Rodenticides Flashcards
Rodenticides
-linked with humans (poor storage, off label use, delayed removal, malicious use)
-baits typically bright colours but no specific coding
Secondary poisoning
“Relay toxicity”
-carcass of poisoned animal poisons the animal that consumes it (dogs and wildlife)
What rodenticides have very high risk of secondary poisoning?
-Strychnine
-Fluoroacetate
-Bromethalin
-Second generation ACRs
What are the 3 neurotoxic rodenticides?
-strychnine
-bromethalin
-fluoroacetate
Strychnine
Strychnos nux vomica (Strychnine tree)
-banned in Canada
How does strychnine poisoning occur?
-consumption of strychnine laced bait
-consumption of strychnine poisoned animal
-malicious poisoning
Who is susceptible to strychnine toxicity?
All species, but most dogs
-very toxicity; targets CNS
Strychnine mechanism of action
Glycine antagonist at post synaptic receptors in the spinal cord and medulla
-prevents inhibition of motor neurons; affects all muscles = uncontrolled stimulation of motor neurons
Strychnine clinical features
-apprehension, anxiety, agitation
-generalized muscle spasms (extensor rigidity, tonic clonic seizures)
-responsive to external stimuli
-cyanosis
-dilated pupils
-sudden death
-No PM lesions
Management of strychnine
-no antidote, need aggressive decontamination and supportive care
-if asymptomatic= activated charcoal, gastric lavage under GA
-seizures= diazepam, GA
-respiration= intubation and mechanical ventilation
-IV fluids
-need to manage hyperthermia, rhabdomyolysis, hypoxia, acidosis
Diagnosis of strychnine
-Exam findings= sudden onset of neuro signs, extensor rigidity, seizures that respond to exxternal stimuli, lack of GI signs
-presence of strychnine in stomach, vomit, urine, liver, bait
Prognosis of strychnine toxicity
poor to grave
-if an animal can survive 24-48 hrs then prognosis improves
Differential diagnosis for strychnine
-other rodenticides
-metaldehyde
-tremorgenic mycotoxins
-tetanus (will have a latent period; strychnine will not)
-high dose stimulants (amphetamines, cocaine)
-Anatoxin-a
-water hemlock
-OP/carbamate insectacides
-non toxic: brain disease, hepatic encephalopathy, severe hypoglycemia, rabies
Bromethalin
-emerged to use against warfarin resistant rodents
-widely available in home and garden stores (pellets, blocks, concentrate)
-extremely toxic to highly toxic
Bromethalin mechanism of action (2 options)
- Uncouples oxidative phosphorylation in mitochondria, decreasing ATP production and Na-K ATPase, loss of oncotic pressure in brain
Where does bromethalin target?
- Cerebral edema
- CNS: long nerve demyelination, accumulation of fluid within myelin sheath and increases in CSF pressure = intramyelinic edema
Toxicokinetics of bromethalin
Metabolism: Bromethalin metabolized to desmethylbromethalin in liver
Distribution: highly lipophilic
Elimination: long half life; enterohepatic recirculation
What animal is resistant to bromethalin?
Guinea pigs
-do not undergo metabolization of bromethalin in liver
What does a high dose of bromethalin in dogs cause?
Convulsant syndrome
-asymptomatic for 2-12hrs then acute progression
-muscle tremors
-hyperesthesia
-agitation/hyperexcitability
-running fits
-seizures responsive to external stimuli
-obtundation
-death due to resp paralysis
What does a low dose of bromethalin in dogs and any dose in cats cause?
Paralytic syndrome
-delayed onset (1-several days)
-hindlimb paresis, ataxia, decreased proprioception
-cats= abdominal distention
-progresses to:
loss of deep pain sensation, UMN bladder, CNS depression, decerebrate posture, obtunded, seizures
Clinical pathology of bromethalin
-mild hyperglycemia (may be hypernatremic)
-increased CSF pressure
-normal CSF cytology= no inflammation, normal specific gravity and protein
Management of asymptomatic bromethalin toxicity
-no antidote
-early GI decontamination (activated charcoal, emesis)
-low renal excretion so diuresis not helpful
-intravenous lipid emulsion?
Management of symptomatic bromethalin toxicity
-manage cerebral edema
-seizure control
-supportive care
Diagnosis of bromethalin antemortem
-history of exposure and compatible clinical signs
*cases of progressive hindlimb paresis
-detection of desmethylbromethalin in fat, serum, brain, kidney, liver
Diagnosis of bromethalin post mortem
Histology
-diffuse white matter spongiosis
-intramyelinic edema
Differentials for bromethalin
-Convulsant syndrome: strychnine, fluoroacetate, tremorgenic mycotoxins, intracranial diseases, antifreeze, anatoxin-a
Paralytic: botulism, tick paralysis, IVD
Prognosis for bromethalin
Guarded to grave
-poor if symptomatic with neuro signs
-mild symptoms=guarded
-asymptomatic and decontamination= good
