Oleander toxicity

Common oleander (Nerium oleander) is widely used as an ornamental landscape shrub or tree in mild climates.  It likes full sun, has pink flowers, tolerates dryness, and reaches 8 to 20 feet in height.  Yellow oleander (Thevetia peruviana) has similarly shaped yellow flowers, but is a different species.  Both are commonly used as a trouble free hedges in Florida,  California and Hawaii.   In northern climates common oleander is increasingly being sold as an indoor houseplant or summer patio plant, posing a risk to indoor pets as well as ones outside.

Medicinally common oleander has been used externally for skin diseases and leprosy, but early Greeks, Romans and Hindus knew the shrub to be highly toxic.

Toxic Elements

Cardiac glycosides found in common oleander include: oleandrin, digitoxigenin, neriin, folinerin, rosagenin. Toxins in yellow oleander include thevatin A, thevatin B, thevetoxin, peruvoside, ruvoside and neriifolin.

These inhibit a sodium-potassium ATPase  pump in a manner similar to digitalis derived glycosides such as digitoxin and digoxin affecting the gastrointestinal, nervous and cardiac systems.  See Foxglove / Digitalis  for more information on mechanisms of action.

The entire common oleander plant should be considered poisonous with the highest concentrations of cardiac glycosides are in the seeds, stems and roots and lesser amounts in leaves and fruity.  Extracts have been used as both insecticides and rodenticides.  A number of case reports exist of deaths and illness caused by roasting meat on sticks made of oleander – it is thought that heat enhances absorption of toxins.  A fatal case of leaf oleander poisoning in an adult human resulted in estimates that 5 to 15 leaves contained lethal levels of toxins.

Oleandrin appears to have a half- life in compost of ~6 days.  Oleandrin has been detected in lettuce mulched with oleander material, albeit at low levels.

In contrast, the highest levels of cardiac glycosides in yellow oleander are in the leaves and then the fruit.  Thevetia glycosides seem to concentrate in heart tissue over blood.  It is estimated that the absorption of 2 leaves would be sufficient to kill a child of ~12.5 kg.


Initially nausea and vomiting, weakness, rash, trembling, depression, hyperkalemia, bradycardia, progressing to other arrhythmias, heart block, atrial fibrillations, cardiac arrest.  Animals on cardio-active medications may have worse effects.  Excessive salivation and hypertonia have also been seen in early stages of Thevetia toxicity.


Diagnosis in animals is usually based on history and symptoms, examination or analysis of vomit. In humans, digoxin and digitoxin assays have been used to diagnose oleander poisoning with both oleandrin and oleandrigenin exhibiting binding activity, but correlations between toxin levels and clinical effects in animals have not been fully validated.


See your veterinarian for treatment to support cardiac function and to monitor and address hyperkalemia and other electrolyte disorders.  Cardiac abnormalities may require treatment with multiple drugs and may only be partly responsive to any one drug.

In humans, Digibind (Digoxin-Immune Fab), a product made from antigen binding fragments of anti-digitoxin antibodies (usually generated in sheep) has been used to treat life threatening cardiac abnormalities.  It has been used successfully in oleander toxicity in humans. Dogs have been used as a model for human oleander toxicity.  In one study, 3 of 5 control dogs died. All treatment dogs that received 60 mg/kg IV survived and all converted to a normal rhythm within 10 minutes, though 3 of the 5 subsequently experienced dysrhythymias.    Expense can limit availability in veterinary medicine.

There is experimental evidence that fructose-1,6, diphosphate can mitigate oleander toxicity in dogs as well.  See Foxglove/Digitalis for more information on drugs that have been documented to interact with digoxin – there may be similar effects with these glycosides.

More information

USDA Plants Database


Bandara, et. al., A review of the natural history, toxicology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning. Toxicon. 2010, Sep 1; 56(3):273-81

Clark, et. al, Digoxin-specific Fab fragments in the treatment of oleander toxicity in a canine model. Ann. Emerg. Med. 1991 Oct;20(10):1073-7.

Dasgupta A and Datta P., Rapid detection of oleander poisoning using digoxin immunoassays: comparison of five assays. Ther. Drug Monit.  2004 Dec;26(6):658-63.

Downer, et al., Toxic potential of oleander derived compost and vegetables grown with oleander soil amendments.  Vet Hum Toxicol. 2003, Aug; 45(4)

Jortani, et. al Inhibition of Na,K-ATPase by oleandrin and oleandrigenin, and their detection by digoxin immunoassays. Clinical Chemistry: 42 (10). 1996. 1654-1658.

Markov, et. al., Fructose-1,6-diphosphate in the treatment of oleander toxicity in dogs, Vet Hum Toxicol, 1999; 41(1): 9-15.

Szabuniewicz, et. al,., Treatment of experimentally induced oleander poisoning Arch Int. Pharmacodyn 1971: 189:12-21

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