4.5 Insecticides and Rodenticides Flashcards

1
Q

are most herbicides, pesticides, insecticides and fungicides very toxic? what is the prognosis? are there exceptions?

A
  • 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
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2
Q

what is rotenone? what is it used for? what species is it toxic for? what is the mechanism of toxicity?

A

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)

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3
Q

clinical signs of rotenone toxicity?

A

vomiting (low dose) but may progress to lethargy, tremors, seizures (high dose) ➝ respiratory failure, dyspnea and death

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4
Q

how do we diagnose rotenone toxicity?

A

history, pulmonary congestion, GI irritation

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5
Q

how do we treat rotenone toxicity? what is the prognosis?

A

 Treatment:
-minimize absorption: bathe with detergent; nonspecific detoxification
-correct acidosis if present
-diazepam for seizures
 Prognosis: good

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6
Q

what are pyrethrins/pyrethroids? what are they used for? what is their toxicokinetics and mechanism of toxicity?

A

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

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7
Q

clinical signs of pyrethrin/pyrethroid toxicosis?

A

 Paresthesia, abnormal behaviour
 Irritation: Salivation, vomiting, diarrhea
 Hyperexcitability, tremors & seizures,
dyspnea, weakness & death
 Highly toxic to cats and fish

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8
Q

how can we diagnose pyrethrin/pyrethroid toxicosis?

A

History; no specific clinical or anatomic pathology lesions; tissue analysis not useful

  • CBC: stress leukogram
  • biochemistry: hyperglycemia
  • R/O: Organophosphates, metaldehyde
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9
Q

treatment for pyrethrin/pyrethroid toxicity? prognosis?

A

 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)

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10
Q

how would a cat with pyrethrin toxicity look at on presentatoin? what is the mechanism that results in this?

A

Binds to sodium channel on nerves
> Prolonged opening of Na+ channels ➝ repetitive sensory nerve impulses

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11
Q

what is the source of organophosphates and organocarbamates? what are they used for and how can animals be exposed?

A

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

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12
Q

what are the toxicokinetics of organophosphates and organocarbamates?

A

Toxicokinetics:
 Rapidly absorbed *by any route
 Do not accumulate in fat
 Metabolized by plasma esterases
 Rapidly excreted in urine

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13
Q

Mechansim of toxicity of organophosphates and organocarbamates?

A

 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

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14
Q

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?

A

 High acute toxicity, rarely chronic
 Cats more susceptible than dogs
 Poultry have lower tolerance than mammals
 Metabolized & excreted rapidly, AChE regeneration needs 2 wks

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15
Q

clinical signs of toxicity due to organophosphates and organocarbamates

A

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

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16
Q

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?

A

 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

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17
Q

how do we treat a case of organophosphates and organocarbamates toxicity? what is the prognosis?

A
  • 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)

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18
Q

public health considerations for organophosphates and organocarbamates?

A

-Avoid exposure when washing/bathing
-Meat residues are not a problem since they are rapidly excreted
-Hold milk until no residues present

19
Q

what is metaldehyde used for? what animals ingest it more commonly?

A

Sources/Exposure: slug & snail bait
 Used in coastal/lowland wet areas
 Pets are attracted to baits
 Common in dogs, also in cats & sheep

20
Q

toxicokinetics of acetaldehyde?

A

 Acetaldehyde liberated by gastric acid
 Odor like mild formaldehyde
 Both metaldehyde and acetaldehyde are readily absorbed from the GI tract

21
Q

mechanism of metaldehyde

A

– Role of both metaldehyde and acetaldehyde is unclear,
may be due to decreased [serotonin] & [GABA] in brain

22
Q

clinical signs of metaldehyde toxicity?

A

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)

23
Q

diagnosis of metaldehyde toxicity?

A

– No specific lesions
– Acetaldehyde in stomach (odour), submit contents frozen
– Test blood cholinesterase to R/O OP toxicosis
– Acidosis due to acetaldehyde production

24
Q

treatment of metaldehyde toxicity? prognosis?

A

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

25
Q

what is amitraz? how are animals exposed to it?

A

Formamidine insecticide (Mitaban for demodecosis; Preventic, tick-repellent collars)

Source/Exposure:
 Topical miticide; flea collars, ectoparasite control in
swine
 Careless use of spray or dip
 Dogs may eat flea collars
 Contraindicated in horses

26
Q

toxicokinetics of amitraz

A

 Readily absorbed orally
 Excreted in urine

27
Q

mechanism of action of amitraz? what is the antidote?

A

Most of the adverse effects in mammals is related to alpha2 agonist effects in CNS (yohimbine or atipamezole reverses) < antidote!

28
Q

clinical signs of amitraz toxicity. how fast do they come on?

A

– Signs within 2-4h of exposure
– Bradycardia, sedation, hypotension (α2 effect), ataxia, depression, vomiting, diarrhea, seizures
– Horses are very susceptible to ileus and colic

29
Q

how to diagnose amitraz toxicity?

A

– Hyperglycemia, few specific lesions, amitraz in stomach contents

30
Q

how to treat amitraz toxicity? prognosis?

A

– Detoxification: bathe, emetics (early), activated charcoal
– Yohimbine/atipamezole to treat α2 effects
– IV fluids, diazepam for seizures

prognosis:
– Good with prompt and appropriate Rx

31
Q

what are macrolide endectocides? what is their mechanism?

A

 Source: Ivermectin (Ivomec, Heartgard, Eqvalan), abamectin, dormectin (Dectomax), milbemycin oxime (Interceptor), moxidectin (ProHeart, Quest), selamectin (Revolution)

 Mechanism: GABA agonist (GABA in CNS in mammals)
-GABA found in PNS in arthropods & nematodes

32
Q

what is the toxicity of macrolide endectocides? what animals are susceptible?

A

 Very safe in most breeds of dog (toxicity at 200x Rx dose)
 Collies, shelties & border collies are most susceptible (15x Rx dose)
 Collies have a mutation in mdr gene that codes for a P-glycoprotein drug efflux protein in the blood-brain barrier – inhibits ability to restrict entry ivermectin into brain

33
Q

clinical signs of macrolide endectocide toxicity

A

 Tremors, mydriasis, depression, ataxia, coma & death

34
Q

treatment of macrolide endectocide toxicity? prognosis?

A

Treatment:
 Decontamination: charcoal & cathartic if recent oral exposure
 Supportive care
 Epinephrine for acute anaphylactic reactions

Prognosis: therapy may be prolonged but prognosis good

35
Q

what is fipronil and what does it cause? how can we treat toxicity and what is the prognosis?

A

Fipronil (Frontline) -spot-on & spray (binds GABA gated Cl channels)
-Dermal hypersensitivity reactions;
-Tremors/seizures in rabbits (off-label)
-Bathe with detergent; diazepam for seizures
-Prognosis good for most exposures; guarded for seizing rabbits

36
Q

what is imidacloprid and what does it do? what can it cause in toxic doses and how do we treat?

A

Imidacloprid (Advantage) -spot-on
-ACh receptor agonist; higher affinity for insect receptors
-Acute oral toxicity: salivation or vomiting
-Dermal hypersensitivity –bathe with detergent
-Antihistamines or steroids in extreme cases

37
Q

what is 4-aminopyridine (Avitrol)? what is it used for?

A

Avicide

  • Sources:
    – Bird control agent, usually in corn
    – Bait has 0.5-3.0% 4-aminopyridine
    – Pigeons or starlings often presented
    – Abnormal behaviour; distress cry
    – Intent is to poison a few, frighten the rest away
    – Infrequently ingested by dogs and horses
38
Q

toxicokinetics of 4-aminopyridine (Avitrol)

A

– Rapidly absorbed by GIT
– Rapid hepatic metabolism, excreted in urine

39
Q

mechanism of action of avitrol

A

– Increased release of ACh ➝ increased cholinergic neurotransmission
– Blocks K+ current of repolarization
– Resembles toxicity by cholinesterase inhibitors

40
Q

what is avitrol toxic for?

A

– Highly toxic to birds and mammals
– LD50 of 3.7 mg/kg (dogs)
– i.e. LD50 dose for 25 kg dog = 20 g of 0.5% bait

41
Q

clinical signs of 4-aminopyridine (Avitrol) toxicity?

A

Mammals:
– Nervous system overstimulation (like OPs):
> Hyperexcitability, salivation, tremors, incoordination, tonic clonic seizures
– Cardiac arrhythmias, tachycardia (unlike OPs)

Birds:
– Disorientation, seizures, vocalization

42
Q

how can we diagnose 4-aminopyridine (Avitrol) toxicity?

A

Ddx: OP insecticides, metaldehyde, tremorgenic mycotoxins No specific pathology lesions; 4-AP in stomach, liver, kidney

43
Q

treatment for 4-aminopyridine (Avitrol) toxicity? prognosis?

A

– Detoxification, before signs
– Pancuronium bromide (neuromuscular blocker) as antagonist
– Diazepam for seizures

  • Prognosis
    – Favourable if survive 4h after onset of signs