Rodenticides Flashcards
What are the possible sources of anticoagulant rodenticides?
- used as prepared baits, or powders for mixing with bait material
- some used as medical anticoaguants
How can animals be exposed to anticoagulant rodenticides?
- ingestion of baits or eating contaminated food
- relay toxicosis (secondary)
- malicious poisoning
What are the properties of anticoagulant rodenticides?
- odorless and tasteless
- resistant in environment for weeks to months
- slow action
What factors can enhance the toxicity of anticoagulant rodenticides?
- vitamin K deficiency
- pre-existing liver disease
- enzyme inhibitors
- concurrent factors causing hemorrhage
- drugs displacing anticoagulant from binding sites
- steroids or thyroxine may increase receptor site affinity
Describe the mechanism of action of anticoagulant rodenticides
- inhibit vitamin K epoxide reductase
- leads to depletion of reduced vitamin K
- reduced carboxylation and activation of precursors of clotting factors
Which are the precursor clotting factors?
II, VII, IX, X
When is the onset and what are the clinical signs of anticoagulant rodenticide toxicosis?
- onset in 1-5 days
- hemorrhage signs: epistaxis, bloody discharge, hematuria, weakness, shock, hematomas, anorexia
- abortion in cattle
How do you diagnosis anticoagulant rodenticide toxicosis?
- detection in blood, serum, or plasma in live animal
- postmortem: liver, GI contents, vomitus, sample of bait
How would you treat anticoagulant rodenticide toxicosis if exposure is recent and the animal has a normal coagulation panel?
decontamination
- emesis, charcaol
How would you treat anticoagulant rodenticide toxicosis if there are no clinical signs, but prolonged coagulation?
- give vitamin K1 orally
- consider giving clotting factors
How would you treat anticoagulant rodenticide toxicosis if the animal is bleeding, but PCV is > 15-20% and stable?
- start with vitamin K therapy
- give clotting factors
- consider giving RBCs
How would you treat anticoagulant rodenticide toxicosis if the animal is bleeding, and PCV is < 15% and unstable?
- give clotting factors and RBCs
- start vitamin K therapy
What are possible sources of/ways of exposure to Cholecalciferol?
- ingestion of pesticides for rats/mice
- relay toxicosis
- vitamin D toxicosis: large doses, poisonous plants, ingestion of psoriasis medications
What are the properties of Cholecalciferol?
- Cholecalciferol = vitamin D3
- insoluble in water
- soluble in most organic solvents/oil
- no bait shyness
Describe the mechanism of action of cholecalciferol
- absorbed from GI tract
- binds to vitamin D binding protein in plasma and transported to liver
- metabolized in liver to calcidiol
- calcidiol transported to kidneys and metabolized to calcitriol
What are the effects of cholecalciferol toxicity?
- increased serum Ca
- causes hypercalcemia and hyperphosphatemia
- deposition of Ca in soft tissues
- tissue damage, hemorrhage, increased capillary permeability, and renal ischemia
- increased loss of Na and K
When is the onset and what are the clinical signs of Cholecalciferol toxicity?
- onset is 24-36 hours
- depends on tissues affected
- GI: anorexia, vomiting, ab pain, constipation
- Renal: PU/PD
- CV: arrhythmias, hypertension
- CNS: depression, weakness, seizures
What are the lesions of Cholecalciferol toxicosis?
- hemorrhagic gastroenteritis
- mineralization in affected tissues
How is Cholecalciferol toxicosis diagnosed?
- elevated serum Ca/P
- elevated calidiol and calcitriol
- radiographs: mineralization
How is Cholecalciferol toxicosis treated?
- emesis and activated charcoal if recent
- IV lipid therapy
- restrict Ca/P in diet
- avoid sunlight
- supportive therapy
- treat the hypercalcemia
How can you treat hypercalcemia?
- saline diuresis
- furosemide
- sodium bicarbonate
- glucocorticoids
What are the properties of Bromethalin?
- effective against warfarin-resistant rodents
- no bait shyness
What are the toxicokinetic features of Bromethalin?
- highly lipophilic
- rapidly absorbed orally
- widely distributed
- lethal synthesis in liver
- excreted in bile
Describe the mechanism of action of Bromethalin
- uncoupling of oxidative phosphorylation
- lack of adequate ATP
- insufficient energy for Na/K pumps
- leads to fluid imbalance, edema, and increased pressure (brain and spinal cord)
What are the acute clinical signs of Bromethalin toxicosis?
- severe muscle tremors, hyperthermia
- extreme hyperexcitability
- generalized seizures
What are the subacute clinical signs of Bromethalin toxicosis?
- hind-limb ataxia, proprioceptive deficits, and paresis (can progress)
- CNS depression
- focal motor or generalized seizures
- death due to respiratory failure
What are the lesions of Bromethalin toxicosis?
- cerebral edema
- diffuse white matter vacuolization
How is Bromethalin toxicosis treated?
- emesis (if within 1 hour)
- activated charcoal with cathartic
- supportive care
- treat cerebral edema, seizures
What are the properties of Strychnine?
- bitter taste, white powder
- moderately water soluble
- persists in environment up to 40 days
What are the toxicokinetic features of Strychnine?
- rapidly absorbed from the GI tract
- crosses the BBB
- metabolized in liver
- excreted in urine
What is the mechanism of action of Strychnine?
- blocks post-synaptic effect of glycine in the spinal cord
- leads to: exaggerated reflexes, muscle spasms, extensor rigidity, and tonic seizures
When is the onset and what are the clinical signs of Strychnine toxicosis?
- rapid onset of 10 min - 2 hours
- early: apprehension, panting, nausea
- stiffness, muscle twitching, hyperthemia
- progresses to tonic seizures and opisthotonos
- death due to respiratory failure
What are the properties of zinc phosphate?
- grey-black powder
- acetylene, garlic, or “dead fish” odor
- stable when dry, decomposes in environment within 2 weeks
- when exposed to acid, liberates phosphine gas
When is the onset, and what are the clinical signs of zinc phosphate toxicosis?
- rapid onset (min-hrs)
- anorexia, vomiting
- ab pain and bloat in cattle
- increased RR, wheezing, dyspnea
- dogs may show CNS excitation
- death due to tissue anoxia
Where is zinc phosphate absorbed?
- zinc phosphate and phosphine gas absorbed in GI tract
- gas can also be inhaled
What lesions are caused by zinc phosphate toxicosis?
- gastroenteritis
- congestion of liver/kidneys/lungs
How is zinc toxicosis treated?
- emesis, gastric lavage, antacids, mineral oil
- supportive care
What are the properties of Fluoroacetate?
- odorless
- water soluble
- degraded by soil microbes and plant enzymes
- irritant
What are the toxicokinetic features of Fluoroacetate?
- absorbed from GI tract, lungs, or open wounds (not intact skin)
- distributed throughout the body
- excreted in urine
What is the mechanism of action of Fluoroacetate?
- competes with citrate in citric acid cycle
- slows TCA cycle and decreases cellular respiration and energy
- build up of unused citrate
When is the onset, and what are the clinical signs of Fluoroacetate toxicosis in dogs?
- 30 min to 22-4 hours
- CNS stimulation: seizures, yelping, running
- GI signs: diarrhea, vomiting
- hyperthermia
- death from respiratory failure/anoxia
What are the clinical signs of Fluoroacetate toxicosis in horses, cattle, and goats?
- cardiac signs in horses
- heart failure, staggering, arrhythmias
- colic and terminal convulsions
What are the clinical signs of Fluoroacetate toxicosis in sheep?
- disoriented running, blindness, weakness, ataxia, coma, death
What are the clinical signs of Fluoroacetate toxicosis in cats and pigs?
- bradycardia and other arrhythmias
- CNS depression or excitement, vocalization, hyperesthesia, hypothermia
What are the properties of Metaldehyde?
- irritant, flammable
- poorly soluble in water
What are the toxicokinetics features of Metaldehyde?
- absorbed from GI tract
- cross the BBB
- metabolized in liver by enzymes
What is the mechanism of action of Metaldehyde?
- decreases brain GABA, NE, and serotonin
- causes direct GI irritation
- causes metabolic acidosis
- CNS excitation
When is the onset and what are the clinical signs of Metaldehyde toxicosis?
- onset within 3 hours
- acute neurotoxicosis and hyperthermia
- salivation, vomiting, diarrhea
- incoordination, muscle tremors, seizures
- nystagmus, mydriasis in cats
What are lesions of Metaldehyde toxicosis?
- formaldehyde odor in stomach contents
- petechiae/ecchymosis in GI mucosa
- congestion, edema, hemorrhage in lungs, liver, and kidneys
