Rodenticides Flashcards
What type of rodenticide is warfarin?
Anticoagulant rodenticide
Are anticoagulant rodenticides environmentally stable?
Resistant in environment for weeks and months
What is the order of species susceptibility to anticoagulant rodenticides?
Pig > dog > cat > ruminant > horse > chicken
What factors increase toxicity of anticoagulant rodenticides?
Vit K deficiency Liver disease Enzyme inhibitors Presence of drugs that cause hemorrhage, anemia, hemolysis, methemoglobinemia, or increase capillary permeability Administration of steroids or thyroxine Trauma or surgery Renal insufficiency and fever Newborn and debilitated animals
What factors decrease anticoagulant rodenticide toxicity?
Pregnancy and lactation
Enzyme inducers
Where are anticoagulant rodenticides metabolized?
Liver by hydroxylation
Second-generation compounds (brodifacoum or diaphacinone) have long half lives
T/F: anticoagulant rodenticides cross the placenta and are excreted in milk
True
What is the MOA of anticoagulant rodenticides?
Inhibit vit K epoxied reductase
-> no reduced vitK
Reduced carboxylation and activation of precursors of clotting factor 2,7,9,10
Tachypnea/dyspnea
Anorexia and lethargy
Signs of hemorrhage- epistaxis, bloody discharge, melena, hematuria
DDX?
Anticoagulant rodenticide
Spoiled sweet clover (cattle and horse)
Vit K deficiency (swine and poultry)
Other conditions associated with hemorrhage like ricin, saponins, monocrotaline, gossypol, inorganic arsenic, iron, and zinc phosphide
What would you see in laboratory tests with anticoagulant rodenticides and what is the best sample?
Blood
Prolonged coagulation parameters
- activated coagulation time (ACT)
- activated partial thromboplastin time (APTT)
- prolonged PT
Treatment of anticoagulant rodenticide toxicity?
Symptomatic
- fresh whole blood/fresh frozen plasma
- fluid therapy
- oxygen therapy
- thoracocentesis
Vit K (oral and bioavailability is increased with fatty meal)
What is cholecalciferol toxicosis?
Large dose of vit D —> excessive calcium and phos
What are sources of cholecalciferol toxicosis?
Feeding on poisoned rodents
Large doses of vit D
Ingestion of human psoriasis meds with vit D
Poisonous plants containing vit D analogs
What is the oral LD50 of cholecalciferol ?
88mg/kg Moderately toxic (50-500mg/kg)
What are predisposing factors to cholecalciferol toxicosis?
Renal disease
Hyperparathyroidism
Ingestion of high Ca and Phos in diet
How is cholecalciferol transported in the body?
Binds to serous vitD binding protein and transported to the liver
The highest concentrations of cholecalciferol are found where?
Plasma, liver, kidney, and fat
How is cholecalciferol metabolized?
Liver: cholecalciferol —> 25-hydroxycholecalciferol
Kidney: 25-hydroxycholecalciferol (calcifediol) —> 1,25-dihydroxycholecalciferol (calcitriol)
Where is cholecalciferol excreted?
Bile and feces
Can be excreted in milk in toxic levels
What is the MOA of cholecalciferol ?
VitD -> increase GI absorption and tubular reabsorption of calcium
Hyperphosphatemia
Deposition in kidney, cardiac, lung, vascular, and stomach tissues
Anorexia, bloody vomit, abdominal pain, dehydration
PU/PD
Cardia arrhythmia and hypertension
DDX?
Hypercalcemia
- lymphoma
- pseudohyperparathyroidism
- primary hyperparathyroidism
- ingestion of calcinogenic plants
- cholecalciferol (Vit D)
PU/PD
- diabetes mellitus/insipidus
- hyper/hypo-adrenocortisism
- renal disease
Anorexia, bloody vomit, abdominal pain, dehydration
PU/PD
Cardiac arrhythmia and hypertension
You suspect cholecalciferol toxicosis, what would you expect to see on lab data?
Hypercalcemia
Hyperphosphatemia
elevated BUN, crea, azotemia
Hyperproteinemia, proteinuria, and glucosuria
Decreased PTH
What is the treatment for cholecalciferol toxicosis ?
GI tract decontamination —>emetic, activated charcoal, cathartic
Reduction of serum Ca —> saline IV, furosemide, glucocorticoids, calcitonin
Pamidronate disodium —> inhibitor of bone resorption
T/F: secondary poisoning of non target animals by bromethalin rodenticide may be possible in cats
True
Who is more sensitive to bromethalin toxicosis?
Cats (1.8mg/kg) > Dog ( 4.7mg/kg)
Highly toxic
What speices is resistant to bromethalin rodenticide?
Guinea pigs
Is bromethalin hydrophilic or lipophilic?
Highly lipophilic
-> rapidly absorbed orally and reaches high concentrations in fat and brain
Where is bromethalin metabolized and excreted?
Liver: metabolized to desmethylbromethalin (more toxic)
Excreted in bile (possible enterohepatic circulation)
Small amount excreted in urine
What is the MOA of bromethalin?
Uncouple oxidative phosphorylation
Lack of ATP
Insufficient energy for Na and K ion pump
Cerebral and spinal cord edema
Cerebral damage due to lipid peroxidation
Severe muscle tremors, hyperthermia, extreme excitability, running fits, generalized seizures that are triggered by light/noise
DDX?
Bromethalin
Neurotoxins -
Zinc phosphide
Strychnine
Organic aresenic, lead, organophosphate, metaldehyde, urea
What are the subacute signs that can develop with bromethalin toxicosis ?
Hindlimb ataxia and paresis that progress to hindlimb paralysis, loss of deep pain response, patellar hyper-reflexive ,severe CNS depression and vomiting
What lesions are seen in bromethalin toxicosis?
Cerebral edema
Diffuse white matter vacuolization in the CNS
What is the treatment for bromethalin toxicosis?
Decontaminate: Emetic, activated charcoal, saline cathartic
Mannitol and dexamethasone for cerebral edema
Diazepam and phenobarbital to control seizures
T/F: cats are more sensitive to strychnine toxicosis than dogs
False
Dogs 0.75mg/kg -extremely toxic
Cats 2.0mg/kg - highly toxic
Horses, cattle, and pig also very sensitive
T/F: small amounts of strychnine ingested over time may not cause poisoning
True
Rapid elimination
Where is strychnine distributed in the body?
Does not accumulate, but significant amounts can be found in liver and kidney
Crosses BBB
Metabolized in liver
Where is strychnine metabolized and excreted?
Met: liver
Ex: urine
What is the MOA of strychnine?
Blocks the post synaptic effect of glycine in the spinal cord
Stimulation of spinal cord causes tonic seizures
What are clinical signs seen with strychnine poisoning ?
Early - apprehension, panting, possible nausea and vomiting
Mydriasis, stiffness, muscle twitching, tonic seizure, and opisthotonos
Animal dies from respiratory failure
What sample is used or detection of strychnine?
Urine
Stomach contents
What is the treatment of strychnine toxicosis?
Phenobarbital (dog) and thiobarbiturates (cat) for seizures
Diazepam effect is variable
Methocarbamol, guaifenesin, and xylazine as alternatives
Apomorphine and gastric lavage -prevent further absorption
Ammonium chloride and fluid therapy - enhance renal excretion
What drugs are contraindicated in strychnine toxicosis?
Opioid Phenothiazine Butyrophenones NMBD Dissociative anesthetics
What are the properties of zinc phosphide?
Gray-black powder with acetylene odor (dead fish)
Liberates phosphine gas under acidic conditions
Phosphine gas is toxic and flammable
Zinc phosphide is insoluble in water
Both gases are irritants
What is the legal dose for zinc phosphide?
20-40mg/kg
Gastric acid increases toxicity, vomiting decreases toxicity
Gastric acid causes hydrolysis of zinc phosphide to ____________ which is absorbed across the GI tract
Phosphide gas
What is the MOA of zinc phosphide ?
Phosphide gas may inhibit oxidative phosphorylation and cellular energy production —> cell death
Irritation of GI tract and respiratory mucosa
Damage of blood vessels and RBC membrane
What are the main tissues affected by zinc phosphide toxicosis?
Brain Heart Liver Kidney Lung
What are the clinical signs associated with zinc phosphide toxicosis?
Anorexia Vomiting Incresed rate and empty of respiration Wheezy Abdominal pain Bloat (cattle) “Mad dog running”, hyperexcitabiltiy
What lesions are associated with zinc phoside toxicosis?
Odor of acetylene (dead fish)
Gastroenteritis
Congestion of liver and kidney
Pulmonary congestion and edema
What specimens should be collected and how are they handled for testing zinc phosphide?
Stomach content, vomitus, or bait
Rapidly frozen
What lab abnormalities would you see with zinc phosphide toxicosis?
Elevated serum zinc
Metabolic acidosis
Dehydration
Hypocalcemia
What is the treatment of zinc phosphide toxicosis?
Emetic and gastric lavage, sodium bicarbonate, potassium permanganate
Oral antacids
IV anti acidotic agents - sodium bicarb or sodium lactate
Ca gluconate for hypocalcemia
O2 therapy
Symptomatic treatment
Prognosis of zinc phosphide?
Animals that vomit may recover
Signs of tissue damage have guarded to poor prognosis
What is currently the onl used of flouroacetate ?
Currently it is only used in the livestock protection collar
Controls coyotes preying on sheep and goats
What are the properties of flouroacetate?
Odorless and water soluble
Insoluble in most organic solvents
Degraded in soil by microorganisms
Irritant
What is the LD50 for flouroacetate in dogs
0.05mg/kg
Extremely toxic
T/F: flouroacetate is readily absorbed from GI tract, lung, wounds, and intact skin
False
Cannot be absorbed across intact skin
Where does flouroacetate accumulate?
Trick question.. it does not accumulate in any particular tissue
How is flouroacetate metabolized?
Acid hydrolysis makes flouroacetate —> monofluoroacetic acid
What is the MOA of flouroacetate?
Enters cells
Condense with oxaloacetate to fluorocitrate that competes with citrate for active site in CAC —> decreased cellular respiration and energy
Brain and heart most affected
Build up of citrate
Ammonia accumulation in brain —> convulsions
What signs do you see for flouroacetate toxicosis in dogs?
CNS stimulation and GI irritation
Vomiting, diarrhea, urination, hyper irritability, hyper-motility, running in straight line, barking, yelping, intermittent clonic-tonic seizures and opisthotonos
What clinical signs do you see in flouroacetate toxicosis in horse, cattle, sheep, and goat?
Signs of heart failure
Colic, staggering, arrhythmia, Vfib
Terminal convulsions due to cerebral anoxia
What clinical signs do you see in cats and pigs due to flouroacetate toxicosis?
CNS and cardiac signs
Death due to flouroacetate toxicosis is a result of?
Convulsions and respiratory failure that causes cyanosis, hemorrhage on the heart, pulmonary changes, dark blood, and organ congestion
What specimens are best to run lab diagnostics for flouroacetate ?
Gastric contents and vomitus
What is the treatment for flouroacetate toxicosis?
Anticonvulsant for seizures
O2 therapy
Charcoal, milk, limewater
Antidote = acetate donors (glycerol monoacetate, ethanol, and acetic acid)
Calcium chloride - protect against arrhythmias
Sodium bicarbonate IV for metabolic acidosis
Prognosis for flouroacetate toxicity?
Grave
