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TOXICOLOGY 2 > 19/20 - Toxic Range Plants II > Flashcards

19/20 - Toxic Range Plants II Flashcards

1
Q

Lupine

A
  • Toxicity: highest during early growth of plant (Spring)
  • Sheep is most toxic (but not only ones)
  • *Targets: CNS, fetus
  • Mechanism: agonists of nAChR and mAChr
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2
Q

Lupine: clinical features

A
  • **cholinergic toxidrome
  • Anorexia, depression, reluctance to move
  • Hypersalivation/frothing, prolapsed third eyelid
  • Urination, defecation
  • Ataxia, weakness
  • Muscle twitching
  • Dyspnea
  • Collapse
  • Coma
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3
Q

Lupine: management

A
  • *antidote: ATROPINE
  • Symptomatic and supportive care
  • Remove from pasture
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4
Q

Lupine: diagnosis

A
  • Animals grazing pastures with lupine present
  • Plant in rumen/stomach contents
  • No specific PM/histo lesions
  • *prognosis: varies by severity of intoxication
    o Full recover is possible
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5
Q

Death camas

A
  • Mountain foothill rangelands, pastures and meadows
  • Appears early in spring when other forages are sparse
  • Resembles wild onion
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6
Q

Death camas: toxicity, mechanism and target

A
  • *all parts of plants
  • Mechanism: alter membrane potential of electrically excitable cells
  • **Target organs: CNS, heart
  • *sheeps and goats > cattle > other species
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7
Q

Death camas: clinical features

A
  • Often found dead
  • Onset: within hours
    o GI: frothy hypersalivation, anorexia, vomiting
    o Frequent urination and defecation
    o CV
    o CNS tremors
    o Progresses to tachycardia, respiratory distress, cyanosis, coma (death within 12-72hrs)
  • PM: sever pulmonary congestion and edema, thoracic SC hemorrhage
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8
Q

Death camas: management

A
  • No antidote: supportive care only
  • IVFT, antiarrhythmics
  • Low stress handling
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9
Q

Death camas: diagnosis

A
  • Found dead on pasture with death camas present
  • ID plant in rumen/stomach contents
  • *prognosis: poor=animals often found dead
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10
Q

Locoweed

A
  • Major group of poisonous plants in USA (also found in Canada)
  • *species sensitivity: HORSES > cattle, sheep
  • All growth stages and parts of plant are toxic and dangerous year round
  • Found on/in mountains, foothills, plains, semi-arid dessert
  • Herbicides are INEFFECTIVE to control
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11
Q

Locoweed: toxin, target organs, mechanism

A
  • Toxin: SWAINSONINE
  • Target organs: CNS, KIDNEYS, LIVER, HEART, FETUS
  • Mechanism: get mannosidosis=intracellular accumulation of oligosaccharides in lysosomes=VACUOLATION OF CELLS (especially NEURONS)
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12
Q

Locoism

A
  • CHRONIC
  • *Chronic wasting disease with CNS depression
  • Reproduction issues
  • Death due to emaciation or misadventure
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13
Q

Locoism: histo

A
  • CYTOPLASMIC VACUOLATION of neurons and viscera
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14
Q

Locoweed: management

A
  • NO specific antidote
  • Remove from pasture
  • Supportive care
  • Fully neurological recover is UNLIKELY with chronic poisoning
    o Permanent neuron loss
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15
Q

Locoweed: diagnosis

A
  • Affected animals on pasture with locoweed
  • Confirmation: detection of swainsonine in serum, urine, milk
    o Short half-life
  • Decreased alpha-mannosidase activity (not widely available)
  • *Characteristic histologic lesions
  • Prognosis: early in poisoning=fair for survival
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16
Q

Locoweed: differentials

A
  • Yellow start thistle
  • Horsetail/bracken fern (horses)
  • Hepatic encephalopathy
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17
Q

Horsetail

A
  • Throughout NA
  • HORSES (only eat if no other feed is available)
  • Toxic principles: THIAMINASE
    o Target organ: CNS
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18
Q

Horsetail clinical features

A
  • Following >2-3 weeks of ingestion
  • Gradual onset of CNS and wasting disease
  • Lethargy, depression, anorexia, weight loss
  • Progresses to generalized ataxia, cardiac arrythmias, blindness, muscle tremors, convulsions
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19
Q

Horse tail: management

A
  • Antidotes: THIAMINE (need to be given early)
  • Supportive care
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20
Q

Horse tail: diagnosis

A
  • Presence of horsetail on/near pastures OR in bales
    o No send out test
    o Positive response to therapy
    o No specific PM lesions
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21
Q

Horse tail: prevention

A
  • Prevent access
  • Ensure adequate forage available
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22
Q

Bracken fern: toxicity and mechanism (horse)

A
  • Throughout NA
  • Entire plant is toxic
  • **Mechanism:
    o Cattle: carcinogenicity and bone marrow suppression (bone marrow)
    o Horse: thiaminase (CNS)
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23
Q

Bracken fern: clinical features (horse)

A
  • “bracken staggers”
  • Following consumption for >30days
  • Clinically indistinguishable from horsetail poisoning
  • Most common sign: incoordination
  • Progressive CNS signs
  • Terminal stages: opisthotonos, clonic seizures with tachycardia
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24
Q

Bracken fern: management and diagnosis (horse)

A
  • Management: same as horsetail
  • Diagnosis:
    o Plant ID
    o No send-out test
  • *prognosis: good if poisoning IDed early and thiamine therapy is started early
    o Poor with severe neuro signs
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25
Selenium
- Essential trace mineral antioxidant - Content in soil is variable - Deficiency in livestock >> poisoning - Exposure o Grazing pastures with selenium accumulating plants o Iatrogenic over-supplementation
26
What are the 3 broad categories of selenium accumulating plants?
1. Se hyperaccumulators a. *Astragalus (milkvetch) 2. Facultative Se accumulators a. *Brassica spp. 3. Passive Se accumulators
27
Selenium: toxicity and target organs
- Target organs: HEART (acute), KERATINIZED TISSUES (chronic), SPINAL CORD (pigs, acute, chronic) - Pigs a bit more susceptible
28
Selenium: clinical features
- ACUTE SELENOSIS o Sudden death possible, livestock found dead - Onset: within hrs to a few days - Lethargy - GI - Cardiorespiratory - Weak and wobbly gait - Tetany, death
29
Selenium: clin path, gross pathology, histopath
- Evidence of muscle damage - Gross: myocardial necrosis, pulmonary hemorrhage - Histo: focal myocardial necrosis - *surviving animals may develop myocardial fibrosis and subsequent heart failure - Lesions similar to selenium/vit E deficiency (“white muscle disease”)
30
Chronic selenium toxicosis
- *’alkali disease’ or ‘bob tail disease’ - DYSTROPHIC KERATINIZATION in horses, cattle, pigs o Hair loss, hair fragility, unthrifty o Claw deformities, circumferential hoof cracks - Liver damage, emaciation - Development of heart failure: brisket edema, jugular pulse
31
Selenium clinical features: pigs
- *POLIOMYELOMALACIA - Acute: ASCENDING PARALYSIS progressing to all limbs affected, death - Chronic: skin changes and progressive hindlimb proprioceptive deficits - PM: yellow-brown bilater malacic regions of cervical and lumbar intumescences - Histo: motor neuron necrosis, microcavitation, melin vacuolation
32
Selenium: management
- Acute: no specific antidotes, CV supportive care - Chronic: remove from pasture, provide high quality diet, supportive care for hoof changes - Selenium is SLOWLY excreted
33
Selenium: diagnosis
- Supported by presence of selenium-accumulating on pasture o Selenium content of forages o Acute: liver Se, ID plants o Chronic: clinical signs and whole blood Se - *prognosis: poor for acute, guarded for chronic
34
Selenium: differentials
- Acute myocardial necrosis: ionophores, cardiotoxic plants o Nutritional deficiencies - Acute polioencephalomalacia: botulism, salt poisoning - Chronic: gangrenous ergotis o Mineral and vitamin deficiencies
35
Sweet clover
- Cattle > sheep >> horses - Mycotoxin: DICOUMAROL o Target: BLOOD o Inhibition of vit K epoxide reductase=depletion of clotting factors “1972” (same as anticoagulant rodenticides)
36
Moldy sweet clover: course of disease and how might it present?
- Weeks of consuming contaminated hay or silage - 24-48hrs: once depleted=acute course of disease o Pale MM, weakness o Melena o Prolong hemorrhage following castration or dehorning o Large hematomas o Bleeding into brain, joints, pericardium, etc. - **young calves can be severely affected with normal dams o Excretion in milk - Increased PT and PTT, decreased PCV - PM: extensive hemorrhage, pale carcass
37
Sweet clover: management
- *antidote: oral or injectable VITAMIN K1 for multiple weeks - Remove suspected feed - Low stress handling - Blood transfusion may be required
38
Sweet clover: diagnosis
- Bleeding outbreak in cattle herd (ex. massive hemorrhage from minor trauma)
39
Sweet clover : DDx
- Bracken fern - Anticoagulant rodenticides - Trichothecene mycotoxins - Liver failure
40
Sweet clover: prognosis
- Generally poor with significant bleeding/blood loss
41
Bracken fern: ptalquiloside (cattle)
- **Mechanism: o Cattle: carcinogenicity and bone marrow suppression (bone marrow) o Horse: thiaminase (CNS) - Cumulative toxicity - Eliminated in urine and milk
42
*Bracken fern: clinical features (cattle): ACUTE BRACKEN FERN POISONING
o Dull, listless, decreased appetite o Increased RR o Petechial hemorrhages o Bleeding: internal and external o Sudden death possible - PM: hemorrhage, pallor throughout carcass - *primary hemostatic disorder: petechial hemorrhages - PANCYTOPENIA
43
*Bracken fern: clinical features (cattle): BOVINE ENZOOTIC HEMATURIA
- following months of ingestion in cattle 3-4 years old - bladder tumours that bleed readily: intermittent hematuria - straining, chronic weight loss - anemia possible - UA: proteinuria, RBCs, WBCs
44
Bracken fern (cattle): management
- Acute: no specific treatment or antidote (blood transfusion, supportive care) - Bovine enzootic hematuria: no antidote - (horse: bracken staggers: thiamine)
45
Bracken fern (cattle): diagnosis
- Acute: clinical signs, clin path, plant parts in rumen - Bovine enzootic hematuria: bladder ultrasound, inflammatory CBC/chem/UA o PM: thickened bladder wall with proliferative lesions, desquamated regions of mucosa - (bracken staggers: response to thiamine)
46
What are some nephrotoxic range plants?
- Plants containing soluble oxalates - Oak
47
Soluble oxalates
- Sodium and potassium salts of OXALIC ACID o Common in plants (rhubarb, dock, shamrock – ‘deserts’) o Highest in leaves o Become more toxic as growing season progresses - *mostly a livestock problem (due to lack of other feed)
48
Soluble oxalates: toxicity and mechanism
- Consumption of plants >10% soluble oxalates induces renal damage - High oxalic acid ingestion=binds and sequesters calcium and magnesium o Hypocalcemia o Formation of calcium oxalate=deposition of crystals in renal tubules
49
Soluble oxalates: clinical features
- Acute poisoning: due to consumption of large quantity - Onset: several hours - *hypocalcaemia: weakness, muscle tremors (resembles milk fever, can die) - If animal survive early phase: develop acute renal failure - UA: calcium oxalate monohydrate crystals - PM: pale, swollen kidneys, rumenitis, serosal hemorrhages and edema
50
Soluble oxalates: characteristic histopathology
- **calcium oxalate crystals in renal tubules
51
Soluble oxalates: ‘bighead’ in horses
- Nutritional secondary hyperparathyroidism o Long term hypocalcaemia o Can also be related to abnormal Ca:P in feed o Osteopenia, secondary fractures o Weakness, stiffness, lameness, weight loss o **Bony changes: fibrous osteodystrophy
52
Soluble oxalates: management
- Correct hypocalcemia: IV calcium followed with oral calcium o Does NOT prevent renal failure development - Removal from pasture - Symptomatic and supportive care: fluids
53
Soluble oxalates: diagnosis
- ID of oxalate containing plants - Hypocalcemia - CaOx crystals in urine or in kidney - Send out test for feed
54
Soluble oxalates: prognosis
- good for hypocalcemia that responds to treatment - poor for acute renal failure - cannot predict if an animal will develop renal failure
55
Oak
- horses and ruminants - toxicity follows consumption of oak forage for more than 2 days o all parts (but usually just the parts they can easily munch on) o lack of alternative feed or acorns fallen from a storm - toxic principles: tannin metabolites o **target organs: KIDNEYS, GIT o Exact mechanism of renal damage is unknow
56
Oak: clinical features
- Anorexia, remen stasis, constipation - Lethargy, weakness, depression, recumbency - PU/PD, dehydration - Bloody diarrhea, colic signs - Ventral edema - Death within days to weeks - Tannins excreted in milk: calves affected before cows
57
Oak: gross pathology
- Perirenal edema - Swollen and pale or dark kidneys - Pinpoint hemorrhages on capsule - Ulcerative hemorrhagic gastroenteritis - Histo: acute tubular degeneration, necrosis, and intratubular hemorrhage
58
Oak: management
- No specific antidote - Symptomatic and supportive care o Fluids to correct severe dehydration and maintain normal acid/base and electrolyte status
59
Oak: diagnosis
- Oak on/near pasture where livestock grazing - Acorns and other plant parts in rumen or stomach contents - GC-MS (send out test) - *prognosis: guarded to grave
60
DDx for acute renal failure
- NSAIDs - Vitamin D - Ethylene glycol/soluble oxalates
61
What are some teratogenic and abortifacient plants?
- Poison hemlock - Corn lily - Lupine - Ponderosa pine
62
Poison hemlock
- Low exposure during first trimester - Mechanism: inhibits fetal movement (neurotoxic) - *clinical features: ARTHROGRYPOSIS, torticollis, scoliosis, cleft palate
63
California false hellebore/corn lily
- Species: SHEEP - Alters craniofacial development - *infestion on day 14 of gestation=CYCLOPIA in offspring o “monkey faced lamb disease” - Management: affected lambs typically euthanized due to welfare concerns, remove ewes from pasture
64
Lupine
- Teratogenic: ingestion in first trimester - Mechanism: inhibition of fetal movement via desensitization of the nAChR - *”crooked calf disease” o Arthrogryposis, torticollis, cleft palate o Abortion, still births, weak offspring
65
Ponderosa pine
- ‘pine needle abortion’ - Species: cattle and bison - Exposure: inadequate forage (usually during winter) - Mechanism: decreases uterine blood flow=fetal stress=premature parturition
66
Ponderosa pine: clinical features
- Can happen as little as one day after consumption - THIRD TRIMESTER ABORTIONS - Retained fetal membranes, metritis - Dull and depressed
67
Ponderosa pine: management and prognosis
- Supportive care toe weak calves - Prognosis: good for fertility o Weak calves: survival depends on maturity at birth
68
Ponderosa pine: diagnosis
- History of inclement weather associated with abortions - Limited access to forage - Poor forage quality - *multiple cattle aborting - *evidence of pine trees having needles stripped by cattle - *detection of ICA metabolites

TOXICOLOGY 2 (13 decks)

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