Venoms & Toxins Flashcards

(54 cards)

1
Q

Venomous animals

A

Actively inject toxins into victim

Venom is used for hunting and defense

Example: brown recluse

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2
Q

Poisonous animals

A

Secrete poisons which are passive defense mechanisms

Example: poison dart frog

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3
Q

Three classes of venom compounds

A
  1. LMW substances
  2. Peptides
  3. Enzymes
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4
Q

What are LMW substances?

A

Substances that often cause pain, inflammation, and hypotension

Examples: Prostaglandins, histamine, epinephrine

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5
Q

What are toxic peptides?

A

Peptides that cause direct toxic effects and allergy

Examples: Melittin, bungarotoxin

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6
Q

What are toxic enzymes?

A

Eznymes that cause toxicity and allergy

Examples: hyaluronidase, collagenase, protease

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7
Q

Hymenoptera

A

Includes bees, wasps/hornets, and fire ants

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8
Q

Crazy Ants

A

Native to Africa
Very aggressive
Numbers growing in Florida

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9
Q

Mechanism of action of bee venom

A

Composed of

50% melittin: acts as detergent, is hemolytic, and causes pain and histamine release

12% phospholipase A2: destroys cell membranes

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10
Q

Mechanism of action of wasp/hornet venom

A

Contain neurotoxins, alarm pheremones (alert the swarm to the intruder), and kinins (the primary pain-inducing substances)

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11
Q

Mechanism of action of ant venom

A

Piperidine causes dermal necrosis
Formic acid causes burning sensation and pain
Both chemicals have cytotoxic, hemolytic, fungicidal, insecticidal, and bactericidal properties

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12
Q

Clinical signs of bee, wasp/hornet, ant stings

A

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)

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13
Q

Treatment of bee, wasp/hornet, ant stings

A

Removal of stinger by scraping (not forceps!)

Cold compress

Antihistamines/corticosteroids

Monitor for anaphylaxis

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14
Q

Genus of ticks that can cause toxicity

A

Dermacentor

Ixodes

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15
Q

Mechanism of action of tick toxin

A

Holocyclotoxin causes impaired neuromuscular junction, causing weakness and paralysis

Also may act on Na+ channels

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16
Q

Clinical signs of tick holocyclotoxin toxicosis

A

Appear 6-14 days after attachment of tick

Loss of appetite and voice, incoordination, flaccid paralysis, excessive salivating, vomiting, respiratory distress, death

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17
Q

Diagnosis of tick holocyclotoxin toxicosis

A

No definitive diagnosis
History of tick infestation
Presence of ticks
Ascending paralysis and loss of voice

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18
Q

Treatment of tick holocyclotoxin toxicosis

A
Supportive therapy
Atropine sulfate
Anti-emetics
Fluid replacement therapy
Oxygen

Prognosis is good if treated

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19
Q

Species of toad that cause poisoning

A

All species of Bufo secrete toxins for defense

B. Marinus in Florida, B. Alvarius (California/Arizona)

Eggs and tadpoles are also toxic

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20
Q

Cane Toad/Giant Toad (B. Marinus)

A

Found in Florida
Secrete potent compounds that can be fatal
Have few predators

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21
Q

Compounds and mechanism of action of toad poisons

A

Biogenic amines: cause vasoconstriction, hypotension, hallucination, GI effects

Bufogenins (bufotalin): inhibit Na/K ATPase and produce toxic arrhythimias

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22
Q

Clinical signs/diagnosis of toad poison toxicosis

A
Hypersalivation, foaming at mouth, head shaking, vomiting
Hyperemic gums (brick red)
Arrhythmias
Convulsions, ataxia, hallucination
Severe hyperkalemia
Death can occur in 15 minutes
23
Q

Treatment of toad poison toxicosis

A

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

24
Q

What are Black Widow spiders (Lactrodectus mactans)?

A

Shiny black spider with red hourglass on bottom
Only females are toxic
Messy web

25
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
26
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
27
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
28
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
29
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
30
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
31
Diagnosis of brown recluse envenomation
Difficult if bite is not witnessed
32
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
33
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
34
Eastern Coral Snake (Micrurus fulvius fulvius)
Red, yellow, black alternating bands Small fangs, small heads, round pupils Shy, non-aggressive, and nocturnal
35
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
36
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
37
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
38
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
39
Examples of pit vipers in Florida
Cottonmouth Timber Rattlesnake Eastern Diamondback Copperhead
40
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
41
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)
42
Garbage/carrion toxicity
Usually from protein-rich foods during warm months Enterotoxins and endotoxins Can be due to bacteria or preformed toxins
43
Mechanism of action of enterotoxins
Bacteria bind intestinal epithelium, increasing permeability, and causing fluid loss (diarrhea) and decreased absorption of nutrients
44
Examples of enterotoxins
Salmonella, E. coli, bacillus, Strep, and C. Perfringens
45
What are Endotoxins?
Lipopolysaccharide from gram negative cell walls
46
Mechanism of action of endotoxins
Activates inflammatory processes and causes release of prostaglandins and histamine
47
Clinical sign of endotoxin toxicity
``` Shock Pancreatitis Activation of clotting cascade Heart effects Lethargy Fever Diarrhea, extremely bad smelling feces Abdominal pain ```
48
Treatment of endotoxin toxicosis
Emesis (if not already occurred) Support cardiovascular function Fluids Antibiotics
49
What is botulism?
Caused by clostridium botulinum | Extremel potent toxin
50
Mechanism of action of botulism toxicosis
Prevents release of ACh, causes paralysis
51
How to diagnose botulism?
Hard to diagnose | Often only circumstantial evidence (access to carrion, garbage, compost piles)
52
Clinical signs of botulism
``` Decreased tongue and tail tone Dropping food from mouth, salivation Weakness, weak vocalization, progressive paresis Bradycardia Constipation, urinary retention ```
53
Differential diagnoses for botulism
Anticholinesterase Ionophores Lead Nitrate poisoning
54
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