Venoms and Toxins Flashcards
(44 cards)
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
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**
26
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
27
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
28
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)
29
what is dead from a snake bite mostly due to?
respiratory paralysis
30
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)
31
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**
32
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
33
diagnosis of coral snake
no definitive diagnostic test
34
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
35
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
36
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
37
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**
38
commonly accused non-venomous snakes
* Black Rat Snakes
* Banded water snake
* Northern water snake
* Eastern Hognose snake
* Scarlet king snake
39
enterotoxins
* **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
clinical signs of enterotoxin ingestion
**vomiting, diarrhea, abdominal pain, stasis with gas accumulation and bowel distention**
41
endotoxin ingestions
* **LPS from gram negative cell walls**
* Activates **inflammatory processes** and causes **release of TNF, prostaglandins, histamine**
42
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**
43
clinical signs of endotoxin ingestion
**lethargy**, **fever** followed by hypothermia, **diarrhea**, **abdominal pain, shock**, **extremely bad smelling feces**
44
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**
