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Journal American Rhododendron Society

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Dr. Glen Jamieson ars.editor@gmail.com


Volume 36, Number 4
Fall 1982

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Thatís Why the Lady is a Tramp
David G. Leach, North Madison, Ohio

       Readers of this and other publications on rhododendrons here and overseas may remember several articles on rhododendron poisoning which appeared a few years ago. One, published in Rhododendron Information, entitled "The Two Thousand Year Curse of the Rhododendron", was a detailed account of the historical impact and medical record of lethal honey produced from rhododendron nectar, and of equally deadly rhododendron tea prescribed by 18th and 19th century doctors, mainly for the cure of arthritis.
       I concluded the article, "...the hazard to humans from any source but honey is infinitesimal." The reassurance was not entirely justified, as later information has demonstrated.
       One reason is that rhododendron poisoning is extremely difficult to diagnose, and even more unlikely to be identified by an autopsy. The poisonous compound is acetylandromedol, which produces a profound depression of blood pressure, shock and death. Such fatalities occur routinely each year overseas, especially on the shores of the EÓlack Sea, where honey is produced by bees from the nectar of R. flavum (syn.: luteum). In the United States, poisonous honey appears only intermittently in about six-year cycles when bees are repelled by flowers near ground level wet from protracted rains. Alternative sources of nectar are then sought, especially R. occidentale; the honey produced from the nectar of that azalea can be extremely dangerous. Each spring, in the doctors' lounges of some hospitals in the Pacific Northwest, bulletins are posted as reminders to consider rhododendron poisoning as a possibility for patients with undiagnosed illnesses.
       The publication of the articles has continued to produce letters reporting cases of rhododendron poisoning, and accounts of allergic reactions suffered by propagators handling cuttings, especially of lepidotes and of azaleas; and of urticaria ("hives") contracted by susceptible persons removing faded flowers trusses or even brushing against rhododendrons in flower. The cultivar, 'Pride of Leonardslee', derived from R. fortunei x R. thomsonii is particularly virulent in its concentration of acetylandromedol. The well known English horticulturist, Geoffrey Gorer, at Haywards Heath in Sussex, wrote that his gardener must avoid any contact with 'Pride of Leonardslee' lest he be afflicted with nettle rash, as the British call it, of the utmost severity. There is no proof that acetylandromedol in rhododendrons also acts as an allergen, but there seems to be a strong association between species and hybrids known to contain a high concentration of it, and the appearance of urticaria among people who are exposed to these rhododendrons.
       Professor Fang Wen-pei, at Szechwan University, has written me that Rhododendron molle has been known to be poisonous since some time before 800 to 1,000 A. D. An authoritative herbal published in the Han dynasty refers to its use in China as a poison, and, in very small quantities, for medicinal purposes.
       Natives of Appalachia often believe that rhododendron foliage is innocuous because deer browse on it when other forage is not available in the winter. However, deer produce in their stomachs an enzyme which renders acetylandromedol harmless. Horses which consume the more virulent species and hybrids die quickly, and most knowledgeable farmers are careful to keep their cattle away from rhododendrons when grazing is poor.
       Perhaps the most dramatic account of contemporary human poisoning has been sent to me by Mr. Robert Hebb, Director of Horticulture at the Cary Arboretum, Millbrook, New York. He was leading a group of American gardeners through the rhododendron collection at Inverewe, Scotland, when he stopped to take a close-up photograph of the pendant salmon-pink flowers of 'Lady Chamberlain.' As he jostled the branch on which they were borne, two drops of nectar fell on his finger. Although he had read at least one of the articles on rhododendron poisoning, he was preoccupied with his camera and he unthinkingly removed the sticky nectar by putting his finger in his mouth.
       Hebb knew almost at once that he had inadvertently created a serious problem. Within one to two minutes the pleasantly sweet tasting nectar produced a tingling "pins and needles" feeling in fingers and toes, accompanied by the numbness and lack of control that occurs when a limb, deprived of blood circulation, "falls asleep." Within five minutes after ingestion of the nectar, his coordination was so impaired that he had great difficulty walking to a nearby bench to rest. He felt weighed down by an overwhelming depression. His mind then became disoriented.
       Hebb's account suggests that his thought processes were disassociated. He had a suffocating foreboding of death; irrationally, he dreaded discovery in his condition by his companions at the same time that he imagined himself floating in space. He relates in his letter how he was unable to speak intelligibly. The syllables of words were not in correct sequence; "rhododendron" became "doderendron".
       The acute symptoms lasted 20 to 25 minutes. He then returned to his tour group, walking with some difficulty. Speaking slowly and with intense concentration, he was able to explain his pale and shaken appearance. In another 20 minutes he became extremely thirsty and then hungry. His mind cleared. An hour and 40 minutes after the incident he became drowsy and a headache which had earlier developed, intensified. After sleeping for about one hour he awakened without symptoms of any kind.
       Many of these are the classic symptoms of acetylandromedol poisoning, first described 2,400 years ago in Anabasis by Xenophon, after his soldiers had eaten poisonous honey.
       'Lady Chamberlain' was doubtless named for a benign and gracious peeress of faultless character. But her wayward predilection makes the Lady truly a femme fatale, if not a tramp. She was bred from R. cinnabarinum, a species so toxic in its tissues that browsing cattle, even goats, are commonly killed in its Sikkimese homeland.
       Acetylandromedol produces a narcotic action upon the higher centers of the brain, as it simultaneously and progressively causes dypsnoea, paralysis, convulsions and, finally, respiratory failure. As little as .28 milligrams kills a rabbit in a few hours.
       It is apparent that Mr. Hebb was an involuntary practitioner of brinksmanship. Several more drops of ingested nectar would almost certainly have been fatal. His graphic account of his brush with death is unique among survivors of rhododendron poisoning.
       As a matter of perspective, it seems appropriate to point out that many plant genera are poisonous in whole or in part, including those that are grown for ornamental purposes. The venomous monkshood is notorious; the common English yew contains an alkaloid, taxine, which is rapidly absorbed and causes sudden death; buxine, found in boxwood, causes respiratory failure; oleander is deadly in all of its parts. The list is long. Even the eating of green and sprouting parts of potatoes may cause severe poisoning.
       So rhododendrons are far from alone as potential killers. The antidote, as always, is foreknowledge and a continuing awareness of the peril of ingesting any part of them. Although not all species and hybrids are poisonous, and, in fact, the flowers of some are candied in honey by natives of the Himalaya, few hobbyists will want to play Russian roulette.
       Readers who are interested in obtaining a detailed history of poisoning by acetylandromedol in honey, and of the misuse of rhododendron extracts in medicine, are referred to Rhododendron Information, published by the American Rhododendron Society and to The Rhododendron and Camellia Yearbook 1968, published by The Royal Horticultural Society.
       The gathering of this information was originally undertaken because of interest in an extract for the possible treatment of high blood pressure. Inasmuch as the Middle East was the repository of medical knowledge during the Middle Ages in Europe, the research began at the library of the University in Istanbul. The trail led from there to the Library of the Palace of Rectors in Dubrovnik, Yugoslavia, and then to the Bibliotheque Nationale in Paris. Additional information was obtained in the Library of the British Museum in London; from the New York Public Library in New York; from the Library of the Museum of Natural History in Philadelphia; and from the Library of the Hunt Institute for Botanical Documentation in Pittsburgh. Most of the sources were named, with their authors, in the article but a complete bibliography was inadvertently omitted. The search required the services of translators in Greek, Latin, Arabic, medieval and modern German, French and Russian.


Volume 36, Number 4
Fall 1982

DLA Ejournal Home | JARS Home | Table of Contents for this issue | Search JARS and other ejournals