Equine Intoxications Flashcards

1
Q

Obj: Familiarity with more common equine intoxications

A
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2
Q

Obj: Understand risk and clinical manifestation for common toxins

A
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3
Q

Obj: Establish diagnosis, treatment and prognosis

A
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4
Q

What is Nigropallidal Encephalomalacia? Cause? symptoms? diagnostics? treatment? prognosis?

A
  • Affects Equids
  • Caused by 2,3-dihydro-3, 5-dihydroxy-6-methyl-4[H]-pyran-4-1
    • yellow star thistle (Centaurea melitensis)
      • CA, OR, Western US
    • Russian knapweed (Acroptilon repens)
  • Continuous ingestion at 80-200% BW for weeks to months
  • Symptoms:
    • Bilaterally symmetric lesions
      • Non-progressive focal necrosis of globus pallidus or substantia nigra
    • Facial hypertonicity increases w/ food being offered - inability to prehend
    • Poor BCS
  • Dx - MRI for antemortem
  • Tx - None
  • Poor prognosis for recovery or survival
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5
Q

What is Tremetol? sources?

A
  • Fat soluble, high molecular weight alcohol
  • toxic at 1-10% of BW and is cumulative!
  • White snakeroot (Eupatorium rugosum)
  • Rayless goldenrod (Isocoma wrightii)
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5
Q

What damage does Tremetol cause in horses? signs/symptoms

A
  • Affects Heart, Kidneys, gut, lungs
  • Toxins concentrate in milk
    • Do not give milk to offspring
  • CBC/Chem/UA: (consistent w/ muscle necrosis)
    • elevated CK, AST
    • Hematuria
    • Hemoglobinuria
    • proteinuria
    • acidosis
    • hyperglycemia
  • Signs/symptoms:
    • Weight loss
    • Tremors, ataxia
    • Depression
    • Cardiac arrhythmias
    • Recumbency
    • Skeletal muscle and myocardial streaking and necrosis
    • Death
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6
Q

What other toxin can cause similar signs to Tremetol poisoning, and needs to be ruled out for Dx?

A

Ionophore contamination

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7
Q

How is Tremetol poisoning managed?

A
  • Symptomatic treatment
  • Supportive care
  • Attempt to evacuate GIT
  • Administer mineral oil or activated charcoal
  • Diuresis
  • Examine all herd mates
  • prognosis is poor to grave
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8
Q

What is Red Maple Toxicity? source? signs?

A
  • Seasonal toxicity - Fall
    • after trimming trees or storm
    • Wilted Red Maple leaves
  • Hematologic toxicity
    • acute severe anemia (intravascular hemolysis)
    • methemoglobinemia
  • Signs: Tachypnea, Tachycardia
    • Depressed
    • anorexic
    • Signs of Intravascular hemolysis (red/brown urine)
    • Cyanotic
    • Death
  • CBC/Chem/Blood:
    • hematacrit drops to 10%
    • numerous Heinz bodies
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9
Q

What are the differentials for Red Maple Toxicity?

A
  • Phenothiazine toxicity
  • Wild onion
  • IMHA, EIA
  • Drug hypersensitivity
  • Ehrlichiosis, Piroplasmosis
  • Endotoxemia
  • Hepatic failure
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10
Q

How is Red Maple Toxicity managed? prognosis?

A
  • Stabilize
  • Blood transfusion
  • Anti-inflammatories
  • Antibiotics
  • Oxygen insufflation
  • Environmental evaluation for affected herd mates
  • Guarded prognosis
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11
Q

What plants contain Cardiac Glycoside?

A
  • Foxglove (Digitalis purpurea)
  • Oleander (Nerium oleander)
  • Azaleas (Rhododendron spp.)
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12
Q

how much foxglove is lethal to horses?

A

~0.05% BW (~0.25kg)

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13
Q

How is Cardiac Glycoside intoxication managed?

A
  • Supportive:
    • IV fluids
      • Avoid calcium and potassium containing fluids
    • Analgesics: NSAIDS (Flunixin meglumine or phenylbutazone)
    • Antioxidants: Vit E, DMSO
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14
Q

What is the difference between primary and secondary photosensitization?

A
  • Primary - Plant directly causes photosensitization
    • Ex: St. John’s wort (Hypericum perforatum)
  • Secondary -
    • plant causes hepatic disease
      • severe hepatic disease leads to phylloerythrin accumulation in skin → photosensitization
    • Ex: Ragwort (Senecio spp)
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15
Q

How are cases of photosensitization managed?

A
  • Rule out significant hepatic disease
    • if hepatic disease is present - treat as primary disorder
  • Determine if/wat plants are in the pasture
  • Remove patient from direct sunlight
  • Lesions should heal in 2-3 weeks
  • Topical silver sulfadiazine (SSD) - soothing and antimicrobial
16
Q

What is Pyrrolizidine alkaloid toxicity?

A
  • Source: Senecio spp, crotalaria spp
  • Ingestion of toxic plant causing hepatic damage
    • alkaloid transformed to toxic pyrrole
    • Reactive metabolites bind cell molecules and cross link DNA preventing mitosis
  • Signs:
    • Poor BCS
    • Icterus
  • Chem - consistent w/ primary hepatic disease
    • Elevated GGT, AST, ALP
    • reduced hepatic function: bile acids
  • Histo:
    • Megalocytosis
    • Bridging Fibrosis
  • Guarded prognosis
17
Q

What fungus may infect hay, forage, or grain? what do they cause?

A
  • Rhizoctonia leguminicola - Slobber toxin
  • Neotyphodium coenphialum - Fescue toxicosis
  • Fusarium proliferatum - Leukoencephalomalacia (ELEM)
18
Q

what are the neurotoxins in Yellow Star thistle?

A
  • aspartic acid
  • glutamic acid
  • sesquiterpene lactones:
    • solstitialin A 13- acetate
    • cynaropicrin
  • dopaminergic neurotoxin (2,3 dihydro-3, 5 dihydroxy-6-methyl-4 (H) pyran-4-1) similar to the compound that induced Parkinson’s in People has been isolated
19
Q

What affect does yellow star thistle have on the nervous system?

A
  • Destroys dopaminergic nigrostriatal pathway
    • coordinates and inhibits the cerebral cortex pathways that control prehension and chewing of food (CN V, VII, IX)
20
Q

How is slobber toxin treated?

A
  • removal of infected forage from the diet
21
Q

What toxin is found in tall fescue grass (Festuca arundinacea)

A
  • Endophytic fungus - Neotyphodium coenophialum
    • Produces ergopeptine alkaloids - primarily ergovaline
22
Q

What endocrine abnormalities are seen with Fescue Toxicosis?

A
  • Depressed prolactin secretion
  • Depressed fetal cortisol secretion
  • Elevated circulating estradiol concentration
    • suppressed final stages of gesation
23
Q

What are the clinical signs of Equine Fescue Toxicosis?

A
  • Delayed gestation
  • Thickened placenta
  • impaired lactogenesis
  • Poor fetal maturity
24
Q

How is Fescue Toxicosis managed?

A
  • Remove mares from pasture 90 days before foaling
  • Treat with D2 antagonist - Domperidone 1mg/kg q24h
    • during pregnancy until foaling
    • after delivery if milk production is poor
25
Q

What is the toxin responsible for Moldy Corn Toxicity?

A
  • Mycotoxin - Fumonisin B1, B2, B3
    • interferes with sphingolipid metabolism which disrupts endothelial cell walls and basement membranes
26
Q

What lesions are seen with Moldy Corn Toxicosis?

A
  • Long term, low dose
    • Leukoencephalomalacia - liquefactive necrosis and degeneration of the cerebral white matter
  • High dose
    • liver toxicity
27
Q

What are the signs of Moldy Corn Toxicosis?

A
  • CNS signs predominate:
    • blindness
    • hypermetria
    • depression
    • disorientation
  • Serum Chemistry for hepatic enzymes
28
Q

What is the treatment for Moldy Corn Toxicosis

A
  • Supportive care
  • Prognosis is guarded to grave
29
Q

What are the signs of Ionophore intoxication in horses?

A
  • Anorexia
  • Colic
  • Acute death
  • Weakness
  • Myocarditis
    • Congestive heart failure
    • DCM
30
Q

What is the MOA of Ionophore Intoxication?

A
  • Lipid soluble transports monovalent cations preferentially across cell membranes
    • Monensin is very potent in transporting Na+ across lipid membranes
  • Proton exchange for sodium, leading to acidosis and potassium loss
  • High intracellular sodium leads to secondary intracellular calcium overload
  • This leads to mitochondrial swelling, catecholamine release, and increased myocardial cell and diaphragm cell contractility
    • early positive ionotropyh
    • later negative inotropy and contracture
  • Results include skeletal muscle and cardiac muscle dysfunction with potential failure
31
Q

How is Ionophore Toxicosis diagnosed

A
  • History
  • Feed evaluation (stomach contents)
  • Liver and Muscle enzymes
    • ALP, CK, AST
  • Cardiac isoenzymes
    • Troponin I
    • CK-MB, LDH-HBD
  • Cardiac evaluation
    • ECG
    • Echocardiogram
    • Reduced fractional shortenting
  • +/- thoracic radiographs
32
Q

How are cases of Ionophore Toxicosis treated?

A
  • Remove suspected feed
  • Mineral oil or activated charcoal
    • no digoxin or calcium
  • Supportive
33
Q

What would be the presentation of a horse with a low level of ionophore exposure

A
  • Exercise intolerance
  • cough
  • weight loss
  • congestive heart failure
34
Q

What is the toxin in Blister Beetles?

A

Cantharidin

35
Q

What issues does Cantharidin Toxicosis cause?

A
  • Pseudomembranous inflammation of GIT
  • hemorrhagic cystitis
    • occult blood in urine
  • Myocarditis and necrosis
36
Q

How is Cantharidin toxicosis managed?

A
  • Empty stomach, activated charcoal
  • IV fluid for hypocalcemia
  • Plasma transfusion for Hypoproteinemia