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Snake venom is a highly toxic saliva containing zootoxins that facilitate the immobilization and digestion of prey. The toxins in snake venom can cause neuromuscular paralysis, which can range from mild weakness of the eyelid and facial muscles to fatal paralysis of bulbar and respiratory muscles. The most common toxins that cause paralysis are the non-enzymatic α-neurotoxins and the enzymatic β-neurotoxins. The β-neurotoxins produce effects on both the pre-synapse and post-synapse, resulting in paralysis and muscle membrane damage. The degree of paralysis caused by snake venom depends on the quantity of venom injected, the composition of the venom, and the promptness of therapeutic interventions.
| Characteristics | Values |
|---|---|
| Type of venom | Neurotoxic |
| Toxins involved | α-neurotoxins, β-neurotoxins, fasciculins, dendrotoxins, myotoxins, cardiotoxins, phospholipase A2, amino acid oxidases, proteases, hyaluronidase, fasciculins, etc. |
| Mechanism of paralysis | Toxins interrupt neurotransmission at the neuromuscular junction |
| Symptoms | Fixed dilated pupils, reduced eye movements, droopy eyelids, difficulty talking, swallowing, and breathing, bilateral ptosis, ophthalmoplegia, facial muscle weakness, etc. |
| Treatment | Antivenom therapy |
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What You'll Learn
- Snake venom neurotoxins target multiple sites in the neuromuscular junction
- The two dominant, paralytic toxins are the non-enzymatic α-neurotoxins and the enzymatic β-neurotoxins
- The most dangerous venom in the world is that of the box jellyfish, Chironex fleckeri
- The first myotoxin to be identified and isolated was crotamine, discovered in the 1950s by Brazilian scientist José Moura Gonçalves
- Antivenom therapy is currently the standard practice for treating neuromuscular dysfunction in snake envenoming
Snake venom neurotoxins target multiple sites in the neuromuscular junction
Snake venoms contain a cocktail of molecules that work together to interfere with the transmission of nerve impulses. The most dangerous toxins destroy nerves. Snake venom is a highly toxic saliva containing zootoxins that facilitate the immobilization and digestion of prey, as well as providing defence.
Neurotoxic snake venoms primarily affect the neuromuscular junction, causing a disruption of neurotransmission, resulting in paralysis of the skeletal muscles. Snake venom neurotoxins target multiple sites in the neuromuscular junction. The majority of snake venom neurotoxins either act on the motor nerve terminals (presynaptic) or the nicotinic acetylcholine receptor on the motor end plate (postsynaptic). Presynaptic toxins deplete the synaptic vesicles and cause structural damage to the motor nerve terminals. This type of insult is most likely to be treatment-resistant, and recovery depends on the natural regeneration of the nerve terminal.
Beta-neurotoxins (β-toxins) and succinylcholine share the postsynaptic effects of depolarization and flaccid paralysis. However, they differ in that succinylcholine acts exclusively on the postsynapse, while snake venom β-neurotoxins produce effects directly on both the pre- and postsynapse, resulting in paralysis and muscle membrane damage. Postsynaptically, both classes of agents cause hyperactivation of nicotinic receptors (nAChRs) via uncontrolled acetylcholine release.
Α-neurotoxins (3FTx) bind with high affinity to nicotinic acetylcholine receptors at the neuromuscular junction. Nicotinic receptors rendered non-functional by α-neurotoxins are eventually de-phosphorylated, a state that identifies them for internalization. Internalized receptors are then degraded by the proteasome complex.
Myotoxins are small, basic peptides found in rattlesnake and lizard venoms. They act very quickly, causing instantaneous paralysis to prevent prey from escaping and eventually causing death due to diaphragmatic paralysis.
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The two dominant, paralytic toxins are the non-enzymatic α-neurotoxins and the enzymatic β-neurotoxins
Snake venom is a highly toxic saliva containing zootoxins that facilitate the immobilization and digestion of prey. It is usually injected through unique fangs during a bite, although some species can spit their venom. The two dominant, paralytic toxins are the non-enzymatic α-neurotoxins and the enzymatic β-neurotoxins.
Α-neurotoxins fall into the three-finger toxin (3FTx) class, found exclusively in elapid venoms. They cause weakness and paralysis by interrupting neurotransmission at the neuromuscular junction (NMF). Viper venoms, on the other hand, contain paralytic neurotoxins that are exclusively from the β-class. β-neurotoxins, such as svPLA2, produce effects on both the pre-synapse and post-synapse, resulting in paralysis and muscle membrane damage. They cause hyperactivation of nicotinic receptors (nAChRs) via uncontrolled acetylcholine release.
The paralyzing effects of snake venom typically begin with the muscles around the eyes, leading to fixed dilated pupils, reduced eye movements, and droopy eyelids. Without treatment, these early signs progress to difficulty talking, swallowing, and eventually breathing. Some snake venoms, like the mainland tiger snake, contain both receptor-blocking and nerve-destructive neurotoxins. These neurotoxins can take time to repair, during which breathing may not be possible without external support.
In addition to snakes, other venomous creatures like bees, wasps, ants, stinging fish, and jellyfish are known for the pain caused by their stings. The stonefish and box jellyfish are examples of potent venom effects. Jellyfish toxins can disturb the coordinated contraction of the heart muscles, leading to death if left untreated.
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The most dangerous venom in the world is that of the box jellyfish, Chironex fleckeri
Arguably, the most dangerous venom in the world is that of the box jellyfish, Chironex fleckeri. This species of box jellyfish is considered the most venomous marine animal. It is the largest of the box jellyfish, with body sizes reaching up to one foot in diameter and thick, bootlace-like tentacles up to 10 feet long. The Chironex fleckeri is a highly venomous creature that can kill a healthy adult human in minutes. This is due to the powerful toxins that are injected into the skin through millions of tiny venom-filled harpoon-like weapons on the jellyfish's tentacles.
Once in the circulation, these toxins seem to target the outer membrane of heart muscle cells, punching holes in them. These holes disturb the smooth contraction of the heart muscles, leading to cardiac arrest. If left untreated, this form of venom toxicity can cause death soon after a person has been stung. The Chironex fleckeri has caused at least 79 deaths since the first report in 1883, with the most recent fatality occurring in 2022.
The venom of the Chironex fleckeri contains a complex mixture of proteins, enzymes, and other substances with toxic and lethal properties. Bioactive fractions have been isolated from the venom, and researchers have identified highly abundant venom proteins belonging to a family of taxonomically restricted cnidarian toxins. These toxins have been found to cause profound effects on the cardiovascular system, leading to cardiac issues and even death.
In addition to the lethal effects of the Chironex fleckeri's venom, the stings from this species are also extremely painful. The pain is caused by the injection of venom into the skin through the jellyfish's tentacles. The nematocysts, or tiny darts loaded with poison, on the tentacles deliver the venom, resulting in severe pain and potential necrosis of the skin.
While box jellyfish are found in warm coastal waters worldwide, the lethal varieties, including Chironex fleckeri, are primarily located in the Indo-Pacific region and northern Australia. The lethal nature of their venom, combined with the swimming ability and vision of box jellyfish, makes them a significant threat to humans and other animals.
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The first myotoxin to be identified and isolated was crotamine, discovered in the 1950s by Brazilian scientist José Moura Gonçalves
Snake venoms can cause paralysis by interrupting neurotransmission at the neuromuscular junction. They can also cause muscle destruction, known as myotoxicity, which can lead to fatal damage to the normal rhythm of the heart.
Myotoxins are small, basic peptides found in rattlesnake and lizard venoms. They act very quickly, causing instantaneous paralysis to prevent prey from escaping and eventually resulting in death due to diaphragmatic paralysis.
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Antivenom therapy is currently the standard practice for treating neuromuscular dysfunction in snake envenoming
Snake venoms are highly toxic saliva containing zootoxins that facilitate the immobilization and digestion of prey. They are usually injected through unique fangs during a bite, though some species can also spit venom. The toxins in snake venom can cause severe skeletal muscle necrosis, leading to instantaneous paralysis and eventually death. The toxins may also cause heart failure by disturbing the smooth coordination of heart muscle contractions.
Myotoxicity, a form of muscle destruction caused by snake venoms, can lead to massive increases in blood potassium levels, which can further cause fatal damage to the normal rhythm of the heart. Some venoms contain a cocktail of molecules that act in different ways to interfere with the transmission of nerve impulses, with the most dangerous toxins destroying the nerves themselves.
Antivenom therapy is currently the standard practice for treating neuromuscular dysfunction caused by snake envenoming. The main site of snake neurotoxins is the neuromuscular junction, and they can act as either pre-synaptic or post-synaptic neurotoxins. Pre-synaptic neurotoxins irreversibly damage the presynaptic terminal, while post-synaptic neurotoxins bind to the nicotinic acetylcholine receptor. While antivenom therapy is the standard practice, there is a lack of randomized placebo-controlled trials to support its efficacy in treating neuromuscular dysfunction. However, several comparative trials have been conducted, and numerous cohort studies and case reports are available. These studies have demonstrated the efficacy of antivenom therapy in clearing circulating venom and preventing neurotoxicity, especially when administered early.
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Frequently asked questions
The early signs of paralysis caused by venom are typically fixed dilated pupils, reduced eye movements, and droopy eyelids.
The two dominant paralytic toxins are the non-enzymatic α-neurotoxins and the enzymatic β-neurotoxins. The toxins cause paralysis by different biochemical mechanisms but both result in interrupted neurotransmission at the neuromuscular junction.
Toxins interrupt neurotransmission by binding to the agonist-binding sites of the nicotinic acetylcholine receptors on the motor end-plate with high affinity and poor reversibility.
