Recent print news about the deliberate and malicious poisoning of a dog and two horses with oleander baits was confirmed in the April 2016 California Food Animal Health and Food Safety (CFAHS) bulletin.1 An 18-year-old draft horse and a dog died after ingesting baits placed along a fence line and in a horse paddock. A second horse developed clinical signs but recovered. The baits appeared to be cookies and contained “oats, shredded apples, carrots, and molasses” as well as “very small green leaf fragments throughout.”1 Analysis of the baits showed large amounts of oleandrin, one of the toxins found in the shrub Nerium oleander.1
Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) are the two most common species of oleander in the dogbane family Apocynaceae.2,3Nerium oleander is native to the Mediterranean region and T. peruviana to tropical America regions. Both species are currently grown as ornamental evergreen shrubs in many tropical and subtropical areas, but N. oleander is the prevalent species in the United States. Although a few hardy varieties exist elsewhere in the United States, N. oleander is found primarily in the Southern states and California.4 Little T. peruviana is present in these areas. More frequently it is used as an ornamental shrub in many parts of Mexico and Central American countries. Let’s concentrate on N. oleander.
Nerium oleander is well-described as a shrub or small tree growing to heights of six to 12 feet.2,3 The narrow leaves, often described as lancet-shaped, are dark green with rather distinct yellowish veins and grow in pairs or whorls of three.
Clusters of two- to three-inch-diameter, five-lobed, fringed, white-, pink-, salmon- or red-colored flowers are found at the branch ends. Fruits are present as a long, slender pod or capsule with downy seeds, and the sap is clear and sticky.
All parts of the N. oleander plant are toxic.2,3,5 Cardiac glycosides, the known toxins, are found in the roots, stems, leaves, flowers, seeds and fruit as well as sap, plant nectar and even water in which oleander leaves have been floating.2,6 Roots and stems contain the highest amount of toxin, with the amount in leaves and flowers following closely behind.2,3 Interestingly, the total cardiac glycoside content is reported to be highest in plants with red flowers.2,5 A number of different cardenolide glycosides have been identified in N. oleander, with some references suggesting there may be as many as 30 separate glycosides.3,7 Oleandrin, however, with a mechanism of action similar to digoxin or digitoxin, remains the most widely recognized cardiac glycoside in most scientific papers.2,3
A little goes a long way
The toxic dose of N. oleander varies depending on the plant part and concentration of toxin. It is difficult to find a single toxic dose that includes all animal species. Most suggested toxic doses are related to leaves, although it is often hard to know whether they are green or dry leaves. An ingested dose of 0.005% of an animal’s weight in dry leaves is generally considered lethal to horses and ruminants.4,5 This amount is equal to about 10 to 20 leaves for a mature horse. Other ruminant studies suggested a minimal lethal dose of 50 mg leaves/kg.8 This information is complicated by a suggested lethal dose in sheep of 110 mg dry leaves/kg6 and much larger amounts in goats.8 Recently, a suggested dose of 0.25 mg green leaves/kg was associated with poisoning in dogs.7
Heart-stopping effects, among others
Cardiac glycosides act at the cellular level to inhibit the sodium-potassium-ATPase pump present on cardiac myocytes.2-4 The overall change is an increased concentration of intracellular sodium and corresponding increase in extracellular potassium. In addition, an influx of extracellular calcium along with release of bound intracellular calcium from the sarcoplasmic reticulum results in an increased force of cardiac contraction (positive inotropic effect).2-4 The accompanying increase in sympathetic outflow causes a decrease or alteration in normal electrical conduction causing atrioventricular (AV) blocks, ventricular arrhythmias and asystole.
The cardiovascular, gastrointestinal (GI) and neurologic systems are all affected. Clinical signs in all animal species generally occur with 30 minutes to a few hours of ingestion. GI signs include hypersalivation, vomiting, abdominal pain and diarrhea. Horses may show decreased GI motility, colic and evidence of renal failure.4,9 Recently, clinical signs consistent with hypoglycemia were reported in a dog ingesting oleander leaves.9 Sinus bradycardia, AV block, atrial fibrillation or ventricular fibrillation are commonly reported cardiovascular dysrhythmias.2,4,7,9 Neurologic signs include lethargy, drowsiness, weakness, tremors, ataxia and mydriasis.
Fingering the guilty party
The diagnosis is based on a history of plant ingestion, description of plant and parts ingested and time of ingestion. The history of plant ingestion, presence of hyperkalemia, and electrocardiographic abnormalities support oleander toxicosis but are not a definitive diagnosis. Several toxicologic methods of diagnosis are currently available but take some time to obtain and may not be effective in guiding clinical care. Currently several different immunoassays are available for confirming the presence of N. Oleander cardiac glycosides in blood.2,4,9 Of these, the specific digoxin immunoassay (Digoxin III—Abbott Laboratories) is a rapid and sensitive test for the determining presence of oleandrin and therefore N. Oleander in blood.2 The definitive diagnosis for legal cases, however, is liquid chromatography mass spectrometry analysis of biological fluids.
Ameliorating the effects
If animals are physiologically capable of vomiting and are not already doing so, emesis should be induced if presented within the first hour or so after ingestion. This should be followed with a single dose of activated charcoal with a cathartic and two additional doses of activated charcoal administered every six to eight hours. In animals, such as horses, that are unable to vomit, mineral oil via a nasogastric tube followed one to two hours later with activated charcoal is recommended. Hospitalization is required for all animals with known ingestions, as is close electrocardiographic monitoring for 24 hours if clinical signs are present. Baseline blood glucose and electrolyte (including serum potassium) concentrations and serum chemistry profile results (including BUN and creatinine concentrations) are useful for guiding therapy.4,7,9 Digoxin specific FAB fragments (Digibind—GlaxoSmithKline) have been used successfully to reverse the cardiac effects of N. oleander exposure, but their high cost may preclude use.2,4,9
Further therapy is supportive and based on clinical signs. Early but cautious use of intravenous fluids is needed to maintain blood pressure yet not overload the cardiovascular system. Atropine or glycopyrrolate are options for treating bradycardia, although in some severe situations a temporary pacemaker may be needed. Lidocaine or procainamide may be needed if the animal is persistently tachycardic and nonresponsive to intravenous fluids, has severe ventricular dysrhythmias or has evidence of poor perfusion (hypotension, pulse deficits, tachycardia, pale mucous membranes, prolonged capillary refill time). Antiemetics and gastric protectants are indicated in most cases. Fructose-1,6-diphosphate has been used successfully in experimentally poisoned dogs to lessen the severity of cardiac effects, but clinical use has not been examined.7 Calcium channel blockers and beta-blockers are contraindicated as they can have additive effects on AV conduction and may result in complete heart block.
Is there hope?
It is difficult to provide a prognosis, as each case is unique. Many animals, in particular large animals such as horses and cows, are often found dead in the pasture. Survival is increased in those animals provided with timely intervention and appropriate care. The occurrence of severe cardiac arrhythmias complicates recovery but is not insurmountable.
Animal caretakers, in particular those with small animals, are advised to learn to identify N. oleander, recognize the environmental presence and keep animals far from it. Nerium oleander grows wild in many parts of Texas, Arizona, Nevada and California, and off-leash pets should be watched closely for any signs of exposure. Those individuals with large animals should be cognizant of what is growing in their pasture and along the fence lines. Shrub clippings, a common source of equine poisonings, should not be disposed of in the pasture or left along the fence line but discarded in areas away from any susceptible animals. It is only through continued vigilance that animals can be kept safe from this beautiful, yet deadly shrub. Sadly, even under the best of circumstances, poisonings continue to occur.
1. CAHFS Connection, April 16, 2016. Available at: www.vetmed.ucdavis.edu/cahfs/local_resources/cahfs_connection/2016/CAHFS_Connection_201604.pdf
2. Bandara V, Weinstein SA, White J, et al. A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning. Toxicon 2010;56:273-281.
3. Kiran C, Prasad DN. A review on Nerium Oleander Linn. (Kaner). Int J Pharmacog and Phytochem Res 2014; 6:593-597.
4. Smith PA, Aldridge BM, Kittleson MD. Oleander toxicosis in a donkey. J Vet Intern Med 2003;17:111-114.
5. Soto-Blanco B, Fontenele-Neto JD, Silva DM, et al. Acute cattle intoxication from Nerium oleander pods. Trop Anim Health Prod 2006;38:451-454.
6. Aslani MR, Movassaghi AR, Mohri M, et al. Clinical and pathological aspects of experimental oleander (Nerium oleander) toxicosis in sheep. Vet Res Comm 2004;28:609-616.
7. Bellodi C, Socha JJM, Hatayde MR. Experimental poisoning of dogs with green leaves of Nerium oleander and use of fructose 1,6 diphosphate and glucose as treatment. PUBVET 2014;8:Art 1679.
8. Barbosa RR, Fontenele-Neto JD, Soto-Blanco B. Toxicity in goats caused by oleander (Nerium oleander). Res Vet Sci 2008;85:279-281.
9. Page C, Murtaugh RJ. Hypoglycemia associated with oleander toxicity in a dog. J Med Toxicol 2015; 11:141-143.
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Pet Poison Helpline, an animal poison control center based out of Minneapolis, is available 24 hours, seven days a week for pet owners and veterinary professionals that require assistance treating a potentially poisoned pet. The staff provides treatment advice for poisoning cases of all species, including dogs, cats, birds, small mammals, large animals and exotic species. Pet Poison Helpline is available in North America by calling 800-213-6680. Additional information can be found online at www.petpoisonhelpline.com