Musculoskeletal Toxicity

Question 1

phenoxyacetic acid herbicides

Answer 1

• 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

Question 2

clinical signs of phenoxyacetic acid herbicide toxicity

Answer 2

• 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

Question 3

Diagnosis of phenoxyacetic acid herbicide toxicity

Answer 3

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

Question 4

Treatment of phenoxyacetic acid herbicide toxicity

Answer 4

• 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

Question 5

ergot alkaloids

Answer 5

• 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

Question 6

MOA of ergot toxicity

Answer 6

• 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

Question 7

Clinical signs of ergotism in cattle

Answer 7

• 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

Question 8

clinical signs of ergotism in horses

Answer 8

primary problem is abortions, weak foals, and prolonged gestation

Question 9

clinical signs of ergotism in pigs

Answer 9

infertility and early parturition
decreased milk production

Question 10

diagnosis of ergotism

Answer 10

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

Question 11

treatment of ergotism

Answer 11

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

Question 12

ionophores

Answer 12

• 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

Question 13

MOA of Ionophores

Answer 13

• 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

Question 14

Clinical signs of ionophores in horses and cattle

Answer 14

• 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

Question 15

clinical signs of ionophores in poultry, dogs, and cats

Answer 15

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

Question 16

diagnosis of ionophores

Answer 16

• 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

Question 17

treatment of ionophores

Answer 17

• 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

Question 18

tetanus

Answer 18

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

Question 19

MOA of tetanus

Answer 19

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

Question 20

clinical signs of tetanus

Answer 20

• 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

Question 21

treatment of tetanus

Answer 21

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

Question 22

Common respiratory toxins that cause ventilatory muscle paralysis

Answer 22

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

Question 23

Common respiratory toxins that can cause respiratory center depression

Answer 23

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