Plants Flashcards
Name and main system affected
Oleander (Nerium) Heart
Name and main system affected
Foxglove (Digitalis) Heart
Name and main system affected
Milkweed (Asclepias) Heart
Name and main system affected
Rhododendron, azalea, laurel (Rhododendron, Kalmia, Pieris) Heart
Name and main system affected
Yew (Taxus) Heart
Name and main system affected
Death Camas (Zigadenus) Heart
Name and main system affected
Western False Hellebore (Veratrum) Heart
Name and main system affected
Avocado (Persea) Heart
Name and main system affected
Kalanchoe (Kalanchoe) Heart
Name and main system affected
St. Johnswort, Klamath weed, goat weed (Hypericum) Skin - Primary photosensitizer
Name and main system affected
Allium spp - onions, garlic, chives, shallots Hemolysis
Name and main system affected
Maple (Acer) Hemolysis
Name and main system affected
Mustards (Cruciferae) Hemolysis
Name and main system affected
Sweet Clover (Melilotus) Hemostasis
Name and main system affected
Bracken Fern (Pteridium) Hemostasis
Name and main system affected
Pine (pinus), Juniper (Juniperus), (Abies), (Pseudotsuga), (Picea), (Cupressus) Reproductive
Name and main system affected
Clover (Trifolium), Alfalfa (Medicago) Reproductive
Name and main system affected
Halogen (halogen), shamrock (oxalis) Kidney
Name and main system affected
Oak (Quercus) Kidney
Name and main system affected
Pigweed (Amaranthus) Kidney
Name and main system affected
Some lilies (lilium, hemerocallus) Kidney
Name and main system affected
Bleeding heart, Dutchman’s breeches (Dicentra) Nervous system stimulant
Name and main system affected
Water hemlock (Cicuta) Nervous system stimulant
Name and main system affected
Yellow star thistle (centauria), Russian knapweed (Acroptilion) Nervous system - mixed effects
Name and main system affected
Locoweed (Astragalus) Nervous system - mixed effects
Name and main system affected
Morning Glory (Ipomea) Nervous system - mixed effects
Name and main system affected
Marijuana (Cannabis) Nervous System depressant
Name and main system affected
Jimson weed (Datura) Autonomic Nervous System
Name and main system affected
Lupine (Lupinus) Autonomic Nervous System
Name and main system affected
Poison Hemlock (Conium) Autonomic Nervous System
Name and main system affected
Larkspur (Delphinium) Paralytic
Name and main system affected
Horsetail (Equisetum) Thiaminase containing plant
Name and main system affected
Cocklebur (Xanthium) Liver (2o photosensitizer)
Name and main system affected
Tansy ragwort, groundsel (Senecio), Fiddleneck (Amsinckia), Houndstongue (Cynoglossum) Liver (2o photosensitizer)
Name and main system affected
Alsike and red clover (Trillium) Liver (2o photosensitizer)
Name and main system affected
Sago palm and cycad (cycas) Liver (2o photosensitizer)
Name and main system affected
Buttercup (ranunculus) GI tract
Name and main system affected
English Ivy (Hedera) GI tract
Name and main system affected
Bulbs (Narcissus, Iris, Hyacinthus, Amaryllis) GI tract
Name and main system affected
Nightshade, Potato, Tomatoes (Solanum) GI tract
Name and main system affected
Oxalate containing plants (dieffenbachia, philodendron, colocasia, mostera) GI tract
Name and main system affected
Castor bean (Ricinus) Gi tract
Name and main system affected
Hairy vetch (Vicia villosa) Skin
Name and main system affected
Black walnut (Juglans), Hoary alyssum (Berteroa) Skin
Name and main system affected
Cyanogenic Glycosides Hypoxia
Name and main system affected
Flatweed Musculoskeletal - Stringhalt
Name and main system affected
Moldy Sweet Potato Resp - Fog fever
Name and main system affected
Perilla mint and mustards Resp - Fog fever
Name and main system affected
Lush young green grass Resp - Fog fever
Plant characteristics of sweet clover?
Adult is tall and fragrant (3-9 feet)
Leaves are trifoliate and alternate.
Flowers are small and are yellow or white.
Toxic principle of Sweet Clover?
Coumarin
Mechanism of action of sweet clover?
If sweet clover is put up wet, mold (aspergillus and others) on the clover causes coumarin to become dimeried and oxidized to dicoumarol (only the moldy/dry product is toxic, not fresh plant)
Dicoumarol interferes with vitamin K epoxide reductase
Interferes with clotting factors 2, 7, 9, and 10 and causes bleeding disorders and hemorrhage
Animals affected by sweet clover and lesions seen?
Livestock, esp cattle
Bleeding disorders, hemorrhage
Signs, clinpath depend on site of bleeding
Treatment for sweet clover toxicity?
Supportive (Vitamin K1, fluids, blood transfusions, etc)
6 toxins, MOAs, and clinical signs of mustard (cruciferae) toxicosis?
- Goitrin/thiocyanate - interfere with thyroid hormone synthesis and iodine uptake - goiter and young born weak and may die.
- Thiaminase-like activity or high sulfur - polioencephalomalacia and secondary copper deficiencies - lethargy, incoordination, muscle tremors, blindness, recumbancy, convulsion, death.
- S-methyl cysteine sulfoxide converted to dimethyl disulfide - hemolysis and Heinz bodies - jaundice, hemoglobinuria, anoreixa, splenomegaly, hepatic and renal hemosiderosis and degeneration/necrosis
- Equine Dysmaturity Syndrome - prolonged gestation but foal still immature with incomplete ossification, tendon ruptures, prognathism, etc.
- Bloat and other GI issues
- APEE and nitrate accumulation - reproductive inefficiency and enterotoxemia
How much sweet clover does an animal need to eat to see toxicity?
A LOT
Generally a historical problem, not seen much currently
How much mustard plants does an animal have to eat to see toxicity
Lots!!!
Toxic principle in maple leaves?
Unknown, but whatever it is it is only in the dry not the fresh leaves.
Seems to be most common in Red Maples?
Mechanism of action of maple leaves
Acute hemolytic anemia, methemoglobin, Heinz body formation
Species affected by maple leaf toxicity and lesions in those animals?
Mostly equine and alpaca
Technically all species susceptible
Hemolysis - icterus, splenomegaly, hepatomegaly (centrilobular degeneration), hemiglobinuric nephrosis.
How many dried maple leaves does an animal need to eat to become toxic?
Lots.
Toxic principle in allium spp and where is it concentrated in the plant?
Numerous disulfides
Oxidizing agents
Most concentrated in the bulb
Mechanism of action of allium spp?
Oxidant damage of the red blood cells leads to Heinz body hemolytic anemia.
Clinical signs of allium spp toxicosis?
Hemolysis that begins after a few days and peak at 5 days
Icterus, lethargy, odor to tissues, hemoglobinuric (hypoxic) necrosis chronically, abortions in cattle due to hypoxia.
Species most susceptible to allium spp?
Cats, Cattle
Technically all animals susceptible but wide variation in susceptibilities
Species most resistant to allium spp?
Sheep and goats
Technically all species susceptible but onions can be fed as 100% of diet to some sheep.
Prognosis for animals with allium toxicosis?
Good with supportive care if the animal is not moribund.
Of the allium spp, what is the most potent form?
Dried garlic!
How much allium spp does an animal have to eat for toxicity?
Depends on the animal
Cat = small amount
Sheep = enormous amount
What are the 5 clinical diseases of bracken fern, and what species do these diseases present?
- Equine - neurotoxicosis from Type I thiaminase - weight loss with good appetite, incoordination, bradycardia, tremors/convulsions, recumbency, death.
- Bovine - Bone marrow suppression - first of the platelets causing bleeding disorders, last of the red blood cells causing weakness.
- Bovine - Enzootic hematuria - cyclic inflammation, urinary bladder papillomas, other neoplasms.
- Sheep - Retinal degeneration - glassy eyed appearance and dilated pupils.
What are the toxic principles in bracken fern and where are they located in the plant?
Most toxic principle in young plants (fronds and crizomes) and rhizomes (green or dry) but technically is in all parts of the plant.
Equine diseases: Type I thiaminase
Cattle: Ptaquiloside
Treatment for bracken fern toxicosis?
Ruminants: Antibiotics and supportive care
Equine/monogastrics: Thiaminase HCl
How much bracken fern does an animal need to eat for a toxic dose?
A lot!
25% of diet composed of fern for 3 weeks or more.
How is bracken fern eaten by humans?
Fiddleheads are eaten.
Must cook to get rid of carcinogenic properties.
What are some characteristics of the St. Johnswort plant?
Erect perennial found in dry sandy soils.
Leaves have small translucent glands in them.
Leaves are opposite one another.
5-petaled bright yellow flowers with small black dots along flower margins.
What is the toxic principle in St. Johnswort?
Hypericin - a primary photodynamic pigment.
Which animals are affected by St. Johnswort and how much plant material do the animals have eat?
Any grazing animal.
Have to eat LOTS.
Lesions caused by St. Johnswort?
Inflammation of the white areas of the skin, cornea, and conjunctiva.
Why do humans take St. Johnswort? What effects can St. Johnswort ingestion have on humans?
Taken as a mood stimulant
Hyperforin inhibits many neurotransmitters including GABA.
Can interfere with the metabolism or excretion of over 50 drugs
Cardiotoxins also generally have profound effects on what other bodily system?
The GI tract.
What are some characteristics of oleander plant?
Evergreen found mainly in the SW US.
Long, narrow spear like leave with central veins, and very leathery
Flowers are brightly colored (any color but often pink)
Toxic principle in oleander?
Cardiac glycosides (specifically oleandrin)
Mechanism of action for oleander?
Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.
May also increase vagal tone leading to bradycardia
How much oleander does an animal need to eat to see toxicity?
Small amount!
5-10 leaves can be lethal to an adult cow
How do grazing animals get access to oleander?
Generally by feeding animals tree clippings, lawn mower clippings, or by material getting into silage or hay
Clinical signs of oleander toxicity
Less than 8 hours: salivation, lethargy, diarrhea
Progresses to arrythmias, weakness, hypotension, bradycardia, dyspnea, coma, death.
Lesions of oleander toxicity
Myocardial vacuolation, degeneration, and necrosis
Ischemic renal necrosis
Diagnosis of oleander toxicity
Oleandrin residue analysis of GI contents and serum
ELISA test for digoxin may cross react with this test
Treatment of oleander toxicosis
Toxins excreted slowly, so prolonged treatment (2-3 wks)
Multiple AC doses
Symptomatic care
Digibind: Digoxin specific Fab antibody fragments to bind toxin.
How are humans commonly exposed to oleander?
Roasting food on oleander sticks while camping
What is more dangerous to dogs: dried oleander or fresh oleander?
Dry
Both have the same toxicity but dry is more palatable (bitter when fresh)
Describe foxglove flowers
Bell shaped with dark spots on the inside.
Toxic principle of foxglove and where it is found in the plant
Cardiac glycosides (specifically digoxin and digitoxin)
Found in entirety of plant
What animals are susceptible to foxglove toxicity?
All species
Mechanism of action for foxglove
Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.
May also increase vagal tone causing bradycardia.
Diagnosis of Foxglove toxicosis
Can use ELISA test for digoin on serum, blood, GI contents
Histological lesions on the myocardium (vacuolation, degeneration, and necrosis)
Treatment of foxglove
Treat for 2-3 wks (toxin excreted slowly)
Multiple activated charcoal doses
Digibind: Digoxin-specific Fab antibody fragments to bind toxin
Symptomatic treatment.
Where is foxglove native to?
Western Washington
How much foxglove needs to be ingested for toxicosis?
Small amount
What is the toxic principle in Rhododendron, azaleas, laurels, and Japanese pieris?
Grayanotoxics
Where in rhododendrons is toxin located?
Grayanotoxins in the entire plant but especially the leaves
Rhododendrons are toxic to all species, but in what species is toxicity most commonly seen?
Goats - clearing an area they mow down a lot of rhodies.
Toxicities also common if clippings given to other grazing animals.
What are the clinical signs of rhododendron toxicity?
PROMINENT GI SIGNS: Vomiting, anorexia, lethargy in 6 hours
24 hours: bradycardia, hypotension, dyspnea, recumbency, convulsions, death.
How much rhododendron does an animal have to eat to see toxicosis?
Small amount
Lesions for rhododendron toxicity
Gastroenteritis
Renal cortical and tubular necrosis from hypoxia
Diagnosis of rhododendron toxicity
History - or leaves easy to see in GI contents
Can test for grayanotoxins in GI contents
Treatment for rhododendron toxicosis?
IV lipid therapy
Decontaminate if possible
Supportive care for GI and heart
What are the toxic principles in yew?
Taxines (one of ten types of alkaloids in yew)
What is the mechanism of action of yew?
Taxines interfere with myocardial conduction by affecting Ca and Na channels and altering intracellular K.
How much yew is toxic to an animal?
Small amount
Clinical signs and when signs begin to occur?
Monogastrics: 15 minutes - 4 hours
Ruminants: Can be delayed, up to 38 hours
ACUTE CARDIAC FAILURE: trembling, dyspnea, ataxia, collapse, death.
May see some GI issues as well.
Lesions for yew toxicity?
None
Diagnosis of yew toxicity
GI contents
Test contents for taxine
Treatment of yew toxicosis
Activated charcoal and cathartic
Supportive care for GI and heart
Which part of the yew plant is toxic?
All except for the fruit of the berry (pink and fleshy, seed is toxic)
Describe yew needles
Approximately 1 inch long
Dark on top, light on the bottom
Why do people harvest yew bark?
Harvest taxol - has been used therapeutically as a breast cancer treatment
Describe death camas
Bulb looks like a wild onion but smells wrong and has a black covering.
Top part of the plant just looks like grass with thick blades and a strong V shape.
Toxic principle in death camas?
Steriod alkaloids (zygacine and others)
Where in death camas are toxins found?
Steriod alkaloids in all parts of the plant (esp problematic because top part can be grazed or harvested into hay)
Mechanism of action of death camas?
Peripheral vasodialtion and vagal stimulation leads to hypotension and bradycardia
Clinical signs of death camas
Within 6 hours, vomiting, salivation, muscle tremors, dyspnea, ataxia, weakness, convulsions, and death.
Diagnosis of death camas
Test for zygacine in GI contents
Treatment of death camas
Supportive care for GI and heart
Activated charcoal
Where is death camas commonly found?
Montana and Idaho
Why is milkweed called milkweed?
Generally has a milky sap in the stems and leaves that attracts butterflies.
What is the toxic principle in milkweed?
Cardiac glycosides and cardenolides.
Two species also have neurotoxins.
What is the (main) mechanism of action of milkweed?
Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.
What are the clinical signs of milkweed toxicosis?
Heart signs: abrupt death, dyspnea, tachycardia, etc.
Other toxins in the plant may cause GIT, respiratory system, or nervous system signs.
Also causes skin irritation
How much milkweed does it take to be toxic to an animal?
Depends on species sensitivity (all animals susceptible)
Moderate amount (about 1 kg) for a horse
Small amount for a sheep.
Treatment for milkweed toxicosis
Sedatives, analgesics, other supportive care based on clinical signs.
Control is easy as milkweed tends to grow an obvious, solitary plant.
Describe kalanchoe
Houseplant often seen in grocery stores
thick succulent leaves.
Flowers = clusters, bright, long lasting blooms, 4-petalled.
Toxic principle in kalanchoe, and where is it found
Cardiac glycosides
Found in all parts of the plant but esp. the flowers
How much kalanchoe is toxic to animals?
Pretty large amount
Clinical signs of kalanchoe
GIT upset in a few hours
Arrythmias, tacycardia, dyspnea if dose is high enough, cardiac arrest at extreme end.
What is the main lesion associated with kalanchoe?
Gastroenteritis
Treatment for kalanchoe
Emesis, AC
Supportive care (fluids, antiarrythmic drugs, etc.)
What species are susceptible to avocadoes?
BIRDS
All spp technically susceptible but birds are really the only species we see serious toxicosis in.
What is the toxic principle of avocado and where in the plant is it found?
Persin
All parts of the plant
Clinical signs of avocado toxicosis?
Avian: acute respiratory and cardiac distress
Lactating animals: Non-infectious mastitis and myocardial necrosis.
Horses: Edema of the head and neck which may cause ischemic myopathy / ischemic myelomalacia.
Describe the characteristics of western false hellebore
Large alternating leaves with parallel veins
Produce flowers on a thick unbranched stem
Found in very moist areas.
Smells skunky to most people.
What is the toxic principle of Western False Hellebore?
Glycoalkaloids and Ester alkaloids
Where is toxic principle located in Western False Hellebore?
Concentrated in the young shoots and roots
Decreased concentration in mature leaves
What is the mechanism of action of Western False Hellebore?
Heart: Bradycardia from increased vagal tone and Hypotension from peripheral vasodilation.
Teratogenic: 5 alkaloids
How much Western False Hellebore does the animal eat to see toxicity?
Teratogenesis: Only a little
Lethality: A lot
What are the effects of Western False Hellebore as a teratogen?
Depends on dose and the stage of gestation.
Early embryonic death/Abortions, Cyclopia, Cleft Palate, Arthrogryposis, Tracheal Stenosis, Vertebral column deformities (lordosis, kyphosis, scoliosis)
What are the clinical signs of Western False Hellebore as a cardiotoxin?
GI: Salivation, Vomiting/Regurgitation
Cardio: Weakness, incoordintation, bradycardia, hypotension, convulsions, coma, death.
Treatment for Western False Hellebore
None
In adult animals, if source is removed should be self-limiting in 3-4 hours.
Only treatment for pregnant animals = prevention
What evergreen needle trees have the highest concentration of toxin and how do you recognize them?
Pondarosa pine: long needles in clusters of 3.
Lodgepole pine: long needles in pairs.
Over 25 spp. have toxin but in lower levels and generally unpalatable so not many toxicities seen.
Toxic priniciple in pines? Where is it found?
Isocupressic Acid
In bark and needles.
Mechanism of action of pines?
Isocupressic acid = TONE GENERATING COMPOUND
Causes uterine vasoconstriction (esp. of the uterine artery)
Fetus releases cortisol causing abortion/premature partruition
Often see retained placentas
What stage of gestation are pine needles a biggest problem for?
Risk highest in the last trimester, but fetuses can also be affected in the first or second trimester.
How much pine needs to be eaten to see toxicity in animals.
A large amount.
What species are most susceptible to pine needle toxicity?
Cattle
Lesions from pine needle toxicity?
Vasoconstricution of caruncles with necrosis and hemorrhage.
Diagnosis of pine needle toxicity
Test fetal thoracic fluid and fetal GI contents for tetrahydroagathic acid (metabolite of isocupressive acid)
May also be able to test uterine artery
Prevention of pine needle toxicity
Don’t graze cattle in pine forests
Provide low protein/high energy diet = experimentally produces avoidance
For what species can alfalfa and red clover be toxic?
Most signs are mainly in ruminants
Slobbering disease in all species
What the toxic principles/clinical syndromes seen with alfalfa/redclover toxicity?
Saponin / proteins can cause bloat
Estrogen / coumesterol can cause infertility or cystic ovaries
Unknown agent can cause photosensitivity
Slaframine can cause slobbering disease
Describe halogeton
Reddish stem
Tubular sausage-like fleshy green gray leaves arranged in clumps
Gen in alkaline, dry soil
What plant has the same toxic principles as halogeton?
Shamrock (Oxalis)
(4-leaved clover type plant often with a purplish center)
Toxic principle of halogeton?
Soluble sodium and potassium oxalates
How much halogeton does an animal need to ingest to see toxicity?
Moderate amount
In what species is halogeton toxicity most commonly seen in and why?
Grazing animals (esp sheep and cattle) during the winter - dried plants stick up out of the snow and are palatable, and toxin concentrated in the dry plants.
Mechanism of action of halogeton
Soluble oxalates are a metabolic poison - interfere with lactate and succinate dehydrogenase
Oxalates bind Ca2+ and so cause hypocalcemia
Formation of calcium oxalate crystals in the renal tubles cause renal necrosis
Clinical signs of halogeton?
Generalized hypocalcemic signs early: salivation, lethargy, dyspnea, ataxia, muscle tremors, seizures
Renal signs later
Clin Path and Lesions of halogeton
Clin Path: hypocalcemia and azotemia
Renal tubular necrosis due to calcium oxalate crystals
Treatment of halogeton?
Give dicalcium phosphate orally so that oxalates will be bound in the gut and not get absorbed as much.
Toxic principle of oak and where is it found?
Gallotannins (gallic acid, tannic acid, pyrogallol)
Found in acorns and budding/immature leaves
How much oak does an animal need to eat to see toxicity?
Lots and lots
Clinical signs of oak toxicity?
GI: bloody, mucoid diarrhea
Renal: weakness, weight loss, lethargy, eventual death.
Clinical Pathology of Oak toxicosis
Isosthenuria, proteinuria, azotemia, hyperkalemia, hypoproteinemia, hypocalcemia.
Lesions of oak toxicity
Gastroenteritis
Nephritis - multifocal necrosis of proximal renal tubules
+/ edema, ascites, etc.
Prognois for oak toxicity?
Generally poor - renal damage irreversible
Toxic principle of pigweed
Nitrate accumulator
Also contains soluble oxalates
Treatment for pigweed
Renal = supportive
Nitrates = methylene blue
What are the two types of lillies that are nephrotoxic?
Lillium and Hemerocallus
(Tiger lily, Easter lily, Day lily, Asiatic hybrid lily, Stargazer lily)
What is the toxic principle in nephrotoxic lilies and where is it located?
Unknown but definitely water soluble
All parts of lily
How much lily does an animal need to eat to see toxicity
Tiny amount (a bite)
In what animals are lilies toxic?
CATS only
(Dogs can have some GI upset from the bulb)
Clinical signs of lily toxicity
GI upset
Renal signs in 48-96 hours!
May see facial and paw edema
Lesions of lily toxicity
Severe acute renal tubular necrosis
NO oxalate crystals
Treatment of lily toxicosis
Decontaminate! Emesis, AC, cathartic, etc.
IV fluid diuresis for 48-72 hours
Monitor renal values
What is the toxic principle of bleeding heart and where is it found?
Isoquinoline-like alkaloids
In all parts of the plant
Clinical signs of bleeding heart toxicity?
Gastrointestinal signs first
Muscle tremors, prostration, convulsions.
Prognosis for bleeding heart toxicity?
Usually good - death is very rare and recovery is rapid.
Treatment for bleeding heart toxicosis?
Generally none - animals recover in less than 2 hours in most cases.
Describe some characteristics of water hemlock
Bulbous root with yellow resin in very moist areas or in water.
Adult plant can be 3-10 feet tall with a hollow stem.
Umbrella like clusters of white flowers
Toxic principle in water hemlock and where it is found
Cicutoxin
Mostly in roots and young shoots
How much water hemlock does an animal need to eat to see toxicosis?
Small amt (one root can kill pretty much any animal)
Clinical signs of water hemlock toxicosis
Rapid onset in 15-45 minutes: first pre-ictal uneasiness then violent convulsions and death.
Diagnosis of water hemlock toxicity?
Generally still see the plants in the GI contents because death is so rapid.
Can also test for cicutoxin in GI contents.
Prognosis for water hemlock toxicity?
Grave - fatality so fast.
Describe some characteristics of yellow starthistle
1-3 feet tall
Thin, short, narrow leaves that almost look like needles
Stem and leaves covered with cottony hair
Oviod spiny flower base
Toxic principle of yellow starthistle and where it is located
Pyrone (hypothesized)
Found only in aerial portions of the plant
What species is yellow starthistle a problem?
Horses and other equids
What lesion does Yellow Starthistle cause and what nerves does this lesion affect?
Nigropalladial encephalomalacia
Impairs CN: 5, 7, 9, 12. (Trigeminal, Facial, Glossopharyngeal, Hypoglossal)
How much yellow starthistle does an animal have to see for toxicity?
A LOT.
Mechanism of action of Yellow Starthistle
Binds to dopaminergic receptors and causes necrosis. (Hits same receptors as cocaine does, some young horses seem to be addicted to it)
Dopaminergic areas: Anterior globus palladius, substantia nigra.
Clinical signs of yellow starthistle toxicity
Acute presentation of a chronic problem
Lip twitching, involuntary chewing movements.
Trouble eating and drinking = starvation (wasting, death)
Prognosis for yellow starthistle toxicity?
Grave. Not reversible.
Toxic principles in Locoweed (3)
- Miserotoxin - in all parts of the plant only when FRESH.
- Swainsonine/Swainsonine-N-oxide - mainly in the seeds, thought to be a mycotoxin.
- Selenium accumulator
Mechanism of action of locoweed
Miserotoxin: Both neuro and respiratory effects
Swainsonine (and S-N-Oxide) inhibit Golgi mannosidases which leads to the accumulation of mannose in cytoplasma and vacuoles/lysosomes of neurons, hepatocytes, renal tubules, and other tissues.
Selenium: causes skin and abortions.
Clinical signs of locoweed
Miserotoxin: ataxia (Wallerian degeneration of peripheral nerves and posterior spinal cord), pulmonary edema and emphysema, death.
Swainsonine: Locoism - ataxia, visual impairment, hyperexcitability or lethargy, emaciation.
Selenium: Hoof and hair problems, abortions, unthriftiness.
Diagnosis of locoweed
Can test for swainsonine
Can also evaluate mannoidase activity (for decrease)
Histological lesions of locoweed
Vacuolization of many cell types including neurons, renal epithelial cells, hepatocytes
Toxic principle in morning glory and where it is located
Lysergic acid derivatives
Only in the seeds
How many morning glory seeds does an animal have to eat to see toxicosis?
A LOT.
Clinical signs of morning glory toxicosis?
Vomiting, diarrhea, dilated pupils, hallucinations, disorientation, other bizzare behavior
Treatment of morning glory toxicosis?
Supportive care +/- sedation.
What do you always have to worry about with a pet that came in for eating marijuana?
Dual exposures!! (xylitol, raisins, chocolate, macademia nuts).
Toxic principle of marijuana?
THC - tetrahydrocannabinols
Mechanism of action of marijuana
CNS depression and derangement
Clinical signs of marijuana toxicosis
Ataxia, lethargy, dilated pupils, easily aroused, inappropriate urination, changes in heart rate, hyperexcitability, inappropriate urination.
Prognosis for marijuana toxicity
Good - fatalities very rare and so far only seen with dual toxicities
Treatment for marijuana toxicity
IV lipid therapy for very high exposures
Decontamination
Supportive care
What does the fruit and leaves of a trumpet vine look like?
Fruit = round, spiny
Leaves = simple, alternating, strong odor.
What are the toxic principles in trumpet vine?(3) Where are they?
- Atropine
- Hyoscyamine
- Scopolamine
All parts of the plants toxic but especially the seeds.
Clinical signs of trumpet vine toxicity?
Trembling, excitation, colic, dilated pupils, tacky mucous membranes, tachycardia, blurred vision, decreased intestinal motility
Treatment for trumpet vine toxicity
Decontamination
Physostigmine should theoretically work but not much clinical success
Toxic principles of lupine and which type of plant has most?
Guinolizidine alkaloids
“Bitter” lupines have more alkaloids than “sweet” lupines
Lupine mechanism of action
A nicotinic effect - mimicing acetylcholine at both sympathetic and parasympathetic ganglia, NMJs, and CNS.
This acts as an anesthetic for the growing fetus
What are the clinical signs of lupine in fetal cattle?
Crooked Calf disease: Arthrogryposis, Vertebral column abnormalities (kypohosis, lordosis, scoliosis), Cleft Palate.
Rarely may kill the calf and cause abortions
What is the critical time period for malformations in a cow eating lupine?
Day 40-110 of gestation
How much lupine does an animal need to eat for toxicity?
Generally occurs in animals that eat a LOT but in only a short period of time
What is the essential characteristics of poison hemlock?
Purple spots! (on the stem)
Otherwise looks very similar to water hemlock except in dry land instead of water.
Toxic principle in poison hemlock and where it is located
Piperidine alkaloids
In the whole plant, increasing in concentration as the plant matures.
How much poison hemlock does an animal need to eat to see toxicity?
Small amount
Mechanism of action of poison hemlock
Nicotinic effects (like lupine) can theoretically cause anesthetic effects and fetal malformations.
What animal is most commonly poisoned by poison hemlock?
Humans! Root looks like a carrot.
Then cattle.
Clinical signs of poison hemlock?
Muscle tremors, weakness, ataxia and DUMBSLED signs (salivation, lacrimatin, defecation)
Respiratory arrest
Rare: can see arthrogryposis, cleft palate, and vertebral column abnormalities.
Toxic principle of larkspur?
Polycyclic diterpene alkaloids
When is larkspur most dangerous?
When the plant is the most palatable - from the pre-blooming to the pod-forming stage
Mechanism of action of larkspur
Paralysis: Inhibition of the post-synaptic neuromuscular junction by acting as a competative inhibitor of Acetylcholine. Bind more tightly to nicotinic acetylcholine receptors than others.
Clinical signs of larkspur
Most commonly, cattle just found dead on pasture (acute death)
May see uneasiness, ataxia, muscle stiffness, muscle twitching, and abdominal pain.
Treatment of larkspur
May be able to treat with physostigmine to increase the Ach in the NMJ
Can also use neostigmine for the same reason
Prevention of larkspur toxicity?
Graze only when the plant is not palatable (later in the season after pods formed)
Lithim supplements may induce larkspur refusal?
Toxic principle in horsetail and where in the plant?
Thiaminase-like compounds (breaks down Vit B1)
All parts of the plant
How much horsetail does an animal have to eat to see toxicosis?
Lots!
What species are primarily affected by horsetail?
Horses!
Clinical signs of horsetail toxicosis?
Like polioencephalomalacia (but no gross lesions!)
Weakness, weight loss despite good appetite, hind limb ataxia or paralysis, convulsions, possibly death.
Prognosis for horsetail toxicosis?
Good if animal is not yet recumbant.
Treatment for horsetail toxicosis?
Thiamine HCl (aka, Vitamin B1)
What do the spines on a cockleburr look like?
Curved and hooked!
Toxic principle in cockleburr and where is it found?
Carboxyatractyloside
Found in the seeds within the burr and the dicotyledons (babies) as they grow.
How much cockleburr does it take for toxicity?
Moderate amount
Clinical signs of cockleburr toxicosis?
12 hours to 2 days: Anorexia, weakness, lethargy, nausea, vomiting, dyspnea, muscle contractions, convulsions, death
Ascites
Pathological lesions of cockleburr toxicity?
Mottling of the liver and kidney (due to degeneration/necrosis)
GIT inflammation
IN SWINE ONLY: neuronal degeneration and necrosis
Why is cockleburr an uncommon toxicity?
The burrs are so hard that it is often hard for the animals to get to the seeds. Most commonly a problem when the burrs are cut up and then incorporated into silages and hays.
Name some of the pyrrolizidine alkaloid containing plants (common names)
Tansy Ragwort
Groundsel
Hound’s Tongue
Tarweed
Fiddleneck
How much of a plant containing pyrrolizidine alkaloids would an animal have to eat to see a toxicity?
Lots!
TOXICITY IS CUMULATIVE
Animals susceptible to pyrrolizidine toxicities
Cattle, horses, pigs, poultry
Animals resistant to pyrrolizidine alkaloid toxicities
Sheep and goats (and likely camelids)
Mechanism of action of pyrrolizidine alkaloids
Metabolized to highly active pyrroles
Pyrroles alkalate DNA and impairs cell division
Cell continues to grow until critical mass is reached and then necrosis of the cell occurs
Lesions of pyrrolizidine alkaloid toxicosis
Grossly liver can be large or small.
Histo: hepatic megalocytosis, centrilobular necrosis, bile duct proliferation, and portal fibrosis
Clinical signs of pyrrolizidine alkaloid toxicity
Classic hepatic failure signs + secondary photosensitization and hepatic encephalopathy
Diagnosis of pyrrolizidine alkaloid toxicity
This is the primary cause of megalocytosis (though not pathognomonic)
Can test liver and blood in early stages but this is unreliable.
What is the toxic principle in alsike/red clover?
Unknown principle can cause liver damage.
Slaframine = slobbering disease
Clinical signs of red/alsike clover toxicity
Depending on dose may see secondary photosensitization or hepatic encephalopathy and other liver signs.
Slobbering disease in any animal.
Lesions of red/alsike clover toxicity
Hepatomegaly, perilobular fibrosis and bile duct proliferation.
Prognosis of red/alsike clover toxicity?
Depends on the amount of liver damage it has caused.
In what species is liver damage seen with red/alsike clovers?
Liver damage ONLY in horses
(slobbering disease in all animals)
What are the toxic principles in sago palm? (3) And where are they in the plant?
- Cycasin (and metabolite methylazoxymethanol) - liver
- Beta-methylamino-L-alanine - nervous system
- Unknown
All parts toxic, female parts more so, seeds and nuts are most toxic.
Clinical signs of sago palm toxicity and when they occur
15 min: Intense GI signs
2-3 days: hepatic and nervous signs.
In what species are sago palm toxicities most commonly seen?
Theoretically can affect all species but 90% of toxicities in dogs.
Lesions of sago palm toxicosis?
Focal centrilobular and midzonal necrosis
Treatment of sago palm toxicosis
Decontaminate + multiple AC doses
GI and liver protectants
Monitor chemistry panels
Supportive care
Toxic principle in buttercup and where is it?
Ranunculin converted to GI irritant, protoanemonin.
In entire plant but only when fresh.
How much buttercup does an animal need to ingest to see toxicosis?
A lot
Clinical signs of buttercup toxicosis?
Often see dermatitis (esp in humans)
GI issues mainly
In some spp: muscle weakness, difficulty breathing (esp sheep)
Toxic principles in English Ivy (3) and where they are?
All parts of the plant, esp the berries
- Triterpenoid
- Saponin
- Hederagenin
Clinical signs for English Ivy Toxicity
Severe GI signs: salivation, vomiting, diarrhea.
Prognosis for English Ivy toxicosis
Good - fatalities are rare.
Which bulbs cause GI symptoms?
Lots - tulips, iris, amaryllis, hyacinth!
Toxic principle in tulip bulbs
Alkaloids
Clinical signs of tulip bulb toxicity
Oral irritation and mild or severe gastroenteritis
Rarely serious
What domestic plants are related to nightshade?
Tomato and potato
Toxic principle and mechanism of action in nightshade?
Solanine
This is converted to a sugar or solanidine which affects the purkinje cells of the cerebellum
Some plants contain atropine
Clinical signs of nightshade toxicity?
GI signs
Nervous signs: dyspnea, ataxia, paresis or paralysis
DUMBSLED signs if atropine containing plant
How much nightshade does an animal have to eat for it to be toxic?
Lots
What kind of plants are insoluble oxalate containing plants typically?
House plants
Generally dark green with large broad leaves.
What are the toxic principles in insoluble oxalate plants?
Insoluble oxalates and proteolytic enzymes
Mechanism of action of insoluble oxalate containing plants?
Oxalate crystals irritate the GI mucosa
Proteolytic enzymes trigger the release of kinins and histamines
Clinical signs of insoluble oxalate containing plants?
Salivation, swelling of the oral mucosa
Vomiting and diarrhea
Treatment for insoluble oxalate containing plants?
Supportive, esp. rinsing the mouth and giving fluids.
Often includes anti-histamines to quell release.
Prognosis for insoluble oxalate plants?
Good
If death does occur from insoluble oxalate containing plants, why does it occur?
Hypoxia from swelling of the airways
How do pets get castor beans?
Either from gardens or a lot of times found in jewelry.
Toxic principle in castor beans and where it is located?
Ricin (water soluble and rapidly absorbed)
In the seed inside of the outer shell
How many castor beans are needed to cause toxicity?
Small amount! Just one for a dog.
How can castor beans be used as a biological weapon?
If aerosolized and inhaled, ricin will cause pulmonary pathology
Clinical signs of castor bean toxicity?
GI distress in 12-48 hours
If high enough does, multi-systemic problems: hypotension, muscle twitching, dyspnea, convulsions, coma, death.
Lesions with castor bean toxicosis?
Gastroenteritis
Hepatic, renal, or myocardial necrosis
Treatment for castor bean toxicosis?
Only supportive
Characteristics of hairy vetch?
Terminal tendrils on the end of each vine
Pea-like flowers and seed pods
Toxic principle of hairy vetch?
Unknown
Species commonly affected by hairy vetch?
Cattle and horses
Clinical disease from hairy vetch?
There are four but most commonly seen is systemic granulomatous disease.
How much hairy vetch needed to see toxicity?
A lot!
Pathologic lesions associated with hairy vetch
Multiple granulocytic lesions (eosinic, lymphocytic, or plasmacytic infiltrate with multinucleated giant cells)
Dermatitis and conjunctivitis
Mechanism of action for hairy vetch?
Granulomas due to a Type IV hypersensitivity reaction.
What is the toxic principle for hoary alyssum?
Unknown
What plant has the same mechanism of action as hoary alyssum?
Black walnut
What animals are affected by hoary alyssum/black walnut toxicity?
Equine
Clinical signs of black walnut toxicity?
Limb edema, laminitis, and fever if INGESTED
What happens when dogs ingest black walnut WOOD?
Can see neurologic or musculoskeletal signs - vomiting, lethargy, hind limb weakness, tremors, ataxia, disorientation, pain, seizures
What are the clinical signs of dogs eating black walnuts themselves or the hulls of black walnuts?
GI signs - salivation, vomiting, anorexia, diarrhea.
Should you use fat or water to clean off poison oak/poison ivy lesions?
Both! Toxin is lipid soluble but plant water soluble.
What are some examples of cyanogenic glycoside containing plants?
Chokecherries, apple seeds, cherry pits, most other seed fruits.
What is the mechanism of action of cyanogenic glycosides?
Cyanogenic glycosides broken down to sugar and aglycone (by beta-glycosidase)
Aglycone converted to hydrocyanic acid (by hydroxynitrile lyase)
Cyanide interacts with ferric iron of cytochrome oxidase, which inhibits electron transport and cellular respiraton.
Blood is fully oxygenated but cannot be utilized by the cells.
Clinical signs of cyanogenic glycoside toxicity?
Salivation
Hyperpnea, Dyspnea - death from respiratory paralysis
Weakness and muscle fasciculations, convulsions
Blood may be bright cherry red but rarely observed clinically.
Pathologic lesions of cyanogenic glycosides
Bright red mucous membranes
“Bitter almond” smell to GI contents
Treatment of cyanogenic glycoside toxicity
Cyanokit - contains hydroxocobalamin (precursor to B12) to bind cyanide and have it be eliminated by the urine.
Other care = supportive
What can flatweed cause?
Stringhalt
Name four plants that can cause fog fever (pulmonary emphysema and edema), and how each can cause it.
Lush greens in early spring - contains high levels of tryptophan which is converted to 3-methyl indole in the rumen. 3-MI affects the lungs.
Moldy Sweet Potato - produces 4-ipomeanol, affects the lungs.
Perilla mint
Mustards
