Household Toxin List...
It can be very difficult for a veterinarian to properly diagnosis what toxin your pet got in to and treat it appropriately, usually they will or wont respond to the various counter medications or supportive therapies administered. Therapies for the symptoms are how one usually treats poisoning situations. Although they can run blood panels, these are not specific to an exact toxin/overdose and will only show if there is any organ involvement that needs to be addressed. There are certain toxicology labs that can be run but these are not only very costly but can take days to get the results. Because of this, it is vital that the owner always pay attention and not leave toxic items or items that a pet can easily overdose on, out for the animal to easily get to. If your pet has managed to get in to something it should not have and you now what it is, grab the box, vial, can, or the item, place it in a sealable bag and take it with you to the vet or when calling poison control. Having the items label can prove to be a life saver in really negative situations.
Here are some every day household items that one needs to always keep out their pets reach, this list does not include plants. All toxic plants can be found in charts at the bottom of this page.
Rodent Poisons
Antifreeze
Motor Oils
Most Human RX Medications
Molds
Algae (in excess)
Insecticides
Herbicides (if not already dry)
Heavy Metals
Batteries (especially lithium)
Chewing Too Much on Treated Lumbar
Expanding Foams or Glues
Snail and Slug Bait
Paint balls
Mothballs
Nicotine (over 20 mg)
Chocolate
Macadamia Nuts
Xylitol (in chocolate and chewing gum)
Cold Medicines
Play Dough (salt toxicity)
Liquid Potpourri Products
Air Fresheners
Silica Packets (Moisture removers from packaging)
Brewing Hops
Excessive Mulch Ingestion
Fermented Compost
Cattle Feeds Containing Xenobiotics
Benzyl Alcohol (animals rarely ingest this chemical found in insecticides)
Acorns (In excess, will cause major blockage)
Jodi Register (2015)
Toxic Plant List...
*Toxic plants that affect Potbelly Pigs, compiled by Stephanie Matlock. (2015)
Grasses that Cause Trauma
Common Name Scientific Name
Foxtail barley Hordeum jubatum
Needle grasses Stipa spp.
Squirrel tail Sitanion hystrix
Bristle grass Setaria spp.
Sandbur Cenchrus longispinus
Medusahead rye Taentherum asperum
Prairie three-awn Aristida oligantha
Tanglehead Heteropogon contortus
Miscellaneous plants cause irritation to the mouth of animals through the action of oxalate crystals present in the plants leaves and stems. The oxalate crystals become embedded in the mucous membranes of the mouth causing severe inflammation and swelling, excessive salivation, and difficulty in swallowing. In addition the soluble oxalates in the plants can induce kidney failure.
Common Nightshades with the Potential for Causing Poisoning
Common Name Scientific Name
Black nightshade Solanum nigrum
Huckleberry, wonderberry S. americanum
Hairy nightshade S. sarrachoides
Cutleaf nightshade S. triflorum
Silverleaf nightshade S. elaeagnifolium
Horse nettle, bull nettle S. carolinense
Sodom apple S. sodomaeum
Buffalo bur S. rostratum
Tropical soda apple S. viarum
Bittersweet, climbing nightshade S. dulcamara
This large family of plants with some 88 genera and more than 2300 species has long been associated with poisoning of humans and animals. Deadly nightshade or belladona (Atropa belladona) was used in ancient times to dilate the pupils of women to enhance their beauty, and it has found use as a potent hallucinogen. The black berries of belladona, the showy red berries of Jerusalem cherry (Solanum pseudocapsicum), and bittersweet (S. dulcamara) have caused poisoning in people who eat them. Animals are rarely poisoned by belladona and are more likely to be poisoned by various genera that include Solanum spp. (nightshades), Datura stramonium (jimson weed), Hyoscyamus niger (black henbane), Lycopersicon spp. (tomato), Cestrum spp. (jessamine), and Physalis (ground cherries or Chinese lanterns). The more common members of the nightshade family associated with poisoning in animals are presented in the table above. Livestock may be poisoned if they are fed potatoes (Solanum tuberosum) after they have sprouted and the skins turned green. Similarly green tomato vines may cause poisoning if fed to livestock. Potato plants, however, can be effectively used as a source of food for livestock if ensiled, or fed with grass hay or cereal grains
Miscellaneous Plants Infrequently Associated with Gastrointestinal Poisoning
Scientific Name Symptoms Common Name
Achillea milleform Colic, diarrhea Yarrow
Baccharis halimifolia Eastern baccharis Colic, diarrhea, staggering, trembling
Brassica spp. Mustards Colic, hemorrhagic diarrhea
Cephalanthus occidentalis Button bush Vomiting, weakness, death
Datisca glomerata Durango root Anorexia, diarrhea, depression, death
Hedera helix English ivy Colic, diarrhea
Hydrangea spp. Hydrangea Hemorrhagic diarrhea
Iris spp. Iris Colic, diarrhea
Phoradendron spp. Mistletoe Severe colic and diarrhea
Tulipa spp. Tulips Colic, diarrhea
Spurges are usually not eaten by cattle when other forages are available. Sheep and goats, however, will eat the plants without apparent problem. Spurges cause excessive salivation in some animals due to the irritant effects of the plant sap. Cattle frequently develop diarrhea if they are compelled to eat leafy spurge. Recovery is rapid once animals are provided more nutritious food.
Note
Leafy spurge is a noxious weed that should be vigorously controlled to prevent its rapid invasion of pastures and rangeland where it will displace nutritious forbes and grasses. Sheep are effective biologic controls for leafy spurge and can be profitably used to graze rangeland heavily infested with leafy spurge. Sheep can eat diets containing up to 40 to 50 percent leafy spurge without any evidence of disease or decrease in weight gain. The sheep can reduce the plant's biomass and density but will not eradicate it. Approximately 5 percent of leafy spurge seeds eaten by sheep remain viable in the feces, and, therefore, sheep can help spread the plant if not appropriately managed. Ideally sheep should be used to graze the leafy spurge before it flowers and the seeds are produced. If sheep are grazing the plant when it has seeds, they should be kept confined for at least 5 days before they are moved to leafy spurge-free areas
Plant Toxins That May Affect Milk Quality
Common Name/ Principal Toxin
Scientific Name
White snakeroot Eupatorium rugosum Acetylbenzofurans (tremetol)
Rayless golden rod Isocoma pluraflora Acetylbenzofurans (tremetol)
Groundsels, senecio Senecio spp. Pyrrolizidine alkaloids
Rattle pod Crotolaria spp. Pyrrolizidine alkaloids
Hound's tongue Cynoglossum spp. Pyrrolizidine alkaloids
Fiddleneck Amsinckia intermedia Pyrrolizidine alkaloids
Comfrey Symphytum spp. Pyrrolizidine alkaloids
Heliotrope Heliotropium spp. Pyrrolizidine alkaloids
Viper's bugloss Echium spp. Pyrrolizidine alkaloids
Mustards, rape, cabbage Brassica spp. Glucosinolates*
Horse radish Amoracia spp. Glucosinolates*
Radish Raphanus spp. Glucosinolates*
Water cress Nasturtium officinale Glucosinolates*
Poison hemlock Conium maculatum Piperidine alkaloids (coniine)
Tobacco Nicotiana spp. Piperidine alkaloids (coniine)
Locoweeds Astragalus, Oxytropis spp. Indolizidine alkaloids (swainsonine)
Lupine Lupinus spp. Quinolizidine alkaloids (anagyrine)
Bitterweeds Helenium, Hymenoxys spp. Sesquiterpene lactones*
Bracken fern Pteridium aquilinum Ptaquiloside
Buttercups Ranunculus spp. Protoanemonins*
Onions, garlic Allium spp. N-propyl disulphide*
Autumn crocus Colchicum spp. Alkaloids (colchicine)
Avocado Persea americana Unknown toxin
Sage Artemisia spp. Monoterpenes, diterpenes*
Marijuana Cannabis sativa Cannabinol
* These plants impart an abnormal flavor to milk.
Where lactating animals gain access to avocado leaves or fruits (Persea americana), they may develop a noninfectious mastitis, with a marked decrease in milk production. Cattle, horses, goats, and rabbits have been affected by this unique plant toxicity [24]. Goats fed as little as 31 g/kg body weight of avocado leaves showed dramatic reduction in milk production and developed hard swollen udders 24 hours after they had eaten the leaves. The milk was of a cheesy consistency and contained clots. The milk somatic cell counts also became markedly elevated. If no further avocado leaves were fed, the udder edema regressed and milk production returned, but not to the levels prior to feeding the avocado leaves [25]. Generalized necrosis of the mammary gland epithelium with sloughing of necrotic cells and minimal inflammation was the principle histologic finding
Plants Known to Accumulate Nitrates
Botanical Name Common Name
Ambrosia spp. Ragweeds
Amaranthus spp. Pigweed
Avena fatua Wild oat grass
Chenopodium spp. Lamb's-quarter
Cirsium arvense Canada thistle
Convolvulus arvense Field bindweed
Datura stramonium Jimsonweed
Echinochloa spp. Barnyard grass
Helianthus annuus Sunflower
Kochia scoparia Kochia weed
Malva spp. Cheese weed
Melilotus spp. Sweet clover
Polygonum spp. Smart weed
Rumex spp. Sorrel, curly leafed dock
Salsola kali Russian thistle
Solanum spp. Nightshades
Solidago spp. Goldenrods
Sorghum halapense Johnson grass
Crop Plants
Avena sativa Oats
Beta vulgaris Sugar beets
Brassica napus Rape
Glycine max Soybean
Linum spp. Flax
Medicago sativa Alfalfa
Pennisetum glauca Pearl millet
Secale cereale Rye
Sorghum vulgare Sudan grass
Triticum aestivum Wheat
Zea mays Corn
There is considerable variation as to what constitutes a safe level of nitrate in animal feeds because of different factors that influence nitrate metabolism. Under normal circumstances, nitrate is reduced in the rumen in a series of steps from nitrate to nitrite, to ammonia, and eventually to microbial proteins. It is the rapid formation and absorption of large quantities of nitrite (NO2) and not nitrate (NO3) that causes poisoning. The rate at which nitrate is converted to highly toxic nitrite depends on the rate of adaptation of rumen microorganisms to nitrate, the rate and amount of nitrate ingested, and the amount of carbohydrate available in the rumen. Experimental data suggest that nitrate poisoning is more likely to occur in ruminants after several days of feeding forages high in nitrate. Other investigators have demonstrated that nitrate-adapted rumen microflora more completely reduce nitrate beyond nitrite to ammonia thereby reducing the potential for poisoning. Similarly, when carbohydrates such as corn and molasses are present in the rumen, nitrates are more rapidly converted to ammonia and microbial proteins without the accumulation of nitrite. On the other hand, low-energy diets increase an animal's susceptibility to nitrite poisoning.
The amount of nitrate that can be safely consumed in forages (45 g nitrate/100 lb body weight) is three times greater than the amount of potassium nitrate (KNO3) that can be given orally as a drench. Similarly sheep can be fatally poisoned by a single oral dose of KNO3, although the same dose has no ill effects when incorporated in the feed. The lethal dose of nitrate given as a drench is 0.5 g KNO3 kg body weight. From this information it is apparent that nitrate produced in plants is far less toxic than the pure chemical present in fertilizer. Plants or hay containing more than 1 percent nitrate (10,000 ppm) dry matter are potentially toxic and should be fed with caution. Forages containing more than 1 percent nitrate should only be fed if the total nitrate intake can be reduced to less than 1 percent by diluting the nitrate forage with nitrate-free forages. Because nitrate is often reported in different units, care must be exercised in interpreting nitrate values. Conversion factors for nitrate and nitrite compounds are given
Common Toxic Milkweeds
Common Name Scientific Name Toxicity *
Labriform milkweed Asclepias labriformis 0.05
Western whorled milkweed subverticillata 0.2
Eastern whorled milkweed A. verticillata 0.2
Woolypod milkweed A. eriocarpa 0.25
Spider antelopehorn milkweed A. asperula 1 - 2
Plains or dwarf milkweed pumila 1 - 2
Swamp milkweed A. incarnata 1 - 2
Mexican whorled milkweed A. mexicana 2.0
Showy milkweed A. speciosa 2 - 5
Broad leaf milkweed A. latifolia 1.0
Narrow-leafed milkweed A. stenophylla -
Butterfly Weed A. tuberosa 1.5
Antelope horn milkweed A. viridis 1
* Amount of green plant as a percent of the animal's body weight that is lethal.
The relative toxicity of the more common milkweeds is shown in Table 2 - 1. Fatal poisoning of an adult horse (450 kg) may occur with the ingestion of as little as 1.0 kg of green milkweed plant material. As little as 0.1 to 0.2 percent body weight of plant on a dry matter basis of A. labriformis and A. subverticillata, respectively, induced fatal poisoning in sheep. In addition to the cardiotoxic effects of the cardenolides common to most milkweeds, other glycosides and resinoids identified in milkweeds have direct effects on the respiratory, digestive, and nervous systems causing dyspnea, colic and diarrhea, muscle tremors, seizures, and head pressing].
The presence of cardenolides in milkweeds, as many as 20 in A. eriocarpa, is apparently a defense mechanism for the plant to discourage most animals and insects from feeding on the plant. Some insects, however, including the larvae of the monarch butterfly (Danaus plexippus) have the ability to feed on milkweeds and store the cardenolides in their own tissues as a protective mechanism. The adult monarch butterfly retains the cardenolides as a defense mechanism. Birds that feed on the monarch butterfly that has fed on toxic milkweeds will experience the intense emetic effects of the cardenolides, and by association, avoid eating the insect in the future.
Clinical Signs
Signs of poisoning usually begin within 8 to 10 hours of the milkweed plants being eaten; the severity of symptoms depends on the quantity of plant consumed. In acute milkweed poisoning the animal may be found dead without any prior symptoms.
Poisoned sheep show a labored and slow respiratory rate, pain and inability to stand, muscular tremors, staggering gait, a weak, rapid pulse, bloating, colic and dilated pupils prior to death. A variety of cardiac dysrhythmias may be detected using electro- cardiography. Once recum- bent, the poisoned animals exhibit periods of tetany and chewing movements. Postmortem signs in animals poisoned by milkweeds consist of nonspecific congestion of the lungs, stomach, and intestines, with hemorrhages present on the surfaces of the lungs, kidneys, and heart.
Primary Photosensitizing Plants
Botanical Name Common Name
Ammi majus Bishop's weed, greater ammi
Cooperia pedunculata Rain lily
Cymopterus watsonii Spring parsley
Fagopyrum esculentum Buckwheat
Heracleum mentegazzianum Giant hog weed
Hypericum perforatum St. John's wort, Klamath weed
Thamnosma texana Dutchman's britches
Photosensitization, resembling but distinct from sunburn, is a severe dermatitis of animals resulting from a complex reaction induced by plant pigments exposed to ultraviolet (UV) wave length sunlight in the skin of animals that have eaten certain plants. This reaction is most severe in nonpigmented skin where these reactive compounds are most directly exposed to light in the UV spectrum. The precise mechanism of this reaction is unknown, but it is thought to be a light-enhanced oxidation reaction. The amino acids (histidine, tyrosine, tryptophan) are particularly susceptible to oxidation and once oxidized evoke an intense inflammatory response in the blood vessels and surrounding cells that results in tissue necrosis. In addition to plant pigments, fungal toxins, chemicals, and occasionally congenital diseases affecting porphyrin metabolism in the liver may induce photosensitization. Quite frequently horses and cattle develop photosensitization while on pasture with no determinable cause.
Photosensitization may be conveniently classified into two basic types - primary and secondary. Primary photosensitization is associated with photodynamic compounds in certain plants, which once absorbed from the digestive tract, react in the nonpigmented with UV light to cause a severe dermatitis. Also in this category are the congenital photosensitivity diseases associated with defective pigment (porphyrins) metabolism in the liver of animals. Secondary or hepatogenous photosensitization, as the name implies, results when an animal's liver is sufficiently diseased to be unable to remove plant by-products that can react with UV light to cause photosensitization. Phylloerythrin, a bacterial breakdown product of chlorophyll, is the photosensitizing compound. Normally phylloerythrin is removed by the liver and is excreted in the bile, but if the liver is severely diseased, it accumulates in the blood to cause photosensitization if a white skinned animal is exposed to UV light. Hepatogenous photosensitization can be further subdivided into that attributable to liver disease as opposed to that caused by biliary system disease that causes a backup of bile. Secondary photosensitization is much more common in livestock than primary photosensitization, and because of the severity of the underlying liver disease, it always carries a poor prognosis.
Primary photosensitization develops when animals eat plants containing polyphenolic pigments. These compounds are at highest concentration in the green plant and are readily absorbed from the gastrointestinal tract to circulate in the blood. In nonpigmented skin these compounds react with UV light to produce radiant energy that oxidizes essential amino acids in the skin's cells. The cells die in the photosensitization process, and the affected skin eventually sloughs off. Two plants associated historically with primary photosensitization are buckwheat (Fagopyrum esculentum), and St. John's wort (Hypericum perforatum). Both plants contain polyphenolic pigments capable of causing primary photosensitization. Several plant species including bishop's weed (Ammi majus), spring parsley (Cymopterus watsonii), and Dutchman's breeches (Thamnosma texana) contain photodynamic furanocoumarin compounds that have been associated with photosensitivity through ingestion and direct contact with the skin. In southeast Texas, a seasonal photosensitivity of cattle is associated with the consumption of the dead leaves of Cooperia pedunculata, a lily of the Amaryllis family. Photosensitivity has also been reported in Europe as a result of exposure to giant hogweed (Heracleum mantegazzianum). Cow parsnip (Heracleum spp.), which occurs in North America, has the potential to cause photosensitivity.
Plants Containing Pyrrolizidine Alkaloids
Scientific Name Common Name
Amsinckia spp. Fiddle neck, tarweed
Crotolaria spp. Rattle box
Cynoglossum officinale Hound' tongue
Echium vulgare Blue weed, viper's bugloss
Heliotropium spp. Giant hog weed
Hypericum perforatum Heliotrope
Senecio spp. Groundsels, Senecio
Symphytum officinale Comfrey
Secondary or hepatogenous photosensitization in animals occurs more commonly than primary photosensitization. Liver disease, the underlying cause of secondary photosensitivity, results from ingestion of plants containing compounds toxic to the liver. A variety of compounds toxic to the liver are found in plants, the most important of which are the pyrrolizidine alkaloids (PAs). Once 80 percent or more of the liver is destroyed by these alkaloids, it is unable to eliminate phylloerythrin, a bacterial breakdown product of chlorophyll. Phylloerythrin then accumulates in the blood, and as it circulates through the skin and is exposed to UV light, it fluoresces and causes oxidative injury to the blood vessels and tissues of the skin. The resulting intense inflammatory response is most severe in the nonpigmented skin. In severe cases of PA poisoning, acute liver failure and death may result before signs of photosensitization have time to develop.
Plants Associated with Photosensitization
Scientific Name Common Name
Agave lecheguilla Agave
Avena sativa Oats
Brachiaria decumbens Signal grass
Bassia hysopifolia Basssia
Brassica spp. Rape, kale
Cenchrus spp. Sandbur
Cynodon dactylon Bermuda grass
Descurainia pinnata Tansy mustard
Daucus carota Wild carrot
Euphorbia maculata Milk purslane
Hordeum spp. Barley
Kalstroemia Caltrops
Kochia scoparia Kochia, Mexican fire weed
Lantana camara Lantana
Lolium perenne Perennial rye grass
Medicago sativa Alfalfa
Microcystis spp. Blue-green algae, water bloom
Narthecium ossifragum Bog asphodel
Nolina texana Sacahuiste
Panicum coloratum Klein grass
Panicum spp. Panic grasses
Pastinaca spp. Parsnip
Psoralea spp. Scurf pea
Polygonum spp. Knottweed
Ranunculus bulbosus Buttercup
Sorghum vulgare sudanensis Sudan grass
Tetradymia spp. Horsebrush
Thamnosma texana Dutchman's breeches
Tribulus terrestris Puncture vine, caltrop
Trifolium spp. Clovers
A wide range of animal species including wild and domesticated ruminants, horses, and pigs are susceptible to PA poisoning. Pyrrolizidine alkaloids are readily absorbed from the digestive tract and are bioactivated to toxic pyrroles and possibly other reactive metabolites by the liver's mono-oxygenase system. It is the active pyrroles that affect the endoplasmic reticulum of the liver cells inhibiting mitosis and the replication of hepatocytes. Animals experiencing poor nutrition, pregnancy, and other metabolic stress are more susceptible to PA poisoning. At high doses, PAs cause hepatocellular necrosis, while at lower doses necrosis is less severe allowing time for the characteristic pathologic changes of megalocytosis, bile duct hyperplasia, and fibrosis to occur. Similar changes may also be seen in the kidneys. In low doses PAs cause endothelial changes in the capillaries of the lungs with resulting pulmonary hypertension and right heart failure. In the case of monocrotaline found in Crotolariaspecies, the highly toxic metabolite dihydromonocrotaline not only affects the liver, but also the lung and possibly other tissues. Horses develop an acute fatal fibrosing alveolitis after eating feed contaminated with crotolaria seeds.
The PAs have been reported to be carcinogens, teratogens, and abortifactients. Feeding toxic quantities of S. jacobaea to pregnant cows through the 15 to 30th days of gestation causes no detectable changes in the fetus, which may indicate PAs are not teratogenic in early gestation. The PAs are secreted in the milk of cows and in very low quantities can cause mild liver changes in calves and kids consuming the milk. The effects of PAs on people consuming milk containing PAs have not been established. Bees feeding on tansy ragwort (S. jacobaea), and Paterson's curse (Echium plantagineum) produce honey containing PAs that is potentially hazardous to those consuming it.
Variation in the PA content of plants, the quantity of plant eaten, and individual animal species susceptibility affect the severity of poisoning seen in animals. The PA content of plants varies considerably, generally increasing with maturation of the plant and reaching a maximum just before the flower buds open. Flowers tend to contain the greatest amount of the alkaloid, and seeds of Crotolaria and Amsinckia concentrate high levels of PA]. Senecio redellii, when near maturity, has been reported to contain exceptionally high levels of PA (10 - 18 percent dry weight). The PA content of plants incorporated in hay remain stable for months, but appear to be largely degraded in properly prepared silage. The stability of PAs in plants cured in hay can be a significant cause of poisoning in mid winter when plant toxicity may not be suspected.
Plants Associated with Cyanide Poisoning
Botanical Name Common Name
Acacia spp. Catclaw, acacia
Amelanchier alnifolia Service, June, or Saskatoon berry
Bahia oppositifolia Bahia
Mannihot esculentum Cassava, manihot, tapioca
Cercocarpus montanum Mountain mahogany
Chaenomales spp. Flowering quince
Cynodon spp. Star grass
Eucalyptus spp. Eucalyptus, gum tree
Glyceria grandis Tall manna grass
Hydrangea spp. Hydrangea
Linum spp. Flax
Lotus spp. Bird's foot trefoil
Malus spp. Crab apple
Nandina domestica Heavenly or sacred bamboo
Phaseolus lunatus Lima bean
Photinia spp. Christmas berry
Prunus spp. Choke-cherry, pin cherry
Pteridium aquilinum Bracken fern
Sambuccus spp. Elderberry
Sorghum spp. Johnson, Sudan grass
Sorghastrum nutans Indian grass
Stillingia texana Texas queen's delight
Suckleya suckleyana Poison suckleya
Trifolium repens White clover
Triglochin maritima Arrow grass
Vicia sativa Common vetch
Zea mays Corn, maize
Plants Known to Accumulate Nitrates
Botanical Name Common Name
Ambrosia spp. Ragweeds
Amaranthus spp. Pigweed
Avena fatua Wild oat grass
Chenopodium spp. Lamb's-quarter
Cirsium arvense Canada thistle
Convolvulus arvense Field bindweed
Datura stramonium Jimsonweed
Echinochloa spp. Barnyard grass
Helianthus annuus Sunflower
Kochia scoparia Kochia weed
Malva spp. Cheese weed
Melilotus spp. Sweet clover
Polygonum spp. Smart weed
Rumex spp. Sorrel, curly leafed dock
Salsola kali Russian thistle
Solanum spp. Nightshades
Solidago spp. Goldenrods
Sorghum halapense Johnson grass
Crop Plants
Avena sativa Oats
Beta vulgaris Sugar beets
Brassica napus Rape
Glycine max Soybean
Linum spp. Flax
Medicago sativa Alfalfa
Pennisetum glauca Pearl millet
Secale cereale Rye
Sorghum vulgare Sudan grass
Triticum aestivum Wheat
Zea mays Corn
Hydrogen cyanide (HCN) is highly poisonous to all animals because it rapidly inactivates cellular respiration thereby causing death. The cyanide ion is readily absorbed from the intestinal and respiratory tracts and has a strong affinity for binding with trivalent iron of the cytochrome oxidase molecule, inhibiting its enzymatic action and preventing cellular respiration. The characteristic cherry red venous blood seen in acute cyanide poisoning results from the failure of the oxygen-saturated hemoglobin to release its oxygen at the tissues because the enzyme cytochrome oxidase is inhibited by the cyanide. Normally, small quantities of cyanide are detoxified by cellular enzymes and thiosulfates in many tissues to form relatively harmless thiocyanate, which is excreted in the urine. When large quantities of cyanide are rapidly absorbed and the body's detoxification mechanisms are overwhelmed, cyanide poisoning occurs. In most species, the lethal dose of HCN is in the range of 2 to 2.5 mg/kg body weight. However, if plenty of other plant material and carbohydrates are present in the stomach, formation and absorption of cyanide may be slowed, allowing animals to tolerate higher doses.
There is considerable variation as to what constitutes a safe level of nitrate in animal feeds because of different factors that influence nitrate metabolism. Under normal circumstances, nitrate is reduced in the rumen in a series of steps from nitrate to nitrite, to ammonia, and eventually to microbial proteins. It is the rapid formation and absorption of large quantities of nitrite (NO2) and not nitrate (NO3) that causes poisoning. The rate at which nitrate is converted to highly toxic nitrite depends on the rate of adaptation of rumen microorganisms to nitrate, the rate and amount of nitrate ingested, and the amount of carbohydrate available in the rumen. Experimental data suggest that nitrate poisoning is more likely to occur in ruminants after several days of feeding forages high in nitrate [94,95]. Other investigators have demonstrated that nitrate-adapted rumen microflora more completely reduce nitrate beyond nitrite to ammonia thereby reducing the potential for poisoning. Similarly, when carbohydrates such as corn and molasses are present in the rumen, nitrates are more rapidly converted to ammonia and microbial proteins without the accumulation of nitrite. On the other hand, low-energy diets increase an animal's susceptibility to nitrite poisoning.
Plants Associated with Cyanide Poisoning
Botanical Name Common Name
Acacia spp. Catclaw, acacia
Amelanchier alnifolia Service, June, or Saskatoon berry
Bahia oppositifolia Bahia
Mannihot esculentum Cassava, manihot, tapioca
Cercocarpus montanum Mountain mahogany
Chaenomales spp. Flowering quince
Cynodon spp. Star grass
Eucalyptus spp. Eucalyptus, gum tree
Glyceria grandis Tall manna grass
Hydrangea spp. Hydrangea
Linum spp. Flax
Lotus spp. Bird's foot trefoil
Malus spp. Crab apple
Nandina domestica Heavenly or sacred bamboo
Phaseolus lunatus Lima bean
Photinia spp. Christmas berry
Prunus spp. Choke-cherry, pin cherry
Pteridium aquilinum Bracken fern
Sambuccus spp. Elderberry
Sorghum spp. Johnson, Sudan grass
Sorghastrum nutans Indian grass
Stillingia texana Texas queen's delight
Suckleya suckleyana Poison suckleya
Trifolium repens White clover
Triglochin maritima Arrow grass
Vicia sativa Common vetch
Zea mays Corn, maize
Cyanogenic glycosides are substances present in many plants that can produce highly toxic hydrogen cyanide (HCN) or prussic acid. Specific plant enzymes released when plant cells are damaged when chewed, crushed, wilted, or frozen, hydrolyze the glycosides to cyanide. At least 2000 plant species are known to contain cyanogenic glycosides with the potential to produce HCN poisoning. However, relatively few of these plants are frequent causes of cyanide poisoning in humans or animals because they are infrequent food sources for humans or animals. Plants that have been most frequently associated with cyanide poisoning in animals are listed the table above.Some of these plants are grown as food sources for humans and animals, for example, sorghum (Sorghum spp.), corn (Zea mays), clovers (Trifolium spp.), and manihot or cassava (Manihot esculenta), and can be used safely provided attention is paid to the circumstances under which these plants accumulate cyanogenic glycosides.
Most plant-induced cyanide poisoning in humans occurs in tropical countries where cassava is commonly used as food. The chronic consumption of poorly prepared assava diets produces a disease syndrome in humans known as tropical ataxic neuropathy. Pigs and goats have been similarly poisoned when fed cassava tubers and leaves. Plants such as blue flax (Linum spp.), grown for fiber (linen) and linseed oil, will also accumulate toxic levels of HCN under the right growing conditions.
Cyanide poisoning of livestock is most commonly associated with Johnson grass (Sorghum halapense), Sudan grass (Sorghum vulgare), and other forage sorghums. Choke-cherries (Prunus spp.), service berry (Amelanchier alnifolia), and arrow grass (Triglochin spp.) are less frequent but long recognized sources of cyanide poisoning. Crab apple leaves (Malus spp.), and sugar gums (Eucalyptus cladocalyx) have caused cyanide intoxication in goats, and even wild deer have become victims of cyanide poisoning after eating service berry. Occasionally cattle have consumed lethal doses of cyanogenic glycosides from eating acacia tree leaves and poison suckleya (Suckleya suckleyana). Under some undetermined growing conditions, certain grasses such as tall manna grass (Glyceria grandis) and Indian grass (Sorgastrum nutans) accumulate toxic levels of cyanogenic glycoside.
Cyanogenic glycosides in the leaves and stems of plants are not toxic unless acted on by the plant or rumen microorganism enzymes, b-glucosidase and hydroxynitrile lyase, to form HCN. Enzymatic conversion of the glycosides is enhanced when plant cells are damaged or stressed as occurs when the plant is chewed, crushed, droughted, wilted, or frozen. In the process, the glycosides, which are normally isolated in cell vacuoles, come into contact with the cell enzymes and HCN is formed. Generally most parts of the plant contain cyanogenic glycosides; the young rapidly growing portion of the plant and the seeds contain the highest concentrations. The flesh of the ripe fruits is edible. Drying the plants decreases their cyanogenic potential especially over time. Ensiling plants will reduce cyanogenic glycoside content by as much as 50 percent, with free cyanide being liberated from silage pits or silos in the curing process. The concentration of cyanogenic glycosides in plants varies with the stage of growth, time of year, soil mineral and moisture content, and time of day. Cool moist growing conditions enhance the conversion of nitrate to amino acids and cyanogenic glycosides instead of plant protein. As the glycosides accumulate they further inhibit nitrite reductase in the plant, favoring the conversion of nitrate to cyanogenic glycoside rather than to amino acids [28]. Nitrate fertilization of cyanogenic plants therefore has the potential to increase the cyanogenic glycoside content of plants. Frost and drought conditions may also increase cyanogenesis in some plant species. Young plants, new shoots, and regrowth of plants after cutting often contain the highest levels of cyanogenic glycosides. Application of herbicides (2,4-dichlorophenoxyacetic acid) can also increase the cyanogenetic glycoside content of plants.
At least 55 cyanogenic glycosides are known to occur in plants, many being synthesized from amino acids as part of normal plant metabolism. Some of the better known glycosides include amygdalin (laetrile) from bitter almonds, peach, apricot, cherry and apple seeds; prunasin from choke-cherries and service berry leaves; linamarin and lotaustralin from flax and white clover; dhurrin from sorghum; and triglochinin from arrow grass. In the 1970s, laetrile received considerable attention as a potential cure for cancer, but its efficacy has never been proven, and, in fact, it was shown to have the potential to be highly toxic to humans and animals.
Selective breeding of certain varieties of plant species with naturally low glycoside content has resulted in varieties that are low cyanogenic glycoside; and has increased their food value for humans and animals. The development of sweet almond varieties with low cyanogenic glycoside content has facilitated the human consumption of almond seeds. Similarly sorghum varieties low in cyanide have been developed that have greatly increased the safety of feeding sorghums, such as Sudan grass, to livestock.
Ruminants are more susceptible to cyanide poisoning than other animals because the normally mildly acidic to alkaline rumen contents (pH 6.5 - 7), high water content, and microfloral enzymes in the rumen hydrolyze the cyanogenic glycosides to HCN. Water drunk after animals have eaten cyanogenic plants enhances the hydrolysis of the glycosides. Conversely, ruminants that are on high energy grain rations where the rumen is more acidic (pH 4 - 6) have a slower release of HCN than if they were fed a grass, hay, or alfalfa diet. Humans, pigs, dogs, and horses that have a highly acidic stomach (pH 2 - 4) tend to have a reduced rate of glycoside hydrolysis and cyanide production in their digestive systems and therefore rarely suffer from cyanide poisoning of plant origin. Atypically, donkeys have been reported to develop acute cyanide poisoning from eating the new shoots from wild choke-cherries
Neurotoxic Plants
Scientific Name Common Name
Aesculus spp. Buckeye, horse chesnut
Artemisia filifolia Sand sage
Astragalus spp. Locoweeds
Centaurea solstitialis Yellow star thistle
Acroptilon repens Russian knapweed
Corydalis spp. Fitweed
Equisetum arvense Horsetail
Eupatorium rugosum Snake root
Haplopappus heterophyllus Rayless goldenrod
Karwinskia humboldtiana Coyotillo
Kochia scoparia Kochia weed
Oxytropis spp. Locoweed
Pteridium aquilinum Bracken fern
Sophora secundiflora Mescal bean
A variety of indigenous and exotic plants found in North American affect the nervous system of animals, some being associated with considerable economic losses to the livestock industry. Arguably the most important group of plants affecting the nervous system are those belonging to the genera Astragalus and Oxytropis, collectively known as locoweeds. These plants, found in vast areas of western North America and in many parts of the world, have long been recognized as a problem to livestock.
There are numerous other plants affecting the nervous system such as yellow star thistle (Centaurea solstitialis) and Russian knapweed (Acroptilon repens) that will be discussed in the second section of this chapter. These and a variety of other plants are significant not only because they are poisonous and cause neurological disease in animals, but they also aggressively displace indigenous plants and reduce the value of natural ranges for grazing. Others like white snakeroot (Eupatorium rugosum) have historical and contemporary significance because of their effects on the nervous system. For example, deaths of early settlers in eastern North America who drank the milk from cows with " milk sickness", a fatal disease characterized by severe muscle tremors, is attributed to the toxin in white snakeroot. Once the neurotoxic effects of the white snakeroot were recognized, preventive management measures have largely eliminated this form of plant poisoning in people. The plants listed in Table 6 - 1 cause poisoning when normal forages are scarce, or the plants are accidentally incorporated in hay and grain fed to animals
stragalus and Oxytropis Species Containing Swainsonine
Astragalus Species Oxytropis Species
A. allochrous A. oxyphysus
A. argillophilus A. playanus
A. assymetricus A. praelongus
A. bisulcatus A. pubentissumus
A. didymocarpus A. pycnostachysus
A. dyphysus A. tephrodes
A. earlei A. thurberi
A. emoryanus A. wootonii
A. flavus O. besseyi
A. humistratus O. campestris
A. lentiginosus O. condensata
A. lonchocarpus O. lambertii
A. mollissimus O. saximontana
A. missouriensis O. sericea
A. nothoxys -
Signs of poisoning do not become evident until animals have consumed significant quantities of locoweeds over many weeks and the toxic threshold is reached. Although horses, cattle, and sheep were thought to develop an addiction for locoweeds, it is more correctly termed habituation because there is no dependence on the plants as there would be in the case of addiction. Locoweeds are palatable and of similar nutrient value to alfalfa, which may explain why animals eat locoweed even when normal forages are present.
The quantity of swainsonine in locoweeds varies according to the species, stage of growth, and the growing conditions. The succulent preseed-stage plants appear to be the most palatable, although cattle appear to relish the flowers and immature seed pods. The palatability of locoweed does not have any relationship to the quantity of swainsonine in the plant
Common Astragalus Species Containing Nitroglycosides
A. atropubescens
A. campestris
A. canadensis
A. convallarius
A. cibarius
A. falcatus
A. flexuosus
A. emoryanus
A. miser var. oblongifolius
A. miser var. serotinus
A. miser var. hylophilus
A. praelongus
A. pterocarpus
A. tetrapterus
A. toanus
A. whitnii
The toxicity of the milk vetches is primarily attributed to the nitro compound called miserotoxin, so called because it was first recognized in timber milk vetch (A. miser). Miserotoxin, a glycoside 3- nitro-1-propanol, is hydrolyzed in the rumen to the toxic 3-nitro-1-propanol (3-NPOH). Other species of milk vetch contain 3-nitropropionic acid (3-NPA) and not 3-NPOH. Misertoxin (3-NPOH) is rapidly absorbed into the blood of cattle and sheep where it is converted to 3-NPA. Although the mechanism is not fully understood, poisoning by these nitro compounds appears to occur in two ways. Nitrite (NO2) from 3- NPA oxidizes hemoglobin to methemoglobin (up to 33 percent), which causes severe respiratory distress. Secondly, 3-NPA or other unidentified metabolite also affects the brain and spinal cord causing muscular weakness and collapse. Cattle and sheep are most frequently poisoned but horses are also susceptible. Other legumes, Indigofera spicata (creeping indigo) and Coronilla varia (crown vetch), contain 3-NPA and have been associated with poisoning in horses. Dogs that have eaten the meat from affected horses may also become intoxicated. Crown vetch is toxic to nonruminants, and if diets contain more than 5 percent of the plant, growth and development retardation in the young can be expected.
The nitro compound content of milk vetches varies with the species and the stage of growth, being highest during the flower and seed pod stage. Years with high rainfall not only produce a flush of milk vetch growth, but the level of misertoxin is also increased in the plants. The nitro compound content of Emory milk vetch (measured as nitrite) is in the range of 6 to 9 mg NO2/g plant during the bud to flowering stage. Nitro compounds are stable in the dried green plant but are lost rapidly from the dried, bleached-out plant. The nature and severity of poisoning depends on the quantity and rate of absorption of 3-NPOH from the rumen. Cattle fed 2.2 g dry weight of Emory milk vetch per kilogram body weight daily develop signs of poisoning in 3 to 4 days [93]. Sheep appear to be much more tolerant of nitro compounds in milk vetch than are cattle.
Plants Containing Oxalates
Scientific Name Common Name
Amaranthus spp. Red-rooted pigweed
Bassia hyssopifolia Five hooked bassia
Beta vulgaris Sugar beet
Chenopodium spp. Lambs-Quarter
Halogeton glomeratus Halogeton
Kochia scoparia Kochia, summer cypress
Oxalis spp. "Shamrock," soursob, sorrel
Portulaca oleraceae Purslane
Phytolacca americana Poke berry
Rumex spp. Sorrel, dock
Rheum rhaponticum Rhubarb
Salsola spp. Russian thistle, tumbleweed
Sarcobatus vermiculatus Greasewood
Grasses
Cenchrus ciliaris Buffel grass
Panicum spp. Elephant grass
Pennisetum clandestinum Kikuyu grass
Setaria sphacelata Setaria grass
Common House and Garden PlantsContaining Oxalates
Arisaema spp. Jack in the pulpit
Alocasia spp. Elephant’s ear
Anthurium spp. Anthurium, flamingo flower
Arum spp. Lords and Ladies, Cuckoo-pint
Calla palustris Wild calla, water arum
Caladium spp. Caladium
Dieffenbachia sequine Dumb cane
Epiprenum spp. Pothos, variegated philodendron, taro vine
Monstera spp. Monstera, cutleaf philodendron, bread fruit vine
Philodendron spp. Philodendron
Spathephyllum spp. Peace lily
Schefflera spp. Umbrella tree
Zantedeshia aethiopica Calla lily
Within a few hours of consuming toxic levels of oxalate, sheep and cattle develop muscle tremors, tetany, weakness, reluctance to move, depression, and recumbency resulting from hypocalcemia and hypomagnesemia. Coma and death may result within 12 hours. Animals that survive the acute effects of oxalate poisoning frequently succumb to kidney failure. As animals become uremic (increased serum creatinine and urea nitrogen levels), they develop severe depression, stop eating, and after a few days become comatose and die.
Plants Associated with Livestock Abortion
Scientific Name Common Name
Amaranthus spp. Red-rooted pigweed
Agave lechequilla Lechuguilla
Astragalus spp. Milk vetch, locoweeds
Brassica spp. Rape
Conium spp. Poison/spotted hemlock
Cupressus spp. Cyprus
Festuca spp. Fescue
Gutierrezia sarothrae Broomweed, snakeweed
Halogeton spp. Halogeton
Indigofera glomeratus Juniper
Juniperus spp. Juniper
Medicao sativa Alfalfa
Oxtropis spp. Locoweeds
Phytolacca americana Poke weed
Pinus ponderosa Ponderosa pine
Solidago spp. Goldenrods
Tanacetum spp. Tansy
Trifolium spp. Clovers
Veratrum spp. False hellebore, skunk cabbage
Cattle and sheep, and to a lesser extent horses, are the most susceptible to the reproductive and teratogenic effects of chronic locoweed poisoning. Unlike most teratogens, swainsonine may exert its effects on the dam and the fetus at any time during gestation, causing a variety of problems. These reproductive problems are most likely due to the combined effects of swainsonine on the pituitary gland affecting gonadotrophin production, the ovary affecting estrogen and progesterone levels, the uterus and placenta, and directly on the fetus. Abortion, infertility, fetal deformity, and disturbances in placental circulation that results in massive accumulation of fluid in the uterus (hydrops). Some calves and lambs may be born weak and do not thrive. Abortions can occur at anytime during gestation [9]. Animals that have aborted tend to cycle normally and will conceive again provided they are kept from eating more locoweed, and there is not a chronic secondary uterine infection resulting from the abortion.
Known and Suspected Teratogenic Plants
Scientific Name Common Name
Astragalus spp. Milk vetch, locoweed
Blighia sapida Akee
Colchicum autumnale Autumn crocus
Conium maculatum European or spotted hemlock
Cycadaceae spp. Cyads
Datura stramonium Jimson weed
Indigofera spicata Creeping indigo
Lathyrus spp. Wild pea
Leucaena leucocephala Mimosa
Lupinus spp. Lupine
Nicotiana glauca Wild tree tobacco
Nicotiana tabacum Tobacco
Oxytropis spp. Locoweed
Papaveraceae Poppies
Senecio spp. Groundsel
Veratrum californicum Western false hellebore
Vinca rosea Periwinkle
Freshly aborted fetuses and the placenta when examined histologically may show the characteristic cellular vacuolation of swainsonine poisoning. The alkaloid itself can be detected in the serum of animals if they have been eating locoweed within 2 days of sampling because the serum half-life of swainsonine is only about 20 hours.
Lupine Species Known to Contain Anagyrine
Scientific Name Common Name
Lupinus. argenteus Silvery lupine
L. caudatus Kellog's spurred lupine
L. erectus Tall silvery lupine
L. evermanii Evermans lupine
L. laxiflorus Douglas spurred lupine
L. leucophyllus Wooly leafed lupine
L. nootkatensis Nootka lupine
L. serecius Silky lupine
Nervous Syndrome
Lupines have been associated with three different syndromes of poisoning in livestock. In North America, lupine poisoning is most commonly associated with a teratogenic syndrome that most frequently affects cattle, and is commonly referred to as "crooked calf disease" . Occasionally lupines have caused an acute fatal neurologic disease in sheep, and rarely in cattle and horses. The toxins responsible for the neurotoxicity are a variety of alkaloids other than anagyrine. Sheep ingesting from 0.25 to 0.5 percent of their body weight of seeds from certain lupines found in the western United States develop an acute neurologic disease characterized by muscle tremors, noisy labored breathing, convulsions, coma, and death. Species of lupine that have been incriminated in this neurologic syndrome include L. leucophyllus, L. argenteus, L. leucopsis, and L. siriccus. A third syndrome, lupinosis, is associated with livestock grazing lupine pods and stalks infected with a fungus Phomopsis leptostromiformis (Diaporthe toxica) that produces a mycotoxin (phomopsin) capable of causing severe liver, kidney and muscle disease. The fungus persists in the lupine stubble after harvesting and causes severe liver disease and poor growth in sheep and occasionally cattle that graze the stubble. Lupinosis is especially important in those parts of the world where lupines are grown for the purpose of harvesting their seeds for animal consumption.
Obligate Selenium Accumulator Plants
Plants That Accumulate Selenium
Scientific Name Common Name
Astragalus (24 spp.) Milk vetches
Conopsis spp. Golden weeds
Xylorhiza spp. Woody aster
Stanleya pinnata Princes plume
Secondary Selenium Accumulators
Scientific Name Common Name
Acacia spp. Acacia
Artemisia spp. Sages
Aster spp. Asters
Atriplex spp. Saltbrush
Castilleja spp. Paintbrush
Penstemon spp. Beard tongue
Grindelia spp. Gumweed
Toxicity
Selenium has numerous complex effects on cellular function, many of which are poorly understood. It is well known that selenium inhibits cellular enzyme oxidation reduction reactions, especially those involving sulfur-containing amino acids. This effect of selenium on sulfur alters the metabolism of sulfur-containing amino acids (methionine, cystine) thereby affecting cell division and growth. This causes degeneration and necrosis of the cells that form keratin (keratinocytes). By replacing sulfur in the keratin molecule, the primary constituent of the hooves and hair, selenium weakens the keratin structurally at the site of selenium incorporation into its structure. Consequently the hair and hoof wall tend to fracture at this site when subjected to mechanical stresses.
Selenium poisoning in animals is variable and depends on the amount and rate of absorption of selenium from the intestinal tract. Horses appear to be more susceptible to chronic selenosis than are cattle and sheep. Some animals such as pronghorn antelopes appear capable of consuming diets high in selenium (15 ppm) for long periods without ill effect. Individual animal susceptibility, the chemical form of selenium present, and the bioavailability of selenium as a result of the interaction with other elements such as sulfur or arsenic present in the diet are also important in the pathogenesis of selenium poisoning
Selenium-Accumulating Astragalus Species
A. albulus
A. argillosus
A. beathii
A. bisulcatus
A. confertiflorus
A. crotalariae
A. diholcos
A. eastwoodae
A. ellisiae
A. grayi
A. haydenianus
A. moencoppensis
A. oocalycis
A. osterhouti
A. pattersonii
A. pectinatus
A. praelongus
A. preussii
A. racemosus
A. recedens
A. sabulosus
A. toanu
