Lupine AKA blue bonnets mech and species/ target organ
Highest during early growth of the plant (Spring)
* Toxicity: 0.25-1.5% BW in sheep
- Targets: CNS, fetus
- Mechanism:
- Acute: agonists of nAChR and mAChr
- Sheep»_space; horses, cattle
- Teratogenic: inhibition of fetal movement
lupine clinical features
- Acute lupinosis – within minutes to hours post-ingestion
- Cholinergic toxidrome**
- Anorexia, depression, reluctance to move, nervousness/agitation
- Hypersalivation/frothing, prolapsed third eyelid
- Urination, defecation
- Ataxia, weakness
- Muscle twitching progressing to seizures with extensor rigidity
- Dyspnea
- Collapse
- Coma, death
lupine management and diagnosis
Antidote: atropine
* Symptomatic and supportive care: seizure control
* Remove from pasture
* Diagnosis: animals grazing pastures with lupine present, plant in rumen/stomach contents
* Detection of lupine alkaloids in stomach contents, blood
-no PM lesions
prognosis: varies by severity of ingestion
death camas mech and tox/ target organ
-appears in early spring, resembles wild onion
* Toxins: cevanine alkaloids
* Toxicity: all parts of plant toxic
- Mechanism: altered membrane potential of electrically excitable cells → prolonged opening
- Target organs: CNS, heart
- Species differences: sheep and goats( due to low grazing) > cattle > other species
- 500 grams of plant can kill an adult sheep
death camas clinical features
-animals often found dead
Onset: within hours of ingestion
* GI: frothy hypersalivation, anorexia, vomiting and retching, colic, bruxism
* Frequent urination and defecation
* CV: bradycardia, hypotension
* CNS: tremors, ataxia (hindlimbs > forelimbs), staggering, severe depression, profound weakness
* Abnormal posture: low head, drooped ears, arched back
* Progresses to tachycardia, respiratory distress, cyanosis, recumbency, terminal convulsions, coma
* Death within 12-72 hours
* PM: severe pulmonary congestion and edema, thoracic SC hemorrhage
death camas - management and diagnosis
- No antidote - supportive care only
- IVFT, antiarrhythmics, atropine for bradycardia, sympathomimetics for hypotension
- Diagnosis: found dead on pasture with death camas present, identification of plant in rumen/stomach contents
- Detection of zygadenine in rumen contents, serum (send-out)
- DDx: cyanobacterial toxins, lead, nitrate, cyanide, other cardiotoxic plants (oleander)
- Prognosis: poor → animals often found dead
- If animal survives >24 hours, likely to survive
locoweed species/ parts of plant toxic
- Oxytropis spp., Astragalus sp group of plants
- Species sensitivity: horses > cattle, sheep
- All growth stages and parts of plant are toxic + dangerous year-round
- Palatable in spring and fall, and as dried stalks in winter
- Found on/in mountains, foothills, plains, semi-arid desert regions, marginal soils
- Herbicides are ineffective to control locoweeds
locoweed mechanism + toxicity and target organs
- Toxin: swainsonin
- Toxicity: 0.3 mg/kg BW in horses
- Target organs: CNS, kidneys, liver, heart, fetus*
- Mechanism: similar structure to mannose → competitive inhibition of a-mannosidase and mannosidase II in lysosomes and Golgi bodies → mannosidosis
- Intracellular accumulation of oligosaccharides in lysosomes → vacuolation of cells **(characteristic)
- Especially: neurons
loco weed clinical LOCOISM
Onset: chronic → a few weeks to months of grazing
* Chronic wasting disease with CNS depression
* Anorexia, weight loss, dull/harsh haircoat, unthrifty
* Behaviour + temperament changes: depression, nervousness, reluctance to move
* CNS/neuromuscular: proprioceptive deficits, staggering gait, abnormal posture, intention tremors
* Inability to blink → dull-eyed appearance
* Repro issues: polycystic ovaries
* Death due to emaciation or misadventure
clin path of locoweed
- Clinical pathology
- Hypoproteinemia (hypoalbuminemia)
- Decreased T3, T4
- Elevated AST, LDH
- Vacuolated cytoplasm of lymphocytes
- PM: non-specific gross lesions; adipose atrophy (cachexia)
- Histo: cytoplasmic vacuolation** of neurons and viscera
Teratogenic: abortions, arthrogryposis, small/weak neonates
* Reproductive: reduced fertility, decreased libido
locoweed management and diagnosis
- No specific antidote
- Remove from pasture
- Supportive care
- Full neurological recovery is unlikely with chronic poisoning
- Permanent neuron loss
- Diagnosis: affected animals in pasture with locoweed
- Confirmatory: detection of swainsonine in serum, urine
-characteristic histo vacules of neurons
loco weed DDx and prognosis
- DDx: progressive onset of neurologic signs → yellow star thistle, horsetail/bracken fern (horses),
hepatic encephalopathy
Prognosis: early in poisoning → fair for survival
* Visceral vacuolation can be reversible, but neuronal changes can be permanent
* Severe neurologic impairment: poor
horsestail= species, target and toxicity
-Equisetum spp
-Dstribution: throughout North America
* Moist, sandy/gravely soils: sandbars, ditches, streams, ponds
- Species affected: horses
- Horses do not typically eat horsetail unless other feed is not available
- Toxic principle: thiaminase decreasing thiamine
- Target organ: CNS
- Toxicity: consumption of hay with >20% horsetail for 3-4 week
horsetail clinical features
- Following >2-3 weeks of ingestion
- Gradual onset of CNS and wasting disease
- Unthriftiness, lethargy, depression, anorexia,
weight loss, mild ataxia, diarrhea - Look “scruffy”
- Progresses to generalized ataxia, cardiac
arrythmias, blindness
-death due to exhastion
horsetail management and diagnosis/ ddx
Antidote: thiamine
* 500 mg to 1 g per day IV
* The earlier the better
* Supportive care – high quality feed
* Diagnosis: presence of horsetail on/near pastures, in bales and positive to therapy
- DDx – toxic plants: yellow star thistle, locoweed, bracken fern
- Prevention: prevent access, ensure adequate forage available
brakcken fern toxin/ plant parts/ target
- Toxin: ptalquiloside (cattle), thiaminase (horses)
- All plant parts are toxic
- Mechanism of action and targets
- Cattle: carcinogenicity and bone marrow
suppression (bone marrow)* - Horses: thiaminase (CNS)*
- Cumulative toxicity
- Eliminated in urine and milk
bracken fern clinical features
- “Bracken Staggers”
- Following consumption for >30 days
- 20-25% of diet for 3 weeks can induce this syndrome
- Clinically indistinguishable from horsetail poisoning
- Most common sign: incoordination
- Progressive CNS signs: weakness, depression, ataxia-> recumbency
Terminal stages: opisthotonos, clonic seizures with tachycardia
bracken fern management and diagnosis
- Management: Antidote: thiamine
- 500 mg to 1 g per day IV
- The earlier the better
- Supportive care – high quality feed
- Diagnosis
- Plant identification – evidence of grazing, lack of other feed
- No send-out test
- Prognosis: good if poisoning identified early and
thiamine therapy is started early - Poor with severe neuro signs
selenium
Essential trace mineral: antioxidant (glutathione peroxidase), immune function, thyroid hormone synthesis
- Deficiency in livestock»_space; poisoning
- Exposure scenarios:
- Grazing pastures with selenium accumulating plants
- Iatrogenic over-supplementation (parenteral or dietary)
selenium accumulating plants
Se hyperaccumulators : Astragulus (milkvetch)
faculative Se accumulators: brassica spp
selenium mech and target organ
- Target organs: heart (acute), keratinized tissues (chronic), spinal cord (pigs, acute and chronic)
- Mechanism of action:
- Acute: oxidative injury via glutathione depletion + generation of reactive oxygen species → acute myocardial necrosis
selenium clinical features
- Acute selenosis
- Most common: over-supplementation or overdose of parenteral supplement
Sudden death possible; livestock found dead - Onset: within hours of exposure to a few days
- Lethargy, anorexia
- GI: diarrhea (watery, dark), abdominal pain
- Cardiorespiratory: dyspnea, tachypnea, tachycardia, weak and
rapid pulse - Weak and wobbly gait, depression, head down, drooped ears
- Tetany, death within 72 hours
chronic selenium toxicosis
- “Alkali disease” or “bob tail disease:
- Consumption of high selenium forage or over- supplementation in diet over weeks to months
- Dystrophic keratinization: in horses, cattle, pigs
- Hair loss, hair fragility, unthrifty
- Claw deformities, circumferential hoof cracks, swelling of coronary band → lameness
- Liver damage, emaciation
- Development of heart failure: brisket edema, jugular pulse
selenium clinical features in pigs
- Pigs: poliomyelomalacia
- Acute: ascending paralysis progressing (hindlimbs > forelimbs)
progressing to all limbs affected, death - Pigs are BAR and willing to eat
- Chronic: skin changes and progressive hindlimb proprioceptive deficits
- Swelling at coronary band region, claw deformity
- PM: yellow-brown bilateral malacic regions of cervical and lumbar intumesences
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midterm87
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management of the poisoned animal75
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teratology28
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insecticides, herbicides, millusicides26
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drugs60
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plants60
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range plants40
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poisoned mushrooms9
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toxic food products19
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lead and copper20
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arsenic and mercury15
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iron, zinc, mg, mn20
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salt and sulfer10
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mycotoxins22
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venomous and poisonous animals16
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household hazards15
