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Houseplants and Ornamentals Toxic to Animals


Renee D. Schmid

, DVM, DABT, DABVT, Pet Poison Helpline & SafetyCall International, LLC, Bloomington, MN

Reviewed/Revised Nov 2023
Topic Resources

For pets, houseplants and ornamentals are a common source of potential toxicosis. Although many plants are harmless in small quantities, large ingestions or ingestion of highly toxic varieties may lead to life-threatening symptoms.


Pet Poison Helpline, an international animal poison control center, receives thousands of calls regarding exposure to potentially poisonous plants. These incidents most commonly involve the following 10 plants:

  • true lilies (Lilium spp)

  • chokecherry/cherry (Prunus spp)

  • azalea (Rhododendron spp)

  • tulip (Tulipa spp)

  • peace lily (Spathiphyllum spp)

  • hydrangea (Hydrangea spp)

  • aloe (Aloe spp)

  • philodendron (Philodendron spp)

  • daffodil (Narcissus spp)

  • pothos/devil’s ivy (Epipremnum aureum)

Many plants that share the same common name are in different families and have different levels of toxicity. Therefore, it is important to identify not only the common name of the plant ingested, but also the scientific name. This will ensure that the patient is correctly assessed and treated.

Toxicity of Plants Containing Soluble Oxalates

Exposure to plants containing soluble oxalate is not common in companion animals; however, life-threatening signs may occur after exposure. Small ingestions, including a taste or nibble, may result in GI upset, including vomiting and inappetence; however, more serious signs are not expected. With large ingestions, soluble oxalates released from the plant initially bind to calcium, resulting in hypocalcemia. Initial clinical signs include vomiting and those consistent with hypocalcemic tetany, including lethargy, ataxia, tremors, and seizures. This is not expected to occur with small ingestions and is more readily seen in livestock grazing large quantities of plants containing soluble oxalates.

There is a concern for calcium oxalates to precipitate in the kidney, resulting in renal failure due to damage to the renal tubules. In cases of renal damage, lethargy, vomiting, anorexia, PU/PD, oliguria, and anuria may occur. For exposures consisting of more than just a small taste or nibble, treatment consists of decontamination with emesis and one dose of activated charcoal with a cathartic followed by intravenous fluids for 24-48 hours. Intravenous calcium gluconate is indicated in cases where hypocalcemia occurs. Renal indices should be monitored during a hospitalization and evaluated if clinical signs develop.

Some examples of plants containing soluble oxalates:

  • rhubarb, garden rhubarb (Rheum rhabarbarum) - stalks are edible and not a concern

  • shamrock (Oxalis spp)

  • sour star fruit (Averrhoa carambola)

  • curly dock, red sorrel, green sorrel, sour dock (Rumex spp)

Toxicity of Plants Containing Insoluble Oxalates

Many household plants contain insoluble calcium oxalates. Insoluble oxalates (raphides) are needle-like crystals found bundled in cells called idioblasts that are scattered throughout the plant. Chewing or crushing the plant material causes these idioblasts to release the raphides into tissues or surrounding material, causing irritation and trauma to any tissue that contacts these raphides.

Common house and ornamental plants that contain insoluble calcium oxalates:

  • Aglaonema commitatum (Chinese evergreen)

  • Anthurium spp (flamingo flower)

  • Caladium spp (caladium, elephant ear)

  • Dieffenbachia spp (dumbcane)

  • Epiprenum spp (pothos)

  • Monstera deliciosa (fruit salad plant)

  • Philodendron spp (philodendron)

  • Schefflera actinphylla (umbrella plant)

  • Spathiphyllum spp (peace lily)

  • Syngonium spp (arrowhead vine)

  • Zantedeschia spp (calla lily)

Insoluble Oxalate-Containing Plants

Clinical signs after ingestion of insoluble oxalate-containing plants include immediate pain, irritation, erythema, hypersalivation, pawing at mouth, edema, lethargy, and anorexia. Supportive care is recommended. This includes removal of the plant material, rinsing or wiping out the patient's mouth to help remove remaining raphides, and, sometimes, use of milk or other calcium-containing dairy products. Insoluble oxalates often bind to calcium-containing dairy products, which aid in the clearance of the oral cavity and esophagus. Care should be taken to ensure edema to the laryngeal region does not cause respiratory distress. Securing an airway and providing oxygen support may be necessary if laryngeal edema occurs. Most cases of exposure to insoluble oxalate-containing plants have a good to excellent prognosis and full recovery is expected, often without veterinary intervention. Unlike plants containing soluble oxalates, insoluble oxalates do not pose a concern for renal injury.

Toxicity to Animals of Plants that Contain Grayanotoxin

Plants that contain grayanotoxin are found both indoors and outdoors as ornamental plants, shrubs, and small trees. Flowering plants are appealing to pets and often a source of toxicosis. Grayanotoxins bind to sodium channels which results in prolonged depolarization of excitable cells, particularly nerve and muscle cells. Cardiac muscle is commonly affected by these toxins. All parts of the plant are considered toxic, although the nectar, flowers, leaves, and stems are of greatest concern. Historically, grayanotoxin-containing plants have been known to cause “mad honey disease” in children sucking the nectar from flowers.

Clinical signs after ingestion of plants containing grayanotoxins develop within 1–4 hours, and occasionally as long 12 hours, after ingestion. Clinical signs include gastrointestinal, cardiovascular, and CNS abnormalities. Transient blindness has also been reported, although less commonly. In small animals ingesting only a few leaves or petals, clinical signs are generally limited to gastrointestinal effects and CNS depression; however, monitoring through the day for the development of cardiac abnormalities is typically recommended. Larger ingestions will result in more severe toxicity.

Treatment consists of decontamination of the asymptomatic patient with emesis followed by an antiemetic and one dose of activated charcoal with cathartic. If clinical signs are present, decontamination should only be performed if the patient is neurologically appropriate. Plant material will often remain in the stomach for many hours, allowing for successful emesis several hours after ingestion. Intravenous fluids will help to provide cardiovascular support in the event of hypotension. Monitoring heart rate and blood pressure should be initiated and continued until patient is discharged. Atropine is recommended for bradycardia. Arrhythmias may be treated with antiarrhythmics, including lidocaine and procainamide. Methocarbamol is recommended for management of tremors and standard anticonvulsants are generally effective with seizure control. Vomiting, diarrhea, and other gastrointestinal signs can be managed well with typical treatment (ie, antiemetics, antidiarrheals, gastroprotectants, bland diet) as needed. Small ingestions that result in gastrointestinal signs have an excellent prognosis. Larger ingestions in which notable cardiovascular or CNS signs develop have a guarded to good prognosis with aggressive care.

Common house and ornamental plants that contain grayanotoxins include the following:

  • Kalmia latifolia (mountain laurel)

  • Lyonia spp (fetterbush, staggerbush)

  • Pieris japonica (Japanese pieris)

  • Rhododenron spp (azalea, rhododendron)

Common Plants Containing Grayanotoxins

Toxicity to Animals of Plants Containing Cardiac Glycoside

Plants containing cardiac glycosides are among some of the most toxic plants and have a narrow margin of safety. Their toxic principles have evolved to serve as protective mechanisms. The monarch butterfly, for example, protects itself from predators by storing cardiac glycosides in its wings after ingestion of milkweed, thus poisoning its unsuspecting predator.

Common houseplants and ornamentals that contain cardiac glycosides include the following:

  • Adenium obesum (desert rose)

  • Asclepias spp (milkweed)

  • Convallaria majalis (lily of the valley)

  • Digitalis lantans (woolly foxglove)

  • Digitalis purpurea (common foxglove)

  • Kalanchoe spp (kalanchoe, mother of millions)

  • Nerium oleander (oleander)

  • Ornithogalum umbellatum (star of Bethlehem)

  • Taxus spp (Japanese yew)

  • Thevetia peruviana (yellow oleander)

Plants Containing Cardiac Glycoside

In general, all parts of the milkweed plant are considered toxic. For yews, in contrast, the red fleshy berry is not considered poisonous; however, the seed inside the berry is toxic. The level of toxicity varies between plants, with oleander and foxglove considered to be most toxic. Cats are believed to be more sensitive than dogs. Most plants containing cardiac glycosides are structurally similar to the cardiac drug digoxin, allowing for cross-reactivity with immunoassays for diagnosis and use of its antidote in poisoning situations. Through different toxic principles, plants containing cardiac glycosides inhibit the Na+/K+ ATPase pump, a necessary component for cardiac function. This inhibition causes a rise in intracellular Ca++ as well as accumulation of extracellular K+ and intracellular Na+. The resulting effects are more forceful, yet slower, cardiac contractions.

Clinical signs of toxicosis include weakness, vomiting, diarrhea, bradycardia or tachycardia, arrhythmias, and hyperkalemia. Onset of clinical signs is expected within the first 2 hours after exposure with clinical signs that may persist for up to 4–5 days.

Treatment of cardiac glycoside poisoning consists of decontamination in the asymptomatic patient with emesis induction and one dose of activated charcoal with cathartic. Due to enterohepatic recirculation, repeating activated charcoal without a cathartic every 6–8 hours for a total of 3 doses is recommended. Intravenous fluid treatment is recommended for hemodynamic support. Digoxin-specific antibody contains antibody fragments (fab) are specific antidotes for digoxin toxicity that work well for cardiac glycoside toxicosis from plants as well. Use of antiarrhythmics such as lidocaine can be administered when antidote access is not available. Atropine and glycopyrrolate have been used successfully for bradycardia. Electrolytes should be monitored closely. Severe hyperkalemia, > 7.5–9mEq/L, should be treated with sodium bicarbonate or dextrose:insulin treatment. Mild hyperkalemia can be treated with intravenous fluid treatment alone. In cases with no development of cardiovascular abnormalities or hyperkalemia, the prognosis is excellent. Patients that develop severe signs of toxicosis with no access to an antidote have a guarded to poor prognosis. Those patients with access to an antidote have a guarded to good prognosis. Fatalities have been reported after oleander and foxglove toxicosis even with aggressive treatment.

Toxicity to Animals of Cyanogenic Glycoside Plants

As the name suggests, cyanogenic glycoside plants contain cyanide. Although several household and ornamental plants contain cyanogenic glycosides, severe toxicity in small animals is uncommon unless large ingestions occur.

Substances generally housed within seeds of the fruit and leaves of the plant are converted to cyanide when the plant or seed is compromised, as in chewing or grinding. Upon release, cyanide binds with ferric (Fe3+) iron and prevents the release of oxygen for cellular use. This results in tissue hypoxia. If a seed is swallowed whole, cyanide is not released; thus, toxicity is not expected.

Although fruits such as apples, cherries, and peaches are included in these groups of plants, those purchased for human consumption contain very low levels of cyanide within their seeds and it would be rare for toxicity to develop in animals consuming these fruits.

Common houseplants and ornamental plants that contain cyanogenic glycosides include the following:

  • Cercocarpus spp (mountain mahogany)

  • Hydrangean spp (hydrangea)

  • Malus spp (apple)

  • Nandina spp (heavenly bamboo)

  • Nandina Photina spp (photina red leaf)

  • Prunus spp (chokecherry, black cherry, cherry laurel, almond tree, plum tree, peach tree, apricot tree)

Clinical signs of toxicity include vomiting, diarrhea, almond-flavored breath, tachypnea, respiratory distress, hypotension, arrhythmias, sudden collapse, cyanosis, seizures, severe metabolic acidosis, coma, and death. A classic sign of cyanide toxicosis is cherry red blood coloring, which also contributes to brick red mucous membranes, although changes to mucous membranes do not always occur in animals. Clinical onset of toxicosis develops very rapidly, often within 10–60 minutes after exposure. Signs of hypoxia develop quickly, and death often occurs before treatment can begin.

Most cases of cyanogenic plant exposure in small animals only need minimal gastrointestinal support. In cases where large ingestions occur, treatment consists of decontamination in the asymptomatic patient with emesis induction and one dose of activated charcoal with cathartic. Obtaining a whole blood cyanide level is helpful with diagnosis. Monitoring metabolic acidosis with venous blood gas should be routinely done and acidosis corrected with sodium bicarbonate, if present. Antidotes for cyanide toxicity include the use of sodium nitrite, which forms cyanomethemoglobin when combined with cyanide, followed by sodium thiosulfate to form thiocyanate. Thiocyanate is water soluble and readily excreted in the urine. Less severe cases may be treated with sodium thiosulfate alone. Hydroxycobalamin has been used as an antidote in Europe and is currently available in the US. Its combination with cyanide forms cyanocobalamin (vitamin B12), which is excreted in urine. If clinical signs are limited to gastrointestinal effects, prognosis is excellent. The prognosis is guarded in patients with more severe effects.

Toxicity to Animals of Lilies

Lilies are a very common plant, both indoors and outdoors. In addition to being popular garden plants, lilies are frequently part of cut flower arrangements. Although lilies are not toxic to most animals, cats are highly sensitive to poisoning. Many plants have “lily” in the name but are not true lilies and do not pose the same toxicity concerns as true lilies. Only lilies within the Lilium and Hemerocallis families are considered true lilies and are toxic. Thus, with any lily exposure, it is important to determine whether the plant is a true lily or an imposter.

True lilies are known to cause nephrotoxicity in cats. Although the specific mechanism is not known, true lilies have been shown to damage renal tubular epithelial cells. If untreated, lily toxicosis results in acute renal failure.

Clinical signs begin within 1–3 hours after ingestion and include salivation, anorexia, lethargy. and vomiting. Over the next 12–30 hours, additional signs develop, including polyuria, dehydration, continued vomiting, and lethargy. As signs worsen, weakness, recumbency, and death occurs within 3–7 days. Seizures are an uncommon sign but occur in severe cases due to substantial uremia.

Treatment consists of decontamination after recent ingestion in the neurologically appropriate cat followed by an antiemetic and one dose of activated charcoal with cathartic. Baseline CBC, chemistry, and urinalysis should be obtained to assess current health status. Monitoring renal values every 24 hours for the first 72 hours is advised to evaluate progression and response to treatment. Intravenous fluid administration at 2–3 times maintenance for 48–72 hours is recommended to offer renoprotection. Gastroprotectants should be administered if gastritis secondary to azotemia is present. If oliguria occurs, aggressive treatment to increase renal output, including mannitol and furosemide, may be of benefit. Once anuria develops, peritoneal dialysis and hemodialysis should be considered. When treatment is initiated early after ingestion and only mild effects develop, prognosis is excellent. Prognosis becomes more guarded to poor if treatment is not begun until after more severe signs, including oliguria or anuria, have developed.

True Lilies

Common true lilies include the following:

  • Hemerocallis spp (daylily)

  • Lilium spp (Asiatic lily, Oriental lily, Easter lily, stargazer lily, tiger lily, trumpet lily, Madonna lily, white lily, rose lily, rubrum lily)

Common imposter lilies include the following:

  • Agapanthus africanus (lily of the Nile)

  • Alstroemeria spp (Peruvian lily)

  • Clivia miniata (fire lily)

  • Convallaria majalis (lily of the valley)

  • Darlingtonia californica (cobra lily)

  • Eucharis grandiflora (Amazon lily)

  • Gladiolus spp (sword lily, gladiolus)

  • Hippeastrum spp (amaryllis )

  • Nymphaeaceae spp (water lily)

  • Scadoxus spp (blood lily)

  • Spathiphyllum wallisii (peace lily)

  • Zantedeschia spp (calla lily)

  • Zephyranthes drummondii (prairie lily)

Imposter Lilies

Toxicity to Animals of Cycads (Sago Palm)

Although many palms in tropical areas are known for their grand size, many smaller varieties are used as ornamental plants indoors, so animals in all parts of the country are at risk of exposure.

Cycad or sago palm plants include the following:

  • Cycad revoluta (Japanese cycad)

  • Cycas cirinalis (sago palm)

  • Zamia floridana (coontie [native to Florida])

  • Zamia furfuracea (cardboard palm)

  • Zamia pumila (coontie plant)

Dogs are extremely sensitive to toxicity of cycads or sago palms, with severe gastrointestinal signs, hepatotoxicity and CNS abnormalities expected.

Seeds are the most toxic part of the plant, however, all parts are considered toxic. Two primary toxins are present within the plant, cycasin and beta-methylamino-L-alanine (BMAA). Cycasin primarily causes gastrointestinal, CNS and hepatoxic effects, while BMAA primarily causes CNS effects. Many fatalities are a result of hepatic necrosis. Clinical signs of toxicosis include vomiting and diarrhea (either of which may be bloody), anorexia, lethargy, abdominal pain, ataxia, tremors, seizures, icterus and petechiae or ecchymotic hemorrhages secondary to liver failure. Initial clinical signs are often evident within the first 4 hours of ingestion and progress to liver failure within 48–72 hours.

Treatment consists of decontamination of the neurologically appropriate patient with induction of emesis followed by an antiemetic and one dose of activated charcoal with cathartic. Two additional doses of activated charcoal without a cathartic administered 6–8 hours apart are recommended due to enterohepatic recirculation. Baseline laboratory tests to assess the patient’s overall health, followed by evaluating liver enzymes daily for 72 hours, is ideal. In-hospital monitoring is preferred due to the potential for major gastrointestinal effects, neurologic abnormalities, and the progression to hepatic failure. Methocarbamol for tremors and standard anticonvulsants should be administered as needed.

Gastroprotectants should be provided based on severity of gastrointestinal signs present. Hepatoprotectants including S-adenosylmethionine (SAMe) and N-acetylcysteine (NAC) are necessary to support liver function and repair if hepatic necrosis is present. Hypoglycemia and a secondary coagulopathy may develop in patients with hepatic necrosis; therefore, monitoring blood glucose and coagulation profile is important in these patients. If hypoglycemia is present, 2.5%–5% dextrose supplementation should be administered as a constant rate infusion. Animals who have prompt medical intervention and aggressive care have a fair to good prognosis. The prognosis is guarded to poor in patients who develop notable clinical signs or have a delay in treatment. Those who do develop hepatic necrosis may need prolonged care.

Toxicity to Animals of Common Gastrointestinal Irritant Plants

Several houseplants and ornamentals contain substances known to cause gastric irritation. These result in only mild to moderate gastrointestinal upset, except in rare instances. Animals can generally ingest large amounts acutely or chronically nibble on leaves without severe repercussions. Clinical signs are generally limited to anorexia, vomiting, and diarrhea. Treatment consists of symptomatic and supportive care with antiemetics, antidiarrheals, and a bland diet. Although most animals recover within 24–48 hours, those with underlying gastrointestinal disease may need a longer course of treatment. Removing the plant source is ideal to prevent re-ingestion. Prognosis with exposure to these plants is excellent.

Common gastrointestinal irritant house and ornamental plants include:

  • Aloe spp (aloe)

  • Euphorbia pulcherrima (poinsettia)

  • Hedera spp (ivy)

Common Gastrointestinal Irritant Houseplants

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