Antiparasitics

Question 1

antiparasitics can be broadly classified in 3 ways

Answer 1

endoparasiticides, ectoparasiticides, endectocides

Question 2

2 ways drugs are different than pesticides: how are they identified? which can be used extra-label?

Answer 2

drugs: DIN, can be prescribed, extra-label permitted
pesticides: PCP (Pest Control Products Act) registration number, can’t be used extra-label

Question 3

what are 3 main reasons for anti parasitic treatment failure

Answer 3

resistance!!
also failure to integrate drug treatment with mgmt strategies and incorrect use due to lack of knowledge

Question 4

what NT activates nicotinic receptors

Answer 4

acetylcholine, ACh

Question 5

where are nicotinic receptors found in mammals

Answer 5

SNS and PSNS ganglia, muscel, CNS

Question 6

where are nicotinic receptors found in nematodes

Answer 6

muscle, neurons

Question 7

where are nicotinic receptors found in insects

Answer 7

CNS

Question 8

both curare and snake alpha-neurotoxin contain _______ which acts as a neuromuscular blocker causing [not red]

Answer 8

nAchR antagonist (block Ach interacting with nicotinic receptors)

Question 9

myasthenia graves results in destruction of nAchRs at NMJ. what does treatment involve, and how does it work

Answer 9

administration of acetylcholinesterase antagonist:

ok. so. Ach acts at nAchRs of spinal cord ganglion of SNS; myasthenia gravis destroys these receptors so that signals.
AchE breaks down Ach. if AchE is INHIBITED, then more Ach stays in synapse, so nerve impulses keep going.
[the drug isn’t helping the destroyed receptors, but it keeps the Ach levels up]

Question 10

give MOA for levamisole and pyrantel

Answer 10

nAch agonists and AchE inhibitors, causing spastic paralysis of nematode muscles.
[weak agonists for mammalian nAchRs and strong agonists of nematode nAchRs]

Question 11

this drug toxicity looks similar to organophosphate poisoning: see muscarinic and nicotinic effects. the is drug is given PO, parenterally, or topically. effective against mature ruminant parasites.
what is the drug? what is the class?

Answer 11

levamisole, an imidazothiazole

Question 12

what are signs of NICOTINIC overstimulation

Answer 12

muscle tremors (first head, then body), tetany, weakness, tachycardia, myadriasis (due to SNS activation by nicotinic overstimulation)

Question 13

what are signs of MUSCARINIC overstimulation

Answer 13

diarrhea, urination, miosis, bradycardia, bronchospasms, emesis, lacrimation, loss muscle strength, salivation, sweating. DUMBBELLSS

Question 14

this drug has same MOA as imidazothiazoles (eg. levamisole), is poorly absorbed from the GIT and is generally very safe, safer than levamisole, acts directly on the worms in GIT. it is only available orally and has lots of resistance.
what is the drug? what is the class?

Answer 14

pyrantel, a tetrahydropyrimidine

Question 15

organophosphates and carbamates are pesticides commonly used in agriculture. toxicosis can occur.
what is the mechanism of toxicity for each?

Answer 15

acetylcholinesterase inhibition (acetylcholine excess)
organophosphate = irreversible
carbamate = reversible

Question 16

organophosphate and carbamate toxicosis acute syndrome: what are the 3 broad categories of clinical signs that can occur?

Answer 16

muscarinic, nicotinic, CNS. C/S vary between cases

(specifically:
- Muscarinic (DUMBBELLS): Diarrhea, Urination, Miosis, Bronchorrhea (also bronchospasm), Bradycardia, Emesis, Lacrimation, Lethargy, Salivation/sweating
- Nicotinic: Muscle tremors (first head, then body), tetany, weakness, tachycardia and mydriasis (because of sympathetic activation by nicotinic receptor overstimulation)
- CNS: Anxiety, restlessness, hyperactivity, depression, seizures, depressed respiration, and coma)

Question 17

organophosphate and carbamate toxicosis acute syndrome: death occurs due to what?

Answer 17

respiratory failure!
massive respiratory secretions, bronchiolar constriction, and intercostal and diaphragm muscle paralysis

Question 18

describe intermediate syndrome of organosphosphate/carbamate toxicosis: what does it results from? what is it caused by/ what do clinical signs relate to?

Answer 18

chronic exposure to single exposure to very lipophilic compound. may follow acute crisis or be the only effect
due to development of Ach tolerance: down regulation of muscarinic Ach receptors, therefore C/S relate to nicotine overstimulation

Question 19

organophosphate and carbamate toxicosis: what are clinical signs in large animals

Answer 19

similar to small animals: nicotinic, muscarinic, and CNS effects. delayed polyneuropathy weeks to months after exposure (weakness, ataxia, progressing to paralysis with loss of tail, anus, and bladder tone) acutely, bloat in cattle

Question 20

organophosphate and carbamate toxicosis: describe treatment

Answer 20

severe muscarinic signs require emergency treatment with atropine!
reactivate AchE in organophosphate toxicity
decontamination: emesis or washing with dish soap

Question 21

increasing the influx of sodium through VGNaCs in axons (excessively) leads to what

Answer 21

excessive depolarization and cell death

Question 22

pyrethrin and pyrethroid MOA

Answer 22

increasing the influx of sodium through VGNaCs in axons leading to excess depolarization and cell death in insect nervous system

Question 23

why is pyrethrin/pyrethroid toxicosis primarily a problem in cats

Answer 23

metabolism of the insecticide requires glucoronidation can cats are bad at it