Plants - Sudden Death

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69 Terms

1
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Why/when do animals eat poisonous plants?

- Limited access to high-quality forage
- Contaminated hay
- Drought
- Seasonal accessibility
- Stress

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Prevention of plant poisoning

-identification/removal
-characterization
-grazing management

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Sudden death differential diagnosis

-infectious dz (anthrax)
-electrocution
-poisoning

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What are the plants causing sudden death?

-nitrate
-cyanide
-diterpenoid alkaloids
-cardiac glycosides
-legumes (rumen bloat)

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Levels elevated in

-rapidly growing
-young
-stalks/stems
-high moisture/early am
-fertilizers
-S/P/Mo deficiencies
-drought/herbicide

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Mechanism

Methemoglobin!

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Clinical signs

-drowsiness
-weakness
-tremors
-tachypnea/tachycardia
-brown mucosae >20%
-hypovic death >80%

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Diagnostics

-aqueous humor, <60hrs, 4-5ppm
-methemoglobin, <2hrs, >40%

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Toxicity forage

>1% dry forage
>0.2% aboriton

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Toxicity water

>1500ppm toxic
>200ppm abortion

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Treatment

Methylene blue IV

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Considerations for treatment

-180d withdrawl period
-horses may develop heinz body anemia

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Prevention

-adaptation
-increase carbs
-ensiling
-decrease monensin
-NOT reduced by drying/haying

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Plants

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Relative nitrate accumulation highest to lowest

-annual weeds
-corn
-sorghums
-cereal grains (oat hay)
-grasses
-legumes

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Levels elevated in

-new growth
-cool/moist
-seeds, leaves, barks, twigs
-drought, frost, wilting, chewing (PLANT STRESS)

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Mechanism

HCN binds iron and blocks cytochrome C = oxygen satyration of Hb = cellular anoxia

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What favors it?

-plant damage
-water
-pH6-7 (ruminants more at risk!)

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Diagnostics

-sudden death 1-2hrs
-cherry red venous blood
-pink mm, prolonged clotting
-generalized clotting/hemorrhage on necropsy

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Toxicity

2mg/kg, >200ppm

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Treatment

Sodium thiosulfate/sodium nitrate IV

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If unsure between cyanide and nitrate poisoning, what should you give as treatment?

Methylene blue

23
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Sudan grass poisoning

-CHRONIC
-urinary incontinence
-hindleg weakness
-may present as goiter

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Plants

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25
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Which plant are we most worried about?

Sorghum

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Which one is most toxic?

Tall larkspur

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What makes it more toxic?

-early growth
-more sun
-all parts of plant are toxic

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Mechanisms

-norditerpenoid alkaloids
-methyllycaconitine

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Differences in species

Cattle > horses > sheep > goats

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Age

Younger cattle may consume more and have reduced metabolism

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Sex

Heifers more susceptible than steers/bulls

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Breed

Dairy more susceptible

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Clinical signs

-sudden death 3-4hrs
-tachycardia
-weakness/staggering
-sternal then lateral recumbency
-death from NM paralysis/bloat
-no signigicant postmorten signs besides plant in rumen

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Treatment

-none proven
-place with head/chest uphill
-treat bloat
-Acetyl cholintesterase inhibitors (neostigmine)
-grazing management (mineral salt)

35
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MONKSHOOD

-hooded flower/woody stem
-all parts toxic
-similar to larkspur
-inhibits VG Na channels
-symptomatic/supportive care

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Toxin

Cicutoxin

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Mechanisms

Noncompetitive inhibitor of GABA A receptors

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Clinical signs

-sudden death 2-3 hrs
-violent convulsions 10-15min
-tongue biting/chewing
-bloat
-dilated pupils
-resp failure

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Pathological findings

-pale areas in heart/skeletal mm
-myofiber degeneration
-elevated LDH/AST/CK

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Treatment

-unlikely
-control seizures with diazepam

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Mechanism

Depolarize Na+ channels causing them to remain open = hypotension/cardiovascular collapse

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Toxicity

-5-60g green plant/kg
-0.6-0.7% body weight

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Treatment

2mg atropine and 8mg picrotoxin per 100lbs may be effective

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Toxicity

-taxine A/B
-horses > rabbits-pigs > cow-dog-sheep > goat
-.2-12 g leaves/kg
-2.3g/kg lethal dogs
-toxic when dry

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Clinical signs

-sudden death
-muscle trembling
-slow heart rate/arrythmias
-V/D/convulsions

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Treatment

None but can do rumenotomy, mineral oil, electrolytes, activated charcoal, IM atropine

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CARDIAC GLYCOSIDES

-fox glove
-lily of the valley
-milkweeds
-oleander
-yellow oleander
-avocado

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Mechanism

Block Na/K ATPase

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Clinical signs

-sudden death
-cardiac arrythmias/first and second degree heart block
-abd pain/D+

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Postmortem

-acute poisoning
-hemorrhage/congestion/edema/cellular degeneration
-multifocal myocardial degeneration

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Treatment

-induce emesis
-oral activated charcoal
-cathartic
-monitor serum K+, IVF
-anti-arrythmic drugs

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Fox glove toxin

Digitalins

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Lily of the valley

-convallerin
-exposure through yard waste

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Milkweeds

Exposure in hay, symptoms 8-10hrs

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Oleander

0.005% BW LD, oleandrun/neriin

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Yellow oleander

-thevitin
-concentrated in fruit

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Avocado

-persin (inhibits Na/K+ ATPase)
-leaves are toxic, ripe fruit is nontoxic
-myocardial necrosis
-sterile mastitis
-horses = edema head/neck
-sudden death

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GRAYANOTOXINS

-rhododendrons
-azaleas
-mountain laurel
-japanese pieris

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Mechanism

Inhibit VG Na channel, 0.2% BW leaves

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Clinical signs

-disrrythmias
-heart block
-projective V+
-D+
-ataxia/prostration
-death

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Rhododendrons

-native perennial
-woody shrubs
-common to NW/SE/E

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Japanese Pieris

-woody shrup
-common E/W

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Treatments

-activated charcoal
-supportive care such as atropine for bradycardia

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LECTINS

-castor beans
-rosary pea
-black locust

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Mechanism

-glycoproteins bind to cell surface carbs to faciliate entry into cell
-inhibit ribosomal protein synthesis

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Caster beans princible toxins

-ricin (mech above)
-ricinine (piperidine alkaloid found in leaves/seeds)
-ricinoleic acid (unsaturated fatty acid)

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Clinical signs

1. Pyrexia, depression, anorexia, colic
2. 1-2 day lag period
3. V/weakness/hemorrhagic D+

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Rosary pea

Lectin, tropical

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Treatment

-emetics/laxatives
-activated charcoal
-fluid/electrolytes
-vitamin C can improve survival