Poisonous Plants of Indiana and Kentucky
BIOL L564 Local Flora: Summer Flowering Plants
Indiana University Southeast
Poisonous plants contain a substance that, when consumed by a herbivore in sufficient quantity, can cause damage or illness (James et al. 2019). Some poisonous plants can cause harm when touched or handled by humans or animals. Poisonous plants are responsible for illness and death in humans and wild and domesticated animals. These plants also cause damages and losses to farmers in Indiana and Kentucky every year (Heron & LaBore 1964). There are around 100 species of plants growing in Indiana and Kentucky that are considered poisonous, many of which can cause harm to livestock. Around one-third of these can cause serious illness or agricultural problems (Heron & LaBore 1964).
In this paper, I examine poisonous plants and why plants are poisonous, how these plants inflict harm on humans and wild and domesticated animals, the defense mechanisms of plants, the evolution of plant poisons and the coevolution of herbivores, the environmental factors which impact poisonous plants, and the spread of poisonous invasive species. In addition, I examine some of the most common poisonous plants from seven plant families that greatly impact the natural ecosystems and agricultural resources of Indiana and Kentucky and pose the greatest threat to humans and pets. I also discuss the poisonous chemicals produced by each plant and how the chemical(s) affect humans and animals.
Poisonous plants are harmful to humans and animals, both wild and domesticated. The poisoning of humans and domesticated animals by toxic plants continues to be a significant risk, especially for children and pets (Panter et al. 2018). When wild animals are exposed to unfamiliar forages or non-native and/or invasive plant species, they are at increased risk for potential poisoning. Plant poisonings are likely to increase in wildlife populations as humans encroach on natural areas, destroy habitats, and interrupt migratory routes (Panter et al. 2018).
Poisonous plants also adversely impact plant and animal agriculture. Even though our knowledge about poisonous plants and their toxins has continued to grow, poisonings continue to occur in livestock (Panter et al. 2018). In general, poisoning by plants only occurs when an animal eats too much of a plant too quickly or continuously grazes on a poisonous plant for an extended period (Panter et al. 2018). Poisoning can also occur when hay or forages are harvested in areas where poisonous plants are abundant. Animals may be poisoned when they are fed contaminated hay containing a high percentage of poisonous plants (Panter et al. 2018).
Plant poisons are secondary metabolites created by plants for a variety of reasons. These chemicals, while not related to the primary physiological functioning of the plant, often play a vital role in its survival. Virtually all plants invest resources in the production of secondary metabolites (Smilanich et al. 2016). The production of these chemicals comes at a cost to the plant, which is generally offset by an increase in the plant’s level of fitness (Smilanich et al. 2016). The toxins found in poisonous plants are from a wide variety of classes of chemicals which, when consumed by animals, affect one or more organs in different ways (James et al. 2019).
These secondary metabolites created by plants play an important role in driving the interactions between plants and other organisms in terrestrial communities (Smilanich et al. 2016). These chemicals defend plants from herbivores and pathogens, are used by herbivores as feeding cues and by insects as oviposition cues, and attract the natural predators of the herbivores feeding on the plants (Smilanich et al. 2016).
Evolution of Defense Mechanisms
Plants have evolved a variety of methods to protect themselves such as physical and mechanical barriers to consumption including the growth of spines or thorns, tough, woody tissues, and hydrophobic cuticles to protect against bacterial or fungal infestations (Pysek & Cock 2007). Plants often use a combination of physical and chemical defense methods. The production of secondary compounds for defense such as tannins, lignins, and proteinase inhibitors is incredibly common (Pysek & Cock 2007). Some plants secrete toxic chemicals that are effective even at low doses, such as alkaloids, cyanogenic glycosides, glucosinolates, non-protein amino acids, coumarins and terpenoids (Pysek & Cock 2007). Plants are often under selective pressure from both specialist and generalist herbivores and therefore may develop multiple toxins or utilize different levels of concentrations of toxins depending on the pressure faced (Smilanich et al. 2016).
When plant poisons were first studied, it was thought that these substances were waste products, however, very few of these poisonous compounds are by-products of or essential for plant metabolism (Laycock 1978; James et al. 2019). Research now shows that the toxic secondary metabolites found in plants are created to be defense mechanisms that protect the plant against insects and other herbivores (Laycock 1978). In some plants, the concentration of poisonous compounds is so high or the compounds are so structurally complex that the cost of producing and storing them would be unreasonable unless the compounds substantially increased the fitness of the plant, such as by serving as a defense mechanism (James et al. 2019). In some cases, toxic substances may provide more than one benefit. For example, the oxalates produced by plants in the Halogenton genus may deter predators, but also help the plants overcome osmotic and moisture stress (James et al. 2019). Further, the number and variety of poisonous compounds and species of plants producing these compounds is too great for their evolution to be coincidental. The fact that herbivores and insects have developed resistance to, methods for sequestration of, and detoxification of plant poisons suggests the coevolution of poisonous plants and herbivores (James et al. 2019).
If poisons did evolve as defense mechanisms in plants, they could function in several different ways: toxicity, palatability, and aversive conditioning, in which animals learn that eating a plant will make them sick and avoid that plant in the future (Laycock 1978). If being poisonous reduces the amount of photosynthetic tissue eaten off a plant and therefore increases chances of survival, it is more likely that plant toxicity evolved as a defense mechanism against specialist insects or disease-causing bacteria and/or fungi rather than generalist herbivores (James et al. 2019). Many poisonous plants are unpalatable, which can be an advantage in communities subjected to pressure by grazing animals. However, palatability is subjective and an unpalatable plant would not necessarily need to be poisonous to reduce its chances of being eaten (James et al. 2019). Being poisonous and unpalatable does not always prevent a plant from being eaten by herbivores (Laycock 1978). It is likely that to be an evolutionary benefit, palatability would need to be linked to aversive conditioning (James et al. 2019). Any of these defenses can function to reduce the amount of poisonous plants being eaten, and therefore make the poisonous plants more competitive (Laycock 1978).
Palatability and Aversive Conditioning
Aversion to toxic substances based on taste has been evidenced in a variety of animals (James et al. 2019). It is concluded that when animals eschew poisonous plants, the toxins are detectable through palatability (James et al. 2019). While no ubiquitous relationships between palatability and chemical compounds exist, most animals have a preference for sweet flavors and avoid the astringency of tannins and the bitterness of cyanogenic glycosides and alkaloids (James et al. 2019).
Bitterness acts as a repellent to most animals. This evasion of bitter substances is a behavioral trait attained through natural selection and coevolution alongside poisonous plants (Hankins et al. 1974). That many poisonous plants are toxic is not what repels animals from eating them. Their palatability, specifically their bitterness, is what repels animals from eating poisonous plants (Bate-Smith 1972).
Coevolution of herbivores
The evolution of plant defenses, including the formation of toxic secondary metabolites, has been heavily influenced by herbivores since they first began interacting 420 million years ago (Smilanich et al. 2016). If plants evolved poisons as defense mechanisms against herbivores, it stands to reason that herbivores have coevolved adaptations to prevent being poisoned by plants. Some of the adaptations herbivores have developed to prevent poisoning include: eating a generalized diet to reduce the chance of eating too much of a toxic species, the ability to detect poisonous plants and avoid them, and the ability to detoxify plant poisons (Laycock 1978).
Most large herbivores are generalists, which likely reduces the chances of eating a toxic amount of a poisonous plant (James et al. 2019). Native animals that coevolve alongside vegetation are better able to avoid poisonous native plants than domesticated animals. Many herbivores have coevolved to avoid eating poisonous plants or have adaptations that allow them to detoxify or sequester the toxins in their body to avoid being poisoned (James et al. 2019).
Detoxification and Sequestration
Some herbivores have coevolved with poisonous plants, developing adaptations that allow them to detoxify plant poisons (James et al. 2019). While detoxification from a toxic compound varies across species, native animals that coevolved with the plant community should be more able to detoxify from poisonous compounds than livestock that did not go through the same coevolutionary process (James et al. 2019). Native animals, including big game animals, tend to avoid poisonous plants but can eat some without serious harm. However, deaths of native animals from poisonings do occur, indicating that abilities to detect and avoid or otherwise detoxify from poisonous plants are not unerring (James et al. 2019).
In addition to the ability to detoxify poisonous compounds, some insects have developed the ability to sequester toxins from plants within their bodies for self-defense. Monarch butterflies are a well-studied example of an insect with this adaptation. As caterpillars, monarch butterflies feed on milkweed plants which secrete a latex substance from damaged tissues that contains a cardiac glycoside known as cardenolide (Roeske et al. 1976). This toxin accumulates in the tissues of the monarch caterpillar but does not poison it. Rather, by selectively sequestering and metabolically altering the cardenolides, the monarch can diminish adverse effects while maintaining the toxins for its own benefit (Roeske et al. 1976). If the monarch has accumulated high enough levels of cardenolide in its tissues, it will cause vomiting in any bird which eats it (Roeske et al. 1976). Much like the aversive conditioning learned by herbivores in response to eating poisonous plants, predators learn to avoid consuming monarchs from this response (Roeske et al. 1976; Laycock 1978).
Resistance to plant poisons in insects is thought to have evolved in response to consuming poisonous plants, however, adaptations to plant toxins may be evolutionarily linked to sequestration and not simply a means to eat toxic plants (Petschenka & Agrawal 2015). The variation in toxins found in poisonous plants is a critically important driver for the co-evolution of poisonous host plants and insects that forces sequestering herbivores to tread a fine line between intoxication and protection from predators (Züst et al. 2018).
Environmental factors impact the effects of poisonous plants
Environmental factors have been observed to impact the effects of poisonous plants. Problems stemming from the ingestion of poisonous plants tend to increase during periods in which rainfall levels are below normal, resulting in a reduction of the amount and variety of vegetation available for grazing (Panter et al. 2018). When typical grazing grasses are reduced due to drought or other environmental factors, animals are more likely to graze on poisonous plants.
The level of toxicity of a plant can also be impacted by environmental conditions, as can the response of an animal to ingested toxins. Factors such as temperature, moisture level, stage of growth, and the part of the plant can impact the level of toxins in poisonous plants (James et al. 2019). Similarly, environmental conditions such as heat or cold, moisture level, wind, and sunlight can exacerbate or ease the response of an animal to ingested toxins from poisonous plants (James et al. 2019).
Climate change could have an impact on the abundance and toxicity of poisonous plants. The increased level of atmospheric CO2 associated with climate change has been shown to increase photosynthesis, growth, and population biomass of poison ivy, with the growth exceeding that of other woody species (Mohan et al. 2006). Not only does increased CO2 lead to an increase in the growth of poison ivy, but plants subjected to high CO2 produce a form of urushiol, the active toxin of poison ivy, that is more allergenic (Mohan et al. 2006). Results from a study by Mohan, et al. indicate that plants in the Toxicodendron genus, which includes poison ivy, poison oak, and poison sumac, will become both more abundant and more toxic as global atmospheric CO2 levels increase (Mohan et al. 2006), Gladman 2006). This could have major implications for forest population dynamics and human health (Mohan et al. 2006).
Many of the poisonous plants found in the states of Indiana and Kentucky are non-native and/or invasive. This is problematic for a variety of reasons. Non-native and invasive poisonous plants are a threat to native wildlife because these animals cannot discern non-native poisonous plants from non-poisonous plants. Further, such poisonous invaders can significantly impact the biodiversity of natural ecosystems and threaten human environments. The spread of invasive species, many of which are poisonous, out-compete native species and lead to a loss of native biodiversity. This can greatly impact forest and agricultural resources (Panter et al. 2018). Invasive poisonous species are often aggressive invaders and impact a wide range of ecosystems and resources including wild areas, managed forests, range and pasture, and agricultural land (Panter et al. 2018). Not only are invasive and poisonous plants a problem for livestock producers and farmers, but they also impact the ecosystem services on which many sectors of society depend (Panter et al. 2018).
Poisonous Plants of Indiana and Kentucky
Plants of the Apiaceae family are rich in secondary metabolites including coumarins, essential oils, flavones, terpenes, and acetylenic compounds (Pysek & Cock 2007). Some of these compounds are used by plants for self-defense (Pysek & Cock 2007). Species in this family have been used as spices, vegetables, or for medicinal purposes, yet some are highly toxic (Pysek & Cock 2007).
The chemical most characteristic for Apiaceae are called furanocoumarins. They are both of pharmaceutical interest and harmful to human health (Pysek & Cock 2007). Furanocoumarins in Apiaceae are concentrated in the oil canals and secretory ducts of all plant organs, with the highest amounts located in the fruits and the roots. (Pysek & Cock 2007)
Water hemlock Cicuta douglasii
Water hemlock is extremely poisonous to humans and animals and contains highly toxic alkaloids that are found in all parts of the plant (Agricultural Extension Service/University of Tennessee 1980). The primary toxins include cicutoxin and oenanthotoxin, which act as central nervous system antagonists (Schep et al. 2009). Ingestion of even a small amount of plant matter can cause serious intoxication (Schep et al. 2009).
The area between the nodes contains the oil in which the toxins are found and the roots contain the highest concentration of toxins (Agricultural Extension Service/University of Tennessee 1980). Livestock is extremely susceptible to poisoning by water hemlock because it grows in damp soil, which enables animals to easily pull up the entire plant and consume the roots (Agricultural Extension Service/University of Tennessee 1980). Most cases of poisoning occur during the spring when the plants are young, small, and easy to uproot (Agricultural Extension Service/University of Tennessee 1980).
The toxins cause the depolarization of neurons in the nervous systems that leads to anxiety, trembling, and convulsions, seizures, and even death (Schep et al. 2009; Agricultural Extension Service/University of Tennessee 1980). Other effects include nausea, vomiting, diarrhea, tachycardia, and cardiac arrhythmia, renal failure, respiratory impairment, and coma (Schep et al. 2009). Animals that have been poisoned may foam at the mouth, exhibit dilation of pupils, and have an increased body temperature (Agricultural Extension Service/University of Tennessee 1980).
Gastrointestinal evacuation is the recommended treatment, along with management of the respiratory system, and control of seizures (Agricultural Extension Service/University of Tennessee 1980)(Schep et al. 2009). If renal failure occurs, dialysis may be required (Schep et al. 2009). With early treatment, the prognosis is good (Schep et al. 2009). However, without treatment, death by respiratory failure will occur (Agricultural Extension Service/University of Tennessee 1980).
Poison hemlock Conium maculatum
Like water hemlock, poison hemlock is extremely toxic. Poison hemlock contains a group of piperidine alkaloids, coniine, and γ-coniceine, along with other toxins that are poisonous to humans and animals (Reynolds 2005). γ-coniceine is more toxic and its levels in relation to coniine vary depending upon variety, environmental conditions, and provenance of the plants (Reynolds 2005)(Herron 1972)(Reynolds 2005). The toxins in poison hemlock can be identified by their mousy smell (Herron 1972). The entire plant is poisonous, including the stems, leaves, and fruit (Agricultural Extension Service/University of Tennessee 1980). The concentration of toxins is highest in the leaves in the spring and the fruit in the fall (Agricultural Extension Service/University of Tennessee 1980).
Poisoning in livestock is most likely to occur in early spring when little other vegetation is available (Herron 1972). While drying reduces the coniine content, hay containing dried poison hemlock plants is not safe (Herron 1972). Chronic but non-lethal poisoning that occurs in pregnant livestock can lead to birth defects and malformations (Reynolds 2005).
There have been recorded cases of human poisonings (Reynolds 2005). Human poisoning has occurred due to mistaking poison hemlock for anise, parsley, or parsnips and eating the seeds, leaves, and roots. (Herron 1972)
The alkaloids found in poison hemlock are neurotoxins (Reynolds 2005). Symptoms of severe poison hemlock poisoning include excessive salivation or slobbering, loss of appetite, and gastrointestinal irritation. An animal might be found down and be unable to get up, and experience twitching, trembling, staggering, incoordination, and muscular weakness (Herron 1972)(Agricultural Extension Service/University of Tennessee 1980)(Herron 1972). Other symptoms include pain, rapid pulse, and nervousness followed by coldness of the extremities, slow heartbeat, and coma (Agricultural Extension Service/University of Tennessee 1980). Death results from respiratory paralysis and failure (Herron 1972)(Reynolds 2005); (Herron 1972).
Wild parsnip Pastinaca sativa
Wild parsnip was brought to North America by European colonists in 1609 as a source of food and was established as common by 1630 (Zangerl & Berenbaum 2005). It escaped cultivation and became invasive quickly. Wild parsnip can rapidly colonize wild prairies and restoration areas, is listed as an invasive species in several states surrounding Indiana and Kentucky, and has spread to all but 5 US states (Zangerl & Berenbaum 2005).
The toxins in wild parsnips are furanocoumarins, which provide defense against specialist webworms (Zangerl & Berenbaum 2005). Consumption of the reproductive structures of wild parsnip by webworms causes the plant to produce increased concentrations of the three main furanocoumarin toxins, xanthotoxin, bergapten, and sphondin (Zangerl & Berenbaum 2005).
Wild parsnip is considered to be phototoxic. The furanocoumarins produced by the stems and leaves of the plant cause reddening, blistering, and hyperpigmentation when they come in contact with human skin (Zangerl & Berenbaum 2005).
Cow parsnip/Giant Hogweed Heracleum lanatum
Like wild parsnip, cow parsnip (also called giant hogweed) contains furanocoumarins in the sap of the plant. Photodermatitis is caused when the sap comes in contact with human skin (Pysek & Cock 2007). Cow parsnip is particularly noxious because the sap causes serious UV-induced photodermatitis 24-48 hours after contact with the skin (Pysek & Cock 2007). Symptoms include mild to severe erythematous reactions in which the skin turns red and painful blisters, depending upon the amount of sap and UV exposure the skin received (Pysek & Cock 2007). Hyper-pigmentation of the skin occurs in burned areas within 3-5 days following contact and can last for months or even years (Pysek & Cock 2007).
To prevent photodermatitis, avoiding contact with cow parsnip is advised. If this is not possible, it is important to wear appropriate clothing which covers exposed skin. If taking management measures such as cutting the plants, all parts of the body should be covered, and gloves and full-face protection should be used (Pysek & Cock 2007). The sap can remain phototoxic for several hours after plants have been cut and will remain toxic on exposed clothes, so clothing should be handled with caution. Skin that comes in contact with the sap should immediately be thoroughly rinsed with water (Pysek & Cock 2007).
Members of the Anacardiaceae family are well-known for causing contact dermatitis. Members of this plant family, which includes cashews, cause more allergic contact dermatitis than all other plants combined (Gladman 2006). In the United States, the Toxicodendron genus, which includes poison ivy, poison oak, and poison sumac, causes the most plant-related medical issues (Gladman 2006).
Poison Ivy Toxicodendron radicans
Poison ivy is one of the most problematic plants in the United States, causing 350,000 cases of contact dermatitis every year (Mohan et al. 2006). About 80% of people who are exposed to the carbon-based oily phenolic compound, urushiol, found in poison ivy develop contact dermatitis (Mohan et al. 2006). Urushiol is a skin and mucous membrane irritant present in all parts of the plant and is the source of allergenic pain caused by the species (Francis 2004a; Agricultural Extension Service/University of Tennessee 1980). Contact dermatitis can occur after exposure to even very small amounts (Francis 2004a). When exposed to the skin, urushiol is metabolized, causing an immune system reaction that results in rash, blisters, and intense itching that can last 1-3 weeks (Francis 2004a). While most people only experience a skin reaction, sensitivity can vary from person to person and over the life of an individual, and severe allergic reactions including anaphylaxis can occur (Francis 2004a).
While the toxin has little to no effect on wild animals and livestock, pets may carry the urushiol on their fur and transmit it to humans (Agricultural Extension Service/University of Tennessee 1980). Some humans experience intense itching, inflammation, and blistering on areas that came in contact with poison ivy (Agricultural Extension Service/University of Tennessee 1980). Burning poison ivy is dangerous because urushiol may be transmitted by smoke (Agricultural Extension Service/University of Tennessee 1980).
Stinging Nettle Urtica dioica
Plants in the genus Urtica are characterized by stinging hairs that produce at the base an urticating substance (Coile n.d.). All parts of the stinging nettle plant are covered with these spine-like stinging hairs that can cause considerable, yet generally short-lived pain when they come into contact with human skin (Francis 2004a). Many chemicals have been proposed as the potential pain-causing toxins including histamine, serotonin, and acetylcholine (Fu et al. 2006). The difficulty in effectively extracting toxins from the hairs has resulted in the toxic effects of extracts from stinging hairs of Urtica not being well characterized (Fu et al. 2006). Fu et al. (2006) identified oxalic acid and tartaric acid, two prevalent constituents of terrestrial plants, as possible pain-causing toxins in the stinging hairs.
When the hair tip is broken, it behaves like a hypodermic needle and injects the toxins which cause intense pain and rashes.” (Coile n.d.) Mild cases generally experience itching, rash, blisters (Francis 2004a). Severe cases can also experience intense pain, fever, swelling, and ulcers (Francis 2004a).
Asclepiadaceae, the milkweed family, contains roughly 200 genera and 2500 species found throughout the temperate and tropical areas of the world (Roeske et al. 1976). Species native to Indiana and Kentucky include Common Milkweed Asclepias syriaca, Swamp Milkweed Asclepias incarnata, and Butterfly Milkweed Asclepias tuberosa. Milkweeds are characterized by the milky latex substance they secrete when a leaf or other organ is damaged (Roeske et al. 1976). This latex contains resinoids, alkaloids, and cardiac glycosides known as cardenolides which act as inhibitors of Na+ /K+ -ATPase in animals (Roeske et al. 1976; Agricultural Extension Service/University of Tennessee 1980; Züst et al. 2018). Cardenolides have been found in plants from 12 genera of the Asclepiadaceae family, yet extensive variation in concentration occurs between species and even within a single species (Roeske et al. 1976).
Cardenolide is used by milkweed as a defense from generalist herbivores, but specialist insects, such as the monarch butterfly and the oleander aphid Aphis nerii, have coevolved to resist poisoning from ingestion and can sequester the toxin for their defense (Züst et al. 2018).
These substances are of pharmaceutical interest for the treatment of cancers, tumors, warts, and bronchitis (Roeske et al. 1976). They are also known to be poisonous and have caused extensive cases of poisoning in cattle and sheep (Roeske et al. 1976).
All parts of the plant both fresh and dried, are poisonous, however, the green plants are rarely eaten due to their bitter taste (Agricultural Extension Service/University of Tennessee 1980). Because the bitterness of milkweed acts as a repellent against grazing, poisonings usually only occur when animals graze the plant due to lack of other vegetation (Agricultural Extension Service/University of Tennessee 1980). Whorled milkweed is more poisonous than the broad-leaved species, and milkweeds of the western plains of the United States are the most deadly (Agricultural Extension Service/University of Tennessee 1980). In addition to cattle, sheep, horses, goats, and poultry are sensitive to milkweed, and consuming just 2% of body weight constitutes a toxic amount and can cause symptoms (Agricultural Extension Service/University of Tennessee 1980).
The first symptoms of milkweed poisoning are gastrointestinal and include loss of appetite and diarrhea (Herron 1972; Agricultural Extension Service/University of Tennessee 1980). Later symptoms include labored breathing, dilated pupils, followed by spasms, staggering, and weakness leading to falling and paralysis. Coma, respiratory failure, and death result (Herron 1972; Agricultural Extension Service/University of Tennessee 1980). The suggested treatment includes laxatives and intravenous fluids (Agricultural Extension Service/University of Tennessee 1980).
Dogbane Apocynum cannabinum
Dogbane contains the glucoside cymarin, along with poisonous resins and other toxic compounds (Herron 1972). Glucoside and resinoids are found in the leaves and stems, but all parts of the plant are considered to be poisonous, both fresh and dried (Herron 1972; Agricultural Extension Service/University of Tennessee 1980). Dogbane is extremely toxic - just ½ to 1 ounce (15-30 grams) of the fresh leaves is enough to kill a cow (Herron 1972; Agricultural Extension Service/University of Tennessee 1980).
Symptoms of dogbane poisoning include an increase in body temperature and pulse, pupil dilation, cold extremities, infrequent bowel actions, discolored mucous membranes, and red and sore mouth (Herron 1972; Agricultural Extension Service/University of Tennessee 1980). Poisoning is treatable if caught early enough by emptying the stomach, administering antidotes and gastric protectants, along with heart stimulants if needed ((Agricultural Extension Service/University of Tennessee 1980)).
Pokeweed Phytolacca americana
Pokeweed contains oxalic acid, a saponin called phytolaccatoxin, along with an alkaloid called phytolaccine (Herron 1972; Agricultural Extension Service/University of Tennessee 1980). The toxins are found in all parts of the plant, but the roots and seeds are especially toxic (Herron 1972).
The young leaves are often used as cooked greens as cooking deactivates the toxins, but the older leaves are much more toxic. Poke salad is considered safe to eat as long as the young leaves are boiled multiple times and the cooking water is poured off (Agricultural Extension Service/University of Tennessee 1980). If not cooked properly, pokeweed can be deadly.
Cattle, horses, and pigs have all been poisoned by pokeweed (Agricultural Extension Service/University of Tennessee 1980). Cattle usually avoid pokeweed due to its unpalatability, but sometimes feed on young leaves in the spring (Herron 1972). There have been reports in Kentucky of cattle dying after herbicide application caused cattle to be attracted to pokeweed. Pigs have died after consuming the roots (Herron 1972).
When small amounts are consumed, the only symptoms are nausea and vomiting (Herron 1972). When larger amounts are ingested, severe gastrointestinal cramping and diarrhea can occur. Spasms, convulsions, and mucosal hemorrhaging, along with liver damage, can occur (Agricultural Extension Service/University of Tennessee 1980). With treatment, most animals recover within 24-48 hours, however, without treatment, respiratory paralysis will lead to death (Herron 1972; Agricultural Extension Service/University of Tennessee 1980).
Plants in the Solanaceae family contain high concentrations of alkaloids. Varying concentrations of tropane alkaloids can be found in all parts of plants in this family including leaves, stems, roots, flowers, fruits, and seeds (Kumar et al. 2009; Miraldi et al. 2001). The principal alkaloids in plants of the Solanaceae are hyoscyamine, scopolamine, atropine may be (Miraldi et al. 2001).
Horsenettle Solanum carolinense
The principal toxin found in Horsenettle is an alkaloid, solanine (Agricultural Extension Service/University of Tennessee 1980). The toxicity of horsenettle depends on the part of the plant, maturity, and environment. The most toxic part of the plant is the berries, which increase in toxicity as they ripen (Agricultural Extension Service/University of Tennessee 1980). The leaves are also toxic, but less so than the berries (Agricultural Extension Service/University of Tennessee 1980). Horsenettle is commonly found in cultivated fields and pastures, but animals do not generally eat the plants unless they have been harvested with hay (Herron 1972).
Poisonings of humans and livestock have occurred (Herron 1972). Poisonings can be classified as acute or chronic (Agricultural Extension Service/University of Tennessee 1980). Chronic poisoning can occur due to eating small quantities of horsenettle over time and results in the failure to properly grow and develop, jaundice, and constipation (Herron 1972; Agricultural Extension Service/University of Tennessee 1980). Acute poisoning can occur after eating a large quantity within a short period and results in gastrointestinal disturbances, lesions, irritation of the mouth, drowsiness, and paralysis Agricultural Extension Service/University of Tennessee 1980; Herron 1972).
Deadly nightshade Solanum dulcamara
Deadly nightshade contains high concentrations of the alkaloidal glycoside solanine, found in the leaves, stems, and unripe fruit, solasodine found in flowers, and β-solamarine found in the roots (Kumar et al. 2009; Herron 1972). Deadly nightshade plants are less toxic when dried (Herron 1972).
All parts of the plant are toxic to horses, sheep, and cattle, but these animals generally will not eat enough to be poisoned (Francis 2004b). For this reason, most poisonings occur in pigs, goats, calves, and poultry (Herron 1972).
When poisoning of animals does occur, symptoms include stupor, staggering, weakness, and constipation (Herron 1972). Later symptoms include dilated pupils and loss of coordination (Herron 1972). The symptoms can progress quickly to cramps, convulsions, and death due to respiratory paralysis (Herron 1972).
Deadly nightshade intoxication has been reported in both children and adults (Çaksen et al. 2003). The flavor of nightshade fruits is so bitter and unpalatable that it is unlikely that a human would eat enough to be severely poisoned (Francis 2004b). However, ripened nightshade berries are one of the most commonly reported plant injections (Hornfeldt & Collins 1990). The ingestion of even a small amount in children is generally treated with syrup of ipecac to induce vomiting (Hornfeldt & Collins 1990).
In humans, the most common symptoms of nightshade poisoning include flushing, speech difficulties, tachycardia, and dilated pupils. These initial symptoms of acute intoxication of deadly nightshade generally do not lead to permanent damage or death. However, meaningless speech, lethargy, absence of tachycardia, and coma indicate more severe poisoning (Çaksen et al. 2003).
Jimsonweed Datura stramonium
Jimsonweed contains the tropane alkaloids atropine, hyoscyamine, and scopolamine (Miraldi et al. 2001; Agricultural Extension Service/University of Tennessee 1980). The levels of atropine and scopolamine vary depending upon the part of the plant and the stage of growth (Miraldi et al. 2001). The highest atropine concentration was found in leaves of the young plant, with the highest scopolamine content found in apical leaves (Miraldi et al. 2001). A study by Miraldi et al. (2001) indicated that atropine is the principal alkaloid found in jimsonweed, with scopolamine concentration decreasing as the surface area of leaves increases.
All parts of the jimsonweed plant are considered poisonous, both fresh and dried (Herron 1972; Agricultural Extension Service/University of Tennessee 1980). The seeds are the most toxic part of the plant containing the highest concentrations of alkaloids (Agricultural Extension Service/University of Tennessee 1980). The entire plant is poisonous, both green and dried (Herron 1972).
Humans may be poisoned by eating the fruits (Herron 1972). Jimsonweed has a strong, unique odor and is extremely bitter to the taste, so the green plant is rarely eaten by livestock, except when other vegetation is unavailable for forage (Nice 2008; Herron 1972; Agricultural Extension Service/University of Tennessee 1980) In addition to cattle, poisonings have occurred in pigs, horses, poultry, and dogs (Agricultural Extension Service/University of Tennessee 1980).
Chronic, mild poisoning can cause birth defects and deformities in pregnant livestock (Agricultural Extension Service/University of Tennessee 1980). Symptoms of acute, severe poisoning can occur quickly (Nice 2008). Initial symptoms include an increase in pulse and respiration, along with pupil dilation and apparent blindness (Nice 2008; Agricultural Extension Service/University of Tennessee 1980). The mouth and mucous membranes will be dry, along with retention of urine or possible frequent urination (Nice 2008; Herron 1972; Agricultural Extension Service/University of Tennessee 1980). Digestive problems, such as nausea and diarrhea can develop (Herron 1972; Nice 2008). Later, respiration will become slow and irregular, body temperature drops, and convulsions and coma can occur (Agricultural Extension Service/University of Tennessee 1980; Herron 1972). The main symptoms of jimsonweed poisoning in pigs are twitching and convulsions (Herron 1972). Sheep tend to have abnormal leg movements, intense thirst, disruptions in vision, and bite at the air (Agricultural Extension Service/University of Tennessee 1980). Death occurs due to asphyxia (Herron 1972).
White Snakeroot Ageratina altissima
The toxin found in white snakeroot is an alcohol called tremetol (Agricultural Extension Service/University of Tennessee 1980). Tremetol is found in all parts of the plant, both fresh and dried (Agricultural Extension Service/University of Tennessee 1980). White snakeroot is poisonous to humans, livestock, and many other animals (Agricultural Extension Service/University of Tennessee 1980). Poisoning can occur from eating the plant directly or by consuming milk from cows, sheep, or horses that have eaten the plant, and has caused sickness and death in humans (Agricultural Extension Service/University of Tennessee 1980).
Trembling is the most common symptom of white snakeroot poisoning (Agricultural Extension Service/University of Tennessee 1980). Animals that have been poisoned become sluggish, still, and will stand with their feet spread wide (Agricultural Extension Service/University of Tennessee 1980). Other symptoms, including slobbering, constipation, vomiting, and uncontrolled urination may also occur (Agricultural Extension Service/University of Tennessee 1980). Humans can become delirious after drinking toxic milk from a poisoned animal (Agricultural Extension Service/University of Tennessee 1980).
All animals can be poisoned by eating fresh buttercup plants (Herron 1972). Buttercups contain protoanemonin, an oil irritant, in the stems and leaves (Agricultural Extension Service/University of Tennessee 1980). Protoanemonin is not highly toxic and concentration can vary across species (Agricultural Extension Service/University of Tennessee 1980). Flowering plants tend to be more toxic than young plants (Agricultural Extension Service/University of Tennessee 1980).
In livestock, symptoms of poisoning include abdominal pain, diarrhea, convulsions, and death (Agricultural Extension Service/University of Tennessee 1980). Milk from poisoned cows will be bitter and might be red or orange-colored (Agricultural Extension Service/University of Tennessee 1980). Buttercup poisoning is generally uncommon, but invasive buttercup species are spreading rapidly, increasing the risk, especially when other vegetation is scarce (Agricultural Extension Service/University of Tennessee 1980)
Larkspur contains multiple highly poisonous alkaloids, with the main toxin being delphinine (Herron 1972). Larkspur is at its most poisonous during early growth stages in the spring (Herron 1972). Because larkspur grows early before other grazing vegetation is abundant, poisoning tends to occur at this time. Poisoning can occur in cattle, along with horses and sheep (Herron 1972).
The severity of intoxication depends on the amount of the plant eaten and the tolerance of the animal. Small amounts can cause symptoms such as loss of appetite and constipation, excitability, and staggering (Herron 1972). When large quantities of larkspur have been consumed, severe symptoms, such as vomiting and bloating, slobbering, and convulsions can occur (Herron 1972). If severe poisoning is left untreated, death due to respiratory paralysis can occur (Herron 1972).
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