Toxic plants (Proceedings)

Insoluble calcium oxalate - containing plants

Insoluble calcium oxalate plants are very commonly kept as houseplants. Some of the more common ones include: Aglaonema modestrum - Chinese evergreen, Alocasia antiquorum or Colocasia -Elephant's ear, Anthurium spp. - Flamingo plant, Arisaema triphyllum - Jack-in-the-pulpit, Caladium spp., Dieffenbachia spp. - Dumb cane, Monstera spp. - Split-leaf or lacy-leafed philodendron or Swiss cheese plant, Philodendron spp. and Spathiphyllum spp. - Peace Lily. The calcium oxalate crystals look like needles and when the plant is damaged, these crystals embed themselves in the oral cavity. Clinical signs include hypersalivation, vomiting and possible swelling of the pharynx (obstruction is rare). Treatment includes milk or water to rinse mouth. Calcium-containing products precipitate soluble oxalates in oral cavity, reducing pain. Prognosis is good and clinical signs usually resolve within 24 hours with no lasting effects.

Dracaena (Dracaena spp).

Common house plant genus that includes the corn plant, dragon tree, money tree and lucky bamboo. It contains various steroidal saponins and glycosides. All parts of the plant are toxic. Clinical signs include vomiting(possibly with blood), hypersalivation, anorexia, depression, and ataxia. In addition, cats may show dilated pupils, dyspnea, and tachycardia. Treatment is symptomatic and supportive.

Poinsetta (Euphorbia pulcherrima)

Poinsettas are overrated as a toxic plant. They do contain diterpenoid euphorbol esters in their sap which can cause vomiting.

Hydrangea (Hydrangea spp.)

Hydrangeas contain hydrangin, a cyanogenic glycoside. However, in dogs and cats, GI signs predominate.

Bulb plants

Common bulb plants include tulips (Tulipa gesneriana), daffodils, narcissus, amaryllis (Narcissus spp.) and hyacinths (Hyacinthus spp.). All parts of the plant are toxic, but the bulb is the most toxic. Ingestion of the flower or stem can cause vomiting. Ingestion of the bulbs can cause hemorrhagic gastroenteritis and neurologic signs.

Sago palms

Sago palms (Cycas and Macrozamia sp.) are ornamental plants found in tropical to subtropical climates, but they can also be grown as houseplants. There are three toxins in cycads. Cycasin is thought to be responsible for the hepatic and gastrointestinal signs. Sago palms also contain two neurotoxins (B-methlamino-L-alanine and an unidentified toxin). The seeds contain the highest amount of cycasin, but the entire plant is toxic. Cycasin causes centrolobular and midzonal coagulative hepatic necrosis along with GI hemorrhage. GI signs begin within a day and laboratory values (ALT, bilirubin, Alk Phos) become abnormal in 24 to 48 hrs. The most common signs are vomiting (+/- blood), depression, diarrhea, anorexia, and seizures. Mortality rate is about 30%.

Treatment is emesis, followed by repeated doses of activated charcoal. Monitor liver enzymes for 48 hours, or until levels return to normal. Seizures and tremors may be controlled with diazepam. Blood or plasma transfusions may be necessary if coagulopathies develop. Prognosis is good if caught early, but guarded in cases where the animal is already showing signs.

Lily

Members of the true lily family (Lilium and Hemerocallis) have been shown to cause acute renal failure in cat. Some examples of true lilies include: Easter lilies (L. longiflorum), tiger lilies (L. tigrinum), rubrum or Japanese showy lilies (L. speciosum, L. lancifolium), and day lilies (H. species). The toxic principle is unknown, but is known to be water soluble. Even minor exposures (a few bites on a leaf, ingestion of pollen, etc.) may result in toxicosis, so all feline exposures to true lilies should be considered potentially life-threatening and should merit aggressive clinical intervention.

Affected cats often vomit within a few hours of exposure, but the vomiting usually subsides after a few hours, during which time the cats may appear normal or may be mildly depressed and anorexic. Within 24 to 72 hours of ingestion, oliguric to anuric renal failure develops, accompanied by vomiting, depression, and anorexia. Elevations in blood urea nitrogen (BUN), creatinine, phosphorus and potassium are detectable as early as 12 hours post ingestion. In some cases, hypoglycemia and mild liver enzyme elevations may occur. Casts, proteinuria, glucosuria, and isosthenuria are usually detectable on urinalysis within 24 hours of ingestion, reflecting lily-induced damage to renal tubular cells. In severe cases, death or euthanasia due to acute renal failure generally occurs within 3 to 6 days of ingestion.

Treatment of lily cats includes decontamination (emesis, one dose activated charcoal with cathartic) and fluid diuresis at twice maintenance for 48 hours. If treatment is started within the first 18 hours after exposure, prognosis is good. Delaying treatment beyond 18 hours frequently results in death or euthanasia due to severe renal failure. Since the tubular injury from lily ingestion spares the renal tubular basement membrane, regeneration of damaged tubules may be possible. In severe cases, peritoneal dialysis may aid in managing renal failure until tubular regeneration occurs.

Cardiac glycosides

Cardiac glycoside containing plants include oleander (Nerium oleander) – toxic principles: oleandrin, neriine; foxglove (Digitalis purpurea) – toxic principle: digitalis; and lily-of-the-Valley (Convallaria majalis) – toxic principle: convallarin. The glycosides are rapidly absorbed from the GI tract and they inhibit the Na+ /K+ ATPase pump, with resultant increase in intracellular sodium. The elevated intracellular Ca++ increases contractility giving fewer, but more forceful contractions.

Ingestion of these plants can cause almost every type of arrhythmia, but bradyarrhythmias are the most common. Hyperkalemia may be noted. Gastrointestinal signs, seizures and sudden death may also be seen. Decontamination should include emesis if appropriate and repeated doses of activated charcoal due to enterohepatic recirculation. Avoid use of calcium containing fluids (LRS, Ringers). Monitor and correct arrhythmias as they arise (atropine, propranolol, lidocaine, phenytoin, etc.). Digibind® (digoxin immune Fab) is produced from specific digoxin antibodies from sheep. It will bind directly to the toxin and inactivate it. Unfortunately, it is expensive. The prognosis is guarded depending upon severity of clinical signs.

Kalanchoe sp. – devil's backbone, mother of millions, Mexican hat plant

This is a common household plant, especially around the holidays. This plant contains a cardiac glycoside, but most dogs and cats only develop GI signs.

Grayanotoxins

The grayanotoxin (andromedotoxin) containing plants include rhododendrons, azaleas (Rhododendron spp.), laurels (Kalmia spp.) and Japanese pieris (Pieris spp.). Grayanotoxins bind to sodium channels in excitable cell membranes of nerve, heart, and skeletal muscle. They increase membrane permeability of sodium ions.

Clinical signs include vomiting, hypersalivation, bradyarrhythmias, tremors, seizures and sinus arrest. Signs can last for 1 to 2 days. Emesis induction and activated charcoal can be given to asymptomatic animals. Atropine should be given for severe bradycardia.

Japanese Yew (Taxus spp.)

Yews are commonly used as landscaping plants. Yews contain taxine alkaloids where have a direct action on cardiac myocyte ion channels. They inhibit normal exchange of Na+ and Ca++ across myocardial cells and depress cardiac depolarization leading to arrhythmias and fatal conduction disturbances. All parts, except for the ripe berry (fleshy red structure surrounding seed), are toxic. Sudden death can occur within hours of ingestion. Treatment includes minimizing stress and administering activated charcoal. Monogastrics that are still alive at 12 hours are likely to survive.

Tropane alkaloids

Tropane alkaloid plants include Jimson weed (Datura stramonium): hyoscyamine, atropine, scopolamine; Belladonna (Atropa belladonna): atropine, hyoscyamine, hyoscine, and Henbane (Hyoscyamus niger): atropine, scopolamine. Clinical signs include tachycardia, dry mouth, mydriasis, hallucinations and possible seizures. The toxins are present in all parts of plant, but most concentrated in the seeds. If signs are life threatening, physostigmine can be given.

Solanaceous plants and solanine

The family Solanaceae includes: Physalis spp. Ground cherry, Cestrum spp. Jessamines and Solanum spp. (the nightshade group): potato, tomato, eggplant. Solanum alkaloids are severe GI irritants and can also contain cholinesterase inhibitors and variable amounts of atropine. Neurological effects from these plants can be mixed depending on the concentrations of solanine and atropine.

Plants containing Lectins

Lectins are plant proteins with an affinity for sugar moieties. They are also referred to as hemagglutinins and toxalbumins. Lectins are found in Ricinus communis (Castor bean) – toxic principle is ricin; Abrus precatorius (jequirity bean, rosary pea, precatory bean) – toxic principle is abrin; and Robinia pseudoacacia (black locust) – toxic principle is robin. Lectins disrupt protein synthesis in ribosomes leading to cell death. Rapidly dividing cells are the most severely affected.

The lectins are found throughout the plant, but the highest levels are found in the seeds. The seed coat must be damaged to release the toxins. Clinical signs include lethargy, vomiting, diarrhea, abdominal pain, and hemorrhagic gastroenteritis. Treatment is symptomatic and supportive.

Autumn Crocus (Colchicum autumnale)

Autumn crocus contain colchicines which inhibits mitotic spindle formation. Ingestion can cause vomiting, diarrhea, weakness and possible death. Do not confuse with spring crocus (Crocus spp.) which is not toxic.

Tobacco (Nicotiana spp.)

Tobacco (cigarettes) ingestion is common in dogs. Tobacco contains nicotine and nornicotine (pyridine alkaloids). Nicotine mimics acetylcholine (ACh) at sympathetic and parasympathetic ganglia, at neuromuscular junctions of skeletal muscle, and at some synapses in the CNS (i.e., at nicotinic receptors). Vomiting is common as nicotine effects the chemoreceptor trigger zone and emetic center. Low doses cause stimulation of receptors similar to Ach, while higher doses cause stimulation followed by blockage at autonomic ganglia and myoneural junctions of skeletal muscle (depolarizing blockade). Death is due to respiratory failure.

Nicotine is poorly absorbed from the stomach, but well absorbed from the small intestine, respiratory tract, and skin. Alkalinization enhances absorption. The canine oral LD50 is 9.2 mg/kg. If the animal is asymptomatic, emesis should be induced followed by active charcoal. Atropine can be given to treat the parasympathetic effects.

Marijuana (Cannabis sativa)

Marijuana is a very common ingestion in dog and cats. It is often co-ingested with other illicit substances or chocolate (brownies). The major active constituent in marijuana is THC (Δ-9-tetrahydro-cannabinol), although as many as 66 cannabinoids have been identified. The concentrations of cannabinoids in plants depends upon environmental conditions. Signs can start within 30-60 minutes and last up to 72 hours. Most animals are lethargic and ataxic, but about 25% are agitated instead. Treatment consists of supportive care. Rarely is marijuana intoxication lethal.

Hops (Humulus lupulis)

Hops are used in beer brewing. Ingestion of hops by dogs causes a malignant hyperthermia-like syndrome. Signs can be seen within three hours. Signs start with agitation, tachypnea, abdominal discomfort, and hyperthermia (104°F). There is a rapid progression to profound hyperthermia (> 108°F) and death. The toxic principle is unknown.

If the animal is still asymptomatic induce vomiting and give a dose of activated charcoal. Start animal on intravenous fluids to prevent myoglobin or hemoglobin induced renal failure. If the dog is already hyperthermic institute cooling measures. Dantrolene (Dantrium®) a direct-acting skeletal muscle relaxant works the best to reduce the temperature, but cyproheptadine can also be tried. Prognosis is poor to guarded, as many affected animals die.

Soluble oxalate-containing plants

Soluble oxalate containing plants include: Oxalis spp. (shamrock), Rheum rhaponticum (rhubarb), Rumex spp. (dock, sour dock, curly dock), Halogeton, Sarcobatus spp. (greasewood) and Chenopodium spp. (lambsquarters). Soluble oxalates are sodium and potassium salts of oxalic acid. They are rapidly absorbed from the gut and hypocalcemia results from oxalic acid complexing with serum calcium. Fatal renal tubular necrosis may occur from crystallization of excreted calcium oxalate in the kidneys.

Mushrooms

Mushroom identification is very difficult and a trained professional should always be consulted. Mycologists at local colleges or schools may be able to help in identification of mushrooms. The toxin content can vary with growing season, location and other environmental factors. As identification can be delayed it is recommended that emesis be induced followed by a dose of activated charcoal.

Isoxazoles mushrooms contain ibotenic acid and muscimol. It is found in Amanita gemmata, Amanita muscaria (fly agaric, mukhomor, woodpecker of Mars), Amanita pantherina (panther mushroom), Amanita smithiana, Amanita strobiliformis and Tricholoma muscarium mushrooms. Animals that ingest ixoxazole mushrooms have fluctuating CNS excitation and depression due to contrasting effects of muscimol and ibotenic acid. Vomiting is common early in the intoxication. Care must be taken when treating the agitated stage as some patients will stop breathing after the administration of a CNS depressant. Signs occur quickly (30 min to 2 hrs) and last for 8 to 24 hours.

Large variety of mushrooms can cause gastrointestinal upset. Members of Agaricus, Albatrellus, Armillaria, Boletus, Chlorophyllum, Entoloma, Gomphus, Hebeloma, Laccaria, Lactarius, Laetiporus, Lampteromyces, Meripilus, Omphalotus,Psalliota, Rhodophyllus, Russula, Scleroderma, and Tricholoma species are all GI toxic. Onset of signs is quick (15 minutes to several hours) and can last for a few hours to couple of days. Treatment is symptomatic (antiemetics, fluids).

Muscarinic mushrooms belong to the Inocybe and Clitocybe spp. Muscarine binds to muscarinic (acetylcholine) receptors in the parasympathetic nervous system, stimulating postsynaptic neurons. Typical SLUDDE (salivation, lacrimation, urination, dyspnea, diarrhea, emesis) signs develop without nicotinic or significant CNS effects. The onset of signs is quick, usually 5-30 minutes; almost never beyond 120 minutes. Signs can persist for several hours if untreated, but resolve quickly with administration of atropine.

Psilocybin or magic mushrooms can cause altered behavior and mentation, hypersalivation, ataxia, and hyperthermia. Psilocybe (liberty caps), Panaeolus, Conocybe,Gymnophilus and some Stropharia species may also contain this type of toxin. The toxin is thought to stimulate serotonin receptors (e.g. 5-HT2A) within the CNS and PNS. Signs occur within 30-180 minutes and can last for up to 3 days. Treatment is symptomatic. Cyproheptadine is a 5-HT2 antagonist that can block the effects of serotonergic drugs (SSRI, LSD) and may be of benefit in cases of psilocye toxicosis.

Gyromitra spp (false morels), Helvella crispa and H. lacuose contain gyromitrin. Gyromitrin is metabolized to monomethylhydrazine, which inhibits g-aminobutyric acid (GABA) synthesis. Decreased GABA inhibition results in seizures. Clinical signs include a gastrointestinal phase followed by neurologic, heptatorenal and/or hemolytic phases. Prognosis is guarded in patients developing signs beyond gastrointestinal upset.

Amanitins and phalloidins are hepatic toxins found in Amanita, Galerina and Lepiota mushrooms. Amanitins are absorbed and taken up by the hepatocytes where they produce liver necrosis. Amanitins inhibit nuclear RNA polymerase II, interfering with DNA and RNA transcription. Animals ingesting amanitins have a triphasic syndrome following latent period of 6-12 hours. Phase 1 (gastrointestinal) vomiting, diarrhea, abdominal pain, dehydration, and lethargy. Phase 2 (hepatotoxic) signs and lab values consistent with hepatic failure leading to coagulopathy. Phase 3 (hepatorenal) hemorrhages, seizures, flulminant hepatic failure, renal failure leading to death in 4-7 days. Most animals do not survive. Animals should be given activated charcoal and started on IV fluids. N-acetylcysteine (Mucomyst) or SAMe should be started to help protect the liver.

Orellanine containing mushrooms are in the Cortinarius spp. They are toxic to renal tubular epithelium. Fortunately, this is rarely reported in the US. Clinical signs include vomiting, polyuria, polydipsia and depression. The lag time between ingestion and development of illness suggests metabolism to active toxin. Animals may never regain full renal function, necessitating life-long management of CRF.

Diagnostic algorithm for signs from mushrooms in humans (Benjamin, 1995)