4.5 Insecticides and Rodenticides Flashcards
(43 cards)
are most herbicides, pesticides, insecticides and fungicides very toxic? what is the prognosis? are there exceptions?
- most herbicides, pesticides, insecticides and fungicides have low toxicity and high success rate of treatment
- Exceptions include organophosphate/carbamate insecticides and rodenticides= these are extremely toxic
what is rotenone? what is it used for? what species is it toxic for? what is the mechanism of toxicity?
Source/Exposure: topical treatment of cattle lice and mites, flea control products (less common),
Excessive use of powders and dips: i.e. cats, grooming & oral exposure
Intentionally in water to kill fish – easily absorbed through gills
Toxicity:
birds, fish and cats are most susceptible
acute toxicity most common
Mechanisms of Toxicity:
Physical irritant
Interferes with nerve conduction (blocks mitochondrial electron transport chain)
clinical signs of rotenone toxicity?
vomiting (low dose) but may progress to lethargy, tremors, seizures (high dose) ➝ respiratory failure, dyspnea and death
how do we diagnose rotenone toxicity?
history, pulmonary congestion, GI irritation
how do we treat rotenone toxicity? what is the prognosis?
Treatment:
-minimize absorption: bathe with detergent; nonspecific detoxification
-correct acidosis if present
-diazepam for seizures
Prognosis: good
what are pyrethrins/pyrethroids? what are they used for? what is their toxicokinetics and mechanism of toxicity?
Source/Exposure: insecticides & flea control
Excessive use of sprays or spot-on products
Inappropriate use (enclosed spaces, open aquariums)
Toxicokinetics:
Lipophilic, partially absorbed orally and dermally Distributed to high lipid tissues (fat, CNS, PNS)
Rapidly metabolized & excreted
Mechanism of Toxicity:
Binds to sodium channel on nerves > Prolonged opening of Na+ channels ➝ repetitive sensory nerve impulses
clinical signs of pyrethrin/pyrethroid toxicosis?
Paresthesia, abnormal behaviour
Irritation: Salivation, vomiting, diarrhea
Hyperexcitability, tremors & seizures,
dyspnea, weakness & death
Highly toxic to cats and fish
how can we diagnose pyrethrin/pyrethroid toxicosis?
History; no specific clinical or anatomic pathology lesions; tissue analysis not useful
- CBC: stress leukogram
- biochemistry: hyperglycemia
- R/O: Organophosphates, metaldehyde
treatment for pyrethrin/pyrethroid toxicity? prognosis?
Treatment: no antidote, try to minimize absorption: bathe with detergent, general detoxification, and control seizures/spasms: diazepam, barbiturates, methocarbamol
Prognosis: generally excellent (cats with spot-on, guarded)
how would a cat with pyrethrin toxicity look at on presentatoin? what is the mechanism that results in this?
Binds to sodium channel on nerves
> Prolonged opening of Na+ channels ➝ repetitive sensory nerve impulses
what is the source of organophosphates and organocarbamates? what are they used for and how can animals be exposed?
Source/Exposure: still widely used
Insecticides: fly, ant & roach baits, shampoos, collars, dips & sprays
Animals can be exposed by contaminated feedstuffs
Improper use: plant insecticides on animals
what are the toxicokinetics of organophosphates and organocarbamates?
Toxicokinetics:
Rapidly absorbed *by any route
Do not accumulate in fat
Metabolized by plasma esterases
Rapidly excreted in urine
Mechansim of toxicity of organophosphates and organocarbamates?
Phosphorylates or carbamylates bind acetycholinesterase (AChE) to inhibit it
> Remember – AChE plays a vital role in the breakdown of the neurotransmitter acetylcholine, which is found in both the peripheral and central nervous systems
> Increased ACh in cholinergic synapses at parasympathetic (muscarinic) & neuromuscular (nicotinic) sites
>neurons continue to fire
OP have higher affinity for AChE than do carbamates
OPs have a reversible bond until “aging” (loss of one of alkyl groups) occurs, then stable bond and irreversible
OCs are reversible/temporarily bound to AchE
what is the nature of of the toxicity of organophosphates and organocarbamates? what species are susceptible? how long does it take for effects to leave?
High acute toxicity, rarely chronic
Cats more susceptible than dogs
Poultry have lower tolerance than mammals
Metabolized & excreted rapidly, AChE regeneration needs 2 wks
clinical signs of toxicity due to organophosphates and organocarbamates
Muscarinic & nicotinic signs; excessive cholinergic stimulation
Acute poisoning can occurs within 30 min, usually 6h
These mnemonic devices can help you remember the signs of organophosphate toxicities (most of these are due to muscarinic overstimulation):
SLUDGE
how do we diagnose organophosphates and organocarbamates toxicity? should we wait for results to treat? what type of sample can be useful to look at after some time has passed?
Evaluation of cholinesterase activity suggestive of exposure
> Remember these compounds phosphorylate or carbamylate acetycholinesterase (AChE) to inhibit it, so activity should be REDUCED
Whole blood (EDTA; cattle), plasma (dogs) or brain
> Also can test urine, hair, GI contents
> Depression of blood cholinesterase does not necessarily correlate with the severity of poisoning, but can help make the diagnosis
Don’t wait for results, treat immediately
If storage necessary, freeze plasma
Decreased blood AChE activity by 25-50% in severe cases
Tissue residues low since not stored i.e. OPs hydrolyzed within hrs, stomach contents useful
how do we treat a case of organophosphates and organocarbamates toxicity? what is the prognosis?
- Decontamination: bathe, emesis, lavage, activated charcoal (esp in cattle)
- Treat seizures (usually with diazepam)
- Atropine (0.2-0.5 mg/kg) 1/4 IV, 3/4 SC repeat in 6h if necessary
- Pralidoxime chloride (2-PAM) 20 mg/kg IM, releases the AChE so it becomes functional again, if OP bonds have not aged (best case scenario given within 24 h!!!)
> Aging of OP increases stability of phosphorylated enzyme and then 2-PAM not effective
Prognosis: very poor, high mortality
-early treatment and minimal exposure improves prognosis
-carbamates have better prognosis (bind less tightly to AChE)
public health considerations for organophosphates and organocarbamates?
-Avoid exposure when washing/bathing
-Meat residues are not a problem since they are rapidly excreted
-Hold milk until no residues present
what is metaldehyde used for? what animals ingest it more commonly?
Sources/Exposure: slug & snail bait
Used in coastal/lowland wet areas
Pets are attracted to baits
Common in dogs, also in cats & sheep
toxicokinetics of acetaldehyde?
Acetaldehyde liberated by gastric acid
Odor like mild formaldehyde
Both metaldehyde and acetaldehyde are readily absorbed from the GI tract
mechanism of metaldehyde
– Role of both metaldehyde and acetaldehyde is unclear,
may be due to decreased [serotonin] & [GABA] in brain
clinical signs of metaldehyde toxicity?
ClinicalSigns: “Shake and Bake”
– All species susceptible, dogs most frequently affected
– Acute toxicity: anxiety, restlessness, ataxia
– Hypersalivation, mydriasis, tremors, ataxia, incoordination
– Severe muscle tremours, opisthotonos, convulsions, hyperthermia (all usually develop within 1–3 hr after ingestion)
diagnosis of metaldehyde toxicity?
– No specific lesions
– Acetaldehyde in stomach (odour), submit contents frozen
– Test blood cholinesterase to R/O OP toxicosis
– Acidosis due to acetaldehyde production
treatment of metaldehyde toxicity? prognosis?
Treatment:
Emesis (if asymptomatic) or gastric lavage
Activated charcoal to reduce enterohepatic cycling of metaldehyde.
Seizure control: diazepam most commonly used
IV fluids
Sodium bicarbonate to reverse acidosis
Monitor temp and cool with wet towels and fans
No specific antidote
Prognosis:
Depends on dosage, time elapsed, speed of treatment
Good with aggressive treatment and supportive care
