What makes a plant poisonous? What effects do poisons delivered by arrow, spear point, knife, or dart have on the victim? Answers to these questions are not as clear-cut as one might think. Botanist Edward R. Ricciuti wrote,
How many species are capable of poisoning people? No one really knows. The toxic properties of hundreds, even thousands, of species may await discovery, and inclusion in the medical literature. The poisons in many common plants may be undetected simply because no one ever has eaten them, or if someone has, the symptoms of poisoning never have been linked to the plants.
The common wisteria exemplifies the on-going discovery of poisonous plants. This woody vine with its cascading blossoms grows in gardens all over the world, but only in 1961 was it discovered that ingesting its pea-like seeds causes severe stomach poisoning.1
The plethora of known poisonous plants and the continuing discovery of those once thought to be chemically passive may clarify conflicting opinions between Native Americans and non-Indian botanists. The succeeding chapters cite plants believed by Native Americans to be poisonous, regardless of the lack of confirmation by modern botanists, for North American Indians had a much more intimate relationship with the flora of their world than contemporary botanists, and for tens of thousands of years longer.
Poisonous plants grow throughout the world and do not seem to be environmentally bound. They appear in most plant families and are so widely and randomly distributed in the plant kingdom that no botanical grouping can be defined exclusively on the basis of poisonous qualities.
Plant poisons number in the hundreds, but generally one or more compounds from a handful of major chemical groups account for the toxicity. Of these, the most important is the alkaloids, complicated organic compounds characterized by the nitrogen they contain.2
Plant chemicals with medicinal value, phytochemicals, are secondary metabolites, a class of chemicals not required for plant activities such as photosynthesis. Most often defensive in nature, secondary metabolites provide plants the nauseous or toxic chemicals to ward off predators.
Alkaloids, of which there are thousands, form the largest group of phytochemicals, with about 10 percent of them occurring in flowering plants. They appear in certain mushrooms and mosses, as well as in a limited number of animals, such as beaver and spotted salamander. The most powerful ingredients in strychnine, caffeine, nicotine, opium, and curare, they generate the hallucinogenic effect of LSD and peyote, the latter comprising thirteen narcotic alkaloids, including mescaline.
Poisonous plants also contain glycosides, resins, and acids. Glycosides are carbohydrates whose poisonous by-products include cyanide, digitalis, and one of the several toxic compounds in solanine, the poison in nightshade, the most notorious of the Solanaceae. The danger in Jack in the Pulpit, for example, is an acid whereas the toxic “milk” of the milkweed is a resin.3
Most ingredients in arrow poisoning were floral in nature, but many societies incorporated insects and animals or animal products, such as scorpions, poisonous ants, spiders, caterpillars, snake venom, and decayed animal organs. Plant poisons exercise their toxic effects through the action of alkaloids, acids, glycosides, and resins, but the poisons derived from animal products generally induce gas gangrene, tetanus, and severe infection because of the presence of those spores in decaying animal matter. Bacterial flora in the mouths and venom glands of poisonous snakes is a crucial factor in understanding snakebite poisoning. “Overwhelming bacterial infections secondary to snakebite wounds frequently produce morbidity and mortality when the venom alone would not have been sufficiently toxic to do so. Poisonous snakebite wounds have been described as contaminated venom-laden, anaerobic puncture wounds, which predispose to infection and tissue destruction.”4 Significantly, many tribes treated arrows with the rapidly acting plant poisons for hunting and those for war with animal poisons.
Snake venom as an arrow poison is widely known. Dozens of North
American Indian groups applied rattlesnake venom, alone or as an ingredient in a complex recipe, to their arrows. Bushmen in southwest Africa mix a resin extracted from the root of Buphane toxicaria (Ox-bane) with the venom of the ringhals that, on the fingernail-sized heads of their arrows, can with one shot kill large game animals over a period of several hours. Another venom-based African poison is concocted from puff adders and crushed beetles, plants, and resins. In eastern India, Bengali tribesmen tie small wads of cotton soaked in cobra venom to the tips of their arrows.5
Although Native Americans used a great variety of plant products (roots, flowers, seeds, twigs, fruits) as poisons, they considered Cicuta spp. (Water Hemlock), Datura spp. (Sacred Thornapple), Veratrum viride (American False Hellebore), and Aconitum spp. (Monkshood) the most poisonous.
The major species of Cicuta used by North American Indians—C. masculata, C. occidentalis, C. virosa, and C. douglasii—exude a yellow, resinous substance called cicutoxin, a highly unsaturated higher alcohol that acts on the central nervous system. Its effects provide it the distinction of being the most poisonous plant genus in North America. It permeates the plant but is most concentrated in the root, and a piece the size of a pea can kill a man.
Within fifteen to thirty minutes of ingesting Cicuta root, the victim experiences sharp stomach pains, vomiting, rapid pulse, dilated pupils, dizziness, diarrhea, and finally convulsions so powerful that he or she often bites off the tongue and shatters teeth. Death comes from respiratory failure after complete paralysis. Thirty to 50 percent of Cicuta poisoning leads to death.
Cicutoxin poisoning has at times resulted from mistaking Cicuta for artichokes, celery, sweet potatoes, sweet anise, wild ginseng, or water parsnip. Since record keeping began in 1900, one death per year has been attributed to this plant. Anecdotal accounts suggest how quickly it can kill.6 A fisherman in Kentucky confused C. masculata and wild parsnips, and a few bites of the root resulted in convulsions thirty minutes later. A French soldier drank soup to which Cicuta had been accidentally added and was dead three hours later. In another case, a man mistook C. masculata for parsley and lived only fifteen minutes after ingesting it.
Datura belongs to the nightshade family, that of tobacco, tomatoes, hot peppers, potatoes, and eggplants. Species used by Native Americans include Datura wrightii (Sacred Thornapple or Southwestern Thorn-apple), D. meteloides (Sacred Datura), D. stramonium (Jimson Weed), and D. Inoxia (Toloache) with D. stramonium more prevalent in the East and D. meteloides in the West.
Datura is extremely toxic. The Centers for Disease Control and Prevention reports that 89 percent of Datura usage results in poisoning, four to five grams of leaf proving fatal to a child. In an adult, as little as half a teaspoon of crushed seeds will produce complete delirium followed by weeks of disorientation, and ingestion of a mere twenty seeds is lethal. The poisonous solanaceous alkaloids (tropane configuration)—including atropine, hyoscamine (isomeric with atropine) and hyoscine (scopolamine)— cause intense thirst, visual disturbances from the atropine that can last from six hours to three weeks, flushed skin, central nervous system hyperirritability, delirium, rapid heartbeat, elevated temperature, violent hallucinations, convulsions, and coma leading to death.
The story of D. stramonium’s popular name, Jimson Weed or Jamestown Weed, offers a dramatic description of poisoning. The account, written in 1705 by Robert Beverly, describes events in 1676 when soldiers were sent to Jamestown, Virginia, to quell elements of the Bacon rebellion. They were served soup, which was accidentally spiced with D. stramonium.
Some of them eat plentifully of it, the effect of which was a very pleasant comedy for they turned into fools upon it for several days. One would blow up a feather in the air; another would dart straws at it with much fury; another, stark naked, was sitting in a corner, like a monkey, grinning and making faces at them; a fourth would fondly kiss and paw his companions and sneer in their faces with a countenance more antic than any Dutch Droll. A thousand such simple tricks they played and after eleven days, returned to themselves again, not remembering anything that had passed.7
Many American Indian groups considered Veratrum viride (American False Hellebore) and V. californicum (California False Hellebore) highly toxic. V. viride possesses sixty toxic steroidal alkaloids, the most potent being jervine, cyclopamine, cycloposine, pseudo-jervine, cevadine, ru-bijervine, and veratralbine. Jervine depresses circulation and the central nervous system and irritates motor centers in the brain, causing convulsions. Veratralbine slows the pulse rate, lowers blood pressure, and impedes respiration. Hellebore roots are five to ten times more poisonous than the leaves or the stems. Symptoms of poisoning include extreme muscular weakness, frequent nausea and vomiting, cold and clammy skin, giddiness, and impaired vision. A powerful cardiac and spinal depressant, Hellebore can paralyze the heart muscle and cause fatality.
Various species of Aconitum, including Aconitum columbianum (Columbian Monkshood), produce aconitines, a group of toxic alkaloids. The scientific name derives from the Greek word for “dart” and suggests its use as an arrow poison. The popular name Wolfsbane is believed to relate to ancient times when Aconitum served as a wolf poison. Its toxicity results from several monobasic alkaloids, including aconine and aconitine. Symptoms, which occur within a few hours of ingestion, include tingling and numbness of the tongue and mouth, a sensation of ants crawling over the body, nausea and vomiting, labored breathing, cold and clammy skin, and giddiness. More powerful than prussic acid, a dose of one to six and a half milligrams causes fatality in an adult.
A fourteen-year-old boy ate leaves of A. napellus (Common Monkshood) and was dead two hours later. A man mistook the root of A. napellus for horseradish, and a small portion on the tip of his knife killed him within a few hours. In 1841, a disgruntled Irish housewife sprinkled A. napellus over her husband’s greens; he died three hours later.8 Many poisons will be surveyed in the succeeding chapters; however, the discussion of Datura, Cicuta, Veratrum, and Aconitum has established that plant poisons can impair body functions, cause excruciating pain for weeks at less-than-lethal doses, or kill quickly and horribly. Particularly in the case of Cicuta and Aconitum, extremely small doses can lead to fatality. Further, plant poisons can kill in a number of ways: they depress respiration to the point of death, they paralyze the heart muscle, and they bring about coma and convulsions. Finally, toxic chemical agents carried in poisonous plants tend to be alkaloids, acids, resins, and glycosides, occurring singly or in combinations.
About five hundred years ago, Theophrastus Paracelso (sometimes identified as Paracelsus), a Swiss biologist who claimed that everything he knew came from a witch, left this axiom: “Dosis sola facit venenum” (“The dose alone makes a poison”). Most North American Indian poisons were also taken medicinally for a variety of ailments. The knowledge of dosage, as well as the general effects of the substance, made the difference between a potion of life and one of death.
World History
