field cases of tera-
livestock and may impact their propensity to graze this togenesis have been reported in cattle and swine and
plant. Seeds, which are very toxic, can contaminate poul- experimentally induced in cattle, sheep, goats, and swine
try and swine cereal grains (Panter and Keeler, 1989). (Panter et al., 1990a). Pigs become habituated to poison
Plants often lose their toxicity upon drying, but seeds hemlock, and if access to the plant is not limited, they
remain toxic as long as the seed coat is intact. will eat lethal amounts within a short time.
An analysis of a single plant of Conium, second-year There are no diagnostic lesions in poisoned animals,
rosette, revealed γ-coniceine levels of 387, 326, 198, 176, and diagnosis is based on clinical history of exposure and/
and 850 mg/g fresh plant for whole plant, root crown, or alkaloid detection in liver, urine, or blood. At necropsy,
stem, leaf, and green seed, respectively. Coniine was only the presence of plant in the stomach and a characteristic
detected in the leaf at 12 mg/g fresh plant (Panter and pungent odor in the contents with chemical confirmation
Gardner, unpublished data, 1994). of the alkaloids may be diagnostic.
The clinical signs of toxicity are the same in all spe-
cies and include initial stimulation (nervousness) resulting Prevention and Treatment
in frequent urination and defecation (no diarrhea), rapid
pulse, temporarily impaired vision from the nictitating Prevention of poisoning is based on recognizing the plant
membrane covering the eyes, muscular weakness, muscle and its toxicity and avoidance of livestock exposure when
fasciculations, ataxia, incoordination followed by depres- hungry. If a lethal dose has not been ingested, the clinical
sion, recumbency, collapse, and death from respiratory signs will pass spontaneously, and a full recovery can be
failure (Panter et al., 1988). expected. Avoidance of stressing animals poisoned on
Conium plant and seed are teratogenic, causing Conium is recommended. However, if lethal doses have
contracture-type skeletal defects and cleft palate like been ingested, supporting respiration, gastric lavage, and
those of lupine. Field cases of teratogenesis have been activated charcoal are recommended. Control of plants is
reported in cattle and swine and experimentally induced easily accomplished using broadleaf herbicides; however,
in cattle, swine, sheep, and goats (Panter et al., 1999a). persistent control measures are recommended because
Birth defects include arthrogryposis (twisting of front seed reserves in the soil will quickly reestablish a
legs), scoliosis (deviation of spine), torticollis (twisted population.
neck), and cleft palate. Field cases of skeletal defects and The mechanism of action of the Conium alkaloids is
cleft palate in swine and cattle have been confirmed twofold. The most serious effect occurs at the neuromus-
experimentally. cular junction, where they act as nondepolarizing blockers
In cattle, the susceptible period for Conium-induced like curare. Systemically, the toxins cause biphasic nico-
terata is the same as that described for lupine and is tinic effects, including salivation, mydriasis, and tachycar-
between day 40 and day 70 of gestation. The defects, dia, followed by bradycardia as a result of their action at
susceptible period of pregnancy, and probable mecha- the autonomic ganglia. The teratogenic effects are
nism of action are the same as those of crooked calf dis- undoubtedly related to the neuromuscular effects on the
ease induced by lupines (Panter et al., 1999a). In brief, fetus and have been shown to be related to reduction in
these alkaloids and their enantiomers in poison hemlock, fetal movement (Panter et al., 1990a). Likewise, cleft pal-
lupines, and N. glauca were more effective in depolariz- ate is caused by the tongue interfering in palate closure
ing the specialized cells TE-671, which express human during the reduced fetal movement and occurs during
fetal muscle-type nAChR, relative to SH-SY5Y, days 30 40 of gestation in swine, days 32 41 in goats,
which predominantly express autonomic nAChRs, in a and days 40 50 in cattle (Panter and Keeler, 1992).
structure activity relationship (Panter et al., 1990a; Lee
et al., 2006, 2008b; Green et al., 2010). In swine, sheep, WATER HEMLOCK (CICUTA SPP.)
and goats, the susceptible period of gestation is 30 60
days. Cleft palate has been induced in goats only when Water hemlock (Cicuta spp.) is among the most violently
plant or toxins were fed from 35 to 41 days of gestation poisonous plants known to humans. It is often confused
(Panter and Keeler, 1992). with poison hemlock because of its name, growth pat-
Field cases of poisoning have been reported in cattle, terns, and appearance. There are distinct differences in
swine, horses, goats, elk, turkeys, quail, chickens, and appearance, as shown in Figure 61.6.