Download GENUS: Lobelia

POISONOUS PLANTS
Introduction to Poisonous Plants
Plants contain a large number of biologically active chemicals. Some of these have
been found to be extremely useful for treating various human and animal diseases.
However, some plant constituents produce adverse health effects following exposure.
The onset of these adverse effects can be quite sudden or take some time to develop.
Fortunately, there are relatively few plants that, when ingested, cause acute lifethreatening illnesses.
The diversity of chemical substances in plants is quite amazing. In many instances,
the role that a particular chemical plays in the normal ecology of the plant is
unknown. In many cases, the presence of certain chemicals in plants is believed to
confer some degree of protection from plant predators such as insects and ruminants.
There are a number of broad categories of toxicologically significant plant
constituents. These include alkaloids (basic substances with nitrogen bound in a ring
structure), amino acids, peptides and proteins, glycosides (chemical groups such as
cyanide linked to sugars), acids (oxalic acid), terpenes (substances that contain the
branched 5-carbon skeleton of isoprene), phenolics and tanlnins, and essential oils
(various steam-volatile, primarily lipophilic plant metabolites stored in special plant
organs and percieved by man through the stimulation of the sense of smell) .
A number of factors can contribute to an animal being poisoned by plants.
Fundamentally, there is the requirement that a sensitive species of animal ingest, or
otherwise be exposed to, a toxic plant at an appropriate time. There are many
examples of species differences with regard to sensitivity to the toxic effects of
plants. In addition, it is possible for species to adapt to a potentially toxic plant if
exposure is allowed to occur over a period of time. For example, ruminants adapted to
oxalate-containing plants such as Halogeton glomeratus can tolerate concentrations
that are lethal to non-adapted animals .
Ingestion of a potentially toxic plant is the number one route of poisoning in animals.
It is important to emphasize that many, but certainly not all, toxic plants are not very
palatable. Therefore, if given the choice, animals will avoid ingesting them even
though they may be prevalent in the environment of the animal. In these situations,
animals will often eat these plants only when other suitable feedstuffs are not
available or when the animal is not able to selectively avoid the plants. The later
situation may occur when toxic plants or plant parts such as seeds are inadvertently
incorporated into hays, silages, or other foodstuffs
The timing of ingestion may be critical. The concentrations of toxic constituents in
plants can vary from year to year, throughout the growing season of the plant, or as a
result of environmental factors such as drought. As one example, the accumulation of
potentially toxic concentrations of nitrate in forages most often occurs during periods
of drought that prevent the normal growth of the plants (Pfister, 1984).
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The diagnosis of plant poisonings can be difficult. Ingestion of many plants produce
non-specific clinical signs that must be differentiated from other disease conditions.
In addition, death due to toxic plant ingestion often does not result in characteristic
post-mortem lesions. Relatively few tests are available to detect plant toxins in either
ante-mortem or post-mortem samples. In many cases, the best way to support a
diagnosis of plant poisoning is to confirm the presence of a toxic plant in the animal's
environment (this will require positive identification of the suspect plant), to confirm
that the plant has been ingested (noting that the candidate plants have been chewed
and/or finding plant fragments in vomitus or gastrointestinal tract samples), and to
correlate clinical findings, where possible, with those know to be associated with the
suspect plant.
Unfortunately, there are few antidotal therapies for treating plant poisonings. The best
approach for treating intoxicated animals often involves routine decontamination
procedures such as induction of emesis (in appropriate species) and the administration
of activated charcoal and a cathartic to hasten elimination of the plant from the
gastrointestinal tract. In addition, symptomatic and supportive care need to be
provided. Obviously, continued exposure to the suspect plant should be stopped. For
a few plant poisonings, specific antidotes may be indicated; the treatment of cyanide
or nitrate intoxicated animals are examples (see Prunus and Nitrate-Containing Plants
for specific treatment protocols).
Information on poisonous plants can be found in a number of books. In addition,
veterinary toxicologists at veterinary schools and/or veterinary diagnostic laboratories
can provide information and identification services.
When submitted plants for identification it is important to collect specimens of the
entire plant, including the roots. Wet newspaper should be wrapped around the roots
of the specimen and the specimen placed in a plastic bag (it is acceptable to bend the
plant along its stem so that it will fit in the plastic bag). The specimen should then be
kept chilled until it arrives at the laboratory. Alternatively, plants can be dried and
pressed, although this will take more time for processing.
Indian tobacco
Lobelia inflata L
FAMILY: Lobeliaceae
Lobelia inflata is the source of the alkaloid lobeline used medicinally as a respiratory
stimulant and in veterinary science as a respiratory stimulant and ruminatonic.
DISTRIBUTION: Lobelias are found in wet soil, along streams, ponds, shores, and
in swamps. They are also cultivated for garden use.
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DESCRIPTION: In Lobelia the corolla is characteristically split to the base on the
upper side; bilabiate, having 2 lobes above and below, the upper lobes erect, the lower
lobes usually spread; stamens: protrude through the split in the corolla; the 2 lower
stamens bearded at the tip; inflorescence: a terminal bracteate raceme, flowers
alternately inserted; leaves: decurrent.
TOXIC PARTS: All parts of Lobelia are poisonous. Lobelia is toxic to animals at
0.5% of body weight.
TOXICITY: Toxicosis develops within 3 days. In livestock, symptoms are
sluggishness, salivation, diarrhea, anorexia, ulceration around the mouth, nasal
discharges, and eventually coma. Also, lesions of hemorrhage and mild gastroenteritis
may be present. In humans, symptoms include vomiting, sweating, pain, paralysis,
depressed temperature, rapid but weak pulse, collapse, coma, and death.
TOXIC PRINCIPLE: Toxins are pyridine alkaloids, especially lobeline.
TREATMENT :- 1- Contact physician and /or poison control centre.
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2- Gastric lavage, emesis ; treat symptoms as they appear,
supportive therapy ; Artficial respiration and oxygen ,
atropine 2 mg IM .
Lolium
Lolium temulentum L
FAMILY: Gramineae (Poaceae)
DISTRIBUTION: This weed of grain fields and waste places is uncommon in
Pennsylvania. Distribution records indicate sporadic occurrence in the southeastern
corner of the state.
DESCRIPTION: Darnel is an annual grass with stems: solitary or a few clumped
together, 4-8 dm tall; blades: glabrous beneath, scabrous above, 3-9 mm wide; spike:
1-2 dm; spikelets: placed edgewise to the rachis, 5-8 flowered; glume: firm, straight,
5-7 nerved, equalling or surpassing the uppermost lemma, 12-22 mm; lemmas:
obtuse, awned, or awnless.
TOXIC PARTS: The seeds and seed heads are considered poisonous.
TOXICITY: In humans, darnel poisoning is characterized by the sensation of
intoxication, ataxia, giddiness, apathy, various abnormal sensations, mydriasis,
nausea, vomiting, gastroenteritis, and diarrhea. It is rarely fatal.
TOXIC PRINCIPLES: The alkaloids temuline and loliine possibly are responsible
for toxicity of darnel. It also has been suggested that toxicity may be due to a parasitic
fungus living within the seed head.
TREATMENT: 1- Contact physician and /or poison control centre
2- Gastric lavage, emesis ; treat symptoms as they appear,
supportive therapy ;
Artficial respiration and oxygen
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Wild lupine
Lupinus perennis L
FAMILY: Fabaceae (Leguminosae)
DISTRIBUTION: Wild lupine is found in a diversity of habitats ranging from dry
open woods and clearings to moist sandy soil.
DESCRIPTION: Wild lupine is an erect, perennial shrub: 2-6 dm tall, thinly
pubescent; leaves: palmately lobed; lower leaves: 5 cm long, 7-11 leaflets; petioles:
2-6 cm; racemes: erect, 1-2dm, numerous, blue varying to pink or white flowers;
flowers: 2-lipped; calyx: the upper lip. 4 mm, 2-toothed; the lower entire, 8 mm;
corolla: standard, 12-16 mm, half as wide; wings united toward the summit;
stamens: 10, monadelphous; filaments forming a closed tube for half their length;
pod: pubescent, 3-5 cm long, oblong, flattened
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TOXIC PARTS: The foliage and seeds are considered poisonous. The vast literature
on toxicity of Lupinus spp. mainly involves western taxa, e.g rangeland species.
Toxicity may vary among species, produce different symptoms in various classes of
livestock, and fluctuate according to season and habitat.
TOXICITY: The reactions to ingestion are paradoxical. Some animals show
depression, others excitation. Respiratory problems generally develop with labored
breathing, coma or convulsions, and death.
TOXIC PRINCIPLES: The majority of the more than 20 alkaloids isolated from
Lupinus are quinolizidine alkaloids with some piperidine and other components
known Lupanine and lupinine are well-studied compounds from Lupinu;, spateine
appears less well characterized. In Europe, the disease called lupinosis is attributable
to mycotoxins produced by the fungus Phomopsis leptostomiformis, which grows on
Lupinus species.
N.B. Because alkaloids remain toxic in dried plants, contaminated hay also is
poisonous. Alkaloids are generally more concentrated in plants after flowering,
perhaps due to higher concentrations in the seeds..
TREATMENT: as
in case of Lolium
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Foxglove
Digitalis
Digitalis purpurea L.
FAMILY: Scrophulariaceae
DESCRIPTION: Biennial herb, erect to 4 ft tall. Leaves vary with species.
Flowers tubular-bell shaped, spotted on inside, borne in pendant raceme,
from plant stalk. Color varies from white, yellow, lavender, violet, to purple.
Wild type - purple. Fruit is a small dry capsule containing many seeds.
DISTRIBUTION:Common flowering garden plant. Common in open rich
land, roadsides in northern California to British Columbia.
TOXIC PRINCIPLES :Toxic principles are many cardiac or steriod
glycosides, including digitoxin, digoxin, and gitoxin. Dry plants still toxic,
flowers, seeds, leaves, and vase water toxic.
Primary mechanim is thought to be inhibition of the Na+ - K+- ATPase.
Decreases intracellular K+ levels. Leads to high grade cardiac block, and
increased vagal tone. Loss of pacemaker function.
TOXICITY: In humans toxic reactions include gastric upset, nausea, diarrhea,
abdominal pain, severe headache, pulse and cardiac rhythm abnormalities, mental
irregularities, drowsiness, tremors, convulsions, and death. In livestock symptoms are
similar and include bloody stools, lack of appetite, and the urge to urinate. . Lethality
due to cardiac arrhythmias
TOXIC PARTS: The herbage, both fresh and dried, contains powerful, highly toxic
compounds.
TREATMENT
Emesis if recent exposure, in animals that can vomit. Atropine for
bradycardia to prevent additional vagal stimulation during passage of
endotracheal tube to establish respiration. Activated charcoal, saline
cathartic, cholestyramine (for enterohepatic circulation). Administration of
antidigitalis antibody fragments (Digibind). Monitor potassium levels
hourly. Phenytoin to to improve AV conduction, increase heart rate, treat
complete heart block. Avoid calcium containing solutions.
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English ivy
Hedera
Hedera helix L
FAMILY: Araliaceae
DISTRIBUTION: Hedera helix is a cultivated plant grown indoors as a pot subject
or outside, usually as a wall or ground cover.
DESCRIPTION: English ivy is a trailing or climbing vine with a diversity of leaf
shapes ranging from ovate, rotund to variously 3- to 5-lobed or angled, leaves: firm,
evergreen; flowers: small, greenish, produced only when the branches reach a height
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of more than 15 feet; sepals: 5, very short; petals: 5, fleshy; stamens: 5; ovarv: 5celled, 1 style; fruit: a round, 3- to 5-seeded berry.
TOXIC PARTS: The black berries and leaves of English ivy are poisonous if
consumed in quantlty.
TOXICITY: Hedera helix is a purgative that produces local irritation, excessive
salivation, nausea, excitement, difficulty in breathing, severe diarrhea, thirst, and
coma.
TOXIC PRINCIPLES: The toxic substance is hederin, a glycoside of the steroidal
saponin hederagenin.
TREATMENT: - Gastric lavage, emesis ; paraldehyde (2-10 cc) IM; Artificial
respiration and oxygen
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Ergot
Claviceps
Claviceps spp.—
FAMILY: Ascomycetes
OCCURRENCE: Claviceps parasitizes the ovary of grasses, especially rye, wheat
(durum is most susceptible), barley, and some wild species. Infection occurs when
host flowers begin to open.
DISTRIBUTION: Ergot occurs on pasture land grasses or hay and cereal grains from
cultivated fields.
TOXIC PARTS: The poisonous part is the sclerotium (ergot body), a grain-shaped
mass that replaces the grass ovary. This varies in size from the same as the grain to 4
times larger. The fungal mass, homogeneous and white when cut open, is shed with
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the grass and acts as the overwintering phase of the fungus. Federal law prohibits use
of cereal grains containing more than 0.3% sclerotia by weight.
TOXICITY: Two syndromes are produced by ingestion: 1) gangrenous, and 2)
convulsive. Ingestion of small amounts daily over a short period results in necrosis of
tissues in the extremities, producing dry gangrene. Gangrene is caused by constriction
of the blood vessels with blockage of circulation. This results in lameness, coldness,
and insensitivity to pain of the affected part. In some instances, serum seepage can
cause secondary infection, which may be associated with nausea, vomiting,
abdominal pain. and constipation or diarrhea. Pregnant animals spontaneously abort.
Mucus membranes of the oral cavity may be inflamed or damaged. In humans
gastrointestinal distress and headache may be present. Fowl may lose their combs and
beaks. Convulsive ergotism results from ingestion of large quantities of ergot. In
addition to the above syndrome, nervous symptoms appear, which are characterized
by hyperexcitability, paranoia, rapid pulse, and belligerence. In livestock, death may
result from dehydration or starvation within a few days or a month. In humans, whole
body spasms and delirium may be present,.
TOXIC PRINCIPLES: Alkaloids, amines, and other organic compounds are present
in ergot. The antihemorrhagic alkaloids probably are the major problem. Chemical
formulas are known for two dozen alkaloids, derivatives of lysergic acid. Compounds
include ergocryptine, ergocornine, ergocristine, ergotamine, ergosine, and ergonovine.
TREATMENT: Gastric lavage, emesis ; treat symptoms asw they appear, supportive
therapy.
Autumn crocus
Colchicum
Colchicum autumnale L.—
FAMILY: Liliaceae—the Lily Family (see Amianthium)
DISTRIBUTION: Autumn crocus is cultivated around homes and in gardens. It
rarely escapes and becomes naturalized.
DESCRIPTION: The flowers of Colchicum are chalice-shaped, with stamens: 6;
and styles: 3, long and slender. The large leaves appear in the spring with the
previous season’s seed-pod and die back during summer.
TOXIC PARTS: All parts are toxic, especially the bulb and seeds, Leaves are toxic
at about 0.1 % of an animal's weight.
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TOXICITY: Toxicosis includes vomiting; purging; weak, quick pulse;
gastrointestinal irritation; burning pain in mouth, throat, and stomach; and kidney and
respiratory failure.
TOXIC PRINCIPLES: The alkaloid colchicine and related compounds are
responsible for poisonings.
AFFECTED ANIMALS: Children have been poisoned by eating the flowers;
poisoning has been reported in all classes of livestock.
TREATMENT: Gastric lavage, emesis ;shock tjherapy; treat symptoms asw they
appear, supportive therapy.
Poison hemlock; spotted hemlock; deadly hemlock; poison parsley
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Conium
Conium maculatum L.
FAMILY: Umbelliferae (Apiaceae)
DISTRIBUTION: It is found in disturbed or waste areas such as roadsides and the
edges of cultivated fields. Poison hemlock was introduced into North America from
Europe and is and can be found in all areas of the U.S. except for dessert areas. Poison
hemlock can be found growing in the same kind of habitats as the water hemlock.
DESCRIPTION
Glabrous, branching, biennial herb, to 2 m tall with smooth, purple-spotted, hollow
spotted stems arising from a thick taproot. Very similar to the much more poisonous
Cicuta maculata and often confused with it. However, it usually has only one fleshy
taproot; there are no pithy partitions in a hollow area at the juncture of the root; stem
and upper stem leaves are divided. Also, the leaf veins of the poison hemlock run to
the tip of the teeth: those of the water hemlock run to the notches between the teeth.
flowering umbel: 4-6 cm wide (umbels are numerous); fruit: broadly ovoid, about 3
mm, laterally constricted; petals: white
Toxic PARTS: All parts of Conium maculatum are extremely poisonous. Some
studies reveal toxicosis at 0.25% (green-weight basis) of a horse's weight; 0.5% for a
cow's. In contrast, experimental feeding studies on a cow showed symptoms at 2% of
the animal's weight and produced death at about 4%.
TOXICITY:Gastrointestinal irritation, bloating, rapid but feeble pulse, nervousness,
trembling, staggering, coldness of thee extremities. Animals will also display
evidence of muscular incoordination and appear to have great abdominal pain. In
animals that die, breathing ceases due to respiratory paralysis before cardiac arrest.
Unlike water hemlock convulsions do not occur after eating poison hemlock.
Teratogenic effects due to ingesting poison hemlock that occur in calves and piglets
include crooked legs, cleft plate and kinked tails. Arthrogrypotic skeletal
malformations occur in calves when poison hemlock is ingested by pregnant cows
between 40-70 days of gestation. Similar skeletal lesions occur in pigs between days
40-61 of gestation. Cleft plates can occur in piglets if pregnant swine ingest poison
hemlock between days 30-45 of gestation.
TOXIC PRINCIPLES: Alkaloids Gamma-coniceine, coniine, N-methylconiine,
conLydrine, lambbaconiceine, and pesudoconhydrine. Toxicity levels vary with the
stage of growth (time of year), plant part, and the plant's geographic location. The
Conium alkaloids are similar in structure and function to nicotine. Gamma-coniceine
appears to be the major alkaloid in the vegetative stage. Flowers and immature fruit
contain coniine and N-methylconiine. In mature fruit the alkaloid is Nmethylconiine.
The root contains the least amount of toxins; mature seeds contain the greatest. It has
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been shown experimentally that the toxic principles in a plant vary even from hour to
hour.
TREATMENT: Gastric lavage, emesis ;Saline catharic;Artificial respiration and
oxygen;Anti-convulsents(e.g. parental short acting barbiturates).
Rattlebox
Crotalaria
Crotalaria sagittalis L
FAMILY: Fabaceae (Leguminosae)
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DISTRIBUTION: Occurs on dry open soil, waste places, and dry forest clearings.
DESCRIPTION: Crotalaria sagittalis is a small plant growing to less than half a
meter tall, with spreading hairs; leaf stipules: decurrent on the stem; leaves: simple,
entire, sessile, lanceolate flower on the stem to linear toward the top, 3-8 cm, to l.5 cm
wide; inflorescence: 2-4 flowered racemes; flowers: yellow standard, 8 mm;
stamens: 10, filaments fused; fruits: oblong, sessile pods, 2-3 cm. very inflated,
when dry the seeds rattling in the pods; seeds: flat, kidney-shaped, brown beans, 2.5
mm long.
TOXIC PARTS: The herbage and seeds are considered toxic. Monocrotaline is
present in the entire plant.
TOXICITY: Livestock show signs of stupor, labored breathing, weakness,
emaciation, paralysis, and death. Postmortem: gross lesions: hemorrhag, petechiae,
or large ecchymoses; organ congestion; abomasum, omasum, and gallbladder are
edematous; cirrhosis of liver in prolonged cases; histological lesions: pulmonary
changes, including emphysema, alternate with atelectasis and hemorrhage.
TOXIC PRINCIPLES: The presence of pyrrolizidine alkaloid monocrotaline. The
additional alkaloids, fulvine and cristpatine, have been isolated and identified as
macrocyclic esters of retorsine, which is also a toxic factor in the composite genus
Senecio (see Arctium).
TREATMENT: Gastric lavage, emesis ; treat symptoms asw they appear, supportive
therapy.; possibly treatment with crystalline methionine.
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Moon-lily
Datura
Datura stramonium L.—Jimson-weed; thornapple; Jamestown weed
FAMILY: Solanaceae
DISTRIBUTION: Jimson-weed occurs over the entire state, usually as an inhabitant
of dry soil and waste places, dumps, abandoned fields, and in cultivated crops,
especially soybeans and corn.
DESCRIPTION: This is an annual plant, 1.5 m tall with a pungent, "heavy" scent,
often branching in two equal forks; leaves: 2 x 1.5 dm, with a few teeth; calyx:
strongly angled in cross section (prismatic) and narrowly 5-winged; petals: fused into
a tube, white, opening in cloudy weather or evenings, 7-10 cm long; seed pod: 3-5
cm, ovoid, with prickles, opening by 4 valves.
TOXIC PARTS: All parts are poisonous~ especially seeds and leaves. Lethal
dosages for cattle may be 10-14 oz (0.06-0.09% of the animal's body weight). It is
estimated that 4-5 g of leaf or seeds would be fatal to a child.
TOXICITY: In the past several years Datura is one plant reported by the U.S.
National Clearinghouse for Poison Control Centers as the cause of death. Overdose
can occur from excessive ingestion of the herbal medicine Stramonium U.S.P., by
accidental poisonings, or intentional ingestion for illicit drug use. Symptoms vary in
time of appearance (a few minutes for decoctions to several hours for ingestion of
seeds). They include intense thirst, visual disturbance, fushed skin, and central
nervous system hyperirritability. Victims become delirious, incoherent, and perform
insensible antics. Heart beat may be rapid with elevated temperature. Subjects may be
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prone to violence, hallucination, convulsions, coma, and death, Ingestion of small
amounts produces symptoms; larger amounts, death. Symptoms in livestock
approximate those in humans Postmortem: gross and histological lesions are
nonspecific.
TOXIC PRINCIPLES: Solanaceous (tropane)
alkaloids including atropine,
hyosayamine (isomeric with atropine), and hyoscine (scopolamine). Datura alkaloids
are useful in medicine. Total content of alkaloids in a plant may be high, varying from
0.25-.0.7%. Concentration varies in different parts of the plant, during various stages
of development, and under varied growing conditions. The alkaloids are fewer
following a rainy period than during clear, dry weather, and concentration decreases
during the day but increases at night.
TREATMENT: Gastric lavage, emesis ; treat symptoms asw they appear, supportive
therapy.Artificial respiration and oxygen: Paraldehyde(2-10 cc)IM.
Mustards
Brassica
Brassica spp.
FAMILY: Cruciferae (Brassicaceae)
DISTRIBUTION: Some species of Brassica are cultivated plants; others are
troublesome weeds of fields, waste places, gardens, and roadsides.
DESCRIPTION: Taxonomically the genus has been organized in several different
fashions. Most members encountered in the Commonwealth bear saccate sepals,
yellow petals, and have 4 rounded staminal glands at the base of the ovary. The fruit
is terminated by a conspicuous beak, sometimes containing a basal seed.
TOXIC PARTS: Seeds and plants with seed capsules are poisonous.
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TOXICITY: The effects of Brassica poisoning vary depending upon the species of
plant consumed Brassica Kaber(DC) L. (charlock; wild mustard) is known to cause
gastroenteritis, pain, salivation, diarrhea, and upper digestive tract disturbances,
including irritation of the mouth. These symptoms also are associated with B. hirta
Moench. (white mustard) ingestion. Some cultivated mustards such as Brassica
oleracea var acephala DC (common kale), B. o. var capitata L. (cabbage), and B. o.
var. gemmifera Zenker, (Brussels sprouts), cause hemolytic anemia and
hemoglobinuria in some livestock. Goitrogenic substances (LS-vinyl-2thioaxazolidone) are known in kale, cabbage, and turnip (Brassica rapa L.),
TOXIC PRINCIPLES: The substance responsible for toxicosis is sinigrin, which in
the presence of the enzyme myrosinase, is converted to glucose, allyl isothiocyanate
(mustard oil), and potassium hydrogen sulfate. Mustard oils are poisonous. The
toxicity, by ingestion, of allyl isothiocyanate has been determined (in cattle) to be
0.001% of the body weight. Also, mustards occasionally contain toxic concentrations
of nitrate that may complicate toxicosis.
TREATMENT:; treat symptoms asw they appear, supportive therapy.
Fly amanita; fly mushroom; fly agaric
Amanita
Amanita muscaria (Fr.) S.F. Gray
Amanita phalloides Fries—Death cap
FAMILY: Amanitaceae
DISTRIBUTION: The amanitas are found singly or in numbers under hardwoods
and conifers from the spring through the fall.
DESCRIPTION: A. muscaria: cap: 8-24 cm across, convex or flat bright yellow to
orange red, surface rough with white or yellow wartlike spots; gills and stem: white;
stem: 8- 15 cm long and 20-30 mm thick; base of stem: bulbous; veil: white and
persistent.
A. phalloides: This species is taxonomically complex, and occasionally several
species are lumped under this name, The group includes A. verna (Bull ) Quel., A.
virosa (Fr.) Quel, and A, bisporiger Atk. Recent evidence suggests that A. phalloides
is rare and often confused with the more common A. brunnescens, which also is
poisonous. True A. phalloides has a yellowish-green to green cap and white veil and
gills; it is deadly poisonous. In A. brunnescens the cap is dark brown; in the deadly
poisonous A. virosa the fruiting body is pure white and the cap is devoid of warts.
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TOXIC PARTS: All parts of the amanitas are poisonous.
TOXICITY: The characteristic, well-defined symptoms of A. muscaria poisoning
may occur within 3 hours after ingestion. They include increased secretions from
salivary, lacrimal, and other glands; perspiration; and possible severe gastroenteritis;
much watery diarrhea plus retching and vomiting; possible labored breathing; pupils
that are rarely responsive; and possible auditory or visual hallucinations or confusion
occurring before or during the digestive upset. For A. muscaria, deaths are rare, but in
such cases delirium is followed by convulsions, then coma with death from
respiratory failure. In some severe cases, the patient may experience a profound sleep
lasting a few hours, then awake without symptoms or memory of the illness that
preceded.
Symptoms for the more deadly poisonous amanitas include a 10-hour lag period (6-15
hours) before onset of conditions. They begin as sudden, severe abdominal pain.
vomiting, and diarrhea. Blood, mucus, and undigested food are present in vomitus and
stool. Thirst, anuria, prostration. and restlessness are also present. If quantities of
mushrooms are consumed, death ensues in 2 days; more typically the disease lasts 6
to 8 days before death in adults, 4 to 6 days in children. Fever, hematuria, tachycardia,
hypotension, rapid volume depletion, and fluid and electrolyte imbalance also may be
present.
TOXIC PRINCIPLES: A. muscaria. The toxins are choline, muscarine, and
muscaridine The LD50 i.v. in mice is 0.23mg/kg. A. phalloides and other deadly
amanitas contain amanitine and phalloidine (complex polypeptides). The toxins
amanitin and amanin, also present, are highly toxic; the LD50, i.p. in albino mice is 0.1
mg/kg; for phalloidine it is 3 3 mg/g i.m.
TREATMENT: A. muscaria: (Gastric lavage with 1:2,000 tannic acid or 1:10,000
potassium permanganate) or emmesis); (5 – 0.1 to 0.5 mg either IM or IV, repeated as
necessary). Atropine sulfate is antidotal.
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A. phalloides: Mortality is 50-90%. First empty the stomach, then: (1-1 to 2
tablespoons in H2O): corticosteroids and both peritoneal dialysis and hemodialysis to
eliminate toxins and circumvent kidney failure. A high protein diet and intravenous
doses of protein hydrolysate may prevent liver damage, Antiphalloidian serum is
effective only when administered at the onset of symptoms; (26); thioctic acid,
charcoal hemoperfusion, and vitamin C may be useful.
Black nightshade
Solanum
Solanum nigrum L —; deadly nightshade; common nightshade; garden
nightshade
FAMILY: Solanaceae
DESCRIPTION : Annual, thornless, essentially glabrous herb, .1 to 1 m tall.
Leaves alternate, sinuately or coarsely toothed, 5 to 10 cm long, 2 to 5 cm
wide. Flowers white, 6 to 8 mm broad. Fruit shiny, black when ripe, several
seeded, 5 to 9 mm in diameter.
DISTRIBUTION
Found throughout the south, in gardens croplands, and the edge of
woodlands.
TOXICITY
A toxic glycoalkaloid and a steroidal alkaloid, solanine and solanidine, have
been isolated from this group of plants. Toxicity of a given species varies
with environment, portion of plant ingested or degree of maturity. Green
berries are more toxic than red or black berries which are more toxic than
leaves which are more toxic than stems or roots. The berries of both
Carolina horse nettle and black nightshade are green when immature.
However, horse nettle berries turn yellow when mature and nightshade
berries become black.
All classes of livestock and humans have been poisoned. The acutely
poisoned animal is characterized by irritation of the mouth and
gastrointestinal lesions or nervous signs such as lethargy, drowsiness,
salivation, dyspnea, weakness, paralysis, coma, death. Chronically poisoned
animals may demonstrate unthriftiness, jaundiced mucous membranes,
ascites and constipation.
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TOXIC PARTS: The berries and vegetation are poisonous. The toxicity is not lost in
drying and may be toxic in hay.
TOXIC PRINCIPLES: Solanine, a saponic glycoalkaloid that breaks down into a
sugar (solanose) and an alkamine (solanidine), is responsible for poisoning. The
alkamines are steroidal. Concentration of solanine may increase 10 times with
maturity.
TREATMENT: Gastric lavage, emesis ; treat symptoms asw they appear, supportive
therapy. Paraldehyde (2-10 cc)IM.
False hellebore
Veratrum
Veratrum viride Ait.
FAMILY: Liliaceae
DISTRIBUTION: This plant grows in swamps, low wet places, meadows, pastures,
and open woods.
DESCRIPTION: Veratrum viride is a coarse, tall, unbranched herb, 3 to 6 feet,
perennial from a short rhizome; leaves: large (appearing pleated), alternate in 3-ranks,
broad, the bases sheathing the stems; panicle: terminal, composed of greenish-yellow
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to purple, hairy flowers, about 1.5 cm across; tepals: 6, narrowed at base, not
glandular; stamens: 6, filaments free from the perianth; ovarv: tri-lobed, each lobe
terminating in a short style; fruit: an ovoid capsule, surrounded by the withered
perianth; seeds: large, flat, the embryo small and surrounded by a broad wing. See
Amianthium for illustration.
TOXIC PARTS: All parts are poisonous, especially the young, succulent growth in
spring.
TOXICITY: Species vary in physiologically active principles, yet symptoms of acute
poisoning are constant: salivation, vomiting, diarrhea, stomach pains, prostration,
depressed heart action, general paralysis, spasms, and dyspnea. Death may result. In
addition, hallucinations, headache, and a burning sensation of mouth and throat have
been reported. A species of Veratrum from western United States is known to cause
congenital malformation in lambs, including cyclopia (single median eye) and cranial
and lower jaw abnormalities. Ewe embryos in the primitive streak stage (12th and
14th day of gestation) develop deformities; fetal pituitary may be absent,
Postmortem: gross and histological lesions: not reported in acute toxicity.
TOXIC PRINCIPLES: The numerous known alkaloids exist as glyco - or ester
alkaloids and include jervine, pseudojervine, rubijervine, cevadine, germitrine,
germidine, veratralbine, and veratroidine. Plants also may contain cardiac glycosides.
TREATMENT: Gastric lavage, emesis ; Charcoal; Atropine; hypotensive drugs.
Pokeweed
Phytolacca
Phytolacca americana L.
FAMILY: Phytolaccaceae
Native to both America and Africa, this family is composed of plants with leaves:
alternate. entire; flowers: in racemes, bisexual (or unisexual); calyx: 4- to S- parted;
petals: absent; stamens: 3 to many; ovary: superior (or partly inferior); fruit:
drupelike berries. Phytolacca americana is the only plant of the Phytolaccaceae found
in Pennsylvania.
DISTRIBUTION: Found in rich, disturbed soils such as barnyards, lowlands. fields,
fencerows. and moist woodland.
DESCRIPTION: Phytolacca americana can be identified by sepals: greenish white
to pink; flowers: 6 mm wide; racemes: 1-2 dm, pedunculate; infructescence:
nodding; stamens: 10; pistils: 10; fruit: 5-15 cells, a 1 cm thick, juicy (inky), shiny,
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dark-purple berry; plants: glabrous, perennial herbs, to 3 m tall, branched above;
leaves: lance-oblong to ovate, 1-3 dm; petioles: 1-5 cm.
TOXIC PARTS: All parts, but primarily the roots, are considered poisonous. Small
quantities (more than 10) of raw berries can result in serious poisoning of adults.
Fatalities in young children can result from the consumption of a few raw berries.
TOXICITY: The more common symptoms are gastrointestinal cramps, vomiting,
diarrhea, and convulsions in severe cases. Perspiration, prostration, weakened
respiration and pulse, salivation, and visual disturbance are possible symptoms. Death
may result. Humans experience an immediate burning sensation in the mouth upon
consumption. Postmortem: gross lesions: mild to severe gastroenteritis; congestion
of internal organs; histological lesions: stomach ulcerations with hemorrhage.
TOXIC PRINCIPLES: The physiologically active principles have been identified.
Suspected compounds include saponin, together with lesser amounts of the alkaloid
phytolaccin.
TREATMENT Gasric lavage and emesis; Treat symptoms as they appear, supportive
therapy; peripheral plasmacytosis with potential immunosuppressive properties.
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May apple
Podophyllum
Podophyllum peltatum L.
FAMILY: Berberidaceae
DISTRIBUTION: Podophyllum is found in open clearings in moist woods and along
road banks as a migrant from adjacent wood lots. It is also encountered in wet or
damp meadows, open fields, and pastures.
DESCRIPTION: Podophyllum can be recognized by sepals: 6, falling early; petals:
6-9, white, 1-2 cm long; stamens: twice as many as the petals; ovary: oval, with a
large sessile stigma; fruit: yellow when ripe, 4-5 cm, fleshy pulp edible, manyseeded; plants: in colonies; perennial from a rhizome; the flowering stem with two,
umbrella-shaped leaves and a short-peduncled, solitary flower in the axil.
TOXIC PARTS: The herbage, rootstock, and seeds are poisonous.
TOXICITY: In humans and livestock symptoms vary and generally involve severe
gastroenteritis, diarrhea, vomiting, and violent catharsis.
TOXIC PRINCIPLES: Podophyllin, a resinoid toxin, is a very complex mixture of
lignins (including podophylloxin, alpha- and beta- peltatins) and flavonols Sixteen
physiologically active, well-characterized compounds have been isolated in
podophyllin. Chemical analysis reveals 3-6% resin and 0.2 – 1.0% podophyllotoxin,
picropodophyllin, quercetin, and peltatins.
TREATMENT: Gasric lavage and emesis; Treat symptoms as they appear,
supportive therapy; Charcoal; Antidiarrheal agents.
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Rhubarb
Rheum
Rheum rhaponticum L.
FAMILY: Polygonaceae
This family of plants contains at least 40 genera and more than 800 species, all with
jointed stems. Other characters include leaf stipules: united into a tubular sheath
called an ocrea; sepals: petaloid; petals: absent; fruit: an achene. The Polygonaceae
are not known for their poisonous members but for useful ones such as buckwheat and
various ornamental plants. Many elements in the family are weedy.
DISTRIBUTION: Rheum rhaponticum is a cultivated plant that occasionally escapes
from the garden.
DESCRIPTION: Rhubarb can be identified by leaves: large, basal, in clumps; ovate
with cordate bases; leaf blades: up to 1.5 m long, margins wavy; petioles: as long as
leaf blades, often red, stout; sepals: 6, greenish, whitish, or reddish; stamens: 6 (9);
fruit: a 3-winged achene.
TOXIC PARTS: The flat leaf blade is toxic.
TOXICITY: Human consumption of the rhubarb leaf results in gastroenteritis,
cramps. nausea, vomiting, weakness, respiratory difficulties, irritation of the mouth
25
and throat, poor clotting of the blood, internal hemorrhaging, coma, and death. In
hogs the symptoms are staggering, salivation, convulsions, and death.
TOXIC PRINCIPLES: Oxalic acid, uncharacterized soluble oxalates, and possibly
other toxins are believed responsible for poisonings.
TREATMENT: Gasric lavage and emesis with lime water, chalk, or calcium salts;
calcium gluconate, parentral fluids; Treat symptoms as they appear, supportive
therapy.
Poison ivy
Rhus
Rhus radicans L.
FAMILY: Anacardiaceae
Many readers will be surprised to learn that the edible cashew nut belongs to the same
family of plants as poison ivy and poison sumac. This predominantly tropical family
has leaves: alternate, compound; flowers: 5-merous, polypetalous, regular, with an
annular disc between the 5 stamens and ovary; ovary: 1-celled, containing I ovule;
fruit: a drupe.
DISTRIBUTION: Rhus radicans is commonly found in disturbed habitats, food
plains, cultivated fields, cemeteries, waste places, along woodland paths, margins of
woodlots, fencerows, roadbanks, along streams, and in urban situations around
buildings and yards.
DESCRIPTION: The species has complex and variable forms. Some are woody
vines that produce aerial roots and grow by straggling and climbing over other
vegetation. Ground-forms usually spread by rhizomes and develop dense colonies
with a few leaves crowded near the summit. Regardless of growth habit, poison ivy
always has three leaflets per leaf, with leaflets: ovate to subrotund, varying to
rhombic or elliptic, terminally acute to acuminate, basally cuneate; entire to
irregularly serrate or crenate; glabrous or thinly pubescent, petiolule of the terminal
leaflet longer than those of the lateral leaflets; panicles: axillary, 1 dm long, bearing
greenish-yellow flowers that mature into grayish white fruits, 5-6 mm; fruits: mature
August through November, conspicuous all winter; birds eat the ripe seeds with
impunity.
TOXIC PARTS: All parts of poison ivy, with the possible exception of the pollen,
contain toxins that cause dermatitis. It has been suggested that extremely sensitive
persons might contract poison from wind-blown pollen in spring when the plant is
flowering.
26
TOXICITY: Dermatitis ranging from minor reddened and itching skin to major
swelling, blisters, and weeping wounds can result from contact. Ingestion of leaves
can cause irritation of the mucosa and digestive tract; gastritis and death may result.
Animals probably are not as susceptible as humans to contact dermatitis due to hair
and fur. Ingestion of leaves or other plant parts by livestock could be dangerous and
result in death.
TOXIC PRINCIPLES: The toxin 3-n-pentadecylcatechol has been isolated from
Rhusradicans.
TREATMENT: For dermatitis: Antihistamines; Steroidal creams;ointments for skin
inflammation; in severe cases steroid injections can reduce the reaction.
Castor bean
Ricinus
Ricinus communis L
FAMILY: Euphorbiaceae
DESCRIPTION
Large, robust, annual (in the south) or perennial (in tropics and subtropics),
woody herb, to 3 m tall. Leaves alternate, up to 40 cm long, simple,
palmately 7 to 9 lobed, serrate with gland-tipped teeth. Flowers green,
27
inconspicuous; staminate flowers near the base and pistillate flowers mostly
near the top of a small panicle. Fruit a three-lobed capsule with a soft, spiny
exterior, 1.5 to 2 cm long; seeds three per capsule, resembling a female tick,
shiny, grayish-brown mottled with reddish-brown, 10 mm long and 6 to 7
mm wide.
DISTRIBUTION Castor bean is native to the tropics of Africa but is plated
in gardens throughout the U.S. for its large, striking appearance. Found
throughout our area and in the south where winters are mild; cultivated and
occasionally escaping and persisting in pinelands, waste places and
roadsides.
TOXICITY
Principle poisonous found in castor bean is a phytotoxin called ricin, also
termed a toxalbumin. Ricin may comprise up to 3% of the seed weight.
Another phytotoxin found in castor bean is ricinine, it is reported to be
goitrogenic, but the significance of this compound is not clearly established.
All parts of the plants re toxic, but the most toxic are the seeds. Horses are
most susceptible to poisoning but all livestock. Seeds ingested at 0.2% of
body weight have cased toxicosis in cattle and 0.01% of body weight was
toxic to horses. Toxicity is seen most often in spring and summer.
TOXIC PARTS: Seeds, and to a lesser extent foliage, are toxic; 1-3 seeds may be
fatal to a child, 2-4, to an adult.
TOXIC PRINCIPLES: The highly toxic glycoprotein ricin is responsible for
poisoning. This phytotoxin, a composite of various amino acids, consists of a
neutral alpha-chain capable of inhibiting protein synthesis and an acidic beta-chain,
which functions as a carrier and moiety that binds the toxin to cell surface.
Phytotoxins may act as antigens eliciting an antibody response.
TREATMENT: Intestinal detoxificaton and intestinal protectants, administered by
stomach tube are indicated. If dehydrated, large amounts of intravenous fluids assist
in recovery. Ascorbic acid increases survival. Support respiration.
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Cannabis sativa
Nomenclature:
Scientific Name: Cannabis sativa L.
Vernacular name(s): marijuana
Scientific family name: Cannabinaceae
General poisoning notes:
Accidental ingestion of marijuana (Cannabis sativa) by pets is an occasional problem.
Family pets or young children may accidentally ingest the plant, which may be stored
in plastic bags. A dog ingested hashish brownies and then exhibited various
symptoms such as hyperactivity, vomiting, somnolence, staggering, and glazed eyes.
In another case, in Edmonton, a pet ferret ingested the plant and became comatose
after experiencing sneezing bouts and ataxia. Although no fatalities of humans have
been reported, the effects on a young child accidentally ingesting marijuana are bound
to be very disturbing to the parents (Jones 1978, Smith 1988).
Geographic Information
Alberta, British, Columbia, Manitoba, Ontario, Quebec
Toxic parts:
The resins in the leaves are psychoactive in mammals, including humans. These
plants are cultivated indoors and outdoors for human use. The plants can overwinter
as seed in warmer parts of the country. The most common form that may be
accidentally ingested by humans and pets is marijuana that has been left in houses for
illegal human use.
flowers
leaves
Toxic principles:
Delta-tetrahydrocannabinol (THC) is the chemical most often cited as causing the
psychoactive compound in marijuana. This chemical affects humans and many other
mammals. Any children or pets that accidentally ingest quantities of marijuana may
show various symptoms, including coma.
Toxicity:-
Agitation, drowsiness, gait ,unconsciousness and vomiting.
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General symptoms of poisoning:
Nijhoff, The Hague, The Netherlands. 1444 pp.
Victorin, M. 1964. Flore Laurentienne. 2nd ed. Univ.
Montreal, Montreal, Que., Canada. 952 pp.
References:
Jones, D. L. 1978. A case of canine cannabis ingestion. N. Z. Vet. J.,
26: 135-136.
Smith, R. A. 1988. Coma in a ferret after ingestion of cannabis. Vet.
Hum. Toxicol., 30: 486.
References:
Bailey, L. H., Bailey, E. Z. 1976. Hortus
third. Revised. MacMillan, New York,
N.Y., USA. 1290 pp.
Boivin, B. 1966, 1967. Énumération des
plantes du Canada. Provencheria 6. Nat.
Can. (Que.) 93: 253-274; 371-437; 583646; 989-1063. 94: 131-157; 471-528;
625-655.
References:
Small, E., Cronquist, A. 1976. A practical and natural
taxonomy for Cannabis. Taxon, 25: 405-435.
References:
Small, E., Cronquist, A. 1976. A practical and natural
taxonomy for Cannabis. Taxon, 25: 405-435.
References:
Smith, R. A. 1988. Coma in a ferret after ingestion of cannabis. Vet. Hum. Toxicol.,
30: 486.
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