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Snake venom is a complex mixture of toxic proteins, enzymes, amines, carbohydrates, lipids, and nucleosides. Some snake venoms contain neurotoxins, which directly attack the nervous system and prevent the brain from sending or receiving signals to the muscles, causing paralysis. The effects of neurotoxic venom can be rapid, with symptoms appearing within 24 hours. If left untreated, neurotoxic venom can lead to death as vital functions such as breathing and heart function are interrupted. Other types of venom, such as hemotoxic venom, attack red blood cells directly, causing hemorrhaging, tissue death, and organ damage. Snake envenoming is a significant health issue, particularly in rural areas of developing countries, resulting in numerous disabilities and deaths annually.
| Characteristics | Values |
|---|---|
| Type of venom | Neurotoxic |
| How it works | Attacks the nervous system, blocking nerve signalling and preventing the brain from receiving or sending signals to the muscles |
| Symptoms | Fixed dilated pupils, reduced eye movements, droopy eyelids, difficulty talking, swallowing and breathing |
| Cause of paralysis | Disruption of neurotransmission in the neuromuscular junction |
| Antivenom | Intravenous administration of snake antivenom |
| Muscle damage | Viper venoms contain metalloproteases that induce permanent muscle damage |
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What You'll Learn
Neurotoxins and their effects on the nervous system
Neurotoxins are a diverse group of over 1,000 chemicals that can adversely affect the nervous system. They are often neurologically destructive but can also be useful in the field of neuroscience. Neurotoxins can be either exogenous or endogenous. Exogenous neurotoxins are usually acquired by the body through ingestion, inhalation, skin contact, or injection, while endogenous neurotoxins originate from and exert their effects in vivo. Endogenous neurotoxins are commonly used by the body in healthy ways, such as nitric oxide in cell communication, but can become dangerous at high concentrations.
Neurotoxins can be natural or human-made and include snake venom, pesticides, lead, ethanol (drinking alcohol), glutamate, nitric oxide, botulinum toxin (e.g. Botox), tetanus toxin, tetrodotoxin, and ethyl alcohol. They can also be found in certain medications, such as antibiotics and antipsychotics, and in cancer-related therapies like chemotherapy and radiation therapy.
Neurotoxicity occurs when exposure to neurotoxicants changes the function of any part of the nervous system, including the brain, spinal cord, and nerves. The nervous system is highly complex and necessary for survival, making it a target for attack by both predators and prey. As a result, venomous organisms have evolved highly specific neurotoxins that can act very quickly to subdue their prey.
Neurotoxic snake venoms primarily affect the neuromuscular junction, disrupting neurotransmission and resulting in paralysis. They can act on the motor nerve terminals (presynaptic) or the nicotinic acetylcholine receptor on the motor end-plate (postsynaptic). Presynaptic toxins deplete synaptic vesicles and cause structural damage to the motor nerve terminals, leading to treatment resistance and requiring natural regeneration of the nerve terminal for recovery. Postsynaptic toxins competitively bind to agonist-binding sites on the nicotinic acetylcholine receptors, blocking neuromuscular transmission.
The effects of neurotoxins can range from mild to severe and can be temporary or long-lasting. In severe cases, neurotoxicity can lead to death. The extent of the impact depends on the toxicity of the substance, the individual's age, and their health at the time of exposure. Young and elderly individuals are particularly vulnerable to neurotoxic chemicals.
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Antivenom treatments
Snake venom is a complex mixture of toxic proteins, enzymes, amines, carbohydrates, lipids, and nucleosides. It is injected through the snake's fangs into its prey. Some snakes even have fangs that fold into their mouths.
Neurotoxic venom directly attacks the nerves and prevents the brain from receiving or sending signals to the muscles. This can cause paralysis and even death when the heart and lungs stop functioning. This type of venom can work quickly, but not always. Symptoms may take up to 24 hours to appear, but by then it may be too late for treatment.
Neurotoxins are not the only type of venom that can cause paralysis. Myotoxins, for example, break down muscles.
Antivenom is a type of antibody therapy that reduces the effects of venom in the body. It can be administered as an injection or through an IV. The type of antivenom used depends on the species of snake involved in the bite. Monospecific antivenoms treat bites from a specific type of snake, while polyspecific antivenoms treat bites from multiple snakes in a particular geographic region.
In addition to antivenom, there are other treatments for venomous snake bites. If the bite caused a larger-than-normal loss of blood, a blood transfusion may be necessary. If blood pressure drops, IV fluids may be required. Aminoglycoside antibiotics such as gentamycin should be avoided, as they can adversely affect neuromuscular function. Cholinesterase inhibitors such as neostigmine can be used to prevent paralysis by increasing synaptic concentrations of acetylcholine, allowing the neurotransmitter to compete with the toxins. However, this treatment should be used with caution or avoided when β-toxin effects are the primary feature of the envenoming snake or if fasciculin-containing venom is suspected.
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How snake venom differs from other animal venoms
Snake venom is a complex mixture of proteins and enzymes, as well as anticoagulants and other substances. Ninety per cent of the venom is protein by dry weight, and most of the proteins are enzymes. There are as many as 25 different enzymes found in various venoms, 10 of which are present in most of them. Snake venom can be classified into three major categories: neurotoxic, hemotoxic, and cytotoxic.
Neurotoxins are common to the Elapidae family of snakes, which include cobras, mambas, coral snakes, and copperheads. They work on the nervous system by disrupting the electrical impulses that our nerves and muscles use to function. Hemotoxins primarily digest tissues and cause internal bleeding, affecting the circulatory system. They can trigger the destruction of red blood cells and affect the clotting factor of blood. Cytotoxins directly damage and kill cells. This type of venom is often found in cobras and other elapids.
The variety of venom types and mechanisms of action means that nearly every snake species needs a tailor-made antivenom. The only effective treatment against snakebites, antivenom can be divided into two types: monovalent, which is effective against a given species' venom, and polyvalent, which can be used for multiple species. However, the non-human origin of the antibodies used in antivenom means there is a heightened risk of allergic reaction, anaphylactic shock, and even death.
Snake venom differs from other animal venoms in its variety and complexity. While other animals may have evolved certain resistances to snake venom, such as the honey badger and domestic pig, the evolution of snake venom itself can be traced back to a single origin approximately 170 million years ago. Since then, it has diversified into the wide range of venoms seen today, with different combinations of enzymes creating deadlier effects.
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The history of snake venom research
Snake venom has been a subject of scientific research for centuries, with the first scientific treatise on snakebite envenoming, the Brooklyn Medical Papyrus, dating back to ancient Egypt. The fascination and fear of snakes is a long-standing human emotion, and snakes have been associated with images of death and treachery. However, the curative capacity of venom has also been recognised since ancient times, making the snake a symbol of pharmacy and medicine.
One of the earliest known attempts to understand and counter the effects of snake venom was made by the Psylli tribe around 60 CE, who are thought to have developed immunity against it. In the 19th century, the French physician Albert Calmette conducted research on the venom of cobras, studying the physiology of envenomation, the physicochemical properties of the venom, and the effect of different chemicals on it. He also attempted, unsuccessfully, to induce immunity against snake venom in animals. Upon his return to France, he successfully immunised rabbits with cobra venom.
In the same century, scientists such as S.W. Mitchell, R.N. Wolfenden, and G. Lamb made significant contributions to the understanding of snake venom. Mitchell focused on the venom of rattlesnakes, while Wolfenden studied the nature and action of the venom of poisonous snakes, including the Indian cobra. Lamb's work centred on the action of snake venom on blood coagulability and the venom's effects on red corpuscles and blood plasma.
The Nobel Prize-winning discovery of serum therapy for treating bacterial infections paved the way for the introduction of antivenom therapies in the 19th century. French scientists developed the first serum therapy for snakebite envenoming in 1894, and other countries with high incidences of snakebites followed suit in the 20th century, including Brazil, Australia, and South Africa. Vital Brazil, a prominent figure in antivenom production, played a crucial role in establishing two major institutes for snake venom research and antiserum production in Brazil.
In the early 20th century, researchers like Hideyo Noguchi and Afrânio do Amaral contributed to antivenom development. The first antivenom against North American rattlesnakes was produced in 1927. In the present day, there is a renewed interest in pursuing snake venom-based therapies, with researchers exploring the potential of venom to create novel drugs and treatments for conditions such as cancer and inflammation.
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The molecular mechanisms of snake venom
Snake venom is a complex mixture of toxic proteins, enzymes, amines, carbohydrates, lipids, and nucleosides. The molecular mechanisms of snake venom vary depending on the snake species, but the majority of snake venom neurotoxins act on either the motor nerve terminals (presynaptic) or the nicotinic acetylcholine receptor on the motor end plate (postsynaptic).
Neurotoxic venom directly attacks the nervous system, including the brain, and prevents the transmission of signals from the nerves to the muscles. This interruption in neurotransmission results in paralysis of the skeletal muscles and can range from mild weakness to fatal paralysis of bulbar and respiratory muscles. In some cases, complete neuromuscular paralysis involving all skeletal muscles of the body can occur. The severity of neuromuscular weakness and paralysis depends on the type and quantity of toxins present in the venom.
Non-enzymatic α-neurotoxins, also known as three-finger toxins (3FTx), are found exclusively in elapid venoms. These toxins mimic the shape of the acetylcholine molecule, binding to the nicotinic acetylcholine receptors of cholinergic neurons and blocking the flow of acetylcholine, leading to numbness and paralysis. On the other hand, enzymatic β-neurotoxins, such as Type I and Type II secretory phospholipase A2s (sPLA2), are found in elapid and viperid venoms. These toxins produce effects on both the pre- and postsynapse, resulting in paralysis and muscle membrane damage.
The transduction mechanisms involved in snake venom toxicity include arachidonic acid, intracellular calcium, cytokines, bioactive peptides, and possibly dimerization of venom and prey protein homologs. The precise mechanism of svPLA2-induced neuromuscular paralysis is not yet fully understood, but it is believed to involve a self-amplifying cycle of endogenous PLA2 activation, arachidonic acid increases, and nicotinic receptor deactivation. This cycle of effects initiated by PLA2 forms a positive feedback loop that contributes to the overall toxicity of snake venom.
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Frequently asked questions
Snake venom contains neurotoxins that disrupt neurotransmission, preventing signals from being sent from the nerves to the muscles. This results in paralysis.
The paralysing effects of snake venom typically start with the muscles around the eyes, resulting in fixed dilated pupils, reduced eye movements, and droopy eyelids.
Snakes known to cause paralysis include the common krait, black krait, banded krait, neotropical rattlesnake, cobra, coral snake, taipan, tiger snake, and death adder.
Treatment for paralysis caused by snake venom typically involves the administration of antivenom. In some cases, neostigmine-atropine may also be used to improve symptoms.
