Toxic plants (Proceedings)

It is not uncommon for veterinarians working with companion animals to run into suspected intoxications where the actual toxicant cannot be identified. There is almost never a lack of potential perpetrators of these dastardly deeds, because of the somewhat morbid, seemingly natural inclination for people to think there is someone who hates them enough to kill their pet. However, clients are often extremely reluctant to consider or are, even possibly, unaware of the wide variety of common and, sometimes, not so common indoor and outdoor ornamental plants, which if consumed in large enough quantities, can result in potentially lethal intoxications. It has been my experience that, like me almost 30 ago, veterinary professional students still seem to think that toxic plants are the exclusive domain of large animal practitioners and that 500 plants can be memorized the night before the exam. Because livestock species are generally herbivorous or, at least, omnivorous and are generally kept as groups of animals, it might be true, to some extent, that equine and food animal veterinarians do encounter larger numbers of animals affected by plant-related toxins than their small animal colleagues. However, there are certainly plant intoxications with which small animal practitioners should be familiar, especially if their patients have access to palatable indoor and/or outdoor plants and are young, small, overly curious, bored, hungry, just plain stupid and destined to eventually be a Darwinian phenomenon, and/or any combination of the preceding factors.

We are often left to believe that if something is "natural" it is at least safe, if not beneficial. While many natural products do, in fact, have inherent benefits and, even, medicinal value, it should not be assumed that chemicals of plant origin are necessarily less potent or safer than synthesized products. Nature is NOT benign!!! Chemical warfare expertise is essential to the survival of some plants because they are immobile and relatively defenseless. The toxic principles in plants include various classes and mixtures of classes of compounds, such as Alkaloids, Proteins, Peptides, Amino Acids, Glycosides, Oxalates, Tannins, Resins, Nitrates, Sulfides and some Unknown Compounds. No mammalian organ system is immune to the effects of plant toxins, and toxic plants and/or plant toxins can affect multiple systems. It should be understood that, as greater quantities of a toxic plant are consumed, more severe clinical signs are likely to be observed. In addition, different syndromes can be seen in different species and with different levels of toxic exposure.

A systems approach will be used in three hours of lecture to cover some of the more relevant plants with which small animal practitioners should have some familiarity. The plants will be grouped as CARDIOTOXIC AND NEUROTOXIC PLANTS, NEPHROTOXIC AND HEPATOTOXIC PLANTS, and, finally, OTHER COMMON AND NOT SO COMMON TOXIC PLANTS, which primarily affect other systems. While plants will be discussed under one system, an effort will be made, when necessary, to mention other systems potentially affected by a particular plant or related species.

Cardiotoxic and neurotoxic plants

It can sometimes be difficult to tell whether an apparent intoxication involves primarily cardiac or neurological abnormalities. Nonspecific clinical signs, such as weakness, tremors, and gastrointestinal upset, can often be observed with exposure to either cardiotoxic or neurotoxic plants. Small doses of cardiotoxins and neurotoxins can also both cause rapid death, without much in the way of premonitory signs or postmortem changes. Careful examination, including auscultation of the heart and ancillary testing procedures, performed in the earliest stages of a suspected intoxication, can often detect cardiac arrhythmias or subtle neurological deficits, which distinguish the effects of cardiotoxins from those of neurotoxins.

Cardiotoxic Plants

Plants containing cardiac glycosides

     • Asclepias species (Milkweeds), Digitalis purpurea (Foxglove), Convallaria majalis (Lily-of-the-Valley), Apocynum species, (Dogbane), Nerium species (Oleander), Adonis species (Pheasant's Eye), Euonymus species (Burning Bush), Kalanchoe species (Kalanchoe or Mother-in-law Plant)

     • Most plant parts are toxic, and toxicity is generally retained with drying.

     • Cardenolide and Bufodienolide (Kalanchoe) cardiac glycosides interfere with NA+ /K+-ATPase, and all degrees of heart block can be induced.

     • Gastrointestinal signs are frequently observed first (plant material in vomitus or feces).

     • Plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, necropsy findings (might be plant material in GI tract), and possible analyses of stomach contents should all be considered for diagnosing intoxications.

     • Cardiac glycoside exposure should be considered when gastrointestinal upset from observed plant ingestion is accompanied by cardiac arrhythmias or when young animals present with persistent heart block.

     • Therapy involves removal from source, prevention of absorption, increased elimination, supportive care, including control of heart block/arrhythmias, and, possibly, digoxin-specific antibody fragments (Fab).

     • High-level K+- and, especially, Ca2+-containing fluids should be avoided.

Plants containing andromedotoxins (Grayanotoxins)

     • Rhododendron species (Rhododendron/Azalea), Pieris japonica (Japanese Pieris), and Kalmia species, (Laurels but NOT Bay Laurel)

     • Leaves, flower nectar, and, even, honey associated with these plants can be toxic.

     • Andromedotoxins bind and modify Na+ channels, causing prolonged depolarization and excitation, as well as Ca2+ influx, as evidenced by hypotension and bradycardia.

     • Severe gastrointestinal signs are often observed (plant material in vomitus or feces).

     • Plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, necropsy findings (might be plant material in GI tract), and possible analyses of stomach contents should all be considered for diagnosing intoxications.

     • Therapy involves removal from source, prevention of absorption, increased elimination, and supportive care, including control of arrhythmias.

     • Calcium-containing fluids should be avoided.

Cardiotoxic plants (Continued)

Plants containing taxine alkaloids

     • Taxus species (American, British, and Japanese Yews) are extremely common ornamental plants.

     • Most plant parts are toxic, and toxicity is generally retained with drying.

     • Taxine Alkaloids inhibit the conduction of the action potential throughout the heart, resulting in heart block and, potentially, death.

     • Gastrointestinal signs can sometimes be observed first, and dogs can exhibit seizures.

     • Plant availability and potential exposure opportunities, evidence of plant consumption (might be plant material in vomitus or feces), clinical signs, necropsy findings (might be minimal except for the presence of plant material in GI tract), and possible analyses of stomach contents should all be considered for diagnosing intoxications.

     • Therapy involves removal from source, prevention of absorption, increased elimination, supportive care, including control of heart block/arrhythmias.

Neurotoxic plants

The explanation of the pathogenesis and diagnosis of plant-associated neurotoxicoses can be challenging. Depending on the relative concentrations of specific toxins, the species and age of the exposed animal, the duration of plant exposure and/or the amount of plant material consumed, some "primarily" neurotoxic plants can be associated with "non-neurological" syndromes. Muscle weakness and/or damage can present as a "neurological" syndrome, and multiple species of potentially "neurotoxic" plants can be consumed simultaneously in some instances. In addition, animals with hepatic encephalopathy often appear to be "neurologic".

Plants associated with GABA inhibition

     • Cicuta species (Water Hemlock or Cowbane) contain the Resinoid compound, Cicutoxin, which is present in the highest concentrations in the roots and young shoots.

     • Dicentra species (Bleeding Heart and Dutchman's Breeches) are common ornamentals and contain isoquinolone alkaloids.

     • Common clinical signs associated with the ingestion of these plants are salivation, tremors, convulsions, and, potentially, death.

     • Plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, necropsy findings (might be minimal except for the presence of plant material in GI tract), and possible analyses of stomach contents should all be considered for diagnosing intoxications.

     • Therapy involves removal from source, prevention of absorption, increased elimination, supportive care, including control of tremors and convulsions.

Plants containing anticholinergic neurotoxins

     • Plants containing Tropane Alkaloids, such as Atropine and Scoplamine, including Hyoscyamus niger (Henbane), Datura species (Jimsonweed, Thornapple or Moon Flower), Brugmansia species (Angel's Trumpet), and Atropa belladonna (Belladonna or Deadly Nightshade).

Neurotoxic plants (Continued)

Plants containing anticholinergic neurotoxins (continued)

     • Toxic compounds are parasympatholytic, and the most common clinical signs observed with the ingestion of primarily the fruits or seeds of these plants are trembling and excitement, tachycardia and increased respiratory rate, mydriasis, blurred vision, delirium, ileus, hyperthermia, coma and possible death.

     • Plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, necropsy findings (might be minimal except for the presence of plant material/seeds in GI tract), and possible analyses of stomach contents or urine for plant toxins should all be considered for diagnosing intoxications.

     • Therapy involves removal from source, prevention of absorption, increased elimination, supportive care, including control of tremors and tachycardia and possible administration of physostigmine.

Plants containing cholinergic neurotoxins

     • Wide range of plants including Delphinium species (especially Tall Larkpur), Nicotiana species (Tobacco), Conium maculatum (Poison Hemlock), Lupinus species (Lupines or Blue Bonnet), Sophora species (Mescal Bean), and Neurotoxic Blue-green Algae (Anatoxin A from Anabaena flos aquae and Oscillatoria species)

     • The cholinergic neurotoxins from these plants belong to various classes of compounds but all bind to cholinergic receptors, potentially causing tremors, convulsions, depolarizing neuromuscular blockade, and death associated with respiratory paralysis.

     • Tobacco products are frequently associated with concurrent vomiting and convulsions, thereby predisposing affected animals to aspiration pneumonia.

     • Plant availability and potential exposure opportunities, evidence of plant consumption (plant material in vomitus and/or feces), clinical signs, necropsy findings (might be minimal except for the presence of plant material/seeds in GI tract), examination of fixed water samples for Blue-green Algae (Anabaena species have algal cells arranged in chains), and possible analyses of source material, stomach contents, or, in some cases, urine for specific toxins should all be considered for diagnosing intoxications.

     • Therapy involves removal from source, prevention of absorption, increased elimination, and supportive care, including control of tremors and convulsions and treatment of any aspiration pneumonia.

     • The Polycyclic Diterpene Alkaloids in Low Larkspur and related compounds in Aconitum species (Monkshood) are more frequently associated with cardiotoxicity.

     • The Blue-green Algal neurotoxin, Anatoxin a(s), is a peripheral acetylcholinesterase inhibitor and is associated with a SLUDD syndrome in exposed animals.

Miscellaneous plant toxins causing hallucinations, CNS depression, and/or ataxia

     • Psilocybin in Psilocybe, Cynocybe, and other Mushrooms, Delta-9-Tetrahydrocannabinol (Δ-9-THC) from Cannabis sativa (Marijuana), and an unknown toxin in Macadamia integrifolia (Macadamia Nut) can cause "hallucinations", CNS depression, aberrant behavior, and/or ataxia, as well as, in the case of Macadamia Nuts, rear limb weakness.

     • Opportunities for and evidence of ingestion and clinical signs can assist in the diagnosis.

     • Therapy involves removal from the source, decontamination, and supportive care.

Nephrotoxic and hepatotoxic plants

CARDIOTOXIC AND NEUROTOXIC PLANTS are often associated with the rapid onset of potentially lethal intoxications arising from acute exposures to relatively small amounts of plant material. NEPHROTOXIC AND HEPATOTOXIC PLANTS, on the other hand, frequently cause intoxications with a longer time course, which often involve exposures to larger amounts of plant material and which are usually characterized by notable biochemical and/or histological alterations

Nephrotoxic plants

While there are a number of plants discussed below which primarily target the kidneys, plant intoxications associated with hypovolemia and hemolysis or rhabdomyolysis can also involve impaired renal function, and some plant toxins reach the kidneys unchanged.

Plants containing soluble oxalates

     • Oxalis species (Shamrocks) and Rheum rhabarbarum (Rhubarb) contain soluble oxalates (Na+ and K+) which are present in the highest concentrations in the leaves.

     • Common clinical signs associated with the ingestion of these plants can include rapid onset of hypocalcemia and inhibition of respiratory enzymes (sudden death is possible if enough is ingested) and oxalate nephrosis from the deposition of calcium oxalate crystals.

     • Plant availability and potential exposure opportunities, evidence of plant consumption (plant material in vomitus and/or feces), clinical signs, clinical chemistry results, oxalate crystals in urine, and necropsy findings (might be minimal if death from severe hypocalcemia; presence of plant material in GI tract) should all be considered for diagnosing intoxications.

     • Therapy involves removal from source and supportive care, including correction of hypocalcemia and diuresis.

Lillies and cats

     • Lillium and Hemerocallis species (True Lilies, Asian Lilies, Stargazer, and Day Lilies) contain an unknown nephrotoxin to which cats appear to be uniquely susceptible.

     • Common clinical signs associated with the ingestion of these plants can include salivation, gastrointestinal signs, depression, polyuria, and renal failure.

     • Plant availability and potential exposure opportunities (Easter; recent death), evidence of plant consumption (plant material in vomitus and/or feces), clinical signs, clinical chemistry (out of proportion elevation in creatinine) and urinalysis results, and necropsy findings (plant material in GI tract) should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source, prevention of absorption, increased elimination, and supportive care, including diuresis for at least 24 to, if possible, 72 hours in order to prevent anuric renal failure.

Grapes and raisins and dogs

     • Vitis and shriveled Vitis species (Grapes and Raisins) contain an unknown nephrotoxin to which dogs appear to be uniquely susceptible.

     • Clinical signs of excessive ingestion of Grapes and/or Raisins by dogs include vomiting and renal disease and/or failure.

Nephrotoxic plants (Continued)

Grapes and raisins and dogs (continued)

     • Plant availability and potential exposure opportunities, evidence of plant consumption (plant material in vomitus and/or feces), clinical signs, clinical chemistry and urinalysis results, and necropsy findings should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source, decontamination, and supportive care, including diuresis to prevent anuric renal failure.

Hepatotoxic plants

While there are a number of plants discussed below which primarily target the liver, plant intoxications associated with hypoperfusion, hypoxia, hemolysis, and/or hemorrhage can also adversely affect the liver. It should also be noted that, for all ingested plants, the liver is the first organ to "see" potential toxins which have been absorbed from the GI tract. The liver is also the primary site of toxin metabolism or biotransformation, which can result in the production reactive oxygen species (ROS) and hepatic oxidative damage, as well as the synthesis of ultimate toxicants which, primarily, adversely affect other organ systems.

Plants containing pyrrolizidine alkaloids

     • Potentially toxic concentrations of Pyrrolizidine Alkaloids are contained, especially, within the seeds of several plant genera, including Senecio (Tansy Ragwort or Common Groudsel), Amsinckia (Fiddleneck), Crotalaria (Rattlebox), Symphytum (Comfrey), and Cynoglossum (Hound's Tongue).

     • .Pyrrole metabolites alkylate cellular macromolecules, such as DNA, leading to mitotic inhibition, and hepatocytomegaly.

     • Pyrrolizidine alkaloids are carcinogenic and are excreted in milk.

     • Chronic intoxications are most common, and clinical signs can take weeks to develop.

     • Clinical signs are generally consistent with hepatic insufficiency and/or failure and sequelae, such as hepatic encephalopathy.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, clinical chemistry results, and, if indicated, liver biopsies with hepatocytomegaly, as well as consistent necropsy findings, should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source and decontamination (although exposure could have very likely been chronic in nature and have been discontinued for quite some time prior to the appearance of overt clinical signs) and supportive care, including dietary management and administration of antioxidants.

Hepatotoxic blue-green algae

     • The primary toxic principles in blooms of Microcystis aeruginosa, which occur in the Spring but are most common in the Summer and early Fall, are the hepatotoxic Cyclic Heptapeptides referred to as Microcystins, which can, potentially, cause death within 24 hours after ingestion.

     • Microcystins cause dysfunctional phosphorylation of cellular keratin, destruction of cytoskeletons and disassociation of hepatocytes, with hepatomegaly, massive hepatic necrosis, and hepatic hemorrhage.

Hepatotoxic plants (continued)

Hepatotoxic blue-green algae (continued)

     • Mycrocystis algal cells are arranged in "clumps" and can be identified microscopically in fixed samples of water.

     • Nodularia species produce a Cyclic Pentapeptide, which acts like the Microcystins.

     • Clinical signs are consistent with hepatic insufficiency and/or failure and sequelae, such as hepatic encephalopathy.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, clinical chemistry and, if indicated, liver biopsy results, necropsy findings (plant material in GI tract), and possible analysis for Microcystins should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source, prevention of absorption, increased elimination, and supportive care, including dietary management.

Cycads and false sago palms

     • The primary toxic principles in Cycas and Zamia species (Cycads and False Sago Palms) are hepatotoxic, glycosidic toxins, such as Cycasin and Macrozamin, which cause hepatic centrolobular necrosis.

     • Clinical signs are consistent with hepatic insufficiency and/or failure but can include gastrointestinal and neurological signs.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, clinical chemistry and, if indicated, liver biopsy results, and necropsy findings (plant material in GI tract) should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source, prevention of absorption, increased elimination, and supportive care, including dietary management and, possibly, antioxidants.

Amanita mushrooms

     • Amanita species of mushrooms are fungi which emerge from litter near base of trees

     • and which produce a variety of toxins, including Cyclic Octapeptides called Amatoxins, which are stable following exposure to heat, acid, and drying.

     • Amatoxins inhibit transcription of DNA to RNA and, therefore protein synthesis.

     • Clinical signs include initial vomiting and bloody diarrhea for 6 to 24 hours after ingestion, which subsequently subside for 12 to 24 hours and are followed by the hepatorenal phase of the intoxication, which is characterized by hepatic insufficiency, hypoglycemia, coma, and, possibly, death.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption (plant material in vomitus and/or feces), clinical signs, clinical chemistry results, and necropsy findings (plant material in GI tract), as well as possible analyses of GI contents for Amatoxins, should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source, decontamination with repeated doses of activated charcoal (enterohepatic recirculation), increased elimination, and supportive care, including penicillin G, silymarin, other antioxidants, and dietary management.

Other common and not so common toxic plants: Common/uncommon plants affecting the blood

Plants causing oxidative damage to red blood cells

     • N-propyl disulfide and related compounds in Allium species (Onion, Garlic, and Chives) and Hydrazines in some Mushrooms cause oxidative damage to red blood cells and/or hemolysis, as well as, especially, in the case of Hydrazines, GI and CNS signs.

     • Clinical signs can include anemia, weakness, lethargy, and hemoglobinuric nephrosis.

     • Toxicity remains in grilled onions and onion soup mixes.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption, clinical signs, hemogram and clinical chemistry results, and necropsy findings (might be minimal except for plant material or odor in GI tract) should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source, decontamination and supportive care, including possible transfusion, treatment with antioxidants, and diuresis to prevent hemoglobinuric nephrosis.

Plants containing cyanogenic glycosides

     • Cyanogenic Glycosides are found in highest concentrations in the seeds, leaves and stems of plants belonging to 250 genera, including Malus (Apple and Crabapple), Prunus (Cherry, Wild Cherry, Plum, Peach, and Apricot), and, even, Hydrangea (Hydrangea or Hortensia).

     • β-Glucosidase and hydroxynitrile lyase activity are involved in Cyanide production from Cyanogenic Glycosides, and both enzymes are released from damaged plant material.

     • Cyanide binds Fe3+ in cytochrome oxidase (more specifically cytochrome c oxidase), thereby blocking the electron transport system and inhibiting cellular respiration (oxygen is not transferred from the blood to the tissues).

     • Ingestion of material from wilted or decaying plants with cyanogenic potential (especially during early growth) predisposes dogs and cats to cyanide intoxication.

     • Clinical signs develop rapidly and include cherry red blood, hyperpnea, weakness, recumbency, respiratory paralysis, terminal convulsions, and death.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption (plant material in GI tract), clinical signs, necropsy findings (might be minimal except for plant material in GI tract), and possible analyses of the source material or stomach contents should all be considered for diagnosing intoxications.

     • Therapy involves immediate removal from the source, decontamination and supportive care, including possible antidotal treatment with sodium nitrite and/or sodium thiosulfate

Common/uncommon plants affecting the gastrointestinal tract

Following ingestion, the first parts of the body exposed to toxic plant material are the oral cavity, oropharynx, esophagus, stomach, and intestines. Any plant toxins present in large enough concentrations to be simple irritants will at least cause adverse health effects involving one or more of these anatomical sites, if nowhere else in the body. While vomiting and diarrhea can certainly be viewed as clinical signs of intoxication, they are also mechanisms by which the body rapidly rids itself of noxious materials.

Common/uncommon plants affecting the gi tract (continued)

Plants containing insoluble oxalates

     • Many ornamentals, such as Arisaema triphyllum (Jack-in-the-pulpit), Arum maculatum (Arum), Begonia species (Begonias), Caladium xanthosoma (Caladium), Dieffenbachia species (Dumbcane), Monstera deliciosa (Ceriman), Philodendron species (Philodendron), Schefflera or Brassaia species (Schefflera), Scindapsus species (Pothos), Spathiphyllum species, (Peace Lily), Symplocarpus foetidus (Skunk Cabbage), and Syngonium podophyllum (Arrowhead Plant), all contain Insoluble Oxalates (Ca2+) and possibly, Histamine and Kinin.

     • Clinical signs include salivation, headshaking, pawing at the mouth, inflammation; death is very unlikely.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption, and clinical signs should all be considered for diagnosing intoxications.

     • Therapy involves removal from the source and supportive care, including local irrigation and the administration of antihistamine and corticosteroids.

Euphorbia species (Spurges)

     • Ornamentals, such as Poinsettia and Snow-on-the-Mountain, with a milky, irritating sap containing resinous Euphorbin, Phorbol, Esters, and Ingenol.

     • Clinical signs are generally mild, arising from the irritation of mucous membranes and include vomiting and diarrhea, and, very rarely, death when a very small and not very intelligent dog eats a very big plant.

     • Previous plant availability and potential exposure opportunities (time of year for Poinsettia), evidence of plant consumption (plant material in vomitus or feces), and clinical signs should all be considered for diagnosing intoxications.

     • Therapy involves removal from the source and supportive care, including alleviation of gastrointestinal upset.

Plants containing toxalbumins (Lectins)

     • Plants, including Ricinus communis (Castor Bean or African Wonder Plant), Abrus precatorius (Precatory Bean or Rosary Pea), Robinia pseudoacacia (Black Locust), Phoradendron species (Mistletoes), which contain, especially in the seeds, Toxalbumins (Ricin, Abrin, Robin, and Phoratoxin, respectively).

     • Toxalbumins are stable proteins resistant to enzymatic breakdown, which inhibit protein synthesis by interfering with ribosomal elongation factor and inactivating 60S ribosomes.

     • Ricin is particularly toxic, with severe clinical signs and chemical warfare potential.

     • Clinical signs generally follow a 12- to 48-hour lag phase and CAN include burning of the mouth/throat and vomiting (especially Ricin), severe abdominal pain, catarrhal to hemorrhagic gastroenteritis, bloody diarrhea, leukocytopenia, hypovolemic and/or endotoxic shock, and, renal and hepatic involvement, as well as convulsions and death.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption (plant material in feces), clinical signs, hemogram and chemistry results, and necropsy findings (might include plant material in GI tract), as well as, especially for Ricin, possible analyses of the source material or stomach contents, should all be considered for diagnosing intoxications.

Common/uncommon plants affecting the gi tract (continued)

Plants containing toxalbumins/lectins (continued)

     • Therapy involves removal from the source, decontamination, and supportive care, including alleviation of gastrointestinal upset, treatment of shock, and correction of acid-base and electrolyte imbalances, as well as management of hepatic and renal complications.

Miscellaneous plants primarily affecting the gastrointestinal tract

     • Plants, including Podophyllum peltatum (Mandrake), Ligustrum species (Privet), Cyclamen species (Cyclamen), Persea americana (Avocado), Tulip species (Tulip), Colchicum autumnale (Autumn Crocus), Gloriosa superba (Gloriosa Lily/Superb Lily), Dianthus species (Carnations and Pinks), Citrus species (Orange, Lime, and Grapefruit), and species of Mushrooms in Amanita, Boletus, Chlorophyllum, and other genera contain a variety of toxic principles, which can be associated with nonspecific oral irritation, vomiting, and/or diarrhea (possibly bloody), as well as, even, occasionally, death.

     • Autumn Crocus and Gloriosa Lily contain Colchicine, which can be associated with shock, multi-organ failure, and bone marrow suppression.

     • Avocado can also be associated with myocardial necrosis, especially in pet birds.

     • Privet can sometimes be associated with renal damage.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption (plant material in vomitus/feces), clinical signs, hemogram and clinical chemistry results, as well as necropsy findings (might include plant material in GI tract), should all be considered for diagnosing intoxications.

     • Therapy involves removal from the source, decontamination, and supportive care, including alleviation of gastrointestinal upset and treatment/correction of complications.

Common/uncommon plant toxins with GI and neurotoxic effects

     • The seeds and or fruits/nuts of plants, including Phytolaca americana (Pokeweed), Aesculus species (Buckeye), Saponaria species (Bouncing Bet), Hedera species (Ivy), Ilex species (Holly), Sesbania species (Coffeeweed or another Rattlebox), and Aloe vera (Aloe), contain the highest concentrations of SAPONINS (Glycosidic Compounds; also a Narcotic-like Alkaloid associated with Buckye-induced CNS signs), which can damage membranes and cause vomiting and diarrhea, as well as tremors, ataxia, abnormal behavior, and, even, discolored urine thought to be associated with hematuria induced by Aloe ingestion, as well as, possibly, death.

     • Solanum species (Nightshades) contain STEROIDAL GLYCOALKALOIDS, such as Solanine, which is associated with GI irritation (abdominal discomfort, vomiting, and diarrhea) and conversion by hydrolysis into the neurotoxic STEROIDAL ALKALOID, Solanidine, which has the potential to cause CNS depression, behavioral changes, paresis/paralysis, and, possibly, death.

     • Species in a related genus, Brunfelsia (Yesterday, Today, Tomorrow or Morning-noon-and night, Lady-of-the-night, and Kiss-me-quick) are thought to contain GI-irritating compounds classified as SOLANINE-TYPE STEROIDAL GLYCOALKALOIDS, in addition to BRUNFELSAMIDINE and HOPEANINE thought to be associated with the tremors and potentially lethal seizures caused by these plants.

Plant toxins with gi and neurotoxic effects (Continued)

     • The bulbs of species of Narcissus (Daffodil or Jonquil), Amaryllis (Naked Lady and Belladonna Lily), Clivia (Clivia Lily, Clivies, or Kaffir Lily) produce LYCORINE and other Alkaloids, can cause vomiting and diarrhea, hypotension, tremors, and seizures.

     • Species of Chrysanthamum (Mum), Melia (Chinaberry Tree), Celastrus (Bittersweet), Rosmarinus (Rosemary), and non-hepatotoxic Amanita contain MISCELLANEOUS TOXINS which can produce GI (vomiting and diarrhea) and neurotoxic effects.

     • Previous plant availability and potential exposure opportunities, evidence of plant consumption (plant material in vomitus/feces), clinical signs, and the hemogram and clinical chemistry results, as well as necropsy findings (might include plant material in GI tract), should all be considered for diagnosing intoxications.

     • Therapy involves removal from the source, prevention of absorption, increased elimination, and supportive care, including alleviation of the gastrointestinal upset, tremor and seizure control, correction of fluid, electrolyte, and acid base deficits, and diagnosis and treatment of aspiration pneumonia.

Toxic Plant References for Busy Small Animal Practitioners

Books

Burrows GE, Tyrl RJ: Toxic Plants of North America. Ames, IA, Iowa State University Press, 2001.

Gfellar RW, Messonnier SP: Handbook of Small Animal Toxicology and Poisoning, 2nd Edition. St. Louis, Mosby, 2004.

Peterson ME, Talcott P (Eds): Small Animal Toxicology. St. Louis, Elsevier-Saunders, 2006.

Plumlee KH: Clinical Veterinary Toxicology. St. Louis, Mosby, 2004.

Websites

http://www.ansci.cornell.edu/plants/index.html

http://www.aspca.org/site/PageServer?pagename=pro_apcc_toxicplants

http://www.aspca.org/pet-care/poison-control/17-common-poisonous-plants.html

www.vth.colostate.edu/poisonous_plants/report/search.cfm

http://cal.vet.upenn.edu/projects/poison/index.html

http://www.library.illinois.edu/vex/toxic/

http://www.ivis.org/