Musculoskeletal Toxicity Flashcards Preview

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Flashcards in Musculoskeletal Toxicity Deck (23):

phenoxyacetic acid herbicides

  • 2,4-D (Scott's weed and feed)
  • Low toxicity in most animals
  • Affected animals usually exposed to concentrate or predisposed through kidney damage or genetics
  • MOA unknown


clinical signs of phenoxyacetic acid herbicide toxicity

  • GI effects (often only signs in dogs)
    • vomiting, diarrhea may be bloody, oral and GI ulcerations
  • Muscle effects
    • hesitates to move, rigid skeletal muscles
    • ataxia, weakness, posterior weakness
    • seizures at high doses
    • myotonia with serious toxicosis***
    • rumen atony
  • Renal tubular degeneration
  • Hepatic necrosis


Diagnosis of phenoxyacetic acid herbicide toxicity

  • oral and GI ulcers
  • enteritis, rumen stasis
  • congestion of kidney/liver
  • hyperemia of lymph nodes
  • clinical pathology (liver damage)
  • chemical analysis of serum, urine


Treatment of phenoxyacetic acid herbicide toxicity

  • GI (emesis, lavage) or dermal (bath) decontamination
  • activated charcoal/cathartic
  • ion-trapping to enhance excretion
    • 1-2 mEq/kg NaHCO3 if kidneys normal
  • Prognosis is good for treated animals


ergot alkaloids

  • Produced in small grains (barley, rye, wheat, oat) by Claviceps purpurea, similar alkaloids produced by endophytic fungus in tall fescue
  • in infected grains, the seeds are replaced by sclerotia (look like mouse droppings)
  • fescue infection not detectable by the naked eye
  • at least 40 alkaloids have been ID'd including ergovaline, ergonovine, ergotamine, and LSD


MOA of ergot toxicity

  • Alkaloids are dopamine serotonin agonists which produce hallucinations
  • Activity at dopamine receptors in pituitary lead to decreased prolactin secretion
  • Smooth muscle contraction, especially in uterus and peripheral vasculature, may be due to alpha-adrenergic antagonist activity - cause abortion and ischemia


Clinical signs of ergotism in cattle

  • reduced feed intake and weight gain, heat intolerance, retain winter coat ("summer slump")
  • necrotizing egotism
    • lameness, gangrene of extremities that may result in sloughing of feet, ears, and tail during cold weather "fescue foot"
  • fat necrosis
  • poor reproductive perfomance


clinical signs of ergotism in horses

primary problem is abortions, weak foals, and prolonged gestation


clinical signs of ergotism in pigs

infertility and early parturition
decreased milk production


diagnosis of ergotism

  • evidence of sclerotia in feed
  • fescue in forage matter
  • chemical analysis of feed and forage for ergot metabolites


treatment of ergotism

  • treat by removing source, prevent secondary infections
  • Metoclopromide and domperidone increase prolactin secretion and normalize gestation in mares



  • Compounds that form lipid soluble complexes with cations
    • facilitate specific ionic transport across membranes
  • Used as antibiotic (monensin, salinomycin)
    • monensin used in beef and dairy industry to prevent coccidiosis and prevent bloat
  • Approved for use in dairy cattle
  • Several marketed and off label uses


MOA of Ionophores

  • Act by increasing intracellular Na and Ca, leads to mitochondrial swelling and cell death, especially in muscle
  • Usually a result of feed-mixing errors
  • Among non-target species, horse most susceptible
    • results from consumption of ionophore containing poultry or cattle feed
  • Poultry are the least sensitive to ionophore toxicity


Clinical signs of ionophores in horses and cattle

  • Usually occur 12-72 hours after ingestion
  • anorexia is a common clinical sign in all animals
  • horses present with anorexia, colic, profuse sweating on flanks
    • may be in-coordinated and weak
  • cattle are similar to horses but with diarrhea and respiratory difficulty


clinical signs of ionophores in poultry, dogs, and cats

  • poultry
    • down with legs and wings stretched out
  • dogs
    • exhibit posterior paresis and paralysis with lasalocid
  • cats
    • developed polyneuropathy from salinomycin


diagnosis of ionophores

  • increased muscle enzymes and myoglobinuria
  • elevated AST, CK, LDH, alkaline phosphatase, BUN, Bilirubin
  • decreased K and Ca (most pronounced in horses)
  • chemical analysis of feeds, liver (not blood)
  • differentiate from other causes of colic: vit E and Se deficiency, white snakeroot, blister beetle, gossypol, botulism


treatment of ionophores

  • No specific treatment or antidote
  • Feed change to non-ionophore must be made immediately until all diagnostic procedures are completed
  • Offer supportive therapy (fluid and electrolyte replacement)
  • Recovered animals may die later due to exercise intolerance



  • Mostly affects cattle
  • Usually caused by spores in puncture wounds, can be ingested


MOA of tetanus

  • Toxin acts by blocking release of GABA and glycine (inhibitory neurotransmitters)
  • Results are overstimulation of muscles leading to stiffness and tetany


clinical signs of tetanus

  • Stiffness and reluctance to move
  • Twitching and tremors of the muscles
  • Lockjaw
  • Unsteady gait with stiff held out tail
  • Bloat is common in ruminants
  • Later signs: collapse, spasm, death


treatment of tetanus

  • Antitoxin is available but only of value at the very early stages
  • Supportive therapy
  • Prognosis is very poor
  • Vaccination available


Common respiratory toxins that cause ventilatory muscle paralysis

  • Botulism
  • tetanus
  • snake venom
  • OP insecticides
  • strychnine


Common respiratory toxins that can cause respiratory center depression

  • Barbituates, opiates/opiods
  • Ethylene glycol
  • hypnotics, sedatives
  • tricyclic antidepressants
  • crude oil