Toxicity of Rhododendrons to People and Animals

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Rhododendron Poisoning


Rhody

 "The first written account of rhododendrons goes back to the 4th Century B. C. in Greece. It relates to the poisoning of ten thousand soldiers by honey of Rhododendron luteum (Azalea pontica). Rhododendron poisoning has since been confirmed repeatedly. A poisonous compound is found in rhododendron nectar, producing low blood pressure, shock and even death."

 Rhododendron luteum

 from the Ozark ARS Chapter Newsletter, September 1998

Historic Accounts of Rhododendron and Azalea Poisoning

In William Watson's 1911 book, Rhododendrons and Azaleas, he has this account of Rhododendron and Azalea toxicity:

According to Professor Sargent, they [Rhododendron] possess bitter, astringent, and narcotic properties. A decoction of R. chrysanthum is employed in Siberia in the treatment of rheumatism and other affections of the joints and muscles, and is now used in some European countries for the same purpose. The buds of R. ferrugineum are used in Northern Italy in the preparation of an anti-rheumatic liniment, and in the United States a decoction of the leaves of R. maximum is occasionally used for the same purpose. Honey obtained from the flowers is believed to be poisonous, yet the flowers of the Indian R. arboreum are eaten fresh or made into a conserve, although the buds and young leaves are said to be poisonous to cattle. Goats and sheep have been poisoned by the leaves of R. cinnabarinum and R. afghanicum. The dried leaves of R. campaulatum are used in India as snuff, and the leaves of R. lepidotum and R. anthopogon as stimulants. The Chinese use the leaves of various species to adulterate tea. In this country [Britain] Rhododendrons are not usually eaten by animals, not even by rabbits and hares, but when they have been eaten by accident their effect has been noxious.

There is [a] Pontic Rhododendron known to gardeners as Azalea pontic and to botanists as Rhododendron flavum [luteum]. It is the deciduous, twiggy, hairy-leaved yellow or orange flowered shrub that grows a yard or so high, is as hardy as Box [Boxwood], and flowers profusely in spring. Seeds of it were first sent to England by Dr. P. Pallas, who collected them in Crimea and gave them to Messrs. Lee and Kennedy of Hammersmith. This is the plant whose flowers are said to poison the honey obtained from them. Mr. H. J. Ross has stated in the Gardeners' Chronicle that the poisonous principle is got rid of by heating the honey. It has never been recorded that honey is affected in this country [Britain] by this Azalea, although the flowers are favourites with bees.

Note: Watson's book is considered the first treatise on Rhododendrons and Azaleas for gardeners. It was soon followed by Monograph of Azaleas, by Ernest Henry Wilson and Alfred Rehder (1921), Rhododendrons for Amateurs by E. H. M. Cox (1924), and Rhododendrons for Everyone by Frank Kingdon Ward (1926). In the 1921 book, Alfred Rehder writes:

Behr (Fl. Vicin. San Francisco, 173) states that the [Rhododendron occidentale] root contains a powerful narcotic, and according to Jepson (Fl. W. Middle Calif. ed. 2, 311) the plant is feared by sheepmen as poisonous.

In 1967, David Leach (author of Rhododendrons of the World) did extensive research on anecdotes in history about rhododendron poisoning and published it in the Brooklyn Botanic Garden Record, Vol. 21, No. 4:

In 401 BC, Xenophon of Athens led 10,000 Spartan soldiers in retreat from an unsuccessful invasion of the Persian Empire. Two days' march from the Black Sea coast of Turkey, they retreated in to a village where the locals gave them honeycombs. They soon "lost their senses and were seized with vomiting and purging, none of them being able to stand on their legs." Those who ate very little were like drunken men. Those who at much were like madmen. Great numbers lay on the ground. The next day none of them had died, but had recovered their senses. By the fourth day they had recovered and the Persians had not discovered their vulnerable predicament.

In 67 BC, 334 years later, Pompey the Great of Rome embarked to defeat the King of Pontus, Mithridates VI. In 66 BC, part of Pompey's army camped in the same area near the Black Sea coast of Turkey where Xenophon's army had been poisoned. History repeated itself. Locals gave Pompey's troops honeycombs. This time, the Pontic army learned of their predicament and massacred Pompey's party. It took Pompey an additional three years to defeat the Pontic army.

Leach also details how for many years, many cultures have attempted to use Grayanotoxins from Rhododendron chrysanthum to treat rheumatism and gout. Such attempts were accomplished their goal but were complicated with severe side-effects and, in some cases, death. Finally a pharmaceutical company in Germany was able to isolate the particular Grayanotoxin, Grayanotoxin I, to successfully treat high blood pressure.


Rhododendron Toxicity

Plant Azalea and Rhododendron
Toxic Agents Grayanotoxin (formerly known as andromedotoxin, acetylandromedol, and rhodotoxin), arbutin glucoside
Type of Poisoning Internal poisoning
Poisonous Part All parts
Symptoms Nausea, salivation, vomiting, weakness, dizziness, difficulty in breathing, loss of balance. 100 to 225 grams of azalea (Rhododendron occidentale) leaves must be eaten to seriously poison a 55 lb child.
From University of Pennsylvania Veterinary School (http://cal.vet.upenn.edu/projects/poison/plants/ppazale.htm)
Plant Azalea and Rhododendron
Toxic Principle Andromedotoxins (grayanotoxins) are water-soluble diterpenoid compounds. Leaves and flower nectar (including honey made from plant nectar) are sources of the toxin.
Toxicity As little as 3 ml nectar/kg body weight or 0.2% of the body weight, as leaves may be toxic or lethal.
Mechanism Andromedotoxins bind to and modify the sodium channels of cell membranes, leading to prolonged depolarization and excitation. Modification of the sodium channels favors calcium movement into cells and results in a positive inotropic effect similar to that of digitalis.
Clinical signs Salivation and a burning sensation in the mouth are followed by emesis, diarrhea, muscular weakness and impaired vision. Bradycardia, hypotension (caused by vasodilation) and atrioventricular block are serious cardiovascular effects that may be lethal. Dyspnea, depression, and prostration develop, and death may occur within 1-2 days. Ruminants often bloat. Aspiration pneumonia can develop secondary to emesis.
Treatment Detoxification: Emesis is used where appropriate. Activated charcoal should be administered repeatedly the first day.
Supportive therapy: Fluid replacement therapy and respiratory support may be necessary. Atropine is recommended for severe bradycardia. Isoproterenol or sodium channel blockers (e.g., quinidine) may be used to treat heart block.
Precautions Honey made from the plants has been reported to cause cardiac arrhythmias, emesis, mild paralysis and convulsions in humans and is known as “mad honey”.
From Purdue University Veterinary School (http://www.vet.purdue.edu/toxic/plant10.htm)
Plant Azalea and Rhododendron
Toxicity Rating Moderate. These plants grow wild in the East and cause significant problems there, the danger from these plants in Indiana is much less.
Poisonous Part All parts, especially leaves.
Symptoms Stomach irritation, abdominal pain, abnormal heart rate and rhythm, convulsions, coma, death.
Mechanism These plants, as well as mountain laurel (Kalmia spp.) contain grayanotoxins (glycosides), that affect the gastroenteric (stomach and intestines) and cardiovascular systems. The older name for this toxin was andromedotoxin.
In order for toxic signs to manifest, 0.2% by weight of green leaves needs to be ingested. Gastroenteric signs develop first, generally within 6 hours of ingestion, including salivating, vomiting (in capable species), diarrhea, abdominal pain, and tremors. Disturbances in cardiac rate and rhythm may then be noted. If sufficient quantities were consumed, convulsions may occur, followed by coma and death. Not all affected animals will die, and livestock may recover without treatment, depending upon amount ingested.
First Aid Prevent further ingestion and provide supportive care. Veterinary attention is needed if ingestion was recent, or if clinical signs are present.

Mad Honey Disease

From U S Food & Drug Administration Center for Food Safety & Applied Nutrition Food borne Pathogenic Microorganisms and Natural Toxins 1992 (Bad Bug Book)

Honey Intoxication (Food And Drug Information)

1. Name of Toxin: Grayanotoxin (formerly known as andromedotoxin, acetylandromedol, and rhodotoxin)

2. Name of Acute Disease: Honey Intoxication

Honey intoxication is caused by the consumption of honey produced from the nectar of rhododendrons. The grayanotoxins cause the intoxication. The specific grayanotoxins vary with the plant species. These compounds are diterpenes, polyhydroxylated cyclic hydrocarbons that do not contain nitrogen. Other names associated with the disease are rhododendron poisoning, mad honey intoxication or grayanotoxin poisoning.

3. Nature of Disease: The intoxication is rarely fatal and generally lasts for no more than 24 hours. Generally the disease induces dizziness, weakness, excessive perspiration, nausea, and vomiting shortly after the toxic honey is ingested. Other symptoms that can occur are low blood pressure or shock, bradyarrhythima (slowness of the heart beat associated with an irregularity in the heart rhythm), sinus bradycardia (a slow sinus rhythm, with a heart rate less than 60), nodal rhythm (pertaining to a node, particularly the atrioventricular node), Wolff-Parkinson-White syndrome (anomalous atrioventricular excitation) and complete atrioventricular block.

4. Normal Course of the Disease: The grayanotoxins bind to sodium channels in cell membranes. The binding unit is the group II receptor site, localized on a region of the sodium channel that is involved in the voltage-dependent activation and inactivation. These compounds prevent inactivation; thus, excitable cells (nerve and muscle) are maintained in a state of depolarization, during which entry of calcium into the cells may be facilitated. This action is similar to that exerted by the alkaloids of veratrum and aconite. All of the observed responses of skeletal and heart muscles, nerves, and the central nervous system are related to the membrane effects.

Because the intoxication is rarely fatal and recovery generally occurs within 24 hours, intervention may not be required. Severe low blood pressure usually responds to the administration of fluids and correction of bradycardia; therapy with vasopressors (agents that stimulate contraction of the muscular tissue of the capillaries and arteries) is only rarely required. Sinus bradycardia and conduction defects usually respond to atropine therapy; however, in at least one instance the use of a temporary pacemaker was required.

5. Diagnosis of Human Illness: In humans, symptoms of poisoning occur after a dose-dependent latent period of a few minutes to two or more hours and include salivation, vomiting, and both circumoral (around or near the mouth) and extremity paresthesia (abnormal sensations). Pronounced low blood pressure and sinus bradycardia develop. In severe intoxication, loss of coordination and progressive muscular weakness result. Extrasystoles (a premature contraction of the heart that is independent of the normal rhythm and arises in response to an impulse in some part of the heart other than the sinoatrial node; called also premature beat) and ventricular tachycardia (an abnormally rapid ventricular rhythm with aberrant ventricular excitation, usually in excess of 150 per minute) with both atrioventricular and intraventricular conduction disturbances also may occur. Convulsions are reported occasionally.

6. Associated Foods: Grayanotoxin poisoning most commonly results from the ingestion of grayanotoxin-contaminated honey, although it may result from the ingestion of the leaves, flowers, and nectar of rhododendrons. Not all rhododendrons produce grayanotoxins. Rhododendron ponticum grows extensively on the mountains of the eastern Black Sea area of Turkey. This species has been associated with honey poisoning since 401 BC. A number of toxic species are native to the United States. Of particular importance are the western azalea (Rhododendron occidentale) found from Oregon to southern California, the California rosebay (Rhododendron macrophyllum) found from British Columbia to central California, and Rhododendron albiflorum found from British Columbia to Oregon and in Colorado. In the eastern half of the United States grayanotoxin-contaminated honey may be derived from other members of the botanical family Ericaceae, to which rhododendrons belong. Mountain laurel (Kalmia latifolia) and sheep laurel (Kalmia angustifolia) are probably the most important sources of the toxin.

7. Relative Frequency of Disease: Grayanotoxin poisoning in humans is rare. However, cases of honey intoxication should be anticipated everywhere. Some may be ascribed to an increase consumption of imported honey. Others may result from the ingestion of unprocessed honey with the increased desire of natural foods in the American diet.

8. Target Population: All people are believed to be susceptible to honey intoxication. The increased desire of the American public for natural (unprocessed) foods, may result in more cases of grayanotoxin poisoning. Individuals who obtain honey from farmers who may have only a few hives are at increased risk. The pooling of massive quantities of honey during commercial processing generally dilutes any toxic substance.

9. Analysis in Foods: The grayanotoxins can be isolated from the suspect commodity by typical extraction procedures for naturally occurring terpenes. The toxins are identified by thin layer chromatography.

10. Selected Outbreaks: Several cases of grayanotoxin poisonings in humans have been documented in the 1980s. These reports come from Turkey and Austria. The Austrian case resulted from the consumption of honey that was brought back from a visit to Turkey. From 1984 to 1986, 16 patients were treated for honey intoxication in Turkey. The symptoms started approximately 1 h after 50 g of honey was consumed. In an average of 24 h, all of the patients recovered. The case in Austria resulted in cardiac arrhythmia, that required a temporal pacemaker to prevent further decrease in heart rate. After a few hours, pacemaker simulation was no longer needed. The Austrian case shows that with increased travel throughout the world, the risk of grayanotoxin poisoning is possible outside the areas of Ericaceae-dominated vegetation, namely, Turkey, Japan, Brazil, United States, Nepal, and British Columbia. In 1983 several British veterinarians reported an incident of grayanotoxin poisoning in goats. One of the four animals died. Post-mortem examination showed grayanotoxin in the rumen contents.


Chronic Mad Honey Intoxication Syndrome (CMHI)

Oxford Journals, Vol. 11, No. 7, Pp 954-56

Department of Cardiology, Division of Pacing and Electrophysiology, Institute of Cardiology, Istanbul University, Haseki-Fatih, Istanbul, Turkey and Department of Cardiology, Cerrahpasa School of Medicine, Istanbul University, Fatih, Istanbul, Turkey

In this study, two hospitals in Turkey evaluated the history of non-commercial honey intake in all patients referred to our institution for investigation of slow heart rate or atrioventricular (AV) conduction abnormalities. Between April 2008 and December 2008, 173 patients were referred to our institution for assessment of sinus bradycardia and various degrees of AV block and/or permanent pacemaker implantation. All patients were questioned about history of honey intake. Detailed evaluation revealed a history of daily honey intake for a long period of time in five of the patients (2.8%). This non-commercial honey was made by different amateur beekeepers in eastern Back Sea region of Turkey. Discontinuation of honey intake resulted in prompt normalization of conduction and significant symptomatic improvement. None of the patients were admitted to hospital and all were asymptomatic during 3 months follow-up. Holter monitoring for 24-h revealed no abnormality at first and third month.


Mad Honey Poisoning in Turkey

European Society of Cardiology 25 June 2013 Press Release

Dr. Ugur Turk, from Central Hospital, Izmir, Turkey, reports on the cases of a 68 year old father and 27 year old son who were both admitted to the Izmir emergency department at the same time with symptoms of vomiting and dizziness. Surface ECGs revealed both patients to have complete atrioventricular block and atrial flutter with slow ventricular responses.

When a history was taken both father and son reported that their breakfasts over the past three mornings had included high amounts of honey from the Black sea region of Turkey. This information immediately triggered Turk and colleagues to consider that their patients could be suffering from ‘mad honey poisoning’.

Mad honey poisoning occurs after people consume honey contaminated with grayanotoxin, a chemical contained in nectar from the Rhododendron species ponticum and luteum. Grayanotoxin is a neurotoxin that binds to the sodium channels in the cell membrane, maintaining them in an open state and prolonging depolarisation.

“It’s like the effect of cholingeric agents, and results in stimulation of the unmyelinated afferent cardiac branches of the vagus nerve which leads to a tonic inhibition of central vasomotor centres with a reduced sympathetic output and a reduced peripheral vascular resistance,”says Dr. Turk, “This in turn triggers the cardioinhibitory Berzold-Jarisch reflex which leads to bradycardia, continued hypotension, and peripheral vasodilatation.”

Mad honey poisoning generally lasts no more than 24 hours, with symptoms of the mild form including dizziness, weakness, nausea, vomiting, excessive perspiration, hypersalivation and paraesthesia. Symptoms of the more severe form include syncope, seizures, complete atrioventricular block and even fatal tachyarrhythmias (due to oscillatory after potentials).

While no specific antidote exists for grayanotoxin poisoning mild cases can be treated with atropine and selective M2 muscarinic receptor antagonists; while for the more severe form treatment options include temporary pacemaker implantation, and vasopressor agents.

The possibility of honey poisoning, says Dr. Turk, should always be considered in previously healthy patients admitted with unexplained hypotension, bradycardia and other rhythm disturbances. The condition occurs most frequently in people who have consumed honey from the Black sea region of Turkey, a major bee keeping area that is also the native habitat of Rhododendron ponticum and luteum.

“The dissemination of honey around the world means that physicians any where may be faced with honey poisoning,” says Dr. Turk. Anyone buying honey from Turkey should first consume a small amount and leave it a few days before eating any more to check that they do not experience strange side effects."

The symptoms of both father and son resolved without the need for any medications and they were discharged from hospital on the fourth day. When their honey was sent away for melissopalynology, (analysis of the pollen contained in honey) the result revealed it did indeed contain pollen from Rhododendron ponticum and luteum..

[U. Turk, E. Tuncer, E. Alioglu. Mad honey: so sweet pass out. FP 1297. Arrhythmias Poster Session. 25 June 2013. 14:00 local time.]


Children in North Korea Die of Azalea Poisoning

North Korea Today No. 154 Jun 2008

Hungry Children in Daehongdan Die from Eating Azalea Flowers

Children in North Korea died after eating azalea flowers in Daehongdan County. In Sambong Middle School, 9 students were dead from azalea poisoning. Adults know what to eat and what not, but young children can’t tell and just put anything in their mouths because they are hungry. After eating three or four potatoes, they are still hungry and they run up to the mountains and pluck anything to eat. This spring, they ate fistful of azalea petals several times and they died of poisoning. Chang Mi-oak says, ‘They pick basketful of azalea petals and eat them, but if they eat too much at one time, it causes gastrospasms. If they eat them when their stomach is empty, they will die foaming in their mouth. I suffered gastrospasms when I ate azalea. Adults like me cannot control hunger; it is needless to say in case of children.’

Lee Sung-ja says, ‘I warn my older child everyday. The older one would not do, but my younger one may eat flowers while I am not around. So whenever they go out together I admonish the older one, ‘don’t let your brother eat flowers’ several times. My older one tells me that many of his classmates die and asks me, ‘Mother, what can I do?’ It pains me greatly. Children who have no parents die so easily.’

http://www.reliefweb.int/rw/RWB.NSF/db900SID/ASIN-7G4NR5?OpenDocument

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Rhododendron ponticum in Sherlock Holmes and Ancient History

Rhododendron ponticum, the plant Sherlock mentions as being in Addlestone, can cause temporary paralysis—or at least it does in Guy Ritchie's Sherlock Holmes movie. In the 2009 film, Sherlock Holmes proposed that the villian Lord Blackwood used hydrated Rhododendorn ponticum as a way to arrange his own fake execution. Some of the symptoms of being dosed with the toxin can make you seem like you’re dead when you’re not and they used the toxin in the 2009 Sherlock Holmes movie for that exact purpose. “Here is a toxin refined from the nectar of Rhododendron ponticum. It’s quite infamous in the region of Turkey, bordering the Black Sea, for its ability to induce an apparently mortal paralysis. Enough to mislead a medical mind.” Sherlock also uses this poison on Gladstone (his dog) to illustrate his point.

It was also mentioned in the third episode of Season 2 of BBC's Sherlock (TV series), and has been speculated to have been a part of Sherlock's fake death scheme. During the search for the missing children, Sherlock identifies the vegetation sample from a footprint as belonging to the same plant that can induce a death-like sleep, reducing a hearbeat to almost nothing. It can also result in watery eyes which is observed in this episode and is very out of character for Holmes.

It’s not terribly poisonous, about 100 grams need to be ingested by a 25 kg child to seriously poison them, but it is a problem for livestock – particularly sheep, goats and cows – who munch on the flowers and get seriously sick. If you boil it down and concentrate the liquid… well that’s a different story. The toxin is water soluble, so it can be extracted from the leaves and flowers.

The toxin is called grayanotoxin. It binds to specific sodium ion channels in the victim's cell membranes and prevents inactivation, causing persistent activation of muscle and nerve cells. This causes a range of symptoms based on where the activated cells are located, such as muscle weakness, vomiting, sweating, salivation, seizures, and either dangerously slow or dangerously fast heartbeat, depending on the dose. In the end, it can cause death.

Honey from Rhododendron ponticum and Rhododendron luteum took out an army in 401 BC lead by Xenophon of Athens against Persia – hundreds of soldiers vomiting and unable to walk for a day. No-one died, unlike in 67 BC, where the army of Mithradates VI killed Pompey the Great’s soldiers while they were incapacitated. Pompey's soldiers consumed honey made from Rhododendron deliberately left behind by Pontic forces. It was biological warfare, defeat had never tasted sweeter.

Rhododendron poison, made a comeback after 2400 years on the big screen!

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Horticulturist Struck by Rhododendron Poisoning

"That Why The Lady is a Tramp" by David G. Leach in the Journal of the American Rhododendron Society, October 1982, pp 151-2

David Leach reported on an incidence of rhododendron poisoning at Inverewe Gardens in Scotland:

Mr. Robert Hebb, Director of Horticulture of the Cary Arboretum, Millbrook, New York, was leading a group of American gardeners through the rhododendron collection at Inverewe Gardens in Scotland. When he stopped to photograph the salmon-pink flowers of 'Lady Chamberlain.', he jostled a branch and two drops of nectar fell on his finger. Preoccupied with his photography, he unthinkingly removed the sticky nectar by putting his finger in his mouth. Hebb knew almost immediately that he had created a serious problem. Within one or two minutes, the pleasantly sweet nectar produced a "pins and needles" tingling sensation in his fingers and toes, accompanied by numbness and lack of control in his limbs, such as when they "fall asleep."

Within five minutes, his coordination was so impaired that he had great difficulty walking to a nearby bench. He felt weighed down by an overwhelming depression. He had a suffocating foreboding of death. He was unable to speak intelligibly, but felt the need to hide his condition from his companions. The acute symptoms lasted 20 to 25 minutes. He then returned to the group, walking with difficulty. Speaking slowly, he was able to explain his pale and shaken appearance.

In another twenty minutes he became extremely thirsty and hungry. His mind cleared. In an hour and forty minutes after the incident, he became drowsy and a headache intensified. After sleeping for an hour, he awakened without symptoms of any kind.

Many of these are the classic symptoms of Grayanotoxin poisoning. It produces a narcotic action on the brain, difficult breathing, paralysis, convulsions, and ultimately respiratory failure. As little as 28 milligrams kills a rabbit in a few hours. Mr Hebb was lucky to recover without medical intervention. Not everyone is as fortunate.

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Rhododendron Toxicity in Animals

From Purdue University (http://vet.purdue.edu/)
  • PLANTS: Azaleas, Rhododendron (Rhododendron spp.) (heath family)
  • TOXICITY RATING: Moderate. These plants grow wild in the East and cause significant problems there, the danger from these plants in Indiana is much less.
  • ANIMALS AFFECTED: All animals may be affected.
  • DANGEROUS PARTS OF PLANT: all parts, especially leaves.
  • CLASS OF SIGNS: Stomach irritation, abdominal pain, abnormal heart rate and rhythm, convulsions, coma, death.
  • PLANT DESCRIPTION: These perennial shrubs have tough, glossy, smooth-margined evergreen leaves. The large, showy flowers are in terminal clusters and have five white, pink, or red petals (fig. 10). Some horticultural varieties have yellow or orange petals. Common and local names for these plants include "lambkill" and "calfkill". These plants have been used by people to commit suicide.
  • SIGNS: These plants, as well as mountain laurel (Kalmia spp.) contain grayanotoxins (glycosides) that affect the gastroenteric (stomach and intestines) and cardiovascular systems. The older name for this toxin was andromedotoxin.
    In order for toxic signs to manifest, 0.2% by weight of green leaves needs to be ingested. Gastroenteric signs develop first, generally within 6 hours of ingestion, including salivating, vomiting (in capable species), diarrhea, abdominal pain, and tremors. Disturbances in cardiac rate and rhythm may then be noted. If sufficient quantities were consumed, convulsions may occur, followed by coma and death. Not all affected animals will die, and livestock may recover without treatment, depending upon amount ingested.
  • FIRST AID: Prevent further ingestion and provide supportive care. Veterinary attention is needed if ingestion was recent, or if clinical signs are present.
  • SAFETY IN PREPARED FEEDS: These plants are not safe in hay nor in any other prepared feed.
  • PREVENTION: Animals should not be allowed to graze these plants. Keep hungry livestock away from areas where these plants grow. Pets may nibble or taste the leaves out of curiosity or boredom, and this is not advised, but seldom leads to clinical toxicosis. Honey made from the nectar of these flowers is also toxic and should not be consumed, so exercise caution when placing beehives.

Rhododendron Poisonng in Ruminants

From Cornell Veterinary Medicine

  • Description: RHODODENDRON can be toxic to ruminants. Outbreaks of toxicosis have been reported when sheep were hungry and had access to the plant. Dx by history and finding the leaves in the vomitus, feces, or rumen. Toxins in this plant were discussed by Casteel and Wagstaff. There may be secondary pneumonia due to regurgitation. Treat by rumenotomy when cost effective and treatment of secondary pneumonia; treatment was discussed by Mayer.
  • Species: Bovine [oxen or cattle], Caprine [goats], Ovine [sheep]
  • Signs: Abdominal distention, Abnormal lung or pleural sounds, Agalactia, Anorexia, Arrhythmia, Ataxia, Bloat in ruminants, Colic, Constant or increased vocalization, Coughing, Cyanosis, Diarrhea, Dullness, Dysmetria, Dyspnea, Excessive salivation, Fever, Generalized weakness, Inability to stand, Increased respiratory rate, Ingesta in nasal passage, Mucoid nasal discharge, Opisthotonus, Pain on external abdominal pressure, Paraparesis, Purulent nasal discharge, Rumen hypomotility or atony, Seizures or syncope, Sudden death, Tachycardia, Tetraparesis, Trembling, Tremor, Vomiting or regurgitation, Weak pulse.

Rhododendron simsii Poisoning in Birds

From Cornell Veterinary Medicine

  • Description: Leaves of Rhododendron (RHODODENDRON SIMSII) have been reported to be toxic to birds (LaBonde). Dx by dietary history.
  • Species: Avian
  • Signs: Anorexia, Diarrhea, Dullness, Generalized weakness, Vomiting or regurgitation.

Antidotes for Rhododendron Poisoning in Goats

From GoatWorld.com

Recipe #1 for Rhododendron Poisoning in Goats

Quantities do not need to be too exact.

Ingredients:

  • ¼ cup cooking oil
  • ½ cup strong/strong cold tea (6 to 8 tea bags removed) ["English" tea]
  • 1 teaspoon ground ginger
  • 1 teaspoon baking soda

MIX ALL TOGETHER and drench the goat with it all.

How does this work?

Oil puts a lining on the stomach preventing more poison going into the system, tea is the antidote, and ginger relieves pain, baking soda helps bring up the gas.


Recipe #2 for Rhododendron Poisoning in Goats

Ingredients:

  • 15 mls Renco (rennet)
  • 15 mls Mylanta (milk of magnesia)
  • 5 mls brandy

Mix all together - This is the adult dose!

  • For kids under 4 months give 5 mls each of Renco and Mylanta and 2 mls brandy.
  • For kids over 4 months give 10 mls of both Renco and Mylanta and 5 mls brandy.
  • Treat goatlings as adults.

Renco is the tradename for junket rennet and you can buy it in any supermarket. It is good for a variety of gastric ailments in goats, and it works even when it is well past its UseBy date, so don't chuck it out just because you can't use it for junket or cheese any more. The action of the rennet is to neutralise the toxins from the rhododendron. Mylanta is the trade name for milk of magnesia. Sometimes you'll find it in a supermarket but more often you have to go to a chemist. Again, it is useful for a number of stomach upsets in goats (as well as humans).

Its action is twofold: it puts a lining on the gut, and it regulates the pulsing of the gut (peristalsis), which often gets out of kilter with poisoning or colic.

The brandy works, but I haven't yet found out why. It is a fortified spirit so has a high alcohol percentage and you don't need much. Alternatively you can use sherry, which is a fortified wine. They are both made from grapes, and work better for medicinal purposes than spirits or wines made from grain or other substances. I got 100 mls of bulk brandy from my local Liquorland. The staff were highly amused when I told them what it was for, although I admit I have nicked the odd tablespoonful for making fruit mince.

It is usual for goats with rhododendron poisoning to vomit rather spectacularly, everything within a 5 metre radius is likely to be covered in green slime. For this reason it is difficult to drench them with an antidote because it is easy for things to go down the wrong hole and either drown the goat within minutes or cause inhalation pneumonia which isn't treatable in the farm situation. That is why I like this recipe because the amounts are small, and you can take 15 minutes over the drenching, a ml or two at a time between sickies, if you have to. One dose is usually sufficient. I've never heard of anyone having to give two although if the goat did not show improvement within an hour after dosing, one could consider a repeat.

It is important to keep the goat warm, but not in the sun, and out of the wind. Have a bucket of fresh warm water available for the animal to drink, and each time it gets fouled by vomit (which has stuck to the face hair) empty and refill it, otherwise the goat will just be drinking up more poison. A goat which is vomiting all over the place is getting rid of the toxins much more efficiently than one which is not, so vomiting is good.

Once the goat is feeling better, offer a mixture of yummies, a handful of various weeds like yarrow, cleavers, dock, prairie grass or twitch, some green pine needles, tree lucerne (tagasaste), willow, and some good plain hay or straw. Don't give much at a time as anything which is fouled will have to be thrown away, so why waste it by being over-generous?

Some other evergreens such as camellias will give similar symptoms to rhododendron, though not usually so severe, and the goat may not vomit. The recipe will work pretty well on most forms of poisoning, including toadstool spores. It also does a good job as a first-aid measure in organo-phosphate poisoning until you can bring goat and vet together. I suggest sticking both Lorraine's and my recipes on the wall beside your telephone so you always know where they are, and you have immediate access if someone else phones you in a panic.

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References on Rhododendron Poisoning

  • Barton, Benjamin Smith. Some Account of the Poisonous and Injurious Honey of North America, Transactions of the American Philosophical Society, vol 5, 1802, pp. 51-70.
  • Lampe, Kenneth F. Rhododendrons, Mountain Laurel, and Mad Honey, Journal of the American Medical Association, Vol. 259, #13, April 1 1988, p. 2009.
  • Leach, David. Ancient Curse of the Rhododendron, American Horticulturist, Vol. 51, 1972, pp. 20-29.
  • Leach, David. That's Why the Lady is a Tramp, Journal of the American Rhododendron Society, October 1982, pp. 151-152.
  • Mayor, Adrienne. Mad Honey! Archaeology, vol 48, #6, November/December 1995, pp. 32-40.
  • Mirkin, Gabe. Side Effects of Raw Honey, Journal of the American Medical Association, Vol. 266, #19, November 20, 1991, p. 2766.

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