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Plant hazards
Vet Clin Small Anim 32 (2002) 383–395
Plant hazards Konnie H. Plumlee, DVM, MS* Veterinary Diagnostic Laboratory, Arkansas Livestock and Poultry Commission, #1 Natural Resources Drive, Little Rock, AR 72205, USA
Toxicosis from plant ingestion is not a frequent occurrence in cats and dogs, because plants are not normally a part of their diet. Because they are typically foreign to the normal diet of dogs and cats, ingestion of most plants, even if they are not toxic, causes vomiting and possibly mild diarrhea. These mild gastrointestinal disturbances must be differentiated from true poisonings. A complete discussion of all plants that are potentially toxic is beyond the scope of one article. This discussion focuses on plants and plant products that pets commonly encounter or that are potentially dangerous.
Foods for human consumption A few plants or plant products used for human consumption are toxic to certain small animals. Toxicosis usually occurs when owners share these foods with their pets as a treat. Macadamia nuts Macadamia nuts are produced by Macadamia integrifolia and Macadamia tetraphylla trees, which were introduced into Hawaii over 100 years ago [19]. These nuts cause a unique syndrome in dogs that eat them. The toxin and mechanism of action are unknown. The clinical signs usually occur within 12 hours of ingestion and typically last less than 24 to 48 hours. The most prominent clinical sign is difficulty or inability to rise and walk. The reported clinical signs, from most to least frequent, are weakness (hind limbs more severely affected than front limbs), depression, vomiting, ataxia, tremors, hyperthermia, abdominal pain, lameness, stiffness, recumbency, and pale mucous membranes. Mild transient
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elevations in serum triglycerides and alkaline phosphatase can be detected. Lipase values can peak at 24 hours but return to normal by 48 hours after ingestion [19]. The dogs return to normal with symptomatic care. No sequelae are expected. Avocado Persea americana is widely cultivated for its fruit, with primarily the Mexican and Guatemalan varieties grown in North America [22]. Toxicity varies among the varieties and hybrids, with the Mexican variety being considered the least toxic [40]. All above-ground parts of the plant can be toxic to rabbits, mice, and caged birds (canaries, cockatiels, and budgerigars). The toxin is not completely defined, but some clinical signs have been reproduced with persin, a compound that has been isolated from avocado leaves [34]. The mechanism of action is unknown. The clinical signs vary with species of animal. Lactating rabbits and mice develop a noninfectious mastitis and agalactia after eating avocado leaves. Rabbits have also developed cardiac arrhythmia, submandibular edema, and acute death. Caged birds have displayed acute respiratory distress and death 12 to 29 hours after ingestion of avocado fruit [22]. Other signs in birds have included resting on the cage bottom, fluffed feathers, and slightly outstretched wings [22]. Necropsy lesions in birds include subcutaneous edema of the pectoral area, hydropericardium, mild pale streaks of the pectoral muscles, and generalized lung congestion [22]. Lesions in mammals include necrosis of the acinar epithelium of the lactating mammary gland and the myocardium [34]. Treatment is symptomatic and supportive. The prognosis is guarded if signs reflective of cardiac disease or respiratory distress are present. The mastitis can resolve, but milk production is decreased. Onion Although pets have been known to chew on raw onions, most exposures occur when the animal is fed cooked onions. Cats have been known to develop toxicosis when fed baby food that contained onion powder [24,39]. Certain dog breeds such as Akitas and Shibas can have hereditary deficits that make them more susceptible to this toxicosis [51]. The primary toxic substance is n-propyl disulfide, an alkaloid found in leeks, wild onions, cultivated onions, garlic, and chives; however, other toxins may also be involved. The toxin(s) oxidize free sulfhydryl groups on hemoglobin [39]. The oxidized hemoglobin precipitates to form Heinz bodies in the red blood cells. Anemia is the result of damaged red blood cell membranes and the removal of cells that contain Heinz bodies by the spleen [39]. The onset of signs may be acute, but most signs likely develop over 1 to 2 days. Clinical signs are primarily the result of anemia, including pale or
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icteric mucous membranes, fast pulse, weakness, depression, and possibly collapse. Hemoglobinuria is often an early sign. Clinical pathologic findings include decreased hematocrit, decreased hemoglobin, mild methemoglobinemia, and the presence of Heinz bodies. Polychromasia, nucleated red blood cells, and reticulocytes are seen as the regenerative response occurs [23,35]. The treatment depends on the severity of the anemia. Mild cases may only require supportive care; however, blood transfusions are necessary if the anemia is severe. The prognosis varies depending on the severity of clinical signs. Fruit seeds The foliage and seeds of some fruit trees (wild and domestic cherries, apricots, peaches, apples, and plums) contain cyanogenic glycosides [16]. The seeds are frequently more toxic than the leaves, especially in apricots and peaches. One source states that peach seeds have much more cyanide than the leaves [28]. A woman ate 20 to 30 raw apricot seeds purchased from a health food store and developed cyanide toxicosis in minutes [47]. Ingestions of 5 to 25 fruit seeds can cause toxicosis [16]. Cyanide binds to and inhibits cytochrome oxidase, thereby preventing cellular respiration. The oxygen-saturated hemoglobin is unable to release its oxygen to the tissues and can cause the venous blood to become a cherry red color [48]. Clinical signs can develop within minutes to 1 to 2 hours after ingestion, and death often occurs within minutes of the onset of clinical signs. Many animals are found dead, but tremors, ataxia, frothing at the mouth, dilated pupils, dyspnea, and convulsions have been reported. Treatment is often not successful because of the quick onset of clinical signs and death. The treatment for cyanide poisoning is sodium nitrite (16 mg/kg of body weight of a 3% solution administered slowly intravenously), which forms methemoglobin that binds with cyanide to form cyanmethemoglobin. This is followed by sodium thiosulfate (1.65 mL of a 25% solution administered intravenously), which converts cyanide to thiocyanate [16]. One half of these initial doses can be repeated in 30 minutes if the animal has not recovered. Sodium thiosulfate is relatively safe and can be used alone in less severe cases. Sodium nitrite is a potent vasodilator, however, which can cause hypotension and excessive methemoglobin formation. As a result, its use should be limited to more severe cases of known cyanide poisoning [16]. Supportive treatment includes 100% oxygen supplementation and intravenous fluids, which may be the only treatment needed if the animal is displaying mild signs.
Holiday plants Several types of plants that are not present during other times of the year are brought into pets’ surroundings during the holidays. The toxicity of these plants is generally overrated by the public.
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Mistletoe Phoradendron species are evergreen parasitic plants that grow on a variety of host trees. The toxicity of the various mistletoe species seems to vary and may be related to the type of host plant [17]. Most human exposures result in no adverse effects, although a few serious cases have been reported and were believed to be related to the plants or berries being used to brew tea [18]. Few incidents have been reported in animals, and efforts to reproduce disease in animals have been unsuccessful. The toxic component of mistletoe is unknown, although a variety of potentially toxic compounds have been isolated, including lectins, proteins, alkaloids, and amines. The most common clinical signs in human beings are gastrointestinal disturbances, including vomiting, diarrhea, and abdominal pain. Drowsiness, incoordination, seizure (in an infant), hypotension, and cardiovascular collapse have been reported rarely in human beings [31,44]. Treatment is symptomatic and supportive, primarily consisting of correction of fluid and electrolyte deficits. Holly Ilex species include hollies known as English or Christmas holly, American or white holly, and winterberry. These plants, especially the berries, contain saponins, which cause direct irritation to the digestive tract [49]. Clinical signs are usually mild to moderate diarrhea and vomiting. Most cases resolve within 24 hours. Treatment is symptomatic, but severe intoxications may require correction of fluid and electrolyte imbalances. Poinsettia Euphorbia pulcherrima has a milky sap that contains diterpenoid esters, which have irritant effects on the skin, mucous membranes, and digestive tract [25]. Clinical signs include increased salivation, vomiting, and, infrequently, diarrhea. Severe disease is rare. Treatment is symptomatic and supportive. Managing fluid and electrolyte imbalances may be necessary with large exposures. Skin exposures can be washed with alcohol and treated with ointments to reduce inflammation.
Trees and shrubs Pets can have access to numerous trees and shrubs. The following is a discussion of those plants that can be particularly hazardous. Cycad palms These palms are also known as sago palms (Cycas and Macrozamia spp.) and naturally grow in tropical and subtropical climates. Young palms are
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also used as houseplants. All parts of the plant are toxic, but the nuts (seeds) seem to be the most toxic part. Male and female plants exist in the same species, but only the female plant has the cone-shaped middle that produces nuts [12]. The plants contain three toxins: cycasin causes hepatic necrosis and gastrointestinal signs, b-methylamino-L-alanine causes neurologic signs, and a third unknown toxin causes neurologic signs [12,41]. The most common clinical sign in dogs is vomiting, with or without blood. Other signs include depression, diarrhea with or without blood, anorexia, and, occasionally, seizures [2]. Hepatic failure and death have occurred. Clinical pathologic findings include elevated serum alanine aminotransferase, bilirubin, and alkaline phosphatase. Electrolyte abnormalities can occur as a result of prolonged vomiting and dehydration. Gastrointestinal signs appear within 24 hours of ingestion, but the laboratory values usually do not change for 24 to 48 hours [2]. Treatment begins with decontamination via emesis and repeated doses of activated charcoal (2–3 doses within 24 hours). Monitor liver enzymes and bilirubin daily for 48 hours or until the values return to normal. Give 5% dextrose IV [26]. Treat the gastrointestinal irritation with sucralfate and cimetidine or another inhibitor of gastric acid secretion. Control seizures and tremors with diazepam. Blood transfusions may be needed if the gastrointestinal tract hemorrhage results in severe anemia [2]. Maintain the dog on a low-protein diet. Continue all therapy until the signs resolve. Chinaberry This deciduous tree (Melia azedarach) belongs to the mahogany family and has become naturalized to the temperate regions of North America. All parts of the tree are potentially toxic, but most cases of poisoning in dogs result from ingestion of the fallen fruit. Toxicosis has also occurred in rabbits, rats, guinea pigs, poultry, and livestock [21]. Several potentially toxic compounds have been isolated from the plant [45]. The principal toxins are meliatoxins, which are concentrated in the fruit and affect the gastrointestinal and nervous systems. The exact mechanism of action is unknown. The gastrointestinal effects are probably a result of direct irritation. The effects on the central nervous system are similar to those of nicotine, with an initial stimulation of the sympathetic and parasympathetic systems followed by persistent depolarization. Within 1 to 2 hours of ingestion, vomiting and diarrhea (with or without blood), abdominal pain, anorexia, and straining to defecate can occur. Some animals hypersalivate. These gastrointestinal signs are followed by a variety of nervous system signs, including ataxia, depression, excitement, seizures, paresis, and coma. Respiratory arrest is most likely the cause of death. A large number of other signs have been reported, including hyperthermia, hypothermia, tachycardia, bradycardia, dyspnea, stranguria, muscle
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rigidity, mydriasis, and miosis [20,21]. Clinical signs can vary widely, making the diagnosis difficult unless the exposure was observed. The clinical pathologic findings and lesions are also nonspecific. Aggressive decontamination procedures should be used before the onset of clinical signs. No antidote exists; thus, treatment is limited to symptomatic and supportive care. The prognosis is poor after adverse nervous system signs are present. Heath family Plants in the heath family include rhododendron, azalea, laurel, and Japanese pieris. These plants are commonly used as ornamental shrubbery and grow in the acidic moist soils of North America, especially in the eastern United States. These plants contain grayanotoxins, which modulate the gating kinetics of sodium channels in cell membranes, resulting in prolonged depolarization of the nervous tissue [9,37]. The toxin is found in the leaves, stems, nectar, and flowers [38]. Clinical signs can appear between 4 and 12 hours after ingestion and can persist for several days. Vomiting is the most consistent finding. Other gastrointestinal signs that can occur include bloating, abdominal pain, and salivation. Diarrhea is not typically seen. Neurologic signs may or may not be seen and include depression, fine muscle tremors, ataxia, and convulsions with opisthotonus and paddling [9,38]. A small percentage of dogs can have tachycardia or bradycardia. Clinical pathologic findings are nonspecific and reflect the clinical signs, including stress leukogram, dehydration, and electrolyte imbalance. Decontamination involves emesis (if the animal is not already vomiting) and activated charcoal. No antidote exists; thus, treatment is symptomatic and supportive. The prognosis is good in animals that have not aspirated or convulsed. Lectins The two plants of most concern in this category are Ricinus communis (castor bean) and Abrus precatorius (rosary pea, precatory bean). The lectin in castor bean is ricin, which is present in all parts of the plant but is most concentrated in the seed. The lectin in the rosary pea is abrin, which is only present in the seeds. Lectins enter cells and cause their death via inhibition of protein synthesis [27,32]. Fortunately, lectins are poorly absorbed from the digestive tract. Furthermore, chewing or breaking of the seed coat seems to be necessary before the lectins can be released from the bean or pea. Despite ricin being one of the most deadly substances known, death in human beings who ingest castor beans is infrequent, perhaps because the bean is swallowed whole and the seed coat is not broken [3,10].
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The major organ affected is the gastrointestinal tract. Clinical signs include vomiting, diarrhea, gastrointestinal bleeding, abdominal pain, and dehydration. In dogs, signs most often develop within 6 hours of ingestion but can be delayed for up to 42 hours [1]. The duration of signs is 1.5 to 5.5 days [1]. No antidote is available for lectins. Early decontamination via emesis and activated charcoal is warranted before the onset of clinical signs, especially if the seeds could have been chewed and the seed coat broken. If clinical signs occur, fluid and electrolyte balance should be closely monitored. Gastrointestinal protectants and other symptomatic care are given as needed. Mortality is low in animals, because the seed coat is not always broken on ingestion and because lectins are poorly absorbed. Nevertheless, all ingestions should be taken seriously because of the high toxicity of these lectins. The prognosis is guarded if clinical signs do develop. Yew Several species of Taxus are commonly used as ornamental shrubs or trees, including Japanese yew, English yew, Florida yew, and ground hemlock. The bark, leaves, and seeds are toxic but not the red fruit that surrounds the seed. These plants contain taxine, a cardiotoxic alkaloid that causes conduction disturbances with a direct action on ion channels of cardiac muscle. Most cases involve livestock, but caged birds have been intoxicated experimentally [42]. Clinical signs in birds include regurgitation, depression, ataxia, dyspnea, weakness, and acute death [42]. Suspected Japanese yew poisoning has been reported in a dog that had intermittent vomiting, seizures, and aggressive behavior [15]. Yew bark was found in the stomach of a 1-year-old dog and believed to be the cause of its death [13]. In livestock, acute death is common, and clinical signs can begin within 1 to 4 hours after ingestion. It is usually too late for treatment once the signs have occurred because of the peracute nature of the disease. Furthermore, restraining the animal for treatment may cause cardiac arrest. No antidote exists. Cardiac glycosides Several different plants contain cardiac glycosides, but those that pets are most likely to be exposed to are oleander (Nerium oleander), foxglove (Digitalis purpurea), and lily of the valley (Convallaria majalis). Cardiac glycosides inhibit the cellular membrane sodium-potassium pump, resulting in decreased electric conductivity. A variety of cardiac arrhythmias can occur [43]. Abdominal pain and diarrhea can also occur. Death can be peracute, or symptoms may persist from a few hours to 2 days before death ensues. Decontamination is recommended before clinical signs begin. Because any type of arrhythmia, tachycardia, or bradycardia is possible, treatment
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varies from case to case. The electrolyte status of the animal should be monitored closely, and fluids should be administered as needed. Treatment with digoxin immune Fab (Digibind), which is used for toxicosis caused by excessive digoxin, may be helpful if administered early in the disease. The usual dose is 1.7 mL of Digibind (administered through a filter over 30 minutes) per milligram of digoxin that was ingested [14]. With plant ingestions, the amount of toxin involved is not known, however.
Ornamental bulbs These plants have roots that form bulbs, tubers, or corms. Most of these plants only cause mild to moderate gastrointestinal signs if the bulb is ingested. The exceptions are autumn crocus, glory lily, and a few other lilies (Lilium spp. and Hemerocallis spp.). Lilies (Lilium spp. and Hemerocallis spp.) Some plants in the Liliaceae family can cause renal toxicosis in cats. These are ornamental plants that bloom in spring and summer. The plants known to be toxic are Easter lily (Lilium longiflorum), tiger lilies (Lilium tigrinum), rubrum or Japanese showy lilies (Lilium speciosum, Lilium lancifolium), day lilies (Hemerocallis spp.), and Asiatic lilies [8,46]. Peace lilies (Spathiphyllum spp.) and calla lilies (Zantedeschia spp.) are not in the Liliaceae family and do not cause renal problems [46]. All parts of the plant, including the flowers, are toxic. Even one bite of the plant can cause toxicosis. Only cats are known to develop renal failure; dogs seem to be resistant. The mechanism of action is unknown, but the renal failure seems to be caused by necrosis of the renal tubular epithelial cells [8]. The basement membrane remains intact, and tubular epithelial cells can regenerate with prompt aggressive treatment [46]. Vomiting, anorexia, and depression often occur within 2 hours of ingestion. The blood urea nitrogen (BUN), creatinine, potassium, and phosphorus are elevated by 24 to 72 hours. Epithelial casts appear in the urine by 18 hours. Creatinine is often disproportionately elevated (as high as 44 mg/dL) compared with the BUN [46]. Treatment begins with induction of emesis if the ingestion could have occurred within the past 2 to 3 hours. This should be followed with two to three doses of activated charcoal within 24 hours. Diuresis with lactated Ringer’s solution administered intravenously at two times the maintenance level for at least 48 hours should be instituted to prevent renal tubular obstruction from necrosis and sloughing of epithelial cells. Obtain baseline BUN and creatinine levels, recheck daily, and continue fluids if they are elevated. Postponing treatment for longer than 18 hours after exposure can result in renal failure and death. Anuric cats have a grave prognosis, but peritoneal dialysis may restore function in a few cases.
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Autumn crocus and glory lily Autumn crocus (Colchicum spp.) and glory lily (Gloriosa spp.) contain colchicine, an alkaloid that has been reported to cause toxicosis in dogs and livestock. All animals are presumably susceptible. The autumn crocus should not be confused with the spring-blooming crocus, which is a member of the iris family. Colchicine is most concentrated in the tuber and the seeds. It is an antimetabolite that inhibits normal cell division, especially in rapidly dividing cells [7]. Initial clinical signs include vomiting and diarrhea (with or without blood), abdominal pain, hypersalivation, and depression. These signs can progress to weakness, ataxia, paresis, or collapse [11]. Multiple organ failure involving the lungs, kidney, cardiovascular system, and nervous system has occurred in human beings [33]. Coagulopathies and myelosuppression are possible sequelae. Emesis can be induced, and activated charcoal can be given before onset of gastrointestinal signs. Treatment is nonspecific and is limited to alleviation of clinical signs. The prognosis is poor if signs involve multiple organ systems. Other bulbs Bulbs that fall into this category include amaryllis, paper whites, springblooming crocus, Narcissus spp. (narcissus, jonquil, daffodil), iris, and tulip. These ornamental bulb plants usually only cause mild gastrointestinal signs. If a significant amount of the bulb itself is ingested, however, severe vomiting and diarrhea can occur. If the bulb is ingested, the animal should be decontaminated before the onset of clinical signs. Treatment consists of alleviation of clinical signs, because an antidote does not exist for these plants.
Houseplants Numerous plants can be used as ornamentals inside the home. Below is a discussion of the more commonly used plants. Kalanchoe This popular houseplant is indigenous to tropical Africa, Madagascar, Asia, and South America [50]. Kalanchoe contains bufadienolides, which are cardiac glycosides similar to those found in foxglove, oleander, lily-ofthe-valley, and various species of milkweed [12]. Cardiac glycosides inhibit Na+-K+ adenosine triphosphatase, resulting in decreased active transport of sodium with subsequent efflux of potassium. Toxicosis has been induced experimentally in livestock dosed with the plant or its flowers; natural poisonings are reported during the flowering season of the plants [4,29,30]. Kalanchoe toxicosis has also been reported in chicks, a rabbit, and a pack rat [50].
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Clinical signs in dogs that have been reported to the author include cardiac signs (tachycardia and increased blood pressure) and neurologic signs (dilated pupils, nystagmus, delirium, mild seizures, weakness, and tetany). Other signs that can be associated with cardiac glycosides include bradycardia, arrhythmias, hyperkalemia, vomiting, and diarrhea [12]. Treatment of cardiac glycoside exposure begins with decontamination. Induce emesis only if clinical signs are absent. Give activated charcoal unless the clinical condition predisposes the patient to aspiration. Treatment focuses on symptomatic and supportive care. Digibind has been beneficial for oleander poisoning but has not been evaluated for kalanchoe poisoning. Calcium oxalate crystals Many houseplants of the Araceae family contain insoluble calcium oxalate crystals (not to be confused with plants that contain soluble calcium oxalate, which can cause renal toxicosis). These plants are popular and include elephant’s ear, schefflera, caladium, dumb cane (Dieffenbachia spp.), pothos, many ivy varieties, philodendron, peace lilies (Spathiphyllum spp.), and calla lilies (Zantedeschia spp.) [5]. Cells in the plant contain spicules of calcium oxalate crystals, which are needle-shaped. When these cells are broken during ingestion, the sharp crystals shoot out of the cells and embed into the mucous membranes, tongue, and throat [5]. The onset of pain can be immediate or can occur up to 2 hours after chewing on the plant. The animal can have increased salivation, vocalization, anorexia, and depression. Swelling inside the mouth can occur, but a significant enough amount to cause airway obstruction is unlikely [36]. Mild vomiting or diarrhea is possible if the animal swallows a large amount of the plant. Treatment involves symptomatic care. The mouth should be rinsed, and the animal can be offered small amounts of milk or soft food to decrease the pain. If the amount of ingestion is unusually large, the animal can be given gastrointestinal protectants and anti-inflammatory drugs. Most animals recover uneventfully within 24 hours. English ivy This ivy (Hedera spp.) is used as a houseplant and even more commonly as a ground cover. Other varieties are known as Persian ivy, Irish ivy, Atlantic ivy, and Nepal ivy. These plants, especially the berries, contain pentacyclic terpenoids, which cause gastrointestinal signs [6]. In general, these types of ivy are more toxic than other varieties such as those that contain oxalate crystals. Many ingestions are not serious, but severe vomiting, salivation, abdominal pain, and diarrhea can occur. Treatment is symptomatic and supportive.
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Summary A variety of plants, seeds, and nuts can cause toxicosis in small animals. Some plants are not as toxic as commonly believed by the general public. Conversely, plants or nuts that are consumed by human beings can be toxic to their pets. Most plant toxins do not have specific treatments or antidotes. As a result, treatment is often limited to decontamination plus symptomatic and supportive care.
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[46] Volmer PA. Easter lily toxicosis in cats. Vet Med 1999;94:331. [47] Wallace KL, Gerkin R, Mitchell RB. Acute cyanide poisoning due to apricot ingestion [abstract]. J Toxicol Clin Toxicol 1996;34:599. [48] Way JL. Cyanide intoxication and its mechanism of antagonism. Annu Rev Pharmacol Toxicol 1984;24:451–81. [49] West LG, McLaughlin JL, Eisenbeiss GK. Saponins and triterpenes from Ilex opaca. Phytochemistry 1977;16:1846–7. [50] Williams MC, Smith MC. Toxicity of Kalanchoe spp to chicks. Am J Vet Res 1984;45:543–6. [51] Yamoto O, Maede Y. Susceptibility to onion induced hemolysis in dogs with hereditary high erythrocyte reduced glutathione and potassium concentration. Am J Vet Res 1992; 53:134–7.
Plant hazards Konnie H. Plumlee, DVM, MS* Veterinary Diagnostic Laboratory, Arkansas Livestock and Poultry Commission, #1 Natural Resources Drive, Little Rock, AR 72205, USA
Toxicosis from plant ingestion is not a frequent occurrence in cats and dogs, because plants are not normally a part of their diet. Because they are typically foreign to the normal diet of dogs and cats, ingestion of most plants, even if they are not toxic, causes vomiting and possibly mild diarrhea. These mild gastrointestinal disturbances must be differentiated from true poisonings. A complete discussion of all plants that are potentially toxic is beyond the scope of one article. This discussion focuses on plants and plant products that pets commonly encounter or that are potentially dangerous.
Foods for human consumption A few plants or plant products used for human consumption are toxic to certain small animals. Toxicosis usually occurs when owners share these foods with their pets as a treat. Macadamia nuts Macadamia nuts are produced by Macadamia integrifolia and Macadamia tetraphylla trees, which were introduced into Hawaii over 100 years ago [19]. These nuts cause a unique syndrome in dogs that eat them. The toxin and mechanism of action are unknown. The clinical signs usually occur within 12 hours of ingestion and typically last less than 24 to 48 hours. The most prominent clinical sign is difficulty or inability to rise and walk. The reported clinical signs, from most to least frequent, are weakness (hind limbs more severely affected than front limbs), depression, vomiting, ataxia, tremors, hyperthermia, abdominal pain, lameness, stiffness, recumbency, and pale mucous membranes. Mild transient
* E-mail address: [email protected] (K.H. Plumlee). 0195-5616/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved. PII: S 0 1 9 5 - 5 6 1 6 ( 0 1 ) 0 0 0 0 6 - 7
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elevations in serum triglycerides and alkaline phosphatase can be detected. Lipase values can peak at 24 hours but return to normal by 48 hours after ingestion [19]. The dogs return to normal with symptomatic care. No sequelae are expected. Avocado Persea americana is widely cultivated for its fruit, with primarily the Mexican and Guatemalan varieties grown in North America [22]. Toxicity varies among the varieties and hybrids, with the Mexican variety being considered the least toxic [40]. All above-ground parts of the plant can be toxic to rabbits, mice, and caged birds (canaries, cockatiels, and budgerigars). The toxin is not completely defined, but some clinical signs have been reproduced with persin, a compound that has been isolated from avocado leaves [34]. The mechanism of action is unknown. The clinical signs vary with species of animal. Lactating rabbits and mice develop a noninfectious mastitis and agalactia after eating avocado leaves. Rabbits have also developed cardiac arrhythmia, submandibular edema, and acute death. Caged birds have displayed acute respiratory distress and death 12 to 29 hours after ingestion of avocado fruit [22]. Other signs in birds have included resting on the cage bottom, fluffed feathers, and slightly outstretched wings [22]. Necropsy lesions in birds include subcutaneous edema of the pectoral area, hydropericardium, mild pale streaks of the pectoral muscles, and generalized lung congestion [22]. Lesions in mammals include necrosis of the acinar epithelium of the lactating mammary gland and the myocardium [34]. Treatment is symptomatic and supportive. The prognosis is guarded if signs reflective of cardiac disease or respiratory distress are present. The mastitis can resolve, but milk production is decreased. Onion Although pets have been known to chew on raw onions, most exposures occur when the animal is fed cooked onions. Cats have been known to develop toxicosis when fed baby food that contained onion powder [24,39]. Certain dog breeds such as Akitas and Shibas can have hereditary deficits that make them more susceptible to this toxicosis [51]. The primary toxic substance is n-propyl disulfide, an alkaloid found in leeks, wild onions, cultivated onions, garlic, and chives; however, other toxins may also be involved. The toxin(s) oxidize free sulfhydryl groups on hemoglobin [39]. The oxidized hemoglobin precipitates to form Heinz bodies in the red blood cells. Anemia is the result of damaged red blood cell membranes and the removal of cells that contain Heinz bodies by the spleen [39]. The onset of signs may be acute, but most signs likely develop over 1 to 2 days. Clinical signs are primarily the result of anemia, including pale or
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icteric mucous membranes, fast pulse, weakness, depression, and possibly collapse. Hemoglobinuria is often an early sign. Clinical pathologic findings include decreased hematocrit, decreased hemoglobin, mild methemoglobinemia, and the presence of Heinz bodies. Polychromasia, nucleated red blood cells, and reticulocytes are seen as the regenerative response occurs [23,35]. The treatment depends on the severity of the anemia. Mild cases may only require supportive care; however, blood transfusions are necessary if the anemia is severe. The prognosis varies depending on the severity of clinical signs. Fruit seeds The foliage and seeds of some fruit trees (wild and domestic cherries, apricots, peaches, apples, and plums) contain cyanogenic glycosides [16]. The seeds are frequently more toxic than the leaves, especially in apricots and peaches. One source states that peach seeds have much more cyanide than the leaves [28]. A woman ate 20 to 30 raw apricot seeds purchased from a health food store and developed cyanide toxicosis in minutes [47]. Ingestions of 5 to 25 fruit seeds can cause toxicosis [16]. Cyanide binds to and inhibits cytochrome oxidase, thereby preventing cellular respiration. The oxygen-saturated hemoglobin is unable to release its oxygen to the tissues and can cause the venous blood to become a cherry red color [48]. Clinical signs can develop within minutes to 1 to 2 hours after ingestion, and death often occurs within minutes of the onset of clinical signs. Many animals are found dead, but tremors, ataxia, frothing at the mouth, dilated pupils, dyspnea, and convulsions have been reported. Treatment is often not successful because of the quick onset of clinical signs and death. The treatment for cyanide poisoning is sodium nitrite (16 mg/kg of body weight of a 3% solution administered slowly intravenously), which forms methemoglobin that binds with cyanide to form cyanmethemoglobin. This is followed by sodium thiosulfate (1.65 mL of a 25% solution administered intravenously), which converts cyanide to thiocyanate [16]. One half of these initial doses can be repeated in 30 minutes if the animal has not recovered. Sodium thiosulfate is relatively safe and can be used alone in less severe cases. Sodium nitrite is a potent vasodilator, however, which can cause hypotension and excessive methemoglobin formation. As a result, its use should be limited to more severe cases of known cyanide poisoning [16]. Supportive treatment includes 100% oxygen supplementation and intravenous fluids, which may be the only treatment needed if the animal is displaying mild signs.
Holiday plants Several types of plants that are not present during other times of the year are brought into pets’ surroundings during the holidays. The toxicity of these plants is generally overrated by the public.
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Mistletoe Phoradendron species are evergreen parasitic plants that grow on a variety of host trees. The toxicity of the various mistletoe species seems to vary and may be related to the type of host plant [17]. Most human exposures result in no adverse effects, although a few serious cases have been reported and were believed to be related to the plants or berries being used to brew tea [18]. Few incidents have been reported in animals, and efforts to reproduce disease in animals have been unsuccessful. The toxic component of mistletoe is unknown, although a variety of potentially toxic compounds have been isolated, including lectins, proteins, alkaloids, and amines. The most common clinical signs in human beings are gastrointestinal disturbances, including vomiting, diarrhea, and abdominal pain. Drowsiness, incoordination, seizure (in an infant), hypotension, and cardiovascular collapse have been reported rarely in human beings [31,44]. Treatment is symptomatic and supportive, primarily consisting of correction of fluid and electrolyte deficits. Holly Ilex species include hollies known as English or Christmas holly, American or white holly, and winterberry. These plants, especially the berries, contain saponins, which cause direct irritation to the digestive tract [49]. Clinical signs are usually mild to moderate diarrhea and vomiting. Most cases resolve within 24 hours. Treatment is symptomatic, but severe intoxications may require correction of fluid and electrolyte imbalances. Poinsettia Euphorbia pulcherrima has a milky sap that contains diterpenoid esters, which have irritant effects on the skin, mucous membranes, and digestive tract [25]. Clinical signs include increased salivation, vomiting, and, infrequently, diarrhea. Severe disease is rare. Treatment is symptomatic and supportive. Managing fluid and electrolyte imbalances may be necessary with large exposures. Skin exposures can be washed with alcohol and treated with ointments to reduce inflammation.
Trees and shrubs Pets can have access to numerous trees and shrubs. The following is a discussion of those plants that can be particularly hazardous. Cycad palms These palms are also known as sago palms (Cycas and Macrozamia spp.) and naturally grow in tropical and subtropical climates. Young palms are
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also used as houseplants. All parts of the plant are toxic, but the nuts (seeds) seem to be the most toxic part. Male and female plants exist in the same species, but only the female plant has the cone-shaped middle that produces nuts [12]. The plants contain three toxins: cycasin causes hepatic necrosis and gastrointestinal signs, b-methylamino-L-alanine causes neurologic signs, and a third unknown toxin causes neurologic signs [12,41]. The most common clinical sign in dogs is vomiting, with or without blood. Other signs include depression, diarrhea with or without blood, anorexia, and, occasionally, seizures [2]. Hepatic failure and death have occurred. Clinical pathologic findings include elevated serum alanine aminotransferase, bilirubin, and alkaline phosphatase. Electrolyte abnormalities can occur as a result of prolonged vomiting and dehydration. Gastrointestinal signs appear within 24 hours of ingestion, but the laboratory values usually do not change for 24 to 48 hours [2]. Treatment begins with decontamination via emesis and repeated doses of activated charcoal (2–3 doses within 24 hours). Monitor liver enzymes and bilirubin daily for 48 hours or until the values return to normal. Give 5% dextrose IV [26]. Treat the gastrointestinal irritation with sucralfate and cimetidine or another inhibitor of gastric acid secretion. Control seizures and tremors with diazepam. Blood transfusions may be needed if the gastrointestinal tract hemorrhage results in severe anemia [2]. Maintain the dog on a low-protein diet. Continue all therapy until the signs resolve. Chinaberry This deciduous tree (Melia azedarach) belongs to the mahogany family and has become naturalized to the temperate regions of North America. All parts of the tree are potentially toxic, but most cases of poisoning in dogs result from ingestion of the fallen fruit. Toxicosis has also occurred in rabbits, rats, guinea pigs, poultry, and livestock [21]. Several potentially toxic compounds have been isolated from the plant [45]. The principal toxins are meliatoxins, which are concentrated in the fruit and affect the gastrointestinal and nervous systems. The exact mechanism of action is unknown. The gastrointestinal effects are probably a result of direct irritation. The effects on the central nervous system are similar to those of nicotine, with an initial stimulation of the sympathetic and parasympathetic systems followed by persistent depolarization. Within 1 to 2 hours of ingestion, vomiting and diarrhea (with or without blood), abdominal pain, anorexia, and straining to defecate can occur. Some animals hypersalivate. These gastrointestinal signs are followed by a variety of nervous system signs, including ataxia, depression, excitement, seizures, paresis, and coma. Respiratory arrest is most likely the cause of death. A large number of other signs have been reported, including hyperthermia, hypothermia, tachycardia, bradycardia, dyspnea, stranguria, muscle
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rigidity, mydriasis, and miosis [20,21]. Clinical signs can vary widely, making the diagnosis difficult unless the exposure was observed. The clinical pathologic findings and lesions are also nonspecific. Aggressive decontamination procedures should be used before the onset of clinical signs. No antidote exists; thus, treatment is limited to symptomatic and supportive care. The prognosis is poor after adverse nervous system signs are present. Heath family Plants in the heath family include rhododendron, azalea, laurel, and Japanese pieris. These plants are commonly used as ornamental shrubbery and grow in the acidic moist soils of North America, especially in the eastern United States. These plants contain grayanotoxins, which modulate the gating kinetics of sodium channels in cell membranes, resulting in prolonged depolarization of the nervous tissue [9,37]. The toxin is found in the leaves, stems, nectar, and flowers [38]. Clinical signs can appear between 4 and 12 hours after ingestion and can persist for several days. Vomiting is the most consistent finding. Other gastrointestinal signs that can occur include bloating, abdominal pain, and salivation. Diarrhea is not typically seen. Neurologic signs may or may not be seen and include depression, fine muscle tremors, ataxia, and convulsions with opisthotonus and paddling [9,38]. A small percentage of dogs can have tachycardia or bradycardia. Clinical pathologic findings are nonspecific and reflect the clinical signs, including stress leukogram, dehydration, and electrolyte imbalance. Decontamination involves emesis (if the animal is not already vomiting) and activated charcoal. No antidote exists; thus, treatment is symptomatic and supportive. The prognosis is good in animals that have not aspirated or convulsed. Lectins The two plants of most concern in this category are Ricinus communis (castor bean) and Abrus precatorius (rosary pea, precatory bean). The lectin in castor bean is ricin, which is present in all parts of the plant but is most concentrated in the seed. The lectin in the rosary pea is abrin, which is only present in the seeds. Lectins enter cells and cause their death via inhibition of protein synthesis [27,32]. Fortunately, lectins are poorly absorbed from the digestive tract. Furthermore, chewing or breaking of the seed coat seems to be necessary before the lectins can be released from the bean or pea. Despite ricin being one of the most deadly substances known, death in human beings who ingest castor beans is infrequent, perhaps because the bean is swallowed whole and the seed coat is not broken [3,10].
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The major organ affected is the gastrointestinal tract. Clinical signs include vomiting, diarrhea, gastrointestinal bleeding, abdominal pain, and dehydration. In dogs, signs most often develop within 6 hours of ingestion but can be delayed for up to 42 hours [1]. The duration of signs is 1.5 to 5.5 days [1]. No antidote is available for lectins. Early decontamination via emesis and activated charcoal is warranted before the onset of clinical signs, especially if the seeds could have been chewed and the seed coat broken. If clinical signs occur, fluid and electrolyte balance should be closely monitored. Gastrointestinal protectants and other symptomatic care are given as needed. Mortality is low in animals, because the seed coat is not always broken on ingestion and because lectins are poorly absorbed. Nevertheless, all ingestions should be taken seriously because of the high toxicity of these lectins. The prognosis is guarded if clinical signs do develop. Yew Several species of Taxus are commonly used as ornamental shrubs or trees, including Japanese yew, English yew, Florida yew, and ground hemlock. The bark, leaves, and seeds are toxic but not the red fruit that surrounds the seed. These plants contain taxine, a cardiotoxic alkaloid that causes conduction disturbances with a direct action on ion channels of cardiac muscle. Most cases involve livestock, but caged birds have been intoxicated experimentally [42]. Clinical signs in birds include regurgitation, depression, ataxia, dyspnea, weakness, and acute death [42]. Suspected Japanese yew poisoning has been reported in a dog that had intermittent vomiting, seizures, and aggressive behavior [15]. Yew bark was found in the stomach of a 1-year-old dog and believed to be the cause of its death [13]. In livestock, acute death is common, and clinical signs can begin within 1 to 4 hours after ingestion. It is usually too late for treatment once the signs have occurred because of the peracute nature of the disease. Furthermore, restraining the animal for treatment may cause cardiac arrest. No antidote exists. Cardiac glycosides Several different plants contain cardiac glycosides, but those that pets are most likely to be exposed to are oleander (Nerium oleander), foxglove (Digitalis purpurea), and lily of the valley (Convallaria majalis). Cardiac glycosides inhibit the cellular membrane sodium-potassium pump, resulting in decreased electric conductivity. A variety of cardiac arrhythmias can occur [43]. Abdominal pain and diarrhea can also occur. Death can be peracute, or symptoms may persist from a few hours to 2 days before death ensues. Decontamination is recommended before clinical signs begin. Because any type of arrhythmia, tachycardia, or bradycardia is possible, treatment
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varies from case to case. The electrolyte status of the animal should be monitored closely, and fluids should be administered as needed. Treatment with digoxin immune Fab (Digibind), which is used for toxicosis caused by excessive digoxin, may be helpful if administered early in the disease. The usual dose is 1.7 mL of Digibind (administered through a filter over 30 minutes) per milligram of digoxin that was ingested [14]. With plant ingestions, the amount of toxin involved is not known, however.
Ornamental bulbs These plants have roots that form bulbs, tubers, or corms. Most of these plants only cause mild to moderate gastrointestinal signs if the bulb is ingested. The exceptions are autumn crocus, glory lily, and a few other lilies (Lilium spp. and Hemerocallis spp.). Lilies (Lilium spp. and Hemerocallis spp.) Some plants in the Liliaceae family can cause renal toxicosis in cats. These are ornamental plants that bloom in spring and summer. The plants known to be toxic are Easter lily (Lilium longiflorum), tiger lilies (Lilium tigrinum), rubrum or Japanese showy lilies (Lilium speciosum, Lilium lancifolium), day lilies (Hemerocallis spp.), and Asiatic lilies [8,46]. Peace lilies (Spathiphyllum spp.) and calla lilies (Zantedeschia spp.) are not in the Liliaceae family and do not cause renal problems [46]. All parts of the plant, including the flowers, are toxic. Even one bite of the plant can cause toxicosis. Only cats are known to develop renal failure; dogs seem to be resistant. The mechanism of action is unknown, but the renal failure seems to be caused by necrosis of the renal tubular epithelial cells [8]. The basement membrane remains intact, and tubular epithelial cells can regenerate with prompt aggressive treatment [46]. Vomiting, anorexia, and depression often occur within 2 hours of ingestion. The blood urea nitrogen (BUN), creatinine, potassium, and phosphorus are elevated by 24 to 72 hours. Epithelial casts appear in the urine by 18 hours. Creatinine is often disproportionately elevated (as high as 44 mg/dL) compared with the BUN [46]. Treatment begins with induction of emesis if the ingestion could have occurred within the past 2 to 3 hours. This should be followed with two to three doses of activated charcoal within 24 hours. Diuresis with lactated Ringer’s solution administered intravenously at two times the maintenance level for at least 48 hours should be instituted to prevent renal tubular obstruction from necrosis and sloughing of epithelial cells. Obtain baseline BUN and creatinine levels, recheck daily, and continue fluids if they are elevated. Postponing treatment for longer than 18 hours after exposure can result in renal failure and death. Anuric cats have a grave prognosis, but peritoneal dialysis may restore function in a few cases.
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Autumn crocus and glory lily Autumn crocus (Colchicum spp.) and glory lily (Gloriosa spp.) contain colchicine, an alkaloid that has been reported to cause toxicosis in dogs and livestock. All animals are presumably susceptible. The autumn crocus should not be confused with the spring-blooming crocus, which is a member of the iris family. Colchicine is most concentrated in the tuber and the seeds. It is an antimetabolite that inhibits normal cell division, especially in rapidly dividing cells [7]. Initial clinical signs include vomiting and diarrhea (with or without blood), abdominal pain, hypersalivation, and depression. These signs can progress to weakness, ataxia, paresis, or collapse [11]. Multiple organ failure involving the lungs, kidney, cardiovascular system, and nervous system has occurred in human beings [33]. Coagulopathies and myelosuppression are possible sequelae. Emesis can be induced, and activated charcoal can be given before onset of gastrointestinal signs. Treatment is nonspecific and is limited to alleviation of clinical signs. The prognosis is poor if signs involve multiple organ systems. Other bulbs Bulbs that fall into this category include amaryllis, paper whites, springblooming crocus, Narcissus spp. (narcissus, jonquil, daffodil), iris, and tulip. These ornamental bulb plants usually only cause mild gastrointestinal signs. If a significant amount of the bulb itself is ingested, however, severe vomiting and diarrhea can occur. If the bulb is ingested, the animal should be decontaminated before the onset of clinical signs. Treatment consists of alleviation of clinical signs, because an antidote does not exist for these plants.
Houseplants Numerous plants can be used as ornamentals inside the home. Below is a discussion of the more commonly used plants. Kalanchoe This popular houseplant is indigenous to tropical Africa, Madagascar, Asia, and South America [50]. Kalanchoe contains bufadienolides, which are cardiac glycosides similar to those found in foxglove, oleander, lily-ofthe-valley, and various species of milkweed [12]. Cardiac glycosides inhibit Na+-K+ adenosine triphosphatase, resulting in decreased active transport of sodium with subsequent efflux of potassium. Toxicosis has been induced experimentally in livestock dosed with the plant or its flowers; natural poisonings are reported during the flowering season of the plants [4,29,30]. Kalanchoe toxicosis has also been reported in chicks, a rabbit, and a pack rat [50].
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Clinical signs in dogs that have been reported to the author include cardiac signs (tachycardia and increased blood pressure) and neurologic signs (dilated pupils, nystagmus, delirium, mild seizures, weakness, and tetany). Other signs that can be associated with cardiac glycosides include bradycardia, arrhythmias, hyperkalemia, vomiting, and diarrhea [12]. Treatment of cardiac glycoside exposure begins with decontamination. Induce emesis only if clinical signs are absent. Give activated charcoal unless the clinical condition predisposes the patient to aspiration. Treatment focuses on symptomatic and supportive care. Digibind has been beneficial for oleander poisoning but has not been evaluated for kalanchoe poisoning. Calcium oxalate crystals Many houseplants of the Araceae family contain insoluble calcium oxalate crystals (not to be confused with plants that contain soluble calcium oxalate, which can cause renal toxicosis). These plants are popular and include elephant’s ear, schefflera, caladium, dumb cane (Dieffenbachia spp.), pothos, many ivy varieties, philodendron, peace lilies (Spathiphyllum spp.), and calla lilies (Zantedeschia spp.) [5]. Cells in the plant contain spicules of calcium oxalate crystals, which are needle-shaped. When these cells are broken during ingestion, the sharp crystals shoot out of the cells and embed into the mucous membranes, tongue, and throat [5]. The onset of pain can be immediate or can occur up to 2 hours after chewing on the plant. The animal can have increased salivation, vocalization, anorexia, and depression. Swelling inside the mouth can occur, but a significant enough amount to cause airway obstruction is unlikely [36]. Mild vomiting or diarrhea is possible if the animal swallows a large amount of the plant. Treatment involves symptomatic care. The mouth should be rinsed, and the animal can be offered small amounts of milk or soft food to decrease the pain. If the amount of ingestion is unusually large, the animal can be given gastrointestinal protectants and anti-inflammatory drugs. Most animals recover uneventfully within 24 hours. English ivy This ivy (Hedera spp.) is used as a houseplant and even more commonly as a ground cover. Other varieties are known as Persian ivy, Irish ivy, Atlantic ivy, and Nepal ivy. These plants, especially the berries, contain pentacyclic terpenoids, which cause gastrointestinal signs [6]. In general, these types of ivy are more toxic than other varieties such as those that contain oxalate crystals. Many ingestions are not serious, but severe vomiting, salivation, abdominal pain, and diarrhea can occur. Treatment is symptomatic and supportive.
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Summary A variety of plants, seeds, and nuts can cause toxicosis in small animals. Some plants are not as toxic as commonly believed by the general public. Conversely, plants or nuts that are consumed by human beings can be toxic to their pets. Most plant toxins do not have specific treatments or antidotes. As a result, treatment is often limited to decontamination plus symptomatic and supportive care.
References [1] Albretsen JC. Evaluation of castor bean toxicosis in dogs: 98 cases. J Am Anim Hosp Assoc 2000;36:229–33. [2] Albretsen JC, Khan S, Richardson J. Cycad palm toxicosis in dogs: 60 cases (1987–1997). JAVMA 1998;213:99–101. [3] Alpin PJ, Eliseo T. Ingestion of castor oil plant seeds. Med J Aust 1997;168:423–4. [4] Anderson LAP, Shultz RA, Joubert JPJ, Prozesky L, Kellerman TS, Erasmus GL, et al. Krimpsiekte and acute cardiac glycoside poisoning in sheep caused by bufadienolides from the plant Kalanchoe lanceolata forsk. Onderstepoort J Vet Res 1983;50:295–300. [5] Burrows GE, Tyrl RJ. Araceae juss. In: Toxic plants of North America. Ames: Iowa State University Press; 2001. p. 105–19. [6] Burrows GE, Tyrl RJ. Araliaceae juss. In: Toxic plants of North America. Ames: Iowa State University Press; 2001. p. 120–4. [7] Capraro HG, Brossi A. Tropolonic Colchium alkaloids. In: Brossi A, editor. The alkaloids. Orlando: Academic Press; 1984. p. 1–70. [8] Carson TL, Sanderson TP, Halbur PG. Acute nephrotoxicosis in cats following ingestion of lily (Lilium spp.). In: Proceedings of the Annual Meeting of the American Association of Veterinary Laboratory Diagnosticians. Grand Rapids; 1994. p. 43. [9] Casteel S, Wagstaff J. Rhododendron macrophyllum poisoning in a group of goats and sheep. Vet Hum Toxicol 1989;31:176–7. [10] Challoner KR, McCarron MM. Castor bean intoxication. Ann Emerg Med 1995;19:1177–83. [11] Chareyre S, Meram D, Pulce C, Descotes J. Acute poisoning of cows by autumn crocus. Vet Hum Toxicol 1989;31:261–2. [12] Cheeke PR. Neurotoxins, cardiac/pulmonary toxins, and nephrotoxins. In: Natural toxicants in feeds, forages, and poisonous plants, 2nd edition. Danville (IL): Interstate Publishers; 1998. p. 365–409. [13] Clay BR. Poisoning and injury by plants. In: Kirk RW, editor. Current veterinary therapy: small animal practice, 6th edition. Philadelphia: WB Saunders; 1977. p. 179–84. [14] Dalefield RR, Oehme FW. Antidotes for specific toxins. In: Peterson ME, Talcott PA, editors. Small animal toxicology. Philadelphia: WB Saunders; 2001. p. 371–85. [15] Evans KL, Cook JR. Japanese yew poisoning in a dog. J Am Anim Hosp Assoc 1991;27:300–2. [16] Fitzgerald KT. Cyanide. In: Peterson ME, Talcott PA, editors. Small animal toxicology. Philadelphia: WB Saunders; 2001. p. 474–80. [17] Fukunaga T, Nishiya K, Kajikawa I, Takeya K, Itokawa H, et al. Studies on the constituents of Japanese mistletoes from different host trees, and their antimicrobial and hypotensive properties. Chem Pharm Bull (Tokyo) 1989;37:1543–6. [18] Hall AH, Spoerke DG, Rumack BH. Assessing mistletoe toxicity. Ann Emerg Med 1986;15:1320–3. [19] Hansen SR, Buck WB, Meerdink G, Khan SA. Weakness, tremors, and depression associated with macadamia nuts in dogs. Vet Hum Toxicol 2000;42:18–21.
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