Plant Cards Flashcards
Nerium oleander (oleander): Toxic Principles, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLES:
- Cardiac glycosides
- all parts toxic and toxicity not lost in drying.
- small amount lethal
ANIMALS AFFECTED:
- All species
CLINICAL SIGNS:
- GI & heart
LESIONS:
- Gastroenteritis
- Myocardial vacuolation, degeneration, and necrosis
- Ischemic renal necrosis.
TREATMENT
- digibind
- decontamination
- supportive care
Digitalis spp. (foxglove) Toxic Principles, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLES
- Cardiac glycosides
- Entire plant is toxic, and not lost in drying.
- small amount is toxic
ANIMALS AFFECTED:
- All species
CLINICAL SIGNS / LESIONS:
- Gastroenteritis
- Myocardial vacuolation, degeneration, and necrosis
- Ischemic renal necrosis.
TREATMENT
- decontamination
- supportive care
Asclepias spp. (milkweed) Toxic Principles, animals affected, clinical signs, treatment
TOXIC PRINCIPLES
- Cardiac glycosides
- Most toxic during their rapid growth phase
- retain some toxicity when dried
- small amount toxic
ANIMALS AFFECTED // CLINICAL SIGNS:
- All animals susceptible
- GI, heart, respiratory system
- some cause nero signs
TREATMENT
- supportive care
Rhododendron and Pieris japonica (rhododendron, Japanese pieris): Toxic Principles, clinical signs, treatment
TOXIC PRINCIPLES:
- Grayanotoxins
- entire plant is toxic and not lost in drying
- small amount toxic
- All animals susceptible.
CLINICAL SIGNS:
- REGURGITATION
- GI and heart
- Onset - 6 hours
TREATMENT
- decontamination w/ IV lipid therapy
- supportive care
Yew Toxic Principles, clinical signs, treatment
TOXIC PRINCIPLES
- Taxine & alkaloids
- interferes w/ myocardial conduction
- All parts, except the red fleshy berry, are toxic
- small amount toxic
CLINICAL SIGNS:
- acute cardiac arrhythmia & death
- quicker in monogastrics than ruminants (up to 38hr)
- trembling, dyspnea, ataxia, collapse, and death due to acute cardiac failure
- GI signs
- Seizures and liver disease in dogs have been
reported
TREATMENT
- AC
- decontamination
- supportive care
Ziganedus (death camas): Toxic Principles, mech of action, clinical signs, treatment
TOXIC PRINCIPLES:
- Steroidal alkaloids - found in all parts of the plant,
- small amount toxic
MECHANISM OF ACTION:
- alter membrane action potential and homeostasis
- impairs sodium transport.
CLINICAL SIGNS:
- Onset: 1-6 hours
- GIT and heart
- excessive salivation, hypothermia, lethargy, nausea, vomiting, retching, colic, grinding teeth, dyspnea, muscle tremors, weakness, ataxia, prostration, convulsions, and death.
TREATMENT
- decontamination
- supportive care
Veratrum (False hellebores): Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLES:
- Glycoalkaloids and ester alkaloids
- concentrated in the young shoots and root.
- Toxicity decreases as the plant matures
- Small amounts cause teratogenicity
- large amounts cause GI & heart
MECHANISM OF ACTION:
- Hypotension due to peripheral vasodilation
- bradycardia due to excessive vagal tone
- Teratogenic.
ANIMALS AFFECTED:
- Mostly sheep and cattle.
CLINICAL SIGNS // PATHOLOGIC LESIONS:
- Onset within 2-3 hours
- excessive salivation, vomition or regurgitation, muscle weakness, incoordination, hypotension, bradycardia, dyspnea, convulsions, coma, and death within 6-18 hours. - early embryonic death, cyclopia, cleft palate, arthrogryposis, tracheal stenosis, abortions.
TREATMENT:
- Most animals recover in 3-4 hours.
- Keep pregnant animals away from the plant
Persea (avocado): Toxic Principles, animals affected, clinical signs, lesions,
TOXIC PRINCIPLE:
- Persin
- all parts considered to be toxic
- toxic and nontoxic varieties.
ANIMALS AFFECTED:
- All species susceptible, especially BIRDS
- Lower dose exposures affect the mammary tissue
- higher exposures affect the heart.
CLINICAL SIGNS // LESIONS:
- Avian - acute respiratory and cardiac distress, with SQ edema and hydropericardium.
- Goats/lactating animals - Noninfectious mastitis
- myocardial necrosis observed in most animals at higher exposure doses.
- Horse - edema of head and chest
Kalanchoe; Toxic Principles, clinical signs, treatment
TOXIC PRINCIPLES:
- Cardiac glycosides
- all parts toxic, especially the flowers.
CLINICAL SIGNS:
- GIT and heart.
- Onset within a few hours
- lethargy, salivation, GI upset, diarrhea >
- arrhythmias, tachycardia, dyspnea >
- weakness, collapse, cardiac arrest, and death.
TREATMENT
- decontamination
- supportive care
Hypericum perforatum (St. John’s Wart); Toxic Principles, animals affected, lesions, treatment
TOXIC PRINCIPLE
- hypericin.
- Reaches cutaneous circulation where reacts with oxygen and sunlight to cause inflammation
- Need a lot to be toxic
- not a very common poisoning to see.
ANIMALS AFFECTED
- Any grazing animal affected.
LESIONS:
- Lesions restricted to nonpigmented areas, including cornea and conjunctiva
- varying degrees of inflammation within 24 hours of ingestion.
TREATMENT
- keep animals out of sunlight.
- Antibiotics and anti-inflammatories
Allium; Toxic Principles, animals affected, clinical signs, treatment
TOXIC PRINCIPLE
- disulfides (oxidizing agent)
- highest concentration in the bulb.
- Heinz body hemolytic anemia. (especially cats)
- cats & cattle > dogs > sheep/goats
- dried > fresh > cooked
- Garlic 5 times more toxic than onions
ANIMALS AFFECTED:
- Cattle and cats most sensitive
- sheep and goats most resistant.
- All animals susceptible.
CLINICAL SIGNS
- peak is 3-5 days to weeks
- icterus, dyspnea, weakness, collapse, Heinz body formation, hemolysis, anemia, hemoglobinuria, hemoglobinemia.
TREATMENT
- PCV & blood smear on day 1 & 3 or 5
- remove plant
Acer (maple); Toxic Principles, mech of action, animals affected, clinical signs, treatment
TOXIC PRINCIPLE:
- Unknown
- wilted or dried senescent leaves
- also pistachio leaves
MECHANISM OF ACTION:
- Acute hemolytic anemia, methemoglobinemia, and Heinz body formation.
ANIMALS AFFECTED:
- Equine (maybe alpaca)
CLINICAL SIGNS
- Within 24 hours
- lethargy, anorexia, tachycardia, tachypnea, brown discoloration to blood and red tinted serum, Anemia, methemoglobinemia, hemoglobinuria, Heinz bodies.
TREATMENT
- decontamination
- supportive care
Cruciferae family (mustard); Toxic Principles, mech of action, animals affected
TOXIC PRINCIPLES // MECHANISM OF ACTION:
- Must eat A LOT for toxicosis
(1) *Goitrin and thiocyanate -> interfere with thyroid hormone synthesis and iodine uptake -> goiter.
(2) Thiaminase-like activity -> polioencephalomalacia
(3) high sulfur content -> secondary copper deficiencies.
(3) disulfide -> hemolysis and Heinz body anemia.
(4) Equine dysmaturity syndrome – prolonged gestation, hyperplastic thyroids, incomplete
(5) GI irritants (bloat).
(6) Atypical pulmonary emphysema and edema (fog fever), nitrate accumulation, reproductive inefficiency,
enterotoxemia.
ANIMALS AFFECTED:
- All species susceptible.
Melilotus (sweet clover); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLE // MECHANISM OF ACTION:
- toxic when moldy
- dicumerol
- Interferes with vitamin K epoxide reductase -> bleeding disorders
ANIMALS AFFECTED:
- Primarily cattle.
CLINICAL SIGNS // CLINICAL PATHOLOGY:
- dependent on where bleeding is occurring //
Anemia, prolonged clotting times.
LESIONS:
- Generalized hemorrhage.
TREATMENT:
- Supportive // vitamin K1, fluids, blood transfusions, alfalfa
bracken fern; Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLE
- Young plants (fronds, croziers) and rhizomes most toxic but all parts are toxic
- Need A Lot for toxic
- ptaquiloside
ANIMALS AFFECTED:
- horses & cows
CLINICAL SIGNS // PATHOLOGIC LESIONS:
- thiaminase -> polioencephalomalacia like (more in horse)
- bone marrow suppression (more in cows)
- bovine enzootic hemturia
- carcinogenic -> neoplasm of GI and urogenital
TREATMENT:
HORSE
- Thiamine hydrochloride may help
RUMINANTS
- Antibiotics, supportive care
Pinus spp. (pine); Toxic Principles, mech of action, animals affected, diagnosis
TOXIC PRINCIPLE
- Isocupressic acid
- present in bark, needles, and early new growth tips
- a lot to be toxic
MECHANISM OF ACTION
pine needle induced abortion (misnomer)
- Isocupressic acid = uterine vasoconstriction ->
decrease oxygen and nutrient supply and maybe cortisol release ->
premature parturition or abortion up to 2-3 weeks post-ingestion
- retained placentas, incomplete cervical dilation,
endometritis when ingest large amount for >3 days
ANIMALS AFFECTED
- only bovine
DIAGNOSIS
- Collect fetal thoracic fluid and fetal stomach contents to test for tetrahydroagathic acid and dihydroagathic acid – biomarkers.
Medicago (alfalfa); Toxic Principles, mech of action, animals affected
TOXIC PRINCIPLES
- Saponins and proteins -> bloat,
- estrogens (coumesterol) -> infertility
- slaframine -> slobbering (very common)
MECHANISMS OF ACTION:
- reproductive failures
- early embryonic death
- cystic ovaries
- photosensitivity
ANIMALS AFFECTED:
- Ruminants mostly
- slobbering can occur in all animals.
Halogeton glomeratus (halogeton) / Oxalis spp. (shamrock); Toxic Principles, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLE
- Soluble sodium and potassium oxalates
- mostly in leaves.
- Toxicity increases as plant matures (dried = most toxic)
ANIMALS AFFECTED:
- Sheep and cattle most affected by halogeton (small amount)
- small animals affected by oxalis but must eat A LOT
CLINICAL SIGNS:
- Onset of 2-6 hours
- excessive salivation, anorexia, lethargy, dyspnea, ataxia,
abdominal pain, muscle tremors, prostration, seizures,
- death within 10 hours.
CLINICAL PATHOLOGY:
- Hypocalcemia, azotemia
PATHOLOGIC LESIONS:
- necrosis of proximal renal tubules and collecting ducts
- calcium oxalate monohydrate crystals.
TREATMENT // PREVENTION:
- Dicalcium phosphate orally will form calcium oxalate in the GIT which is relatively insoluble and nonabsorbable (rare to do).
- Watch management practices.
Quercus spp. (oak); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLE:
- Gallotannins: gallic acid, tannic acid and pyrogallol.
- acorn, immature leaves, and early leaf bud.
- Animals need to ingest at least 50% of diet for several
ANIMALS AFFECTED
- cattle in early spring or late fall.
- companion animals that eat A LOT of acorns.
MECHANISM OF ACTION:
- GI
- renal disease.
CLINICAL SIGNS
- Abdominal pain, anorexia, constipation
- bloody, mucoid diarrhea
- renal disease (weakness, lethargy, weight loss, and eventual death)
CLINICAL PATHOLOGY:
- Low USG,
- azotemia,
- hyperkalemia, hypoproteinemia, hypocalcemia,
- proteinuria.
LESIONS:
- Gastroenteritis (edema & hemorrhage)
- nephritis
- perirenal edema and hemorrhage,
- ascites, hydrothorax
- swollen kidneys, Multifocal necrosis of proximal renal tubules.
TREATMENT:
- Treat for renal failure
- generally poor prognosis.
Amaranthus spp. (pigweed) ; Toxic Principles, clinical signs, lesions, treatment
TOXIC PRINCIPLES:
- accumulate nitrates
- soluble oxalates (not commonly seen)
- unknown toxin responsible for perirenal edema and nephrosis
CLINICAL SIGNS:
- signs of nitrate toxicity
- oxalates
LESIONS:
- Perirenal edema, ascites, hydrothorax, edema of the ventral abdominal wall
- Degeneration & necrosis of the proximal renal tubules
- No lesions w/ nitrate.
TREATMENT:
- Treat for renal disease
- Treat with methylene blue for nitrate (rare)
Lilium spp. and Hemerocallus spp; Toxic Principles, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLE:
- Unknown water-soluble compound
- Bulbs can cause mild GI irritation.
- Leaves and flowers can be a problem
- Pollen and vase water can pose a risk as well.
- any exposure should be considered a risk.
ANIMAL AFFECTED
- renal toxicoses in cat
- GI problems reported in dogs, but not common
CLINICAL SIGNS:
- Acute onset of GI upset, lethargy, and anorexia
- polyuria can be seen within 12 hours
- renal disease and/or failure between 12-24 hours post-ingestion
- No crystals
- May have pancreatitis, elevated liver enzymes, neurologic signs (seizures), facial and paw edema.
LESIONS
- Severe acute renal tubular necrosis, with no oxalate crystals.
- Creatinine often higher than BUN.
- Basement membrane can be disrupted.
TREATMENT:
ASYMPTOMATIC
- Early decontamination
- emesis, activated charcoal, cathartic
- gastric lavage or endoscopy or combinations
- IV fluid diuresis 2x maintenance for 48 hours minimum
- establish baseline and monitor BUN and Cr at 24, 48, and 72 hrs prior to discharge
- USG 24 hours post cessation of fluid
SYMPTOMATIC
- treat for renal disease and failure
Dicentra spp. (Dutchman’s breeches, bleeding-heart); Toxic Principles, mech of action, clinical signs, lesions, treatment
TOXIC PRINCIPLES
- Isoquinoline-like alkaloids
- all parts of the plant.
CLINICAL SIGNS:
- Rapid onset of GI problems
- excessive salivation, vomiting, abdominal pain
- muscle tremors, and seizures.
- Convulsions can occur;
- death is rare.
LESIONS:
- Nonspecific - gastroenteritis.
TREATMENT:
Usually recover in 2 hours.
water hemlock; Toxic Principles, mech of action, animals affected, clinical signs, diagnosis, treatment
TOXIC PRINCIPLE
- Cicutoxin
- root, young shoots, green seeds
- Problem all year when animals are tugging on young shoots.
- 8 oz. root is enough to kill any animal.
ANIMALS AFFECTED:
- All animals susceptible
- mostly seen in cattle and sheep.
MECHANISM OF ACTION
- noncompetitive GABA antagonists in the CNS
- prevent formation of inhibitory postsynaptic potentials
- over-activation of neurons in the CNS.
CLINICAL SIGNS:
- rapid onset of uneasiness, muscle twitching, respiratory difficulty, convulsions
- death 15-45 minutes.
DIAGNOSIS:
- pieces of root, rootlets, and shoots in rumen/stomach contents.
- Can test for cicutoxin in GI contents.
TREATMENT:
- Prognosis is generally poor because animals die so acutely.
yellow starthistle & Russian knapweed; Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLE
- pyrone
- aerial portions of plant.
- Nigropallidal encephalomalacia
ANIMALS AFFECTED
- equine
- needs to eat a lot
MECHANISM OF ACTION:
- Interferes with dopaminergic nigrostriatal pathways
- impairs cranial nerves V, VII, IX and XII
- nigropallidal encephalomalacia.
CLINICAL SIGNS:
- Onset is sudden
- involuntary lip twitching and tongue and chewing movements, upper lip pulled back.
- Animals cannot drink or swallow food
- often die from starvation.
PATHOLOGIC LESIONS:
- Nonprogressive, symmetrical, focal necrosis and malacia of anterior globus pallidus and substantia nigra.
TREATMENT:
- Prognosis grave
- supportive care only.
Astragalus spp. and Oxytropis spp. (locoweed); Toxic Principles, mech of action, animals affected, clinical signs, lesions
TOXIC PRINCIPLES:
LOCOWEED TOXICOSIS
- swainsonine mycotoxin
- toxic fresh or dry
- only toxic principle of Oxytropis
NITROTOXIN POISONING
- toxic only when fresh
- all parts toxic,
- highest concentration in seed
SELENIUM POISONING
- acute and chronic
MECHANISM OF ACTION:
SWAINSONINE
- inhibits Alpha-mannosidase and Golgi mannosidase II
- impairs cellular lysosomal function and glycoprotein metabolism
- accumulation of mannose-rich oligosaccharides in cytoplasmic vacuoles and lysosomes of neurons, renal tubules, hepatocytes, and acinar pancreatic cells
NITROTOXIN (CRACKER HEELS)
- less common
- respiratory and neurologic disease.
SELENIUM
- hyperaccumulator plants
ANIMALS AFFECTED
SWAINSONINE
- horses most sensitive but can occur in all livestock and wildlife
NITROTOXIN (CRACKER HEELS)
- cattle most sensitive
SELENIUM
- negatively impact reproductive rates in ewes.
LESIONS:
SWAINSONINE
- edematous vacuolations of many cell types
SWAINSONINE
- pulmonary emphysema and edema
- Wallerian degeneration of posterior spinal cord & peripheral nerves
OTHER CLINICAL SIGNS
- teratogenic
- reproductive issues
Ipomoea spp. (morning glory); Toxic Principles, animals affected, clinical signs, treatment
TOXIC PRINCIPLE:
- foliage causes diarrhea
- ergot-type alkaloids in seeds cause CNS excitation/hallucinogen
- mold = locoism
- Must eat a LOT of seeds
ANIMALS AFFECTED
- All species susceptible.
CLINICAL SIGNS
- Digestive: diarrhea, lethargy, rough hair coat, weight loss.
- Neurologic: CNS excitation, hallucinogenic, locoism
- Respiratory: fog fever
TREATMENT:
- Symptomatic and supportive.
- Animals that are exposed (neurologic form) for less than 30 days have a good chance for spontaneous recovery.
Cannabis sativa (marijuana); Toxic Principles, clinical signs, treatment
TOXIC PRINCIPLE:
- Tetrahydrocannabinols
- all parts are toxic.
- Need to eat A LOT for lethal dose
- Very few fatalities have been reported
CLINICAL SIGNS:
- ataxia-lethargy
- hallucinations, stuporous and easily aroused,
- inappropriate urination (50%),
- tachycardia/bradycardia,
- vomiting, vocalizing, diarrhea, hypothermia/hyperthermia,
hypersalivation, mydriasis, hyperesthesia,
- seizure (rare), coma, and nystagmus
- maybe longer than 36 hrs depending on dose
TREATMENT:
- Decontaminate emetic, AC, anti-emetic
- IV crystalloids for perfusion
- monitor body T, HR, and BP
- diazepam or acepromazine (monitor BP) for agitation
- Protect from aspiration pneumonia
- IV lipid rescue therapy (high dose exposures)
- OTC urine kit tests – false (-) & (+) occur
- most recover w/o any treatment
Datura spp. (Jimson weed); Toxic Principles, animals affected, clinical signs, treatment
TOXIC PRINCIPLE:
- Atropine, hyoscyamine, and scopolamine
- all parts toxic, especially the seeds.
- incorporated into hay or ingested when no other feed
available.
ANIMALS AFFECTED:
- All species susceptible; seen quite a bit in horses.
CLINICAL SIGNS
- trembling and excitation,
- colic, decreased intestinal motility
- dilated pupils, blurred vision
- dry tacky mucous membranes,
- tachycardia
- hallucinogenic
TREATMENT:
- Decontaminate.
- Physostigmine, slow IV (does not work very well)
Lupinus spp. (lupine); Toxic Principles, mech of action, animals affected
TOXIC PRINCIPLE:
- Over 12 quinolizidine alkaloids
- some piperidine alkaloids
- Toxicity varies
- Toxic fresh or dried.
- large amounts in short period of time.
- most common problem is *‘crooked calf disease’ in cattle
ANIMALS AFFECTED
Cattle are most sensitive and susceptible.
Toxicoses reported in sheep, cattle, horse, and goats
MECHANISM OF ACTION:
- Nicotinic effect mimics acetylcholine at sympathetic and parasympathetic ganglia, neuromuscular junctions, CNS.
- Death from respiratory failure (uncommon).
- 40-120 days of gestation -> anesthetic to the developing fetus & restricts movement of the calf. -> crooked limbs, cleft pallet, crooked vertebral column
- Skeletal muscle myopathy has also been reported
Conium maculatum (poison hemlock); Toxic Principles, mech of action, animals affected, clinical signs
TOXIC PRINCIPLE:
- Piperidine alkaloids.
- All parts of the plant are toxic
- toxicity increases as plant matures.
MECHANISM OF ACTION:
- similar properties to nicotine
- initial stimulatory effect followed by an inhibitory action on nicotinic acetylcholine receptors in CNS.
ANIMALS AFFECTED:
- Most often seen in cattle.
CLINICAL SIGNS:
- 1-2 hours, muscle tremors, ataxia, weakness, excessive salivation
- lacrimation
- urination
- defecation,
- lethargy, recumbency,
- death from respiratory arrest in 2-3 hours.
- Cows, pigs, swine, and goats (babies): crooked limbs, cleft palate, crooked vertebral column
Delphinium spp. (larkspur); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLES:
- Toxic Window: toxic AND palatable in pre-blooming to seed pod stage
MECHANISM OF ACTION
- competitive inhibitors of nicotinic acetylcholine receptors
ANIMALS AFFECTED:
- cows
CLINICAL SIGNS:
- Uneasiness, ataxia, muscle stiffness, bloat, muscle tremors, weakness, recumbency
- death within 3-5 hours.
PATHOLOGIC LESIONS:
- detection of alkaloids in GI contents may be of help.
TREATMENT // PREVENTION:
- Physostigmine or neostigmine; acetylcholinesterase inhibitors ->
- increases acetylcholine concentration in the neuromuscular junction
- re-dosing may be necessary.
- Prevent exposure
- Research trying to find genetic resistance
Equisetum spp. (horsetail); Toxic Principles, animals affected, clinical signs, treatment
TOXIC PRINCIPLE:
- Thiaminase
- all parts of plant, fresh or dry.
ANIMALS AFFECTED:
- Primarily horses
- need to eat a lot
- usually contaminated hay.
CLINICAL SIGNS:
- Polioencephalomalacia-like.
- Acute weakness, weight loss despite good appetite, hind
limb ataxia, prostration, paralysis, convulsions
- death in 1-10 days.
- no lesions in the brain
TREATMENT:
- Thiamine hydrochloride.
- Favorable prognosis if not recumbent
Xanthium (cocklebur); Toxic Principles, animals affected, clinical signs, lesions
TOXIC PRINCIPLE:
- toxin found in seeds
- distributed in palatable dicotyledons
- Poisonings occur in spring if grazing
- need to eat a lot
ANIMALS AFFECTED
- any grazer
CLINICAL SIGNS:
- 12 hours - 2 days:
- anorexia, weakness, lethargy, nausea, vomiting,
dyspnea, spasmodic muscle contractions, recumbency, convulsions, and death.
- Targets the LIVER, kidney, GIT, and nervous system.
PATHOLOGIC LESIONS:
- Ascites,
- mottling of liver and kidney,
- GIT inflammation
- Acute centrilobular necrosis
- renal degeneration and necrosis
- neuronal degeneration and necrosis in swine only.
Senecio, tansy ragwort, hound’s-tongue; Toxic Principles, animals affected, clinical signs, lesions
TOXIC PRINCIPLES:
- pyrrolizidine alkaloids
- need to eat A LOT chronically
- Grazed in pastures or contaminated hay.
- Can contaminate milk, honey, eggs, and pollen products. - DHPA pyrroles may persist in tissues for year
ANIMALS AFFECTED:
- Cattle, horses, pigs, poultry.
- Sheep and goats are relatively resistant (alpacas/llamas).
CLINICAL SIGNS:
- hepatic insufficiency / encephalopathy
- loss of condition, weight loss, weakness
- secondary photosensitivity
PATHOLOGIC LESIONS:
- Liver - enlarged or small
- Centrilobular necrosis, bile duct proliferation and
portal fibrosis, fibrosis around the central veins
- HEPATOCYTOMEGALY
- Can test for presence of pyrroles in liver and blood
alsike clover & red clover; animals affected, clinical signs, lesions
ANIMALS AFFECTED
- Horses.
- Slobbering disease can be seen in any animal.
CLINICAL SIGNS:
- acute or chronic hepatic insufficiency or acute hepatic encephalopathy.
- secondary photosensitivity
- contact dermatitis
- Onset of signs 7-30 days
PATHOLOGIC LESIONS:
- Hepatomegaly
- Perilobular fibrosis, bile duct proliferation
- may even see megalocytosis
sago palm; Toxic Principles, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLES:
- All parts of the plant are toxic
- seeds and nuts contain high amounts of cycasin
CLINICAL SIGNS:
- 15 minutes to several hours:
- mainly GI
- anorexia, hypersalivation, vomiting, diarrhea
- hepatic 2-3 days later
- increased liver enzymes, hepatic encephalopathy
- nervous system
- weakness, ataxia, seizures, tremors
ANIMALS AFFECTED
- dogs
PATHOLOGIC LESIONS:
- Focal centrilobular and midzonal coagulation necrosis
- fibrosis if chronic.
TREATMENT:
ASYMPTOMATIC
- decontaminate; emetic, multiple doses of AC, cathartic, anti-emetics
- CBC, chemistry panel, UA.
- Liver protectants.
SYMPTOMATIC:
- CBC, chemistry panel, UA, coagulation times, bile acids
- control vomiting w/ anti-emetics and/or pro-kinetics
- GI protectants
- liver protectants (SAMe, milk thistle, ursodiol)
Ranunculus (buttercup); Toxic Principles, animals affected, clinical signs
TOXIC PRINCIPLE
- Ranunculin converted to a GI irritant, protoanemonin
- only fresh plant is toxic
- Toxin in entire plant
- large amounts needed to be ingested.
- Rare; buttercups are unpalatable.
ANIMALS AFFECTED:
- All livestock
- especially sheep
CLINICAL SIGNS:
- SHEEP: diarrhea, muscle weakness, difficulty breathing, death
- Excessive salivation, GI irritation, abdominal pain, Ds
Hedera helix (English ivy); Toxic Principles, clinical signs
TOXIC PRINCIPLE:
- All parts toxic, especially the berries.
CLINICAL SIGNS:
- GI
- Excessive salivation, vomiting, diarrhea.
- Fatalities rare.
Bulbs; Toxic Principles, mech of action, animals affected, clinical signs, treatment
TOXIC PRINCIPLES
- All parts of the plant (mostly bulbs)
MECHANISM OF ACTION:
- contact irritants,
- allergens,
- centrally acting emetics
- inhibitors of protein synthesis.
ANIMALS AFFECTED
- dogs and cats
CLINICAL SIGNS:
- oral irritation, vomiting with mild gastroenteritis.
TREATMENT
- anti-emetics, AC, fluids
- cardiovascular monitoring,
- GI protectants in severe exposures only
Solanum spp. (nightshade, potato, tomato); Toxic Principles, animals affected, clinical signs, prevention
TOXIC PRINCIPLES
- Leaves and green fruit toxic
- ripe fruit is toxic on silver leaf nightshade,
ANIMALS AFFECTED:
- All animals affected.
CLINICAL SIGNS:
- GI signs
- high enough dose -> neuro signs
- excessive salivation, anorexia, vomiting/regurgitation, diarrhea, abdominal pain, lethargy,
- muscle weakness, paresis/paralysis, ataxia,
- mydriasis,
- dyspnea, bradycardia, rapid weak pulse,
- coma, and death.
PREVENTION
- Keep percent of diet to less than 5% for horses
- less than 10% for cattle and other ruminants
Insoluble calcium oxalate-containing plants (many house plants); Toxic Principles, clinical signs, treatment
TOXIC PRINCIPLE:
- Insoluble calcium oxalates crystals *irritate GIT mucosa.
- trigger release of kinins and histamines
CLINICAL SIGNS:
- mild to moderate gastroenteritis
- Excessive salivation, head shaking, pawing at the mouth, oral irritation, swelling of pharynx and tongue,
- dyspnea,
- vomiting, diarrhea.
- Fatalities due to hypoxia. (uncommon)
TREATMENT:
- Symptomatic,
SEVERE
- antihistamines, rinse mouth, fluids, oral ice chips,
- dilute with milk or yogurt,
- anti-emetics, GI protectants
Ricinus communis (castor bean); Toxic Principles, clinical signs, lesions, treatment
TOXIC PRINCIPLE:
- Ricin
- All parts of the plant
- present in the seeds at the highest concentration
- One seed potentially is toxic to an average size dog
- Ricin is a biological warfare agent
- If inhaled, causes acute pulmonary pathology
CLINICAL SIGNS:
- 12 to 48 hours
- initially see a lot of *GI distress
- abdominal pain, excessive salivation, lethargy, weakness, trembling, hemorrhagic diarrhea, vomiting
- High dose = multisystemic problems:
- hypotension, muscle twitching, dyspnea, convulsions, coma, and death.
LESIONS:
- Gastroenteritis
- myocardial, hepatic, and renal necrosis.
TREATMENT:
- Symptomatic.
Vicia villosa (hairy vetch); animals affected, clinical signs, lesions
ANIMALS AFFECTED:
- Most reported in poultry, cattle, and horses.
CLINICAL SIGNS:
NEUROLOGIC
- ingestion of seeds
- growth depression and death in poultry
- bellowing, seizures, and acute death in cattle.
CUTANEOVISCERAL (most common)
- reported in cattle and horses
- foliage that has been grazed for several weeks
- abrupt onset of rapidly progressing dermatitis, pruritis, hair loss
- diminished appetite and weight loss due to similar lesions
- hypothesized immunologic Type IV hypersensitivity
PATHOLOGIC LESIONS:
- Affects eyes, GI, adrenal glands, heart, kidney, liver, spleen, lymph nodes and thymus
- Dermatitis, conjunctivitis, multiple granulomatous lesions - Monocytic, lymphocytic, plasmacytic, eosinophilic infiltrate with multinucleated giant cells.
Juglans nigra (black walnut) and Berteroa incana (hoary alyssum); animals affected, clinical signs, treatment
ANIMALS AFFECTED:
- Primarily equine.
- dogs
CLINICAL SIGNS:
- 24 hours
- lethargy, limb edema, laminitis, and fever;
- In dogs GI and neurologic or musculoskeletal
TREATMENT:
- Symptomatic and supportive.
Cyanogenic glycoside-containing plants (choke cherry); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment
TOXIC PRINCIPLE:
- Cyanogenic glycoside
- all parts of plant,
MECHANISM OF ACTION:
- Cyanide rapidly absorbed and reacts with ferric ion of
cytochrome oxidase
- inhibits electron transport and cellular respiration.
- Blood is fully oxygenated but cannot be utilized by cells.
ANIMALS AFFECTED:
- All animals susceptible.
CLINICAL SIGNS:
- Excessive salivation,
- hyperpnea and dyspnea,
- weakness, muscle fasciculations, convulsions
- tachycardia,
- death from cellular hypoxia.
- Blood is bright, cherry red (rarely observed clinically).
PATHOLOGIC LESIONS:
- Bright red mucous membranes
- bitter almond odor to GI contents.
TREATMENT:
- Symptomatic and supportive.
- Cyanokit contains hydroxocobalamin that binds cyanide and allows it to be eliminated harmlessly via the urine.
Hypochaeris radicata (flatweed); what condition can it cause
can cause Stringhalt
Plants affecting resp. system; plants, mech of action, diagnosis
PLANTS
- moldy sweet potatoes
- Perilla mint
- mustards
- Astragalus spp
MECH OF ACTION
- fog fever:
- forages/lush green in early spring
- tryptophan gets converted to 3-methylindole in rumen;
- moldy sweet potatoes producing 4-ipomeanol
DIAGNOSIS
can test urine, kidney, lungs, chest fluid
Humulus lupulus or hops; Toxic Principles, animals affected, clinical signs, treatment
TOXIC PRINCIPLE
- fresh/spent/processed hops
SPECIES
- dogs
CLINICAL SIGNS
- Persistent hyperthermia
- tachycardia, dyspnea, weakness, panting, has only been reported in
- need to get into clinic w/in 3-6hrs
TREATMENT
- decontamination
- IV fluids,
- cooling measures
- dantrolene or cyproheptadine.
