10b: Pesticides

What determines potency of cholecalciferol exposure

Duration; chronic exposure is much more dangerous

Sources of cholecalciferol toxicity

• Supplements

• Dermal patches

• Rodenticide

Cholecalciferol toxicity mechanism of action

Increases Ca and P absorption in but and resorption from bones

CS associated with cholecalciferol toxicity

• GIT signs: ulcers, hematemesis

• PU/PD

• Tissue mineralization

• Arrhythmias

Tissue that is likely to mineralize in dogs with cholecalciferol toxicity

Muscles

Tissue that is likely to mineralize in cats with cholecalciferol toxicity

Lungs

Diagnostics for cholecalciferol toxicity

• High Ca and P with low PTH

• Calciuria

Specific treatment for cholecalciferol toxicity

• Prednisolone

• Diuretics

• Pamidronate

Supportive treatments for cholecalciferol toxicity

• Decontaminate

• AC

• Low Ca diet

• GIT protectants

Parts of the Strychnos plant don’t have strychnine

Fruit

Strychnine chemical class

Terpene alkaloid

Strychnine mechanism of action

Blocks GABA Cl^- channels → forced depolarization → uncontrolled nervous activity

Part of the nervous system particularly affected by strychnine

Spinal cord

Onset of strychnine poisoning

RAPID, seconds after injection

CS associated with strychnine poisoning

CNS effects → muscle spasms → rigidity

Cause of death in strychnine poisoning

Respiratory arrest

Typical diagnostic for strychnine poisoning

Typical clinical signs

Strychnine testing you can do for legal purposes

Test stomach contents

Decontamination methods justified in cases of strychnine poisoning

Emesis and gastric lavage

Treatment for strychnine poisoning

• Control neuro: benzos, methocarbamol, PB

• Support resp if needed

• IVF and diuretics

Zinc phosphide toxic substance

Phosphine gas

Zinc phosphide mechanism of action

Oxidative damage to everything

CS associated with Zn phosphide toxicity

• Vomiting ± hemorrhage

• Multiple organ failure

• Tremors → shock → death

What do owners have to be aware of in cases of Zn phosphide toxicity

Humans are VERY susceptible to phosphine gas toxicity! Vomit in a closed car can be fatal for humans!

Diagnostics for Zn phosphide toxicity

• Freeze stomach contents or vomit to test for phosphine

• May test for Zn in stomach

Treatment for Zn phosphide toxicity

• Antacids: decreases gas release

• Emesis or gastric lavage

• Control muscle tremors and convulsions

Prognosis for Zn phosphide toxicity

Poor, organ failure is irreversible

Toxin that has largely displaced anti-coagulant rodenticide

Bromethalin

Bromethalin mechanism of action

Uncouples ATP production

Toxidrome associated with bromethalin

Generalized CNS depression

Specie that has a much lower lethal dose of bromethalin

Cats (it’s always cats…)

CS associated with low doses of bromethalin toxicity

• CNS depression

• Weakness

• Paralysis

CS associated with high doses of bromethalin toxicity

• Severe CNS dysfunction: hyperesthesia, seizures

• Muscle tremors, excitability

• Hyperthermia

Pathognomonic lesion associated with bromethalin

White matter vacuolation

Gross lesion seen with longer survival during bromethalin toxicity

Cerebral edema

Treatment for bromethalin toxicity

• Emesis: may still be intact!

• Fluid offload: diuretics and corticosteroids

• Control seizures: benzos and PB

In a case of bromethalin toxicity, when can you induce vomiting

While the patient can swallow, before neuro signs have set in

Best tissue to test for bromethalin

Fat

Toxin that is more associated with moluscicides

Metaldehyde

Metaldehyde mechanism of action

Suppresses GABA production → lack of CNS inhibition

Phases of metaldehyde poisoning

GIT signs → CNS excitation

Typical cause of death with metaldehyde poisoning

Respiratory arrest :)

Treatment for metaldehyde poisoning

• Control neuro: benzos, PB

• Control hyperthermia

• Supportive IVF and bicarb for acidosis

Anecdotal evidence supporting a diagnosis of metaldehyde toxicity

• Hyperthermia

• Blue bait material in stomach contents

• Formaldehyde-like smell

Best test for metaldehyde poisoning

GIT contents, sealed and frozen! Volatile!

Toxin associated with predator control

Sodium monofluoroacetate (compound 1080)

Compound 1080 mechanism of action

Inhibits aconitase enzyme in the krebs cycle, blocking ATP production

Syndromes seen with compound 1080 toxicity

CNS effects in “smarter” animals (carnivores) and CV failure in “dumber” animals (livestock)

CS associated with compound 1080 toxicity in dogs

GIT signs → vocalization and generalized CNS signs → resp failure and death

CS associated with compound 1080 in cows

Pre-heart failure condition → acute stress/disturbance → acute heart failure and death

Primary diagnostic for compound 1080

History and CS, can test stomach contents

Gross lesions/conditions associated with compound 1080 toxicity in dogs

Rapid rigor mortis due to lots of muscle movement before death

Treatment for compound 1080 toxicity

• Early and aggressive decontamination

• Supportive fluids and bicarb

Prognosis for compound 1080 toxicity

Poor once CS appear

Specific chlorinated hydrocarbon that was used to eradicate malaria

DDT

Why are DDT sprays way less common today

It causes thinning of bird shells, and almost eradicated certain species of bird

Chlorinated hydrocarbon mechanism of action

Blocks GABA receptors (like strychnine!) → forced depolarization

CS associated with chlorinated hydrocarbon toxicity

• Progressive agitation

• Hyperexcitability

• Ataxia

• Intermittent seizures

Cause of death in chlorinated hydrocarbon toxicity

Respiratory arrest

Treatment for chlorinated hydrocarbon exposure

• Decontaminate (GIT or dermal)

• Control neuro

Why are corn gluten rodenticides marketed as being safe

All the ingredients are Generally Regarded as Safe (GRAS)