Plant Cards Flashcards

1
Q

Nerium oleander (oleander): Toxic Principles, animals affected, clinical signs, lesions, treatment

A

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
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2
Q

Digitalis spp. (foxglove) Toxic Principles, animals affected, clinical signs, lesions, treatment

A

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
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3
Q

Asclepias spp. (milkweed) Toxic Principles, animals affected, clinical signs, treatment

A

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

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4
Q

Rhododendron and Pieris japonica (rhododendron, Japanese pieris): Toxic Principles, clinical signs, treatment

A

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
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5
Q

Yew Toxic Principles, clinical signs, treatment

A

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
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6
Q

Ziganedus (death camas): Toxic Principles, mech of action, clinical signs, treatment

A

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
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7
Q

Veratrum (False hellebores): Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment

A

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
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8
Q

Persea (avocado): Toxic Principles, animals affected, clinical signs, lesions,

A

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
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9
Q

Kalanchoe; Toxic Principles, clinical signs, treatment

A

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
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10
Q

Hypericum perforatum (St. John’s Wart); Toxic Principles, animals affected, lesions, treatment

A

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
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11
Q

Allium; Toxic Principles, animals affected, clinical signs, treatment

A

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
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12
Q

Acer (maple); Toxic Principles, mech of action, animals affected, clinical signs, treatment

A

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
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13
Q

Cruciferae family (mustard); Toxic Principles, mech of action, animals affected

A

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.

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14
Q

Melilotus (sweet clover); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment

A

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

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15
Q

bracken fern; Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment

A

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
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16
Q

Pinus spp. (pine); Toxic Principles, mech of action, animals affected, diagnosis

A

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.

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17
Q

Medicago (alfalfa); Toxic Principles, mech of action, animals affected

A

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.
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18
Q

Halogeton glomeratus (halogeton) / Oxalis spp. (shamrock); Toxic Principles, animals affected, clinical signs, lesions, treatment

A

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.
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19
Q

Quercus spp. (oak); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment

A

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.
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20
Q

Amaranthus spp. (pigweed) ; Toxic Principles, clinical signs, lesions, treatment

A

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)
21
Q

Lilium spp. and Hemerocallus spp; Toxic Principles, animals affected, clinical signs, lesions, treatment

A

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

22
Q

Dicentra spp. (Dutchman’s breeches, bleeding-heart); Toxic Principles, mech of action, clinical signs, lesions, treatment

A

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.

23
Q

water hemlock; Toxic Principles, mech of action, animals affected, clinical signs, diagnosis, treatment

A

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.

24
Q

yellow starthistle & Russian knapweed; Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment

A

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.
25
Q

Astragalus spp. and Oxytropis spp. (locoweed); Toxic Principles, mech of action, animals affected, clinical signs, lesions

A
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
26
Q

Ipomoea spp. (morning glory); Toxic Principles, animals affected, clinical signs, treatment

A

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.
27
Q

Cannabis sativa (marijuana); Toxic Principles, clinical signs, treatment

A

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
28
Q

Datura spp. (Jimson weed); Toxic Principles, animals affected, clinical signs, treatment

A

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)
29
Q

Lupinus spp. (lupine); Toxic Principles, mech of action, animals affected

A

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
30
Q

Conium maculatum (poison hemlock); Toxic Principles, mech of action, animals affected, clinical signs

A

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
31
Q

Delphinium spp. (larkspur); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment

A

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
32
Q

Equisetum spp. (horsetail); Toxic Principles, animals affected, clinical signs, treatment

A

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
33
Q

Xanthium (cocklebur); Toxic Principles, animals affected, clinical signs, lesions

A

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.
34
Q

Senecio, tansy ragwort, hound’s-tongue; Toxic Principles, animals affected, clinical signs, lesions

A

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

35
Q

alsike clover & red clover; animals affected, clinical signs, lesions

A

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
36
Q

sago palm; Toxic Principles, animals affected, clinical signs, lesions, treatment

A

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)

37
Q

Ranunculus (buttercup); Toxic Principles, animals affected, clinical signs

A

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
38
Q

Hedera helix (English ivy); Toxic Principles, clinical signs

A

TOXIC PRINCIPLE:
- All parts toxic, especially the berries.

CLINICAL SIGNS:

  • GI
  • Excessive salivation, vomiting, diarrhea.
  • Fatalities rare.
39
Q

Bulbs; Toxic Principles, mech of action, animals affected, clinical signs, treatment

A

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
40
Q

Solanum spp. (nightshade, potato, tomato); Toxic Principles, animals affected, clinical signs, prevention

A

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
41
Q

Insoluble calcium oxalate-containing plants (many house plants); Toxic Principles, clinical signs, treatment

A

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
42
Q

Ricinus communis (castor bean); Toxic Principles, clinical signs, lesions, treatment

A

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.

43
Q

Vicia villosa (hairy vetch); animals affected, clinical signs, lesions

A

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.
44
Q

Juglans nigra (black walnut) and Berteroa incana (hoary alyssum); animals affected, clinical signs, treatment

A

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.

45
Q

Cyanogenic glycoside-containing plants (choke cherry); Toxic Principles, mech of action, animals affected, clinical signs, lesions, treatment

A

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.
46
Q

Hypochaeris radicata (flatweed); what condition can it cause

A

can cause Stringhalt

47
Q

Plants affecting resp. system; plants, mech of action, diagnosis

A

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

48
Q

Humulus lupulus or hops; Toxic Principles, animals affected, clinical signs, treatment

A

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.