8-Venoms & toxins Flashcards

1
Q

Venomous animals

A
  • actively inject toxins into victim
  • venom used for hunting and defense
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2
Q

Poisonous animals

A
  • secrete poisons, which are passive defense mechanisms
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3
Q

Venom composition

three classes of compounds

A
  • 1) LMW substances
  • 2) Peptides
  • 3) Enzymes
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4
Q

LMW substances

A
  • prostaglandins
  • histamine
  • epinephrine

often cause

  • pain
  • inflammation
  • hypotension
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5
Q

Peptides

A
  • cause many direct toxic effects and allergy
  • mellitin
  • bungarotoxin
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6
Q

Enzymes

A

*cause toxicity and allergy

  • Hyaluronidase
    • spreading and potentiating factor
    • catalyzes the cleavage of glycoside bonds
  • Collagenase
    • breaks down capillary walls
  • Protease
    • degrades proteins and cause necrosis
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7
Q

Hymenoptera

A
  • bees
  • wasps
  • hornets
  • fire ants
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8
Q

Bees

A
  • envenomate by stinging; stinger remains in skin in some spp
  • can only sting once
  • swarms of hives can be fatal
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9
Q

Wasps/hornets

A
  • can sting repeatedly
  • highly social; often attack in groups
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10
Q

Fire Ants

A
  • bite, sting, or both
  • some spray formic acid
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11
Q

Bee venom

MOA

A
  • 63 identified components
    • 50% mellitin
      • acts as detergent
      • hemolytic
      • pain and histamine release
      • cortisol release
    • 12% Phospholipase A2
      • destroys membranes (major allergen)
    • 3% hyaluronidase
      • disrupts cell membranes
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12
Q

Wasps/hornets

MOA

A
  • venoms contain peptides, enzymes, amines
    • designed to trigger pain
  • kinins
    • primary pain-inducing substances
  • some contain neurotoxins/alarm pheromones
    • alerts swarm to an intruder
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13
Q

Ant venoms

MOA

A
  • complex mixtures
    • largely alkaloids
  • Piperidine
    • dermal necrosis
    • cytotoxic
    • hemolytic
    • fungicidal
    • insecticidal
    • bactericidal
  • animals with limited mobility affected most
    • neonates
    • juveniles
    • disabled
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14
Q

Bees, wasps, hornets

Clinical Signs

A
  • Small local
    • swollen, edematous, erythematous plaque at sting site
  • Large local (regional allergic reaction)
  • Anaphylaxis
    • most common cause of death
      • reported in dogs
    • not documented in livestock
  • Systemic toxicity
    • uncommon
    • caused by delayed hypersensitivity
    • shock, hemolysis, rhabdomyolysis, hepatic and renal injury
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15
Q

Bees, wasps, hornets

TX

A

1) Removal of retained stinger by scraping
* grabbing stinger with forceps may inject more venom
2) Cold compress to relieve swelling and pain

  • antihistamines and corticosteroids
    • questionable once lesion formed
    • not contraindicated

3) Monitor patients for anaphylactic reactions

  • treat promptly with epinephrine
  • aggressive fluid therapy with balanced fluids: systemic toxicosis

*exposure to single stings is rarely fatal

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16
Q

Fire Ants

Clinical Signs

A
  • pain at sting site
  • erythematous puritic papules in dogs
    • generally resolve w/in 24 hours
  • No reports of anaphylaxis
  • Multiple stings may cause systemic signs similar to multiple wasp/bee stings
  • Multiple envenomations causing systemic rxns/anaphylaxis manage similar to bee stings
    • epi
    • fluids
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17
Q

Ticks

A
  • Dermacentor, Ixodes
  • Holocyclotoxin
    • produced in salivary glands
    • toxin production inc with time on host
  • Dec ACh release at neuromuscular junction
    • paralysis/weakness
  • Dermacentor toxin may act on Na+ channels
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18
Q

Tick tox

Clinical Signs

A
  • May appear 6-14 days after attachment
    • loss of appetite/voice
    • incoordination
    • ascending flaccid paralysis
    • excessive salivating and vomiting
    • respiratory distress
    • death from respiratory paralysis
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19
Q

Tick Tox

DX

A
  • No def dx
  • hx tick infestation
  • presence of
    • dermacentor
    • ixodes
  • ascending paralysis, loss of voice
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20
Q

Tick tox

TX

A
  • Supportive
  • Atropine sulfate
  • Anti-emetics
  • Fluid replacement
  • Oxygen
  • Prognosis good if treated
21
Q

Toad poisoning

Cane Toad / Giant Toad

A
  • All species of Bufo secrete toxins for defense and possibly protection from microorganisms
  • B. marinus (Florida) and B. alvarius (California/Arizona)
  • Eggs and tadpoles also toxic
  • Dogs most commonly involved in toad toxicosis
    • mouthing stimulates release of toxins
22
Q

Toad Tox

MOA

A
  • Biogenic amines (histamine, etc)
    • vasoconstriction, hypotension, hallucination, GI effects
  • Bufogenins (bufotalin)
    • inhibit sodium-potassium ATPase activity similar to cardiac glycosides (digitalis)
    • potentially toxic cardiac arrhythmias
23
Q

Toad tox

Dx

A
  • Clinical signs begin immediately
    • hypersalivation
    • foaming at the mouth
    • head shaking
    • vomiting
  • Other signs
    • hyperemic gums
    • arrhythmias (bradycardia, sinus tachycardia, sinus arrhythmia
    • neuro signs (convulsions, ataxia, hallucinations)
  • can cause severe hyperkalemia
  • death can occur in 15 minutes
24
Q

Toad tox

TX

A
  • immediate oral decon w/ water
  • activated charcoal if no seizures
  • diazepam/barbiturates for seizures
  • atropine
    • for bradycardia
    • NOT for salivation, may exacerbate arrhythmia
  • propranolol/lidocaine or esmolol for arrhythmia
  • fluid replacement for CV support
  • digoxin specific antigen-binding frags (digoxin immune Fab)
    • for neuro signs/hyperkalemia
    • may be cost prohibitive
25
Q

Black Widow

A
  • Only females are toxic
  • messy web
  • venom contains alpha-Iatrotoxin
    • creates pores in membranes allowing Ca++ entry
    • releases massive amounts of neurotransmitter
    • causes sustained muscle spasms
26
Q

Black widow tox

Clinical signs

A
  • Muscle cramping/spasms
  • rapid weight loss
  • abdominal rigidity
  • restlessness, writhing
  • vocalization
  • hypertension
  • tachycardia
  • cats most sensitive to venom and eat spiders
    • severe pain, vomiting, diarrhea, respiratory collapse
27
Q

Black widow tx

Tx

A
  • Control muscle spasms and pain
  • Calcium gluconate
    • muscle cramps
  • Anti-venom
  • supportive care: respiratory
28
Q

Brown recluse

(Loxosceles reclusa)

A
  • Nocturnal, non-aggressive
    • animals bitten when they lay on spider
    • dogs most susceptible
  • venom contains necrotizing enzymes
    • sphingomyelinase D
      • binds to cell membranes
      • cleaves head off lipids
    • causes tissue necrosis
    • victim’s immune response determines severity of lesion
29
Q

Brown Recluse Tox

Clinical Signs

A
  • Initial bite causes little to no pain
  • 3-8 hours after envenomation
    • red, swollen, tender, blister like formation
    • bulls-eye and non-healing ulcer
    • can be necrotic
  • can cause
    • hemolytic anemia, fever, weakness, leukocytosis
30
Q

Brown Recluse tox

Dx

A
  • Dx difficult if bite not witnessed
  • brown recluse often blamed necrotic lesions of other origin
31
Q

Brown recluse tox

Tx

A
  • Dapsone: for dermal lesion
    • inhibits neutraphil migration
  • Treat with fluids and bicarb: hemoglobinuria
  • Anti-inflammatories
  • Antibiotics to prevent secondary infections
  • Analgesics for pain
  • Necrotic lesion
    • clean with burrow’s soln (aluminum acedate) or hydrogen peroxide
    • debridement of necrotic tissue
      • sx removal if site is questionable
    • bandage
32
Q

Snakes

A
  • Elapidae vs Crotalidae
  • Dogs and horses most common victims
    • 25% bites are dry bites-look for CS plus bite marks
  • Size of victim and amount of venom determine severity
    • death due to resp paralysis
33
Q

Eastern Coral Snake

Micrurus fulvius fulvius

A
  • Small fangs, small heads, red next to yellow bands
  • shy, non-aggressive and nocturnal
34
Q

Eastern Coral Snake

Micrurus fulvius fulvius

MOA

A
  • Venom mostly small polypeptides and enzymes
    • bungarotoxin-neurotoxic
    • prevents binding of ACh (similar to curare)
      • causes paralysis
    • binding of neurotoxin to postsynaptic receptor appears to be irreversible
    • enzymes can cause
      • local tissue decrosis
      • myoglobinemia in cats
      • hemolysis in dogs
35
Q

Eastern Coral Snake

Micrurus fulvius fulvius

Clinical Signs

A
  • Onset of CS may be delayed up to 12 hours: duration of effect prolonged
  • CS
    • Salivation (inability to swallow)
    • Dyspnea, weakness, hyporeflexia, CNS depression, paralysis
  • no def. dx test
36
Q

Eastern Coral Snake

Micrurus fulvius fulvius

TX

A
  • Antivenom if neuro signs
    • anaphylaxis to antivenom possible
  • Ventilation if respiratory function compromised
  • Broad-spectrum antibiotics
  • Symptomatic wound care
  • Monitor patients for minimum of 24 hours
    • cats recover in 7-10 days
  • Prognosis good with prompt care
37
Q

Pit vipers: Copperhead, Cottonmouth, Rattlesnakes

(Crotalids)

A
  • heat sensing pit and hinged fangs, triangular head, elliptical pupils, retractable fangs
  • Copperhead responsible for most bites
  • Rattlesnakes cause most deaths
38
Q

Snake bite

Clinical Signs

A
  • Distinct fang marks
  • Immediate swelling and bruising at site of bite
  • Pain around bite
  • Hypotension, shock, tachycardia, tachypnea
  • Anticoagulation
  • Tissue necrosis
  • Cats
    • more resistant than dogs
    • often hide after bite (present later)
  • Dogs
    • seek companionship after bite, treated earlier
39
Q

Snake bite

Tx

A
  • Antivenom
  • Supportive
  • Copperhead
    • antihistamines for inflammation
  • Rattlesnake and moccasin bites
    • fluids
    • corticosteroids for shock
    • glucocorticoid for inflammation
  • cutting, ice, tourniquets contraindicated
40
Q

Garbage/carrion toxicity

A
  • Usually from protein rich foods during warm months
    • leftovers
    • moist foods
  • Can be due to bacteria or preformed toxins
    • enterotoxins
    • endotoxin
41
Q

Enterotoxins

A
  • Salmonella, E. Coli, Bacillus, Strep, C. perfringens
  • Bind to intestinal epithelium
    • inc permeability
    • causes fluid loss and dec absorption
  • Cause vx/d, abdominal pain, stasis with gas accumulation, bowel distention
42
Q

Endotoxin

A
  • Lipopolysaccharide from G- cell walls
  • Activates inflammatory processes and releases
    • TNF
    • Prostaglandins
    • histamine
  • causes circulatory collapse (shock)
  • activation pancreatic enzymes and autodigestion
    • pancreatitis
    • activation of clotting cascade
    • uncoupling oxidative phosphorylation in heart
43
Q

Endotoxin

Clinical signs

A
  • lethargy
  • fever
  • hypothermia
  • diarrhea
  • abdominal pain
  • shock
  • exremely bad smelling feces
44
Q

Endotoxin

TX

A
  • Limit absorption
    • emesis
  • support CV function
  • Correct fluid/electrolyte imbalance
  • Prevent bacterial proliferation and septicemia
45
Q

Botulism

Clostridium botulinum

A
  • Toxin extremely potent
  • Prevents release of ACh at NMJ causing paralysis
  • Very difficult to dx, can be circumstantial
    • access to carrion
    • garbage
    • compost piles
46
Q

Botulism

Clinical Signs

A
  • Decreased tonge and tail tone
  • weakness, dropping food from mouth, weak vocalization
    • can be down but alert, tail wag still present
  • bradycardia
  • constipation, urinary retention
  • progressive paresis
47
Q

Botulism

DDX

A
  • anticholinesterases
  • ionophores
  • snakeroot
  • lead
  • nitrate
  • botulism
  • atropine-like alkaloids
48
Q

Botulism

TX

A
  • Supportive
  • Parenteral nutrition, IV fluids
  • Resp support, O2
  • Warm water enemas, bladder expression may be necessary
  • determine source
  • treat with antibiotics if theres a wound or toxicoinfectious
  • antitoxin
    • doesn’t neutralize toxins in neurons
    • made from horse serum (can cause hypersensitivity)
    • do intradermal test first
  • prognosis poor