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Veterinary Toxicology > Neuromuscular Toxicants > Flashcards

Neuromuscular Toxicants Flashcards

1
Q

What is the site of action of neuromuscular toxicants?

A

NMJ - motor neurons using Ach to act upon N receptors on skeletal muscle

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2
Q

How do neurons and nicotinic receptors work at the neuromuscular junction?

A

action potential causes a calcium influx, allowing vesicles to bind to the pre-synaptic cleft and release Ach to bind to the N receptor —> sodium rushes into muscle cells with potassium leaving, causing local depolarization

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3
Q

What are the functional and structural mechanisms of neuromuscular toxicosis?

A

FUNCTIONAL - impairment of neuromuscular transmission

STRUCTURAL - peripheral motor neuropathy, axonopathy, and myelinopathy

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4
Q

What is axonal dieback?

A

toxic injury causes the tip of the motor neuron to retract to the cell body (distal to proximal) and no longer communicate with skeletal muscle - axonopathy

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5
Q

What are some common clinical signs of neuromuscular toxicosis?

A
  • atony: lack of muscle tone
  • tetany: intermittent muscular spasms
  • tremors
  • myotonia: prolonged muscle contraction or muscle rigidity
  • paresis/paralysis
  • myasthenia: muscle weakness/fatigue
  • cramps, spasms, twitching
  • convulsions, seizures, ataxia
  • respiratory signs and recumebency
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6
Q

Where is the Black Widow Spider found? How do females and males compare? How can they be identified?

A

continental US - commonly on woodpiles and garages

females are offensive, males are not

red/orange/yellow hourglass mard on abdomen

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7
Q

What is the toxic principle of Black Widow Spiders? What are the 2 mechanisms of toxicity?

A

α-latrotoxin

  1. binds to neurexins and calcium-independent receptor for latrotoxin (CIRL) on motor neurons, causing the release of NT:
    - CALCIUM-INDEPENDENT - direct action of CIRL activates phospholipase, releasing calcium, which allows for the release of ACh, GABA, glutamate
    - CALCIUM-DEPENDENT - neurexin activation causes pore-formation, allowing calcium to enter the neuron, resulting in the release of catecholamines
  2. inhibits presynaptic NT reuptake
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8
Q

What species is most suscpetible to Black Widow Spider toxins? What clinical sign is unique in this species? What are other clinical signs?

A

cats —> abdominal pain causing howling

CNA and muscular
- muscle fasciculation and rigidity
- paresthesia
- ataxia
- cramps
- seizures
- flaccid paralysis —> ascending paralysis
- dyspnea due to involvement of respiratory muscles

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9
Q

What drugs are recommended for pain management and muscle cramping/seizures in Black Widow Spider toxicity?

A

OPIOIDS - Morphine, Meperidine, Butorphanol, Fentanyl

BENZODIAZEPINES - Diazepam
+ Methocarbamol

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10
Q

What antivenin is available for Black Widow Spider toxin? What patients is it recommended to use in? What should be prepared for upon administration?

A

Lyovac antivenin

high-risk patients (neonatal/geriatric) or those not responding to symptomatic treatment

anaphylactic reaction

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11
Q

What is the most potent toxin known to man? What 4 syndromes does it cause?

A

Botulinum neurotoxin (BoNT)

  1. botulism
  2. limberneck
  3. shaker foal syndrome
  4. sausage poisoning
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12
Q

What produced Botulinum neurotoxin? What types of toxins are significant in cattle, horses, and birds?

A

produced under anaerobic conditions by Clostridium botulinum

CATTLE - BCD
HORSES - ABC
BIRDS -ABCE

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13
Q

What are the 3 routes of exposure to Botulinum neurotoxin?

A
  1. oral - ingestion of carrion, poorly preserved food, decaying vegetation, and vertebrates (waterfowl)
  2. inhalation
  3. deep wound contamination
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14
Q

What 4 species are most susceptible to Botulinum neurotoxin? What 2 are resistant?

A
  1. wild birds
  2. poultry
  3. cattle
  4. horses
  • pigs
  • dogs
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15
Q

What is the cycle of Botulinum neurotoxin transmission like?

A

carcass-maggot cycle - duck eats infected maggots and dies; flies lay eggs on carcass; maggots hatch and eat infected meat starting the cycle again

  • common in summer and fall when waterfowl are active
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16
Q

What is the structure of Botulinum neurotoxin? What is its mechanism of toxicity?

A

zinc metalloprotease with a heavy and light chain

enters presynaptic nerve endings by endocytosis and heavy chain binds to synaptotagmin, causing the blockage of ACh release at the NMJ —> flaccid paralysis

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17
Q

How does Botulinum neurotoxin block the release of acetylcholine into the NMJ?

A

inhibits exocytosis by cleaving proteins (SNARE) essential for the fusion of the membrane of synaptic vesicles containing ACh with the neuronal cell membrane

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18
Q

What 3 proteins are targeted by Botuliun neurotoxin? What toxins target each?

A
  1. SNAP-25: A, C, E
  2. synaptobrevin: B, D, F, G
  3. syntaxin: C
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19
Q

Target proteins for BoNT:

A
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20
Q

What is the most common sign of Botulism? What is usually seen?

A

progressive neuromuscular dysfunction causing flaccid paralysis with muscle weakness starting in the rear quarters and ascends to the forequarters, neck, and head
+ ataxia, depression, weak tail and tongue muscles (loose tongue common)

sudden death may be only sign

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21
Q

What 3 poor reflexes of the eye and throat are commonly seen with cranial muscle involvement n botulism? What are 2 additional signs?

A
  1. slow pupillary light response - optic/oculomotor
  2. decreased palpebral reflex - trigeminal/facial
  3. decreased gag reflex - glossopharyngeal/vagus

mydriasis, weak vocalization

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22
Q

What are common ANS signs associated with botulism?

A
  • bradycardia
  • vomiting
  • inability to swallow
  • ileus
  • constipation, ruminal atony
  • frequent attempts to urinate (horses)
  • recumbency
  • death from respiratory paralysis
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23
Q

What unique signs of botulism are seen in foals and waterfowl?

A

SHAKER FOAL SYNDROME - common in KY and mid-Atlantic; tremors

LIMBERNECK - progressive paralysis of legs, wings, and neck with death by drowning

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24
Q

What drugs are recommended to counteract flaccid muscles and muscarinic signs with botulism?

A

Physostigmine - AChE inhibitor

Atropine

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25
Q

What are the 5 ways to treat botulism?

A
  1. remove feedstuff causing toxicosis
  2. provide nutritional support - hand-feeding, watering
  3. administer antitoxin if Dx is made early (polyvalent B/C, monovalent B)
  4. administer antibiotic - Penicillin, Metronidazole, Amoxicilli
  5. debride wound for animals suffering from wound botulism
26
Q

What ticks in USA and Australia can cause paralysis? How is toxicity described? What animals are most susceptible?

A

USA = female Dermacentor andersoni, Dermacentor variabilis
AUSTRALIA = Ixodes and Amblyomma spp.

seasonal with tick activity

cattle, sheep, horses, dogs, rarely cats

27
Q

What is the mechanism of toxicity of tick paralysis?

A

holocyclotoxins secreted from tick salivary glands block ACh release at the NMJ and inhibit depolarization of lower motor neurons —> paralysis

28
Q

What clinical signs are commonly seen with tick paralysis? What 2 cranial nerves are typically affected?

A

(one tick is all it takes)
- ascending flaccid paralysis beginning at pelvic limbs, ascending to whole body
- apprehension
- ataxia
- wide-based stance
- respiratory paralysis = death

  1. decreased gag reflex - glossopharyngeal/vagus
  2. anisocoria - oculomotor
29
Q

What 2 unique clinical signs are seen in dogs with tick paralysis? What causes this?

A
  1. anorexia
  2. changes in phonation

laryngeal paresis

30
Q

How can tick paralysis be diagnosed? Treated?

A

presence of ticks associated with sudden appearance of limb weakness and/or respiratory impairment - tick may no longer be attached, but a bite mark can be seen

  • remove tick —> recovery in 72 hr
  • apply acaricide
  • support respiration in severe cases
31
Q

What is the source of anatoxin-a? What is its mechanism of toxicity?

A

blue-green algae (Anabaena spp.)

nicotinic agonist - similar to succinylcholine overdose

32
Q

What are the most common clinical signs of anatoxin-a toxicity?

A
  • rapid onset of muscle rigidity and tremors
  • cyanosis
  • convulsion
  • paralysis and respiratory distress —> death
33
Q

How can anatoxin-a toxicity be diagnosed?

A
  • history of recent contact of ingestion of blue-green algae and compatible clinical signs
  • compatible blood/plasma biochemical changes showing reduced cholinesterase activity
  • water harboring appropriate algae or toxin
34
Q

What makes anatoxin-a toxicity difficult to treat? What is commonly done?

A

no antidote and rapid/potent onset of symptoms

  • support and symptomatic treatment: respiratory support and seizure control
  • decontamination: induce emesis then administer charcoal and cathartic
  • fence off contaminated ponds and lakes to prevent exposure
35
Q

What is the source, mechanism of toxicity, and clinical signs of tetrodotoxin toxicity?

A

puffer fish, frogs, newts

inhibits hast sodium channels in nerves and muscles

paralysis

36
Q

What are 2 biotoxins that can cause paralytic shellfish poisoning? What is the source and mechanism of toxicity?

A
  1. saxitoxin
  2. neosaxitoxin

cockles, mussels, clams, oysters - secreted by dinoflagellates and blue-green algae

blocks sodium channels, causing paralysis

37
Q

What is the main source of ionophores? What is their mechanism of toxicity?

A

coccidiostats and growth promotants (monensin, lasalocid, narasin, salinomycin, etc.)

bind and preferentially transport cation across cell membranes as ion channels or ion carriers, causing…

  • ion imbalance and deficits in excitable tissue function
  • mitochondrial ion imbalance decreasing ATP
38
Q

What species is most susceptible to ionophore toxicity? What are the earliest signs? What else is seen?

A

horses are 10x more sensitive than cattle

food refusal and watery diarrhea

  • weakness, ataxia
  • paresis/paralysis
  • tremors
  • stumbling, exaggerated stepping
  • dyspnea, sweating
  • tachycardia, jugular pulse
  • hesitation to turn or move
  • recumbency
  • rumen atony
  • dehydration, death
39
Q

How should dogs/cats and farm animals be decontaminated of ionophore toxicity? What unique treatment can be used as supportive therapy?

A
  • emesis
  • activated charcoal and cathartic

antioxidants - vitamin E and selenium

40
Q

Where are Larkspurs (Delphinium) commonly found? What species are most susceptible? What is used for biological control?

A

western USA

cattle

sheep —> tolerate 4-5x amount lethal to cattle

41
Q

What is the main cause of cattle losses in western ranges?

A

Larkspur (Delphinium) toxicity

42
Q

What are the 2 toxic principles of Larkspur (Delphinium)? How do they compare?

A

diterpene alkaloids

  1. methyllycaconitine (MLA)
  2. 14-deacetylnudicauline (DAN)

DAN is more toxic, MLA occurs in greater quantities (high concentrations in early growth)

43
Q

What is the mechanism of Larkspur (Delphinium)? Which toxic principle has extra action? What receptors are most sensitive?

A

act at postsynaptic nicotinic cholinergic receptors and block the action of ACh at the NMJ

MLA also blocks ACh receptors in the CNS

cholinergic receptors of cattle

44
Q

What is the most common sign of Larkspur toxicosis? What else is seen?

A

sudden death

(nervous, muscular, GI)
- hyperirritability
- confusion
- muscle tremors
- convulsions
- stiffness/weakness
- constipation, bloat
- oral irritation, salivation
- nausea, vomiting
- collapse with head downhill
- prostration
- inhalation pnuemonia

45
Q

What is the best way to diagnose Larkspur poisoning in cattle? How are they treated?

A

presence of bloat and ruminal contents in bronchi

  • cholinesterase inhibitors: physostigmine
  • avoid stress and excitement
  • relieve bloat with stomach tube and trocarization
  • give antibiotics for inhalation pnemonia
46
Q

What is the most economically significant toxic plant in the US? Where do most poisonings appear?

A

Locoweeds - Astragalus, Oxytropis (vetches)

Pacific Northwest

47
Q

What is the toxic principle in Locoweeds (vetches)? What is responsible for toxicity?

A

nitropropanol glycosides are hydroluzed into nitrotoxins by rumen microbes —> 3-nitro-1-propanol (3-NPOH), 3-nitropropionic acid (3-NPA)

3-NPOH is absorbed and metabolized in the liver to 3-NPA (if 3-NPA is ingested, most is degraded in the GI tract causing lower toxicity)

48
Q

What species are susceptible to Locoweed (vetch) toxicity? What are most likely to be poisoned? In what 2 of these species is it more acute?

A

cattle, horses, sheep, wild herbivores

lactating cattle

sheep and horses —> especially in midsummer

49
Q

What are the 4 steps in the mechanism of toxicity in Locoweeds (vetches)?

A
  1. 3-NPA inhibits succinate dehydrogenase, fumerase, and aspartase in the Krebs cycle leading to decreased ATP production and loss of cellular homeostasis
  2. axonal degeneration in spinal cord
  3. 3-NPA causes hypotension via vasodilatory and cardiodepressor activity
  4. induces methemoglobinemia by being metabolized into nitrites, which oxidize Hb
50
Q

What are the acute signs of nitrotoxicosis associated with Locoweeds (vetches)?

A
  • constipation
  • ataxia
  • staggering gait
  • recumbency
  • death from cardio-respiratory failure
51
Q

What are the more common gradual signs of nitrotoxicosis associated with Locoweeds (vetches)?

A
  • dyspnea
  • salivation
  • weakness
  • muscular spasms
  • docile temperament
  • goose-stepping
  • cracker heels: clicking dewclaws of rear limbs
  • knuckling fetlocks
  • posterior paresis/paralysis
  • loss of body condition
52
Q

What is the main way to treat nitrotoxicosis associated with Locoweeds (vetches)?

A

cattle tend to avoid locoweeds when other forage is available and toxin concentration decreases rapidly as plants mature —> proper amount of feed and withdraw from source

53
Q

What are the main sources of tremorgenic mycotoxins? What 3 species are most affected?

A
  • tremorgenic forages (ryegrass, Dallis grass, Bermuda grass)
  • moldy cheese, bread, walnuts, and pasta
  • garbage

dogs, sheep, horses

54
Q

What are the 3 main toxic principles of tremorgenic mycotoxins? What species are affected by each?

A
  1. Penitrem A and roquefortine C (Penicillium crustosum, P. roqueforti) - dogs
  2. Lolitrem B (Acremonium loli) - livestock
  3. Paspalitrema (Claviceps paspali) - livestock
55
Q

Where are tremorgenic mycotoxins absorbed? Excreted?

A

rapidly absorbed from GI tract

bile

56
Q

How does the onset of clinical signs of tremorgenic mycotoxins compare in dogs and cattle?

A

DOGS = 15 mins after ingestion (small breed dogs show tremors after ingesting one slice of moldy bread)

CATTLE = 7 days of grazing on contaminated forage

57
Q

What are the 3 mechanisms of toxicity of tremorgenic mycotoxins?

A
  1. cause presynaptic release of ACh and prolong depolarization at the NMJ to facilitate transmission at motor endplate
  2. reduces GABA and glycine to cause CNS stimulation
  3. cerebral vasoconstrictions causing anoxia and CNS signs
58
Q

What are common clinical signs of tremorgenic mycotoxin toxicity? How does this compare in livestock?

A
  • tremors leading to spastic ataxia
  • opisthotonus
  • seizures, tetany, muscle fasciculation
  • tachycardia, hyperexcitation, vocalization
  • recumbency

appear normal at rest, but will exhibit stiff spastic gait, muscle spasms, and tetanic seizures upon excitation

59
Q

How should asymptomatic and symptomatic dogs be decontaminated if tremorgenic mycotoxin ingestion is suspected?

A

emesis, activates charcoal, cathartic

sedate/anesthetize and perform gastric lavage and give activated charcoal and cathartic

60
Q

What symptomatic treatment is recommended in dogs with tremorgenic mycotoxin poisoning? What if they do not respond? Livestock?

A
  • Diazepam to control agitation, seizures, and muscle tremors +/ IV fluids
  • IV fluids

replace contaminated forage and keep animals in a quiet place until recovery

Veterinary Toxicology (29 decks)

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