Oleander is an ornamental shrub that flowers in various colors including white, red, pink and violet. This plant is an evergreen perennial that flowers throughout the summer months. Originally a native plant of the Mediterranean, oleander is a very drought-tolerant ornamental. Oleander is now commonly found in warmer areas of the United States. It is often planted as an ornamental hedge along roads and gardens, although it is occasionally grown as a houseplant. The leaves are thick and leathery and vary from four to twelve inches in length. The veins in the leaf are perpendicular to a prominent midrib down the center of the leaf. The fruit produced by the plant is approximately one to four inches in length and is about the size of a pencil in diameter.

Oleander poisoning has been a serious problem with livestock. Oleander is rarely eaten fresh from a bush. Livestock and horses generally eat clippings from pruned plants once they have fallen to the floor of a field in which they are grazing. Plant portions also remain toxic when they are included in hay and prepared feeds.

The toxic cardiac glycoside of oleander is definitely water-soluble and should leaves fall into a pond, it is conceivable that the water could become toxic. The toxin does however impart a bitter taste to the water.

Oleander contains a cardiac glycoside which is similar in action to digitalis but is more toxic. These toxins include oleandrin, andromedotoxin or grayanotoxin which can cause poisoning at doses as low as 0.2% of the body weight of the animal. The leaves, bark, and stems of the plant are equally toxic.

Clinical signs of poisoning may be delayed for up to three hours following ingestion. Typically nausea and vomiting are seen first followed by diarrhea, sometimes bloody, and tenesmus (straining). The animal will become weak and depressed. Incoordination will occur followed by leg paralysis, recumbency (unable to stand), and eventually coma and death.

The most lethal effects of the poison involve the heart. All of the glycosides alter the sodium/potassium channels within the cell membrane of the heart muscle and interfere with calcium homeostasis. Intracellular potassium is decreased and intracellular sodium is increased in cardiac muscle fibers as a result of this interference. Depending on the stage of the poisoning, the pulse may be rapid and weak or slow and strong. Various cardiac arrhythmias may occur and may include heart block, dropped beats, tachycardia (rapid heart rate), bradycardia (slow heart rate) and in the terminal stages ventricular fibrillation. The circulatory collapse causes anoxia (inability to get oxygen). The extremities are frequently cool to the touch and the body temperature may drop below normal. Clinical signs of toxicity may be seen up to 24 hours after the plant has been evacuated from the gastrointestinal tract.

Non-lethal doses will lead to myocardial necrosis (death of some of the heart muscle). This heart damage will then lead to congestive heart failure. Even those animals receiving a low dose are likely to have impaired endurance and performance.

Lethal dosage for the oleander toxin is extremely small. All plant material should be removed from the digestive tract immediately. Repeated dosages of activated charcoal may be beneficial to prevent absorption following evacuation of the stomach. Digibind®, manufactured by GlaxoSmithKline, may be given as an antidote, usually given as 1.7 ml of Digibind per mg of digoxin equivalent ingested, although this may be cost prohibitive in large patients. Animals receiving Digibind should be monitored for anaphylaxis (severe allergic reaction). Patients should be monitored for hypokalemia (low potassium levels). Lidocaine and phenytoin have been used to correct conduction disturbances of the heart with variable success. Atropine has been used for bradycardia and Propranolol has also been reported as helpful.

References:

Fowler, Murray E. DVM. Plant Poisoning in Small Companion Animals. Ralston Purina Company. 1981. 29-31.

Plumb, Donald. Veterinary Drug Handbook. 5th Edition. Blackwell Publishing. 2004. Pp. 251-254.

Peterson Michael DVM and Patricia Talcott DVM. Small Animal Toxicology. Second Ed. 2006. Elsevier Inc. p.462.

Gupta, Ramesh DVM, ed. Veterinary Toxicology. Elsevier 2007. p.196.