13 - Venom Flashcards
(35 cards)
Layers of specificity of venom
- Prey
- Organ
- Bite site
Medically Important Snake Types
All Elapids:
1. Brown snakes
2. Tiger snakes
3. Mulga and black snakes
4. Taipans
5. Death adders
Brown snakes
- High rate of dry bites
- Main clinical feature: Coagulopathy (usually lethal)
- Bite painless, minimal local/non-specific effect
Tiger snakes (+ others)
Major clinical features:
* Consumptive coagulopathy
* Presynaptic neurotoxicity
* Rhabdomyolysis
* Other bites can be treated with tiger snake antivenom
Mulga and Black Snakes
Very large snakes
Major clinical features:
* Severe rhabdomyolysis
* Anticoagulant coagulopathy
* Antivenom often not necessary with red-bellies
Taipans
High mortality (w/o treatment)
* Major clinical features: Consumptive coagulopathy, presynaptic neurotoxicity, mild rhabdomyolysis
* Intubation may be necessary within 1-2hr
* Antivenom warranted BEFORE systemic envenomation est.
Death adders
Usually hide, painful bite
* Major clinical fetaure: Powerful postsynaptic neurotoxin
* Rx: IV anticholinesterases (neostigmine + atropine)
Characteristics of Bites / Venoms
- Local venom-derived tissue damage effects non-reversible
- Non-specific effects include nausea/vomiting, headache, abdominal pain, diarrhoea, dizziness, collapse
Major effects:
1. Coagulopathy
2. Neurotoxicity
3. Myotoxicity (subsequent renal damage)
Coagulopathy
Haemorrhage/ intracranial bleed or infarction possible
* Usually procoagulant coagulopathy caused by TLE’s (thrombin-like enzymes)
* Prothrombin activators ➔ defibrination (< 30 min)
What are the main cerebral complications of snakebite envenoming?
- Ischemic stroke
- Cerebral hemorrhage
Ischemic stroke
Clot preventing oxygenated blood from reaching brain
Cerebral hemorrhage
Bleeding into tissues in brain
* Rare in snake bites (Aus)
Neurotoxicity
- Pre-synaptic – days to resolve, no response to antivenom
-
Post-synaptic reversed by antivenom
* Progressive descending flaccid paralysis (Ptosis first sign)
* Death by respiratory failure
Ptosis
Droppy eyelids and first sign of neurotoxic effects of venom
Different types of neurotoxins
- α-neurotoxins (post-syn)
-
β-neurotoxins (pre-syn)
Aus Elapids may have one or both
Also:
* k-neurotoxins (neuronal nACh receptors)
* Muscarinic toxins
α-neurotoxins
Post-synaptic inhibition (antagonism)
* Short chain type (4 S-S bridges)
* Long chain type (5 S-S bridges, sticks for longer)
* Long chain e.g. α-Bungarotoxin
Myotoxicity
Mainly phospholipases: PLA2
* Attack muscle cell membrane phospholipids
* Breakdown muscle cells ➔ rhabdomyolysis ➔ myoglobinuria
* Secondary renal failure + hyperkalemia (potassium from muscle cells - lethal)
Immediate treatment for snake bites
- Do not wash bite or catch snake
- Keep patient calm + still
- Pressure immobilisation to limit lymphatic drainage (bandage from bite > up limb)
Monitorring at hospital for snake bite
Watch for signs:
1. Paralysis (ptosis, respiratory effort)
2. Coag (persistent ooze from bite site, cranial irritation, bleeding)
3. Rhabdo (muscle weakness / tenderness)
How to detect myoglobin
Coagulation studies and urine analysis
Snake venom detection kit
ELISA-based assay
* Determines which antivenom required
How is antivenom created?
- Inject venom into animal
- They produce antibodies
- Purified/modified (reduce protein load, enable renal elim.)
How can we enable renal elimination of antivenoms?
Remove Fc region from IgG
* Also decreases half-life
* Can lead to Type 1 immediate hypersensitivity
Immediate hypersensitivity
Antigen cross-linking on endogenous IgE bound to mast cells and basophils ➔ histamine release
* Could be urticaria (hives) or full anaphylaxis (rare)
