Oleander (Nerium oleander) is an evergreen shrub belonging to the Apocynaceae family. There are three species which have leathery, lanceolate leaves with an entire margin, often arranged in whorls. The flowers, which grow in bunches at the end of each branch, can be of various colours.
According to data collected in both Italy and Europe, intoxication by poisonous plants is fairly common, particularly in cats. Oleander is the main cause of intoxication due to plants in dogs, particularly in those animals which live outside.
MECHANISM OF ACTION
All parts of the plant are extremely toxic to both humans and animals. The varieties with red flowers seem to be more toxic because they contain a larger amount of cardioactive glycosides. In fact, the toxicity of the oleander is due to a group of cardioactive glycosides, steroid molecules similar to digotoxin, which can have pharmacological effects on the heart.
At low doses, glycosides have therapeutic effects on the heart, as they increase the contractile force of the myocardium, decrease the heart rate and increase the cardiac output. However, since the therapeutic window is rather narrow, overdosage, with consequent toxic effects, can occur. Toxic doses cause severe arrhythmias and disturbances of myocardial pacemaker conduction, which can lead to a decrease in cardiac output and death. Glycosides act by inhibiting the Na+/K+ ATPase pump, an enzyme system in the heart that acts in synergy with the Na+/Ca++ exchange mechanism and whose correct function enables the sequence of excitation-contraction phases of the cardiac cell. Inhibition of the pump causes an increase in the intracellular concentration of Na+ and Ca++ which induces an increase in the strength of contraction of the myocardium. The increase in calcium ions raises the resting potential of the cell membrane, giving rise to arrhythmias. Following inhibition of the Na+/K+ ATPase pump there are changes in the K+ ion fluxes, with a decrease of intracellular K+ and an increase in the extracellular concentration of the ion (hyperkalaemia).
Dogs, like humans, are particularly sensitive to the effects of cardiac glycosides and this similarity between the two species is also seen in the clinical manifestations following intoxication with these substances. The explanation for this fact probably lies in the structural similarity of the Na/K ATPase pump in the two species, such that the cardiac glycosides bind the two structures with equal affinity, while they have less affinity in other animals (for example, the rat).
The cumulative oral dose considered toxic in the dog is 150-225 mg/kg divided into three doses of 50-75 mg/kg at intervals of 24 hours. Survival varies from 76 to 90 hours. The cumulative oral dose that is toxic in the cat is 220-450 mg/kg divided into three doses of 37.5-75 mg/kg at intervals of 24 hours.
SIGNS
The clinical signs become apparent over a period varying from 1 to 24 hours after exposure and involve the gastrointestinal tract and the heart. Immediately after ingestion there is abdominal tenderness, nausea, vomiting, salivation and local irritation of the mucosae. Diarrhoea, which may be bloody, can occur. The pulse may be slow and strong (early and with moderate digitalis-like intoxication), then fast and weak. Electrocardiography shows disturbances of heart conduction which, when severe, can contribute to causing ataxia, hypotension, cold extremities, dyspnoea, shock, coma and death.
DIAGNOSIS
The diagnosis is made from the history (ingestion of the plant), identification of the plant in the gastrointestinal contents, and the presence of clinical signs. Post-mortem findings include subendocardial haemorrhages (uncommon), congestion, pulmonary oedema, and degeneration and necrosis of the myocardium (rare findings). The detection of glycosides in the serum, urine, tissues or gastric contents by chromatographic techniques can contribute to the diagnosis.
The glycosides of oleander can cross-react with the radioimmunological assay for digoxin.
TREATMENT
The treatment is symptomatic and consists of decontamination of the gastrointestinal tract (through the induction of vomiting and gastric lavage) and administration of activated charcoal and laxatives. An adequate state of hydration should be maintained and any fluid-electrolyte imbalance controlled.
In humans and dogs the administration of Fab fragments of specific antibodies to digoxin which bind oleander-derived glycosides and facilitate their elimination through the kidneys can reduce the amount of circulating glycosides. This is possible due to the cross-reactivity between the glycosides of oleander and the antibodies specific for digoxin. Numerous administrations are, however, necessary.
OTHER PLANTS THAT ARE TOXIC TO THE CARDIOVASCULAR SYSTEM
Cardioactive glycosides are present in 11 plant families: Apocynaceae, Asclepiadaceae, Celastraceae, Brassicaceae, Lilaceae, Moraceae, Fabaceae, Ranunculaceae, Scrophulariaceae, Sterculiaceae, andTiliaceae. The glycosides that have a specific effect on the heart are found in at least 34 genera of these families. The best known cardiac glycosides are digoxin and digitoxin, derived from digitalis (Digitalis lanata).
The table reports other commonly occurring plants that can cause intoxication in small animals and, like oleander, can provoke cardiac effects with involvement of the gastrointestinal system.
|
Scientific name |
Common name |
Details |
|
Digitalis purpurea |
Purple foxglove |
Dogs, cats, rabbits (and large animals). The leaves, flowers and seeds are poisonous and can be fatal if ingested because they contain cardioactive glycosides including digitoxin and digoxin. The water collected in saucers under the vases containing this plant is also toxic. Symptomatic treatment. |
|
Persea americana |
Avocado |
Birds (canaries, parakeets, cockatiels). The toxin, contained in the fruit, leaves, seeds and bark, is fatal to small aviary birds. The main cause of poisoning is owners who integrate the diet of these birds with fresh fruit. Death occurs 24-48 hours after ingestion. Clinical signs: reduced activity, inability to remain perched, dyspnoea. Cardiac lesions found in birds include hydropericardium with subcutaneous oedema and generalised congestion. |
|
Convallaria majalis |
Companion animals. The glycosides are contained in the leaves and flowers. Clinical signs: vomiting, diarrhoea, nausea, anorexia, abdominal cramps. Cardiac signs may be found late. High doses cause weakness, depression, collapse and death. Symptomatic treatment (activated charcoal and cathartics). |
|
|
Taxus baccata |
All species. All the plants contain a mixtures of toxic alkaloids (taxanes). The minimum oral lethal dose of yew leaves in the dog is estimated to be 30 g: considering a mean weight of 13 kg for a dog, the oral LD is about 2.3 g of leaves/kg p.v. The clinical signs appear from 1 to 48 hours after ingestion: tremors, dyspnoea, lack of co-ordination, collapse, bradycardia followed by acute heart failure, subacute meningitis and diarrhoea culminating in death. Symptomatic treatment (activated charcoal and cathartics). |
|
|
Rhododendron spp. |
All species. All parts of the plant, especially the leaves, contain the grayanotoxin (glycoside) that affects the gastrointestinal and cardiovascular systems. Clinical signs (which appear within 6 hours): gastric irritation, salivation, anorexia, depression, uncontrollable vomiting, weakness, ataxia, cardiac arrhythmias. Symptomatic treatment. |
Suggested readings
- Bandara V, Weinstein SA, White J, Eddleston M. A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning. Toxicon 2010;56:273-81.
- Langford SD, Boor PJ. Oleander toxicity: an examination of human and animal toxic exposure. Toxicology 1996;109:1-13.
- Berny P, Caloni F, Croubels S, et al. Animal poisoning in Europe. Part 2: Companion animals. Vet J 2010;183:255-9.
- Baskin SI, Czerwinski SE, Anderson JB, Sebastian MM. Cardiovascular toxicity – toxic plants affecting the cardiac system. In: Veterinary Toxicology. Basic and Clinical Principles. Gupta CG (2007) 1st ed. Academic Press, Elsevier, USA.
- Knight AP, Walter RG. Plants affecting the cardiovascular system. In [11]: A Guide to Plant Poisoning of Animals in North America. Internet Publisher: International Veterinary Information Service, Ithaca NY (www.ivis.org [12]), 2002; http://www.ivis.org/special_books/Knight/chap2/chapter_frm.asp?LA=1 [13]
- Amorena M., Caloni F., Mengozzi G. Epidemiology of intoxications in Italy. Vet Res Commun 2004;28:89-95.
- Ceruti A, Ceruti M, Vigolo G. Botanica Medica, Farmaceutica e Veterinaria con Elementi di Botanica Generale. 1993 Zanichelli Editore.
- Wilson CR, Hooser SB. Toxicity of yew (Taxus spp.) alkaloids. In: Veterinary Toxicology. Basic and Clinical Principles. Gupta CG (2007) 1st ed. Academic Press, Elsevier, USA.
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