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 life-threatening 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).
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.
Lobelia inflata L
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.
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.
2- Gastric lavage, emesis ; treat symptoms as they appear,
supportive therapy ; Artficial respiration and oxygen ,
atropine 2 mg IM .
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
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
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
Digitalis purpurea L.
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.
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.
Hedera helix L
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 of more than 15 feet; sepals: 5, very short; petals: 5, fleshy; stamens: 5; ovarv: 5-celled, 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
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 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.
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.
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
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.
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 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).
Crotalaria sagittalis L
FAMILY: Fabaceae (Leguminosae)
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.
Datura stramonium L.—Jimson-weed; thornapple; Jamestown weed
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 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.
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.
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-2-thioaxazolidone) 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 muscaria (Fr.) S.F. Gray
Amanita phalloides Fries—Death cap
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.
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.
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.
Solanum nigrum L —; deadly nightshade; common nightshade; garden nightshade
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.
Found throughout the south, in gardens croplands, and the edge of woodlands.
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.
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.
Veratrum viride Ait.
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 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.
Phytolacca americana L.
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, 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.
Podophyllum peltatum L.
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, many-seeded; 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.
Rheum rhaponticum L.
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 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.
Rhus radicans L.
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.
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.
Ricinus communis L
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, 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.
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.
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).
Alberta, British, Columbia, Manitoba, Ontario, Quebec
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.
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.
Agitation, drowsiness, gait ,unconsciousness and vomiting.
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.
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.
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; 583-646; 989-1063. 94: 131-157; 471-528; 625-655.
Small, E., Cronquist, A. 1976. A practical and natural taxonomy for Cannabis. Taxon, 25: 405-435.
Small, E., Cronquist, A. 1976. A practical and natural taxonomy for Cannabis. Taxon, 25: 405-435.
Smith, R. A. 1988. Coma in a ferret after ingestion of cannabis. Vet. Hum. Toxicol., 30: 486.