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Flashcards in Venoms and Toxins Deck (44):

venomous animal

Actively injects toxins into victim
venom used for hunting and defense


poisonous animals

secrete poisons which are passive defense mechanisms 


3 classes of venom compounds

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



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



  • Can sting repeatedly
  • Highly social, often group attacks


fire ants

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


bee MOA

  • 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


wasp/hornet MOA

  • 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


ant venom MOA

  • 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)


clinical signs of bees, wasps, hornets 

  • 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)


treatment of bees, wasps, hornets

  • 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


clinical signs of fire ants

  • 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)


toad poisoning

  • 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)


MOA of Bufo toads

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


biogenic amine actions

cause vasoconstriction, hypotension, hallucination, GI effects


bufogenin actions

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


clinical signs of Bufo toxicosis

  • 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


treatment of Bufo toxicosis

  • 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


black widow

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


MOA of black widow

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


clinical signs of a black widow

  • 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)


treatment of black widow

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


brown recluse

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


MOA of brown recluse

  • 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


clinical signs of brown recluse

  • 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


diagnosis of brown recluse

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


treatment of brown recluse

  • 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


most common animal victims of snake bites?

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


what is dead from a snake bite mostly due to?

respiratory paralysis


eastern coral snake

  • 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)


MOA of coral snakes

  • 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


clinical signs of coral snake

  • 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


diagnosis of coral snake

no definitive diagnostic test


treatment of coral snake venom

  • 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


pit viper

  • 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


clinical signs of pit vipers

  • 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


treatment of pit vipers

  • 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


commonly accused non-venomous snakes

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



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


clinical signs of enterotoxin ingestion

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


endotoxin ingestions

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


MOA of endotoxin ingestion

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


clinical signs of endotoxin ingestion

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


treatment of endotoxin ingestion

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