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Toxicology > Venoms and Toxins > Flashcards

Venoms and Toxins Flashcards

1
Q

venomous animal

A
  • *Actively injects toxins** into victim
  • *venom** used for hunting and defense
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2
Q

poisonous animals

A

secrete poisons which are passive defense mechanisms

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3
Q

3 classes of venom compounds

A
  1. LMW substances
    * prostaglandins, histamine, epi: causes pain, inflammation, hypotension
  2. Peptides
    * cause many direct toxic effects and allergy
  3. enzymes
    * cause toxicity and allergy
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4
Q

bees

A
  • envenomate by stinging
  • stinger remains in skin for some species, can only sting once
  • swarm of hive attack can be lethal
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5
Q

wasps/hornets

A
  • Can sting repeatedly
  • Highly social, often group attacks
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6
Q

fire ants

A
  • some bite, others sting, some do both
  • some can spray formic acid
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7
Q

bee MOA

A
  • 63 identified compounds
  • Mellitin: acts as a detergent and hemolytic, causes pain, histamine release, cortisol release
  • Phospholipase A2: destroys membranes (major allergen)
  • Hyaluronidase: disrupts cell membranes
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8
Q

wasp/hornet MOA

A
  • Produce venoms containing peptides, enzymes and amines designed to trigger pain
    • kinins are the primary pain-inducing substances
    • some contain neurotoxins or alarm pheromones that alert the swarm to an intruder
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9
Q

ant venom MOA

A
  • Ant venom MOA
  • complex mixture of compounds
  • Largely consist of alkaloids (>1% proteins)
  • Piperodine causes dermal necrosis when injected in the skin
    • have cytotoxic, hemolytic, fungicidal, insecticidal, and bactericidal properties
  • Animals most likely to be severely affected are those with limited mobililty (neonates, juvenile, disabled)
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10
Q

clinical signs of bees, wasps, hornets

A
  • small local (swollen, edematous and erythematous plaque at the site of sting)
  • Large local (regional allergic reaction)
  • Anaphylaxis (most common cause of death)
    • not documented in livestock, reported in dogs
  • Systemic toxicity (uncommon) caused by delayed hypersensitivity (shock, hemolysis, rhabdomyolysis, hepatic and renal injury)
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11
Q

treatment of bees, wasps, hornets

A
  • removal of retained stinger by scraping (flip out)
  • cold compress to relieve swelling and pain
    • antihistamines and corticosteroids
  • monitor patients for anaphylactic reactions
    • treat properly with epi, treat systemic toxicosis with IV fluids
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12
Q

clinical signs of fire ants

A
  • Intense pain at the site of the sting
  • dogs develop erythematous puritic papules that generally resolve within 24 hours
  • No reported anaphylaxis in animals
  • Multiple stings may result in systemic signs similar to those of multiple bee/wasp sting
  • Multiple envenomations resulting in severe systemic reactions/anaphylaxis should be managed similarly to those of bee stings (fluid, epinephrine)
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13
Q

toad poisoning

A
  • All species of Bufo secrete toxins for defense and perhaps protection from microorganisms
  • B. marinus, B. alvarius are commonly lethal
  • Eggs and tadpoles are also toxic
  • Dogs most commonly involved in toad toxicosis (mouthing of toads stimulates release of toxins)
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14
Q

MOA of Bufo toads

A
  • Secretions contain many compounds including:
    • Biogenic amines (histamines)
    • Bufogenins (bufotalin)
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15
Q

biogenic amine actions

A

cause vasoconstriction, hypotension, hallucination, GI effects

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16
Q

bufogenin actions

A
  • Inhibit Na-K ATPase activity similar to cardiac glycosides such as digitalis
  • Produce potentially toxic cardiac arrhythmias
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17
Q

clinical signs of Bufo toxicosis

A
  • Begin immediately with hypersalivation and/or foaming at the mouth, head shaking, vomiting
  • Hyperemic gums, arrhythmias (bradycardia, sinus tachycardia, sinus arrhythmia)
  • Neurological signs such as convulsions, ataxia, hallucinations
  • Severe hyperkalemia
  • Death can occur in as little as 15 minutes
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18
Q

treatment of Bufo toxicosis

A
  • Immediate oral decontamination via water lavage
  • Activated charcoal if no seizures
  • Diazepam/barbituates for seizures
  • Atropine can be used for bradycardia but shouldn’t be given for salivation due to exacerbation of arhhythmia
  • Propranolol/lidocaine or esmolol for arrhythmia
  • Fluid replacement therapy for CV support
  • Severe neuro signs/hyperkalemia may be treated with digoxin-specific antigen-binding fragments (digoxin immune Fab)
    • may be cost prohibitive
19
Q

black widow

A
  • Shiny black spider with red hourglass on bottom of abdomen
  • Only females are toxic
  • Makes a messy web
20
Q

MOA of black widow

A
  • Venom contains alpha-latrotoxin
  • Toxin creates pores in membranes allowing Ca++ entry releasing massive amounts of NTs
  • Causes sustained muscle spasms
21
Q

clinical signs of a black widow

A
  • Muscle cramping and spasms
  • rapid weight loss
  • abdominal rigidity
  • restlessness, writhing
  • vocalization
  • hypertension
  • tachycardia
  • cats are most sensitive to the venom and often eat spiders (clinical signs are those of severe pain, vomiting, diarrhea, and resp collapse)
22
Q

treatment of black widow

A
  • control muscle spasms and pain
  • calcium gluconate (for muscle cramps)
  • anti-venom
  • supportive care, especially resp.
23
Q

brown recluse

A
  • Nocturnal and non-aggressive
    • animals usually bitten if they lay down on the spider
    • dogs are most susceptible
24
Q

MOA of brown recluse

A
  • Venom contains several necrotizing enzymes
    • sphingomyelinase D is most important
      • binds to cell membranes and cleaves head off lipids
    • causes tissue necrosis
    • victim’s immune response determines severity of the lesion
25
Q

clinical signs of brown recluse

A
  • initial bite causes little to no pain
  • 3-8 hours after envenomation, site becomes red, swollen, tender (blisterlike) and forms a typical “bulls eye” and non-healing ulcer (can become necrotic)
  • Can cause hemolytic anemia, fever, weakness, leukocytosis
26
Q

diagnosis of brown recluse

A
  • Diagnosis is difficult if the bite is not witnessed
  • Brown recluse bite often blamed for necrotic lesions due to other causes
27
Q

treatment of brown recluse

A
  • Dapsone to treat the dermal lesion (inhibit neutrophil migration)
  • Treat with fluids and bicarb if hemoglobinuria, anti-inflammatories
  • Administer antibiotics to prevent secondary infections
  • Give analgesic for pain
  • For necrotic lesion:
    • clean with Burrow’s solution or hydrogen peroxide
    • debridement of necrotic tissue - surgical removal off site is questionable
    • bandage
28
Q

most common animal victims of snake bites?

A
  • Horses and dogs
    • usually bitten on extremities or head (nose, throat, tongue)
    • not all snake bites result in envenomation (25% dry bites)
29
Q

what is dead from a snake bite mostly due to?

A

respiratory paralysis

30
Q

eastern coral snake

A
  • red, yellow, black alternating bands, small fangs, small heads, round pupils
  • Shy, non-aggressive and nocturnal (interactions with domestic animals less common than with pit vipers)
31
Q

MOA of coral snakes

A
  • Venom composed of mostly small polypeptides and enzymes
    • neurotoxic due to bungarotoxin
    • acts by preventing binding of ACh (similar to curare) causing paralysis
    • binding of neurotoxin to postsynaptic receptor appears to be irreversible
    • enzymes can cause local tissue necrosis, myoglobinemia in cats, and hemolysis in dogs
32
Q

clinical signs of coral snake

A
  • Onset of clinical signs may be delayed up to 12 hours
    • duration of effect is prolonged
  • Salivation due to inability to swallow, dyspnea, weakness, hyporeflexia, CNS depression, paralysis
33
Q

diagnosis of coral snake

A

no definitive diagnostic test

34
Q

treatment of coral snake venom

A
  • If neuro signs develop: administer antivenom immediately (anaphylaxis to antivenom is a possibility)
  • Resp. function should be closely monitored
    • ventilator support required if respiration is compromised
  • Broad spectrum abx and symptomatic wound care as necessary
  • Patients should be monitored for a min of 24 h (recovery period of 7-10 days in cats)
  • Prognosis is good when proper care received
35
Q

pit viper

A
  • Copperhead, cottonmouth, rattlesnake
  • Characterized by heat sensing pit and hinged fangs
  • Head is wider than body (triangular shaped)
  • Elliptical pupils, retractable fangs
  • Copperheads responsible for the majority of animal snake bites
    • rattlesnakes cause most deaths
36
Q

clinical signs of pit vipers

A
  • Distinct fang marks
  • immediate swelling and bruising at site of bite, pain around bite
  • Hypotension, shock, tachycardia, tachypnea
  • Anticoagulation
  • Tissue necrosis
  • Cats are more resistant than dogs
    • ​Cats often hide after being bitten and are presented at a later stage of toxicosis
    • dogs seek people
37
Q

treatment of pit vipers

A
  • Every case is different
  • Only proven therapy is antivenom
  • symptomatic and supportive care
  • copperhead bites can often be managed with antihistamines for inflammation
  • Rattlesnake and moccasin bites often managed with fluids and corticosteroids for shock and glucocorticoid for inflammation
38
Q

commonly accused non-venomous snakes

A
  • Black Rat Snakes
  • Banded water snake
  • Northern water snake
  • Eastern Hognose snake
  • Scarlet king snake
39
Q

enterotoxins

A
  • Bind to intestinal epithelium, increasing permeability and causing fluid loss (diarrhea) and decreased absorption of nutrients
  • Salmonella, E. coli, Bacillus, Strep, and C. perfringes
40
Q

clinical signs of enterotoxin ingestion

A

vomiting, diarrhea, abdominal pain, stasis with gas accumulation and bowel distention

41
Q

endotoxin ingestions

A
  • LPS from gram negative cell walls
  • Activates inflammatory processes and causes release of TNF, prostaglandins, histamine
42
Q

MOA of endotoxin ingestion

A

circulatory collapse, activation of pancreatic enzymes and autodigestion leading to pancreatitis, activation of clotting cascade, uncoupling of oxidative phosphorylation in heart

43
Q

clinical signs of endotoxin ingestion

A

lethargy, fever followed by hypothermia, diarrhea, abdominal pain, shock, extremely bad smelling feces

44
Q

treatment of endotoxin ingestion

A
  • limit absorption of material
    • emesis if not already occurred
  • support cardiovascular function
  • Correct fluid and electrolyte imbalance
  • prevent bacterial proliferation and septicemia

Toxicology (8 decks)

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