Link to Plants Educational Resources
Poisonous plants are a large and, in general, less well researched area of toxicology. In many cases the exact toxins are not known and anecdotal reports of toxicity are the major source of information. Most poisonings are not serious, however there are some very important exceptions. Some serious toxins may have a considerable delay in the onset of symptoms (e.g. ricin, abrin, colchicine & amatoxins), so all poisonings should be taken seriously until the plant is identified.
It is important to identify both the genus, species and the part ingested (flower, leaf, bulb, fruit, etc.) as toxicity may vary widely. A botanist or nurseryman may be required to aid in identification. Common names should not be used (there are over ten different species known as “Wandering Jew”, “Creeping Jesus” and “Mother-in-law plant”).
The presence of pesticides or herbicides should always be considered, particularly if patients demonstrate nicotinic or cholinergic signs.
The following lists of plants, grouped by symptom complex, may be helpful to identify possible culprits where an unknown plant has been ingested. They are not meant to be exhaustive. They are divided by their initial or most significant symptoms into:
5-10% of all poison center calls involve plants; 85% of exposures occur in children less than of age six.
Poison Center calls: Routes of Exposure
Common lack of an accurate exposure history; this is partly due to its occurrence in the pediatric population:
Which plant was ingested? Time of exposure? Amount of exposure?
Data from the AAPCC Toxic Exposure Surveillance System
Plants most commonly listed as exposures are houseplants that are easily accessible to inquisitive toddlers. Of the top 10 plant exposures most cause no toxicity or mild gastrointestinal symptoms:
Plants most likely to cause serious poisoning in humans:
a. Nerium oleander (oleander)
b. Datura stramonium (Jimson weed)
c. Abrus precatorius (jequirty pea)
d. Cicuta maculata (water hemlock)
e. Conium maculata (poison hemlock)
f. Aconitum napellus (monkshood)
A. Blighia sapida
1. Large fruit tree from Africa, Jamaica and southern US; yellow/orange fruit opens and is edible when ripe
2. Toxins are hypoglycin A and B; Hypoglycin A (from unripe Ackee) inhibits hepatic gluconeogenesis by forming methylenecyclopropane, a nonmetabolizable carnitine that inhibits transport of fatty acids into liver mitochondria; this produces hepatotoxicity and hypoglycemia (by impairing gluconeogenesis) or Jamaican Vomiting Sickness
3. Early symptoms are benign followed by hypoglycemia; reversible hepatotoxicity may occur
4. Risk of Poisoning: eating unripe fruit or subsisting solely on ackee
B. Capsicum annuum
1. Aka: cherry pepper, cone peppers, cluster pepper, cayenne pepper, red pepper, “pepper mace”
2. Most commonly reported plant exposure; related to the mace product containing capsaicin
3. Capsaicin is an alkaloid that is a mucosal irritant causing severe burning pain, local irritation and edema; produces lacrimation (ocular), airway swelling and bronchospasm if inhaled
4. Risk of Poisoning: most exposures are not dangerous; fatal airway edema/bronchospasm may occur
5. Rx: irrigation of exposed areas and supportive care, irrigation with vinegar (5% acetic acid) may provide some symptomatic relief; bronchodilators
C. Epipremnum aureum
1. Aka: hunter's robe, taro vine, pothos ivy, ivy arum, golden Ceylon creeper (common house plant)
2. All plant parts contain calcium oxalate
3. GI and ocular exposure similar to Dumbcane exposure (see D)
4. Skin: contact dermatitis
5. Risk of Poisoning & Rx: similar to other calcium oxalate containing plants
1. Aka: Mother-in-law's tongue plant, tuftroot, poisonous arum (extremely common houseplant)
2. Primary toxicity is due to the presence of calcium oxalate crystals, these crystals are located within cells that contain bundles of needle-like raphides that following plant injury fire out in a projectile fashion. Raphide penetration of tissue causes release of histamine and resultant pain
3. The stalk has the highest crystal concentration
4. Ingestion results in rapid development of redness, swelling and local pain in the mouth and throat. Immediate development of symptomatology limits exposure. If respiratory compromise develops it should occur in the first 6 hours
5. Ocular exposure causes immediate intense pain, chemical conjunctivitis, corneal abrasions
6. Risk of Poisoning: the extent of toxicity is species dependent and related to crystal concentration Severe oral exposure may produce obstruction of the airway and respiratory compromise
7. Rx: usually demulcents (milk, ice cream, water) and cold packs are adequate; ocular exposure requires irrigation.
1. Water hemlock aka: cowbane, snakeweed, wild carrot, poison parsnip, false parsley; often mistaken for Queen Anne’s Lace; Poison hemlock is fern like
2. Water and poison hemlock exposures occur when the plants are mistaken for wild edible species (e.g. wild carrot), or when Water hemlock’s hollow stem is used as pea shooter
3. Water hemlock: all parts of the plant contain cicutoxin, the root contains the most; Poison Hemlock: all parts of the plant contain conine
4. Cicutoxin is an extremely lethal compound that causes rapid CNS stimulation, seizures (perhaps cholinergic); conine is a cholinergic agonist (predominantly nicotinic) and produces early tachycardia and tremor and subsequent bradycardia and motor paralysis
5. Risk of Poisoning: cicutoxin is considered very toxic, second only to Amanita spp poisoning in reported lethality among plants; conine is extremely toxic and is purported to have been used to kill Socrates
6. Rx: Water hemlock: activated charcoal, benzodiazepines for CNS stimulation or seizures, supportive care; hemodialysis and hemoperfusion have been attempted but the benefit is unclear; Poison hemlock: supportive care.
1. Aka: holly, English holly, American holly (common Holiday plant)
2. Have attractive red or black berries in Fall and Winter
3. Mechanism of toxicity uncertain
4. Ingestion may produce severe gastrointestinal symptoms of nausea/vomiting, abdominal pain, and diarrhea
5. Risk of Poisoning: related to amount ingested. Severe electrolyte imbalance is reported
6. Rx: supportive care
1. No toxin isolated: a non-toxic exposure
2. Risk of Poisoning: none
3. Rx: reassurance
H. Datura stramonium
1. Aka: apple of Peru, tolgacha, Jamestown weed, devil's apple, thorn apple, stinkweed, locoweed, loco seeds
a. Toxic, mind-altering properties known for centuries, references made to it in Homer's “Odyssey” and Shakespeare's “Romeo and Juliet”
b. salad. They were “turned natural fools upon it for several days”
3. are tropane alkaloids (atropine, hyoscyamine, scopolamine), also known as belladonna, which are potent antimuscarinic (i.e. anticholinergic) agents
4. Other plants that contain tropane alkaloids that also produce anticholinergic toxicity:
a. Atropa belladonna : belladonna, deadly nightshade
b. Hyoscyamus spp : henbane, black henbane
c. Mandragora officinarum : mandrake
d. Lycium halmifolium : matrimony vine
e. Cestrum spp : night-blooming jessamine
5. , and ingesting parts of the plant especially the seeds
6. Clinical signs are consistent with anticholinergic poisoning: dry flushed skin, mydriasis, tachycardia, decreased bowel sounds, urinary retention, lethargy, hallucinations, agitation, coma, seizures
7. Risk of Poisoning: depends on amount of toxin ingested. Severe signs such as agitation, seizures, hallucinations may be fatal if inadequately untreated
8. Rx: activated charcoal, physostigmine and/or a benzodiazepine for severe manifestations
I. Digitalis purpurea
1. Aka: common oleander, rose laurel
2. A large flowering shrub used extensively in dry climates having large clusters of white, pink, or red flowers
a. The Greeks considered it poisonous to “all four-footed beasts”
b. In folk medicine used as an abortifacient
c. The Chinese used this to treat mental and cardiac disorders
4. Toxicity related to cardioactive steroids, of which over 400 have been isolated in the plant kingdom; at least 5 have been found in oleander.
5. The following are other plants that contain cardioactive steroids and both manifest similar toxicity:
a. Dogbane family: dogbane (Apocynum cannabinum ) wintersweet, bushman's poison, sea mango
d. Milkweed family: balloon cotton, king's cotton, rubber vine, redheaded cotton bush
6. Highest concentration of toxin is in seeds, stem and root
7. Clinical manifestations related to toxin causing digoxin-like poisoning
a. GI: nausea/vomiting
b. Cardiac: dysrhythmias
8. Laboratory: plant cardioactive steroids may cross react with digoxin radioimmunoassay, absolute levels are difficult to interpret
8. Risk of Poisoning: depends on amount ingested, brady- or tachydysrhythmias or hyperkalaemia (potassium > 5.0 meq/L) are signs of consequential poisoning
9. Rx: activated charcoal, digoxin-specific Fab fragments; sufficient cross reactivity of fragments with non-digoxin cardioactive steroids to warrant their use (same indications as digoxin except serum levels)
1. Aka: peace lily, white anthurium, spathe flower, snowflower, Mauna Loa
2. Contains small amounts of calcium oxalate crystals
3. Risk of Poisoning: mild GI symptoms secondary to calcium oxalate
4. Rx: supportive care
1. Aka: philodendron, panda plant, parlor ivy (common house plants)
2. Ingestion is generally benign, few case reports of GI irritation relate to small calcium oxalate content
3. Skin exposure can produce a delayed contact dermatitis secondary to alkyl resorcinol content
4. Highly toxic to cats
5. Risk of Poisoning: many non toxic reports; at worst the outcomes are mild
6. Rx: supportive care
1. Euphorbiaceae, or spurge family is characterized by the presence of latex (a milky sap)
2. Small amounts of diterpene esters are found in this plant, they are mucosal irritants and contact allergens
3. Ingestion of this plant occasionally causes mucous membrane irritation
4. Skin exposure has been reported to cause contact dermatitis
5. Risk of Poisoning: low risk for toxicity.
6. Rx: supportive care
M. Toxicodendron dermatitis
1. T.radicans (poison ivy; not West coast); T.toxicarium (poison sumac);
2. Similar toxin found in Mango rind and cashew nut shell exposure
3. Urushiol-containing oleoresin that produces a contact dermatitis characterized by pruritis and urticaria, erythema, edema, blisters; rash often takes a linear pattern from brushing against a twig or scratching with contaminated fingernails;
4. Reactivity requires prior sensitization and most people can be sensitized; at least 50% of the population is sensitized but reactivity to the toxin varies substantially
5. Ingestion and inhalation produce internal contact and reactions can be severe.
6. The resin is often transmitted by fomites such as garden tools, pets, clothes; may be transmitted from person to person
7. Remove from continued exposure by washing or discarding possible fomites; Domeboro (aluminum acetate) solution or a lubricating agent such as petrolatum may be best for mild dermatitis; it is probably best to avoid drying antipruritic lotions such as calamine except for weeping lesions; topical steroids (hydrocortisone 1%) may be helpful; severe exposures may require oral steroids; sensitized individuals who cannot avoid exposure may benefit from desensitization therapy.
8. arrier protection is the best prevention; newer skin coatings that supply barrier protection appear minimally effective. Rapid washing shortly (minutes) after exposure can be very helpful
N. Phytolacca americana
1. Aka: pokeweed, pokeberry, poke, inkberry, scoke, pigeonberry, American cancer, garget
2. Often ingested as a salad (pokesalad), after boiling leaves twice and discarding the water
a. Double boiling does not guarantee edibility; the extracted liquid is toxic
3. The root contains the most toxins
4. Phytolaccine is a powerful gastrointestinal irritant, the plant also contains mitogens able to stimulate plasma cell production
5. Ingestion causes severe and immediate symptoms of nausea/vomiting, abdominal pain, and diarrhea, hemorrhagic gastritis, dehydration; elevated white blood cell count (mitogen);
6. Risk of Poisoning: severity of symptoms depends on the amount, part of the plant, and preparation prior to ingestion,
7. Supportive care, activated charcoal (?)
O. Ricinus communis
1. Abrus aka: jequirity bean, Seminole bead, prayer bead, crab's eye, ojo de pajaro
2. seeds are larger, brown and variegated
3. is ricin; both are toxalbumins which are potent inhibitors of cellular protein synthesis.
4. Ricin is a potential biochemical warfare agent. It is stable in water or weak acids and is persistent in the environment. Terrorist delivery would be as a toxic cloud resulting in inhalation, by injection or in foods or drink leading to ingestion. Recognize that inhalational toxicity would require that the ricin be aerosolized in respirable particles, < 5 mm in diameter, and that this is exceedingly difficult to accomplish.
5. Clinical symptoms following ingestion gastrointestinal (N/V/D, abdominal pain); delayed toxicity includes multisystem organ failure (liver, renal, CNS) especially when given parenterally.
6. Following inhalation cough, chest tightness, difficulty breathing, nausea and myalgias develop. Rapid progression to airway inflammation, hypoxia, circulatory failure and death occur in 36-48 hours.
7. Severe symptoms can last up to 10 days. There are several reported deaths from oral exposure although it is unclear if these were simply related to hypovolemia from the severe diarrhea
8. Rx: if ingested activated charcoal; for all exposures supportive care and particularly volume repletion
(adapted from Goldfrank’s Toxicologic Emergencies. 6th edition. Appleton and Lange, Norwalk, CT. 1998, p1246)
1. Plants producing irritation primarily of the mouth and throat: edema, bullae, salivation, dysphagia, and dysarthria; Precipitants: water insoluble calcium oxalate crystals and a proteolytic enzyme
d. Jack-in-the-pulpit (Arisaema triphyllum )
e. Elephant’s ear (Colocasia spp)
f. Rhubarb (Rheum raponticum )
g. Pothos (Scindapsus aureus)
2. Irritation chiefly of gastric mucosa; symptoms: local and centrally initiated emesis
3. Irritation chiefly of intestinal mucosa; symptoms: emesis, abdominal pain, colic, diarrhea, melena
a. Horse chestnut (Aesculus hippocastanum )
b. English ivy (Hedera helix )
c. Pokeweed (Phytolacca americana )
d. Yew (Taxus spp)
e. Baneberry (Actaea spp) 4. Plants producing delayed gastroenteritis
a. Lectin (toxalbumin) group; symptoms: burning in mouth, N/V/D, dehydration, headache, CNS depression, seizures, shock
b. Solanine group, glycoalkaloids; symptoms: N/V/D, headache, muscle weakness
5. Gastroenteritis caused by a cellular toxin, the colchicine group. Symptoms: nausea, crampy abdominal pain, diarrhea, hematochezia
6. Diverse symptoms including gastrointestinal
d. ) B. Plants producing cardiovascular disturbances
1. Cardioactive steroid group: bradycardia, ventricular dysrhythmias
2. ) bradycardia, ventricular dysrhythmias
3. ) bradycardia, ventricular dysrhythmias
4. Grayanotoxins (veratrine and andromedotoxin) group:
Salivation, lacrimation, rhinorrhea, emesis, weakness, bradycardia, hypotension
C. Plants having a nicotine-like action
Salivation, headache, nausea, vomiting, ataxia, coma, seizures, hypotension, respiratory compromise
D. Belladonna alkaloid-containing plants
Anticholinergic symptoms: mydriasis, dry skin, vasodilation, ileus, tachydysrhythmias, altered mental status
Water hemlock (Cicuta maculata)
3. Demyelination: progressive ascending bilateral paralytic neuropathy
Buckthorn (Karwinskia humboldtiana)
F. Cyanogenic plants: amygdalin, cyanogenic glycosides
Delayed onset, vomiting, rapid deterioration with symptoms of tissue hypoxia
G. Hepatotoxic plants
4. Pyrrolizidine alkaloids
H. Miscellaneous Christmas poisonous plants
1. Mistletoe (Phoradendron flavescens )
2. Holly (Ilex spp )
3. Poinsettia (Euphorbia pulcherrima)
I. Plant dermatitis
1. Mechanical injury
2. Chemical injury
3. Contact dermatitis
b. ) Western (T. diversilobum)
4. Contact urticaria
b. Cowitch (Mucuna pruriens)
c. Bull nettle (Cnidoscolus stimulosus)
d. Agave, century plant (Agave americana)
e. Primrose (Primula spp)
In general there are few specific antidotes. Late decontamination with activated charcoal is often useful (up to 24 h or so) as the plant may be poorly digested and many plant toxins undergo enterohepatic circulation.
Supportive care is the only other treatment available for virtually all plant toxins except for those causing toxic effects similar to medication.
These toxins (cardiac glycosides, anticholinergic plants, colchicine containing plants) are dealt with in the modules dealing with those drugs. A detailed account of plant toxicity is beyond the scope of this text.
Many references are written specifically for either Europe or North America. Australian books tend to take a four-footed perspective although they are worth some rumination.
Some useful texts & sites to consult include the following:
Wild Plants of Malta This site has quite detailed information on a lot of plants
Ellenhorn MJ: Medical Toxicology: Diagnosis and Treatment of Human Poisoning. Williams & Wilkens, Baltimore, 1997.
Spoerke & Smolinske. Toxicity of houseplants.
Covacevich J, Davie P, Pearn J (Eds). Toxic Plants & Animals: A guide for Australia. Queensland Museum, Brisbane, 1987.
Newall CA, Anderson LA, Phillipson JD. Herbal medicines: A guide for health-care professionals. The Pharmaceutical Press, London, 1996.
Frohne D, Pfander HJ. A colour atlas of poisonous plants. Wolfe, London, 1984.
Isbister GK, Oakley P, Dawson AH, Whyte IM. Presumed Angel's trumpet (Brugmansia) poisoning: clinical effects and epidemiology. Emerg Med (Fremantle). 2003 Aug;15(4):376-82