Venoms & Toxins Flashcards
Venomous animals
Actively inject toxins into victim
Venom is used for hunting and defense
Example: brown recluse
Poisonous animals
Secrete poisons which are passive defense mechanisms
Example: poison dart frog
Three classes of venom compounds
- LMW substances
- Peptides
- Enzymes
What are LMW substances?
Substances that often cause pain, inflammation, and hypotension
Examples: Prostaglandins, histamine, epinephrine
What are toxic peptides?
Peptides that cause direct toxic effects and allergy
Examples: Melittin, bungarotoxin
What are toxic enzymes?
Eznymes that cause toxicity and allergy
Examples: hyaluronidase, collagenase, protease
Hymenoptera
Includes bees, wasps/hornets, and fire ants
Crazy Ants
Native to Africa
Very aggressive
Numbers growing in Florida
Mechanism of action of bee venom
Composed of
50% melittin: acts as detergent, is hemolytic, and causes pain and histamine release
12% phospholipase A2: destroys cell membranes
Mechanism of action of wasp/hornet venom
Contain neurotoxins, alarm pheremones (alert the swarm to the intruder), and kinins (the primary pain-inducing substances)
Mechanism of action of ant venom
Piperidine causes dermal necrosis
Formic acid causes burning sensation and pain
Both chemicals have cytotoxic, hemolytic, fungicidal, insecticidal, and bactericidal properties
Clinical signs of bee, wasp/hornet, ant stings
Site of sting: swollen, red plaques, edema, regional allergic reaction
Anaphylaxis (most common cause of death)
Systemic toxicity caused by delayed hypersensitivity (shock, hemolysis, rhabdomyolysis, hepatic and renal injury)
Treatment of bee, wasp/hornet, ant stings
Removal of stinger by scraping (not forceps!)
Cold compress
Antihistamines/corticosteroids
Monitor for anaphylaxis
Genus of ticks that can cause toxicity
Dermacentor
Ixodes
Mechanism of action of tick toxin
Holocyclotoxin causes impaired neuromuscular junction, causing weakness and paralysis
Also may act on Na+ channels
Clinical signs of tick holocyclotoxin toxicosis
Appear 6-14 days after attachment of tick
Loss of appetite and voice, incoordination, flaccid paralysis, excessive salivating, vomiting, respiratory distress, death
Diagnosis of tick holocyclotoxin toxicosis
No definitive diagnosis
History of tick infestation
Presence of ticks
Ascending paralysis and loss of voice
Treatment of tick holocyclotoxin toxicosis
Supportive therapy Atropine sulfate Anti-emetics Fluid replacement therapy Oxygen
Prognosis is good if treated
Species of toad that cause poisoning
All species of Bufo secrete toxins for defense
B. Marinus in Florida, B. Alvarius (California/Arizona)
Eggs and tadpoles are also toxic
Cane Toad/Giant Toad (B. Marinus)
Found in Florida
Secrete potent compounds that can be fatal
Have few predators
Compounds and mechanism of action of toad poisons
Biogenic amines: cause vasoconstriction, hypotension, hallucination, GI effects
Bufogenins (bufotalin): inhibit Na/K ATPase and produce toxic arrhythimias
Clinical signs/diagnosis of toad poison toxicosis
Hypersalivation, foaming at mouth, head shaking, vomiting Hyperemic gums (brick red) Arrhythmias Convulsions, ataxia, hallucination Severe hyperkalemia Death can occur in 15 minutes
Treatment of toad poison toxicosis
Immediate oral decontamination (water lavage)
Activated charcoal if no seizures
Diazepam/barbiturates for seizures
Propanolol, lidocaine, esmolol for arrhythmias
Fluid therapy
Digoxin for neuro signs/hyperkalemia
What are Black Widow spiders (Lactrodectus mactans)?
Shiny black spider with red hourglass on bottom
Only females are toxic
Messy web
Venom of black widow spider
Contains alpha-latrotoxin
Created pores in membranes allowing Ca++ entry and release of massive amounts of neurotransmitter
Causes sustained muscle spasms
Clinical signs of black widow spider envenomation
muscle cramping and spasms Rapid weightloss Abdominal rigidity Restlessness, writhing Vocalization Hypertension Tachycardia, respiratory collapse
CATS MOST SENSITIVE BECAUSE THEY EAT SPIDERS
Treatment of black widow spider envenomation
Anti-venom only proven treatment
Control muscle spasm and pain
Calcium gluconate for muscle camps
Supportive care, especially respiratory
Characteristics of Brown Recluse spider (Loxosceles reclusa)
Nocturnal and non-aggressive
Animals bitten when they lay down on spider
Dogs are most susceptible
Venom contains several necrotizing enzymes
Brown Recluse venom
Sphingomyelinase D binds to cell membranes and cleaves head off lipids
Causes tissue necrosis
Victim’s immune response determines severity of lesion
Clinical signs of brown recluse envenomation
Initial bite causes little to no pain
3-8 hours after envenomation, site becomes red, swollen, tender, and forms a “bulls eye” and non-healing ulcer
Can cause hemolytic anemia, fever, weakness, leukocytosis
Diagnosis of brown recluse envenomation
Difficult if bite is not witnessed
Treatment of brown recluse envenomation
Dapsone to treat dermal lesion
Fluids, NSAIDs, glucocorticoids
Antibiotics
Analgesics
For necrotic lesions: clean with burrow’s solution (Aluminum acetate) or hydrogen peroxide, debridement of necrotic tissue, bandage
Characteristics of snake envenomation
Venomous snakes - Elapidae or Crotalidae
Dogs and horses most common victims
Size of victim and amount of venom determines severity
Death due to respiratory paralysis
Eastern Coral Snake (Micrurus fulvius fulvius)
Red, yellow, black alternating bands
Small fangs, small heads, round pupils
Shy, non-aggressive, and nocturnal
Mechanism of action of coral snake envenomation
Venom is composed of polypeptides and enzymes
Neurotoxicity due to bungarotoxin
Acts by preventing binding of ACh causing paralysis
Local tissue necrosis, myoglobinuria in cats, and hemolysis in dogs
Clinical signs of coral snake envenomation
Onset of clinical signs may be delayed up to 12h
Salivation, dyspnea, weakness, hyporeflexia, CNS depression, paralysis
No definitive diagnostic test
Treatment of coral snake envenomation
If neurologic signs develop, administer anti-venom immediately
Respiratory function should be closely monitored
Broad-spectrum antibiotics and symptomatic wound care
Prognosis is good when prompt care received
Monitor for a minimum of 24 hours! Recovery can be up to 10 days
Characteristics of pit vipers (Crotalids)
Copperhead, cottonmouth, rattlesnakes
Characterized by heat sensing pit and hinged, retractable fangs
Head is wider than body (triangular-shaped)
Elliptical/vertical pupil
Copperheads are responsible for majority of animal snake bites but rattlesnakes cause most deaths
Examples of pit vipers in Florida
Cottonmouth
Timber Rattlesnake
Eastern Diamondback
Copperhead
Clinical signs of pit viper envenomation
Distinct fang marks Immediate swelling and bruising Hypotension, shock, tachycardia, tachypnea Anticoagulation Tissue necrosis
Cats often hide
Dogs seek human attention
Treatment of pit viper envenomation
Every case is different!
Only proven therapy is anti-venom
Symptomatic and supportive care
Copperhead bites can be managed with antihistamines
Rattlesnake and moccasin bites often managed with fluids and corticosteroids for shock and glucocorticoids for inflammation
DON’T cut, ice, or tourniquet (these localize effects of toxin to one area so is harder for body to fight)
Garbage/carrion toxicity
Usually from protein-rich foods during warm months
Enterotoxins and endotoxins
Can be due to bacteria or preformed toxins
Mechanism of action of enterotoxins
Bacteria bind intestinal epithelium, increasing permeability, and causing fluid loss (diarrhea) and decreased absorption of nutrients
Examples of enterotoxins
Salmonella, E. coli, bacillus, Strep, and C. Perfringens
What are Endotoxins?
Lipopolysaccharide from gram negative cell walls
Mechanism of action of endotoxins
Activates inflammatory processes and causes release of prostaglandins and histamine
Clinical sign of endotoxin toxicity
Shock Pancreatitis Activation of clotting cascade Heart effects Lethargy Fever Diarrhea, extremely bad smelling feces Abdominal pain
Treatment of endotoxin toxicosis
Emesis (if not already occurred)
Support cardiovascular function
Fluids
Antibiotics
What is botulism?
Caused by clostridium botulinum
Extremel potent toxin
Mechanism of action of botulism toxicosis
Prevents release of ACh, causes paralysis
How to diagnose botulism?
Hard to diagnose
Often only circumstantial evidence (access to carrion, garbage, compost piles)
Clinical signs of botulism
Decreased tongue and tail tone Dropping food from mouth, salivation Weakness, weak vocalization, progressive paresis Bradycardia Constipation, urinary retention
Differential diagnoses for botulism
Anticholinesterase
Ionophores
Lead
Nitrate poisoning
Treatment of botulism
Supportive therapy and IV fluids Oxygen Warm water enemas and bladder expression Antibiotics Antitoxin (not always effective- does not neutralize toxin already in neurons)
Poor prognosis
