Venoms and Toxins Flashcards
1
Q
venomous animal
A
- *Actively injects toxins** into victim
- *venom** used for hunting and defense
2
Q
poisonous animals
A
secrete poisons which are passive defense mechanisms
3
Q
3 classes of venom compounds
A
-
LMW substances
* prostaglandins, histamine, epi: causes pain, inflammation, hypotension -
Peptides
* cause many direct toxic effects and allergy -
enzymes
* cause toxicity and allergy
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
5
Q
wasps/hornets
A
- Can sting repeatedly
- Highly social, often group attacks
6
Q
fire ants
A
- some bite, others sting, some do both
- some can spray formic acid
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
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
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)
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)
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
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)
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)
14
Q
MOA of Bufo toads
A
-
Secretions contain many compounds including:
- Biogenic amines (histamines)
- Bufogenins (bufotalin)
15
Q
biogenic amine actions
A
cause vasoconstriction, hypotension, hallucination, GI effects
16
Q
bufogenin actions
A
- Inhibit Na-K ATPase activity similar to cardiac glycosides such as digitalis
- Produce potentially toxic cardiac arrhythmias
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
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
-
sphingomyelinase D is most important
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
