Poisonous Plants

Chapter 31

Poisonous Plants

INTRODUCTION

Spread over 1,575,107 square miles and endowed by nature with a wide variety of physical and climatological conditions, India possesses what is perhaps the richest and certainly the most varied flora of all other areas of similar size on globe. India has an area of culturable land of about 450 million acres, excluding a forest area of 83 million acres of which the total gross cropped area sown each year is approximately 285 million acres.

Plants are of great importance to us. India abounds in all kinds of food plants, spices, perfumes, timber, fibres, gums, etc., which have been known all over the world from ancient times. There are about 700 species of food and fodder plants including 260 species of valuable fodder grasses. Nearly 2,000 species of medicinally active plants have been found in India.

Many other plants are also present which contain certain constituents which, if introduced in the body in relatively small quantity, act deleteriously and may cause serious impairment of body functions or even death. They primarily injure the basic living principle the protoplasm. These plants are known as poisonous plants.

Recent studies have revealed that in India there are about 700 poisonous species belonging to over 90 families of flowering plants. Some of these are Ranunculaceae, Euphorbiaceous, Leguminosae, Solanaceae, Compositae, Apocyanaceae, Asclepiadaceae, Liliaceae, Gramineae, Arace, etc.

DEFINITION OF POISONOUS PLANTS

A poisonous plant is one which, as a whole or a part thereof, under all or certain conditions and in a manner and in amount to be taken or brought into contact with an organism will exert or cause death either immediately or by reason of cumulative action of the toxic property due to the presence of known or unknown chemical substance in it, and not by mechanical method.

The points which should be borne in mind before terming a plant as poisonous are:

The seeds of certain plants like aristida may pierce the skin giving rise to subcutaneous or intramuscular abscesses. These seed have bored into the salivary ducts of the cattle and caused injury. This action is purely mechanical, so it cannot be termed as poisonous plants.

All parts of the plant may not be poisonous. Seed of family Rosaceae contain dangerous amount of prussic acid but the outer fleshy portion of the fruit is eaten.

Certain plants are poisonous to one species and the same quantity may not affect the other species. Example: Belladonna is poisonous to most species but rodents like rabbit can have it in large quantities.

Some plants if eaten affect only a particular organ of the body. It does not cause serious body harm but render the organ unable to carry on their normal functions, e.g., Senecio of sunflower family causes hepatic cirrhosis in man and animals and prevent the liver from carrying out its normal functioning.

Certain plants lose their toxicity on being dried or cooked, e.g., species of Ranunculaceae is toxic in green state but can be used as food when dried.

Certain plants provide food but under certain conditions produce varying amount of poisonous substance, e.g., potato is a vegetable but at time of sprouting produces dangerous amount of solanine.

Certain plants like khesari (Lathyrus sativus) give rise to pathological conditions when fed in large doses for prolonged use.

TOXIC CONSTITUENTS OF THE PLANTS

By the metabolic activity the plants not only produce food material but also certain other substances such as alkaloids, glycosides, toxic proteins, bitter principles, etc. Many of these constituents are harmful to animal life, at least under certain conditions and the plants containing these principles which are capable of producing harmful effect are known as poisonous plants. These constituents can be divided into different groups:

Vegetable Base:

It constitutes nitrogenous vegetable bases like amines, purines and alkaloids.

Amines: Derived from amino acid and are building materials for proteins. Gives poisonous character to certain mushrooms.

Purines: Form active principle of certain tropical plants such as tea, coffee, guaraila.

Alkaloids: Alkaloids form the most important group of vegetable base. These are complex heterocyclic nitrogenous compounds having a basic nature and are mostly tertiary amines. These have profound physiological action and in many cases are of intense poisonous nature. These plants contain bitter taste and sufficient protection from being eaten by cattle. Some of the poisonous alkaloids are—aconitine from aconite root, morphine from poppy capsules, emetine from ipecachuanha root, strychnine from nux vomica seeds, nicotine from tobacco leaves, curarine from curare, etc.

Glycosides: These are compounds which when split up with help of acids or enzymes yield a sugar and a carbohydrate known as aglycone. Among the glycosides, one of the important classes is cyanogenetic glycosides. These glycosides are harmless but give rise to toxic acids, e.g. amygdalin found in bitter almonds, phaseolunatin found in flax, prunasin found in wild cherry, etc. Some other glycosides which produce harmful components on hydrolysis are sinigrin in black mustard seeds, sinalbin in white mustard seed. Certain glycosides have direct toxic action such as digitoxin in Digitalis, ceberin in cerebra, thevetin in Thevetia, antiarin in Antiaris.

Saponin: Occurs in about 400 species belonging to 50 families. They are particularly toxic to cold blooded animals, such as fishes, frogs, insects, etc. Poisonous saponins are known as ‘sapotoxins’.

Bitter Principles: These possess a bitter taste and are found in a number of plants. Bitter principle include the different aloe bitter, which are found in inspissate juice of several species of aloe. These possess a characteristic nauseous and bitter taste and have purgative action, e.g. Santonin—a lactone found in sonic species of Artemrnmisi, Picrotoxin from Anamirata cocculus.

Toxic Proteins: These are also known as toxalbumin and have been observed in Leguminosae and in Euphorbiaceae, e.g. Abrin from Abrus precatorius, ricinin from Ricinus conmmnis, crotin from Croton tiglium. These toxalbumins are essentially blood poisons and arecharacterized by their property of agglutinating and precipitating the RBC’s.

Fixed Oils: These are compounds of glycerol with different kind of fatty acids containing sterols and other substances dissolved in them when heated they decompose giving of acrid acrolein vapours. These are insoluble in water and sparingly soluble in alcohol, freely soluble in ether, chloroform, benzene, etc. These generally have laxative property. The croton oil expressed from the seeds of Croton tiglium produces irritation to the skin; the vesicating action of croton oil is due to resin dissolved in it.

Essential Oils: These are odourous principles which are generally responsible for the odour of plants. They are generally found in combination with glycosides. They are volatile in steam. They sometime possess sharp burning taste, and locally have an irritating action. Large doses causes irritation to the GIT with diarrhoea, vomiting, pain, etc. They may cause haemorrhage and abortion, e.g. oils of juniper, savin, rue, parsley and pennyroyal. Some plants containing oils with toxic constituents are Artemnisia, Ruta, Mentha, Petroselinum, Anemone, ranunculus, Piper, Ferula, etc.

Organic Acids: Organic acids significant in poisonous point of view is oxalic acid, aprotoplasmic poison occurring in large number of plants in form of oxalates. Formic acid an irritant is also found in some plants especially in family utricaceae.

FACTORS DETERMINING THE TOXICITY OF PLANTS

It is surprising that some plants are fairly harmless to humans and animals under certain conditions, while in certain circumstances, they may prove to be poisonous. Some species of plants when grown in different environment produce different number of active principles. Variability in the poisonous content of the plant depends on various factors. Some of these are:

Correct Identification: Proper identification of the plants is very important and if there are several varieties of some species present each should be carefully examined in order to determine which contain highest number of active principles, e.g., there are two forms of Artemisia maritima present; in early stages of growth, one has deep reddish stem and other grayish. Both form brownish stems at maturity but it is only the form with deep reddish stem at early stages contains santonin.

Stages of Growth: The stages of growth of plants are perhaps the most important factor in determining the toxicity, e.g. sorghum when young and wilte or stunted contain fatal quantity of hydrocyanic acid. The greenberries of Solanum nigrum are harmful while the ripe one is edible. The unopened flower heads of Artemisia maritima yield greater amount of santonin than the opened ones.

Condition of Plant: Certain plants like potato and grasses which normally provide valuable food to man and animal may acquire toxic properties during sprouting; yams and certain aroids are poisonous when fresh, but lose their toxicity on drying or boiling.

Soil and Cultivation: Structure of soil, moisture present and temperature influence the metabolic activity of a plant. The difference in soil modifies the production of poison in plants, e.g. cinchona and oleander cultivation can enhance the active principles of the plants.

Climatic Conditions: Climatic conditions such as temperature, light, humidity may influence the metabolic properties of the plants. Ephedra contains large amount of active principles in areas of low rainfall. Alkaloid contents in these plants are less in rainy areas than in dry areas.

Toxic Part of the Plant: Different part of plant varies considerably in the amount of toxic principals contained in them. Thus the toxicity of the root, stem, leaves, flowers, fruits vary considerably even at same stage of growth. One part of the plant may he poisonous while other may not be, e.g. peach, plum kernels contain dangerous amount of hydrocyanic acid but outer portions of fruit are edible.

CLASSIFICATION OF POISONOUS PLANTS

Poisonous plants have been classified in a number of ways. The commonly acceptable classification is as follows.

Poisoning by Plants with Anticholinergic (Antimuscarinic) Poisons

Examples of plant genera associated with this syndrome:

Toxic Mechanism: Competitive antagonism of acetylcholine at the muscarinic subtype of the acetylcholine receptor, which is primarily located in the parasympathetic nervous system and the brain.

ATROPA BELLADONNA L.

Family

Solanaceae.

Common Names

Belladonna, black nightshade, deadly nightshade, nightshade, sleeping nightshade

Description

These perennial plants are about 3-feet high and are often cultivated in flower gardens. The stems are very branched with 6-inch ovate leaves. Solitary flowers, which emerge from the leaf axils, are blue-purple to dull red and about 1-inch long. The fruit is nearly globular, about 0.5 inch in diameter, and is purple to shiny black when mature. The root is a thick rhizome. The sap is reddish.

Toxic Part

The whole plant is toxic.

Toxins

Atropine, scopolamine and other anticholinergic alkaloids.

Clinical Findings

Intoxication results in dry mouth with dysphagia and dysphonia, tachycardia and urinary retention. Elevation of body temperature may be accompanied by flushed, dry skin. Mydriasis, blurred vision, excitement and delirium, headache and confusion may be observed.

Management

Initially, symptomatic and supportive care should be given. If the severity of the intoxication warrants intervention(hyperthermia, delirium), an antidote, physostigmine, is available. Consultation with a Poison Control Centre should be considered.

Poisoning by Plants with Calcium Oxalate Crystals

Examples of plant genera associated with this syndrome:

Toxic Mechanism: Upon mechanical stimulation, as occurs with chewing, crystalline calcium oxalate needles, bundled in needle-like raphides, release from their intracellular packaging (idioblasts) in a projectile fashion. These needles penetrate the mucous membranes and induce the release of histamine and other inflammatory mediators.

ALOCASIA SPECIES

Family

Araceae.

Common Names

Ahe Poi, ‘Ape, Cabeza de Burro, Chine Ape, Elephant’s Ear, Malanga Cara de Chivo, Malanga de Jardín, Papao-Apaka, Papao-Atolong, Taro.

Description

These erect perennials have single, long-stemmed, spearhead-shaped leaves that are prominently veined and often varicolored. Flowers appear on a spadix subtended by a greenish spathe similar to Colocasia. Individual plants may develop from runners (rhizomes).

Toxic Part

The leaves, stems and tubers may be injurious.

Toxins

Raphides of water-insoluble calcium oxalate and unverified proteinaceous toxins.

Clinical Findings

A painful burning sensation of the lips and mouth result from ingestion. There is an inflammatory reaction, often with edema and blistering. Hoarseness, dysphonia and dysphagia may result.

Management

The pain and edema recede slowly without therapy. Cool liquids or demulcents held in the mouth may bring some relief. Analgesics may be indicated. The insoluble oxalate in these plants does not cause systemic oxalate poisoning. Consultation with a Poison Control Centre should be considered.

Poisoning by Plants with Cardioactive Steroids/Cardiac Glycosides

Examples of plant genera associated with this syndrome:

Toxic Mechanism: Cardioactive steroids, termed cardiac glycosides when sugar moieties are attached, inhibit the cellular Na+/K+-ATPase. The effect is to indirectly increase intracellular Ca2+ concentrations in certain cells, particularly myocardial cells. Therapeutically, this both enhances cardiac ionotropy (contractility) and slows the heart rate. However, excessive elevation of the intracellular Ca2+ also increases myocardial excitability, predisposing to the development of ventricular dysrhythmias. Enhanced vagal tone, mediated by the neurotransmitter acetylcholine, is common with poisoning by these agents, and produces bradycardia and heart block.

CALOTROPIS SPECIES

Family

Asclepiadaceae.

Calotropis gigantea (L.) W.T. Aiton.

Calotropis procera (Aiton) W.T. Aiton.

Common Names

Calotropis gigantea: Bowstring Hemp, crown flower, giant milkweed, mudar, mudar crown plant, pua kalaunu. Calotropis procera: Algodón de Seda, French jasmine, giant milkweed, mudar, mudar small crown flower, small crown flower, tula.

Description

These treelike shrubs have ovate or elliptical thick, glaucous, rubbery, opposite leaves. The flowers appear in clusters along the branches; they have a prominent crown with recurved petals and a sweet, pleasant odor. Colours vary from creamy white to lilac, mauve and purple. The seeds have silky attachments (like other types of milkweed seeds), which emerge from pods as they split on drying. The two species differ in size: Calotropis gigantea grows to 15 feet; C. procera generally grows to under 6 feet and has correspondingly more diminutive plant parts.

Toxic Part

The latex has a direct irritant action on mucous membranes, particularly in the eye. Skin reactions to this plant may be caused by allergy rather than to a direct irritant action. All parts of the plant contain a cardioactive steroid and calcium oxalate crystals.

Toxins

An unidentified vesicant allergen in the latex, calcium oxalate crystals and cardioactive steroids resembling digitalis.

Calotropis gigantean

Calotropis procera

Clinical Findings

Human intoxications from this plant have not been reported in modern times. Ingestion of calcium oxalates causes a painful burning sensation of the lips and mouth. There is an inflammatory reaction, often with edema and blistering. Hoarseness, dysphonia and dysphagia may result. Poisoning would be expected to produce clinical findings typical of cardioactive steroids. Toxicity has a variable latent period that depends on the quantity ingested. Dysrhythmias include sinus bradycardia, premature ventricular contractions, atrioventricular conduction defects or ventricular tachydysrhythmias. Hyperkalemia, if present, may be an indicator of toxicity.

Management

Calcium oxalate toxicity: The pain and edema recede slowly without therapy. Cool liquids or demulcents held in the mouth may bring some relief. Analgesics may be indicated. The insoluble oxalate in these plants does not cause systemic oxalate poisoning.

Poisoning by Plants with Convulsant Poisons (Seizure)

Examples of plant genera associated with this syndrome:

Toxic Mechanism: A convulsion is the rhythmic, forceful contraction of the muscles—one cause of which is seizures. Seizures are disorganized discharges of the central nervous system that generally, but not always, result in a convulsion. There are various toxicological mechanisms that result in seizures including antagonism of gamma-aminobutyric acid (GABA) at its receptor on the neuronal chloride channel, imbalance of acetylcholine homeostasis, excitatory amino acid mimicry, sodium channel alteration or hypoglycemia. Strychnine and its analogues antagonize the postsynaptic inhibiting activity of glycine at the spinal cord motor neuron. Strychnine results in hyperexcitability of the motor neurons, which manifests as a convulsion.

AETHUSA CYNAPIUM L.

Family

Umbelliferon (Apiaceae).

Common Names

Dog parsley, dog poison, false parsley, fool’s cicely, fool’s parsley, lesser hemlock, small hemlock.

Description

This carrot-like plant is 8–24 inch high. The leaves resemble parsley but have a glossy shine on both sides and an unpleasant garlic-like odor. The white flowers and seedpods are inconspicuous and are formed on the stem tips. As the common name suggests, this plant may be consumed if mistaken for parsley.

Toxic Part

The whole plant is poisonous.

Toxin

Unsaturated aliphatic alcohols (e.g., aethusanol A) closely related to cicutoxin (from Cicuta species) and traces of coniine.

Clinical Findings

Ingestion can cause nausea, vomiting, diaphoresis and headache. Toxicity resembles poisoning from cicutoxin. However, the concentration of toxin is insufficient to cause serious effects in most cases. If poisoning occurs, onset of effect is rapid, usually within 1 h of ingestion. Symptoms include nausea, vomiting, salivation and trismus. Generalized seizures also may occur. Death may occur if seizures do not terminate.

Management

If toxicity develops, supportive care—including airway management and protection against rhabdomyolysis and associated complications (e.g. electrolyte abnormalities and renal insufficiency)—is the mainstay of therapy. Rapidly acting anticonvulsants, (i.e. diazepam or lorazepam) forpersistent seizures may be needed. Consultation with a Poison Control Centre should be considered.

Poisoning by Plants with Cyanogenic Compounds

Examples of plant genera associated with this syndrome:

Toxic Mechanism: Cyanogenic compounds, most commonly glycosides, must be metabolized to release cyanide. Cyanide inhibits the final step of the mitochondrial electron transport chain, resulting rapidly in cellular energy failure.

MALUS SPECIES

Family

Rosaceae.

Common Names

Apple, Crabapple, Manzana, Pommier.

Description

The apple is a deciduous tree with flowers that form in simple clusters. The fruit is a pome with seeds.

Toxic Part

Seeds are poisonous.

Toxin

Amygdalin, a cyanogenic glycoside.

Clinical Findings

Apple seeds that are swallowed whole or chewed and eaten in small quantities are harmless. A single case of fatal cyanide poisoning has been reported in an adult who chewed and swallowed a cup of apple seeds. Because the cyanogenic glycosides must be hydrolysed in the gastrointestinal tract before cyanide ion is released, several hours may elapse before poisoning occurs. Abdominal pain, vomiting, lethargy and sweating typically occur first. Cyanosis does not occur. In severe poisonings, coma develops and may be accompanied by convulsions and cardiovascular collapse.

Management

Symptomatic and supportive care should be given. Antidotal therapy is available. Consultation with a Poison Control Centre is strongly suggested.

Poisoning by Plants with Gastrointestinal Toxins

Many and various plant genera are associated with this syndrome.

Toxic Mechanism: Several different mechanisms are utilized by plant toxin to produce gastrointestinal effects, generally described as either mechanical irritation or a pharmacologic effect. Irritant toxins indirectly stimulate contraction of the gastrointestinal smooth muscle. The pharmacologically active agents most commonly work by stimulation of cholinergic receptors in the gastrointestinal tract to induce smooth muscle contraction, e.g. cholinergic, including nicotine-like alkaloids. Some plant toxins, e.g. mitotic inhibitors, toxalbumins alter the normal development and turnover of gastrointestinal lining cells and induce sloughing of this cellular layer. Hepatotoxins may directly injure the liver cells, commonly through the production of oxidant metabolites. Indirect hepatotoxicity may occur, as with the pyrrolizidine alkaloids.

SAPINDUS SPECIES

Family

Sapindaceae.

Sapindus Saponaria L.

Sapindus Drummond Ii.

Common Names

Sapindus Saponaria: A’e, Bois Savon Nette, False Dogwood, Indian Soap Plant, Jabon Cillo, Manele, Savon Nier, Soapberry, Wild China Tree, Wing leaf.

Sapindus Drummond Ii: Western Soapberry, Soapberry.

Description

Sapindus Drumond Ii: A deciduous tree growing to 50-feet tall with pinnate leaves containing eight to ten leaflets, each about 3-inch long. Flowers are small, yellowish white, in panicles. Fruits are yellow, turning black, up to 0.5 inch long.

Sapindus Saponaria: A tropical evergreen tree growing to 30 feet, leaves with seven to nine leaflets, each 4-inch long. Flowers are white and fruits are shiny orange, brown, about 0.75 inch in diameter. The fruit of these species has been employed as soap.

Toxic Part

The fruit is poisonous.

Toxin

Saponin, a gastrointestinal irritant, and a dermal irritant/ sensitizer.

Clinical Findings

Most ingestions result in little or no toxicity. The saponins are poorly absorbed, but with large exposures gastrointestinal effects of nausea, vomiting, abdominal cramping and diarrhoea may occur. Allergic sensitization to this plant is common and can cause severe dermatitis.

Management

If severe gastrointestinal effects occur, intravenous hydration, antiemetics and electrolyte replacement may be necessary, particularly in children. Consultation with a Poison Control Centre should be considered.

Poisoning by Plants with Mitotic Inhibitors

Examples of plant genera associated with this syndrome:

Toxic Mechanism: These agents interfere with the polymerization of microtubules, which must polymerize for mitosis to occur, leading to metaphase arrest. Rapidly dividing cells, e.g. gastrointestinal or bone marrow cells typically are affected earlier and to a greater extent than those cells that divide slowly. In addition, microtubules are important in the maintenance of proper neuronal function.

CATHARANTHUS ROSEUS

Family

Apocynaceae.

Common Names

Madagascar periwinkle, Bigleaf Periwinkle, Large Periwinkle, Periwinkle, Vinca (formerly known as Vinca rosea).

Description

The Madagascar periwinkle is a perennial herb with milky sap that is often cultivated on an annual basis. It has erect stems that bear dark glossy green, opposite, oblong-lanceolate leaves, 1–2 inch long, and bear solitary rose pink to white flowers about 1.5 inch across.

Toxic Part

The whole plant is poisonous. A tea made from the leaves and stems is used in folk medicine in the Caribbean and elsewhere.

Toxins

Vinca alkaloids, e.g. vincristine, clinically similar to colchicine—a cytotoxic alkaloid capable of inhibiting microtubule formation.

Clinical Findings

Ingestion may cause initial oropharyngeal pain followed in several hours by intense gastrointestinal symptoms. Abdominal pain and severe, profuse and persistent diarrhoea may develop causing extensive fluid depletion and its sequelae. Vinca alkaloids may subsequently produce peripheral neuropathy, bone marrow suppression and cardiovascular collapse.

Management

Aggressive symptomatic and supportive care is critical, with prolonged observation of symptomatic patients. Consultation with a Poison Control Centre should be strongly considered.

Poisoning by Plants with Nicotine-Like Alkaloids

Examples of plant genera associated with this syndrome:

Toxic Mechanism:

These agents are direct acting agonists at the nicotinic subtype of the acetylcholine receptor in the ganglia of both the parasympathetic and sympathetic limbs of the autonomic nervous system (NN receptors), the neuromuscular junction (NM receptors) and the brain.

NICOTIANA SPECIES

Family

Solanaceae.

Nicotiana attenuata Torr. ex S. Watson.

Nicotiana glauca Graham.

Nicotiana longiflora Cav.

Nicotiana rustica L.

Nicotiana tabacum L.

Common Names

Paka, Tabac, Tabaco, Tobacco.

Description

Nicotiana species may be annual or perennial; the latter generally are large shrubs or small trees. The five-lobed flowers,in large terminal panicles, are distinctively tubular, flare at the mouth, and may be white, yellow, greenish-yellow or red. The fruit is a capsule with many minute seeds. The leaves are simple and alternate, usually have smooth edges and often are broad, hairy and sticky.

Toxic Part

The whole plant is poisonous.

Toxin

The specific toxin depends on the species but involves chemically related alkaloids, for example, nicotine in Nicotiana tabacum and anilazine in N. glauca.

Clinical Findings

Acute intoxications result from ingestion of the leaves as a salad (particularly Nicotiana glauca) from the use of N. tabacum infusions in enemas as a home remedy, from the cutaneous absorption of the alkaloid during commercial tobacco harvesting, or from the ingestion of cigarettes or purified nicotine. Initial gastrointestinal symptoms may be followed by those typical of nicotine poisoning; these include hypertension, large pupils, sweating and perhaps seizures. Severe poisoning produces coma, weakness and paralysis that may result in death from respiratory failure.

Management

Symptomatic and supportive care should be given, with attention to adequacy of ventilation and vital signs. Atropine may reverse some of the toxic effects. Consultation with a Poison Control Centre should be strongly considered.

Poisoning by Plants with Pyrrolizidine Alkaloids

Examples of plant genera associated with this syndrome:

Toxic Mechanism: Pyrrolizidine alkaloids are metabolized to pyrroles, which are alkylating agents that injure the endothelium of the hepatic sinusoids or pulmonary vasculature. Endothelial repair and hypertrophy result in veno-occlusive disease. Centrilobular necrosis may occur following acute, high-dose exposures, presumably caused by the overwhelming production of the pyrrole. Chronic use is also associated with hepatic carcinoma.

SESBANIA GRANDIFLORA

Family

Leguminosae (Fabaceae).

Common Names

Bucolo, Coffee Weed, Colorado River Hemp, Egyptian Rattlepod, Gallio, ‘Ohai, ‘Ohai-Ke‘Oke‘O, ‘Ohai-‘Ula’Ula, Pois Valiere, Rattlebox, Scarlet Wisteria Tree, Serban, Vegetable Hummingbird.

Description

These annuals have green stems 3–8 feet tall that become woody; the entire plant can be shrublike. The compound leaves have numerous linear leaflets. The small, sweetpeashaped flowers are yellow dotted with purple. The fruits are curved seed pods.

Toxic Part

All parts of this plant are poisonous.

Toxin

Pyrrolizidine alkaloids.

Clinical Findings

There are no adequately documented human poisonings, and clinical descriptions are based on the nature of the toxin. Substantial short-term exposure may cause acute hepatitis, and chronic exposure to lower levels may cause hepatic veno-occlusive disease (Budd—Chiari syndrome), and in some cases pulmonary hypertension.

Management

There is no known antidote. Supportive care is the mainstay of therapy. Consultation with a Poison Control Centre should be considered.

Poisoning by Plants with Sodium Channel Activators

Examples of plant genera associated with this syndrome:

Toxic Mechanism: These agents stabilize the open form of the voltage-dependent sodium channel in excitable membranes, such as neurons and the cardiac conducting system. This causes persistent sodium influx (i.e. persistent depolarization) and prevents adequate repolarization leading to seizures and dysrhythmias, respectively. In the heart, the excess sodium influx activates calcium exchange, and the intracellular hypercalcemia increases both ionotropy and the potential for dysrhythmias.

ACONITUM SPECIES

Family

Ranunculaceae.

Aconitum columbianum Nutt.

Aconitum napellus L.

Aconitum reclinatum Gray.

Aconitum uncinatum L.

Common Names

Aconite, Friar’s Cap, Helmet Flower, Monkshood, Soldier’s Cap, Trailing Monkshood, Wild Monkshood, Wolfsbane.

Description

These perennial plants are usually erect, sometimes branched, 2–6 feet in height and have tuberous roots. They resemble delphiniums. The char act eristic helmet-shaped flowers grow in a raceme at the top of the stalk and appear in summer or autumn. The flowers are usually blue but may be white, pink or flesh toned. The dried seedpods contain numerous tiny seeds. Aconitum nacelles is the commonly cultivated monkshood.

Toxic Part

The whole plant is poisonous, especially the leaves and roots.

Toxin

Aconitine and related alkaloids, sodium channel activators.

Clinical Findings

Exposures are relatively uncommon. However, these plants are utilized in some herbal products (e.g. chuanwu, caowu, fuzi). Symptoms are predominantly neurological and cardiac. There is transient burning in the mouth after ingestion, followed after several hours by increased salivation, vomiting, diarrhoea and a tingling sensation in the skin (paresthesia). The patient may complain of headache, muscular weakness and dimness of vision. Bradycardia and other cardiac dysrhythmias can be associated with severe blood pressure abnormalities. Coma may develop, and convulsions may be a terminal event.

Management

Fluid replacement should be instituted with respiratory support if indicated. Heart rhythm and blood pressure should be monitored and treated with appropriate medications and supportive care. Recovery is generally complete within 24 h. Consultation with a Poison Control Centre should be strongly considered.

Poisoning by Plants with Toxalbumins

Examples of plant genera associated with this syndrome:

Toxic Mechanism: The protein toxins derived from these plants work specifically by inhibiting the function of ribosomes—the subcellular organelle responsible for protein synthesis. The toxins typically have two linked polypeptide chains. One of the chains binds to cell surface glycoproteins to allow endocytosis into the cell. The other chain upon cell entry binds the 60S ribosomal subunit and impairs its ability to synthesize protein.

RICINUS COMMUNIS L.

Family

Euphorbiaceae.

Common Names

African Coffee Tree, Castor Bean, Castor Oil Plant, Higuereta, Higuerilla, Koli, La‘Au-‘Aila, Man’s Motherwort, Mexico Weed, Pa‘Aila, Palma Christi, Ricin, Ricino, Steadfast, Wonder Tree.

Description

The annual growth is up to 15 feet or higher in the tropics. The large, lobed leaves are up to 3 feet across. It is also grown as a summer ornamental in temperate areas, where, depending on the cultivar, the leaves can be green to redpurple. Spiny fruits form in clusters along spikes. The fruits contain plump seeds resembling fat ticks in shape, usually mottled black or brown on white. The highly toxic seeds have a pleasant taste.

Toxic Part

The toxin is contained within the hard, water-impermeable coat of the seeds. The toxin is not released unless the seed coats are broken (e.g. chewed) and the contents digested.

Toxin

Ricin.

Clinical Findings

Ingested seeds that remain intact as they pass through the gastrointestinal tract generally do not release toxin or cause toxicity. However, if the seeds are chewed, pulverized or digested (i.e. if passage through the gastrointestinal tract is delayed), then the toxin is absorbed by intestinal cells causing mild to severe gastrointestinal toxicity. Effects depend upon the amount of toxin exposure and include nausea, vomiting, abdominal cramping, diarrhoea and dehydration. Variations in the severity of toxicity may be related to the degree to which the seeds are ground or chewed before ingestion. Parenteral administration (such as by injection or inhalation) or perhaps a large ingestion may produce life-threatening systemic findings, including multisystem organ failure, even with small exposures.

Management

Ingestion of intact seeds does not cause toxicity in the majority of cases and requires no therapy. Cases associated with gastrointestinal effects need to be assessed for signs of dehydration and electrolyte abnormalities. Activated charcoal should be administered. Intravenous hydration, antiemetics and electrolyte replacement may be necessary in severe cases, particularly in children. Consultation with a Poison Control Centre should be strongly considered.