Snake Venom Enzymes Proteins Substances Neurotoxic Effect Coagulants Biology Essay


Snake venom is adapted saliva that is formed by distinct glands of only certain species of snakes. The gland which secretes the zootoxin is an alteration of the parotid salivary gland of other vertebrates, and is usually located on each side of the head underneath and at the back of the eye, capitalized in a muscular case. It is offered with large alveoli in which the venom is stored before being transported by a vessel to the base of the fang across which it is expelled. Snake venom is a mixture of different enzymes and proteins which many of it not harmless to humans, but some are very toxic. Snake venoms are ordinarily not dangerous once ingested


Snake venom involves enzymes, proteins and substances with a cytotoxic, neurotoxic effect and coagulants:

Phosphodiesterases are used to affect the target's cardiac system to decrease the blood pressure.

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Phospholipase A2 lysing the cell membranes of red blood cells leads to hemolysis

Snake venom hinders cholinesterase causes loss of muscle control.

Hyaluronidase enhances permeability of tissue that boosts the rate of incorporation of other enzymes into the target's cells.

Snake venom frequently contains ATPase which promote the hydrolysis of ATP

Amino acid oxidases responsible for the yellow color of the venom of some species

Some are Neurotoxins: Fasciculins Dendrotoxins α-neurotoxins

And other is Cytotoxins: Phospholipases Cardiotoxins Haemotoxins

(Snake venom)

Uses of snake venom :


Snake venom contains molecules with hemostatins (coagulation modifiers) that may be activators or inhibitors of coagulation process and some are basis for hemostasis tests

Such as Prothrombin Activators which are the best considered snake venom hemostatins. They are presently termed according to the taxonomic name of the snake of origin and advanced classification according to their cofactor condition




Group A (no cofactor requirement)

Echis Carinatus

Ecarin A

Group B (requires calcium)

Echis Carinatus

Carinactivase B

Group C (requires calcium and phospholipid)

Pseudonaja textilis

Oxyuranus scutellatus

Pseutarin C

Oscutarin C

Group D (requires calcium and phospholipids and Factor Va)

Pseudonaja textilis

Pseutarin D

Less Common Uses:

Thrombin-like enzymes (SVTLE) snake venom is used for fibrinogen breakdown assay and for the fibrinogen dysfunction detection. SVTLE are not repressed by heparin and therefore used for assaying antithrombin in heparin-containing testers. (Snake venom uses)

Effect of Snake Venom on Human Body

When human is bitten with hemotoxic venom by a snake, the venom decrease blood pressure and increase blood clotting. The venom also hits the heart muscle may causing death.

Cytotoxic venom causing death of tissues. Many cytotoxic types of venom also extent through the body increasing permeability of muscle cells.

Neurotoxic venom interrupts brain function and nervous system it produces paralysis or deficiency of muscle control.

Some animals have normal protection to snake venom, and immune bodies can be brought through cautious applications of managed venom; this technique is used to make the anti-venom treatments. (Effect of Snake Venom)

Types of snake venom

As mentioned, snake venom is modified saliva which contains a variety of proteins and enzymes. Not all snake venoms are dangerous to humans as they contain phosphodiesterase, cholinesterase, hyalurinodase, ATPase. The venom is a clear, limpid fluid of a pale straw or amber colour, or it can be greenish, but very rarely and sometimes with a certain amount of suspended matter. The snake venoms that exist are categorized into several types such as hemotoxic venoms, neurotoxic venoms, cytotoxic venoms and myotoxic venoms. These venoms will be discussed in the next few paragraphs.


One of the major families of snake venom is the neurotoxins venoms; which means it's the venom which attacks the central nervous system and brain. What happens when a snake bites? An exchange of ions across the nerve cell membrane sends a depolarising current towards the end of the nerve cell. When the depolarising current arrives at the nerve cell terminus, the neurotransmitter acetylcholine (ACh), which is held in vesicles, is released into the space between the two nerves (synapse). It moves across the synapse to the postsynaptic receptors.

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If ACh remains at the receptor, the nerve stays stimulated, causing incontrollable muscle contractions. This condition is called tetany. So an enzyme called acetylcholinesterase destroys the ACh so tetany does not occur. It is subdivided into three groups: Fasciculins, dendrotoxins and α-neurotoxins.

1) Fasciculins:

These toxins attack cholinergic neurons (those that use ACh as a transmitter) by destroying acetylcholinesterase (AChE). ACh therefore cannot be broken down and stays in the receptor. This causes tetany, which can lead to death.

Snake example: Black Mamba

2) Dendrotoxins:

Dendrotoxins inhibit neurotransmissions by blocking the exchange of + and - ions across the neuronal membrane ==> no nerve impulse. So it paralyses the nerves.

Snake example: Mambas

3) α-neurotoxins:

α-neurotoxins also attack cholinergic neurons. They mimic the shape of the acetylcholine molecule and therefore fit into the receptors → they block the ACh flow → feeling of numbness and paralysis.

Snake examples: 1- Kraits use erabutoxin (the Many-banded krait uses Bungarotoxin)

2- Cobras use cobratoxin.

They often result in respiratory paralysis and heart failures. Their effect can range between mild seizures to death. Cobras, mambas, sea snakes, kraits and coral snakes are known to possess this venom. The king cobras (ophiophagus hannah) are the most infamous carriers of this venom. Neurotoxic venom is essentially nerve destroying. Hence, one can see speech and swallowing difficulties, drooling, difficulty in breathing, respiratory arrests, convulsions and sometimes even prolonged unconsciousness in the victims. The milder symptoms are dizziness, tunnel vision, blurred vision and increased sweating. This venom causes a very fast degeneration of the synaptic nerves and this is the reason for the blockage of nerve impulses sent to and from the brain to the muscles.

2- Cytotoxics

1) Phospholipases:

Phospholipase is an enzyme that transforms the phospholipid molecule into a lysophospholipid (soap) ==> the new molecule attracts and binds fat and rips a hole in the cell membrane. Consequently water flows into the cell and destroys the molecules in it. That is called necrosis.

Snake example: The Japanese Habu snakes (low toxicity)

2) Cardiotoxins:

Actually cardiotoxins are muscle venoms. They bind to particular sites on the surface of muscle cells causing depolarisation ==> the toxin prevents muscle contraction. For example the heart muscle: the heart will beat irregularly and stop beating, which will cause death.

Snake example: King Cobra and some other cobras

3) Haemotoxins:

The toxin destroys red blood cells (erythrocytes). This symptom is called haemolysis. As it is very slowly progressing venom it would probably not kill a human - another toxin in the snake's venom would most certainly have caused death by then.

Snake example: most Vipers and the members of Naja genus

This is milder venom that generally causes only localized symptoms at the location of the bite. This is a cell destroying venom that destroys everything in it's path - blood vessels, cells and tissues. The symptoms of the invasion of this venom are generally seen around 10-15 minutes after the snake encounter (I meant bite, not the spotting). The results are generally localized pain accompanied by severe swelling and bleeding. One can easily spot the formation of red blisters near the bite area. This venom causes blue/black spotting due to limited blood circulation. The body often revolts against the invasion of this venom by causing nausea and vomiting. If this venom is not treated within four hours, it generally needs an amputation. Puff adders (bitis arietans) are the snakes to be avoided if one is pain phobic.

3-hemotoxic venoms

They are toxins that destroy red blood cells, disrupt blood clotting, and/or cause organ degeneration and generalized tissuedamage. The term hemotoxin is to some degree a misnomer since toxins that damage the blood also damage other tissues. Injury from a hemotoxic agent is often very painful and can cause permanent damage. Loss of an affected limb is possible even with prompt treatment.

Hemotoxins are frequently employed by venomous animals, including pit vipers. Animal venoms contain enzymes and other proteins that are hemotoxic or neurotoxic or occasionally both (as in the Mojave Rattlesnake, the Japanese mamushi, and similar species). In addition to killing the prey, part of the function of hemotoxic venom for some animals is to aid digestion. The venom breaks down protein in the region of the bite, making prey easier to digest.

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The process by which a hemotoxin causes death is much slower than that of a neurotoxin. Snakes which envenomate a prey animal may have to track the prey as it flees. Typically, a mammalian prey item will stop fleeing not because of death, but due to shock caused by the venomous bite. This venom causes the poisoning of blood and affects the blood clotting mechanism to such a grave extent, that the victim can die of internal bleeding. Usually, neither pain nor any other symptoms can be observed for almost 1-3 hours (sometimes even 8). This makes it deadlier, as the victim is usually beyond medical help, by the time the cause is even ascertained. The effects of this venom can be seen as lethargy, headaches, nausea, vomiting, etc. The most scary observations of the outcome of a snake bite of this kind are bruising or blood spots beneath the victim's skin. In extremely bad cases, blood is known to ooze out from all possible bodily openings. It is these venoms that usually cause excessive (and hideous) scarring, gangrene and permanent or temporary loss of motor skills. Worst cases can even result in the amputation of the affected limb. Dependent upon species, size, location of bite and the amount of venom injected, symptoms in humans such as nausea, disorientation, and headache may be delayed for several hours. Hemotoxins are used in diagnostic studies of the coagulation system. Lupus anticoagulans is detected by changes in the dilute Russell's viper venom time (DRVVT), which is a laboratoryassay based on-as its name indicates-venom of the Russell's viper.


This venom is found in the 'bothrops moojeni' snakes, commonly known as the Brazillian lancehead snakes. This venom is known to cause muscular necrosis. Its symptoms are a thickened-tongue sensation, dry throat, thirst, muscular spasms and convulsions. It also causes the stiffness of the jaw, neck, trunk and limbs along with severe pain in movement. The victims often start with drooping eyelids and then turn to more austere results like loss of breath and blackish brown urine discharge. Myotoxic venom contains peptides that destroy the muscle fiber proteins and result in myonecrosis (muscle destruction).

In the very later stages (when treatment is delayed) of the spread of this venom, the muscle proteins enter the blood stream. The kidney overworks in trying to filter out this junk and often gives up trying. This kidney failure is the reason for the dark coloration of urine.

Signs & symptoms of snake venom:

There is a variable symptom of snake venom poisoning, depending on the following criteria:

Snake size and species.

The quantity and degree of toxicity of the injected venom.

The location of bite (As it is far away from the head and trunk, it will be less dangerous)

The age of the person (since very old and very young people are in much more risk)

The person with medical problems.

Pit Vipers:

Most pit vipers Bites cause pain immediately and usually within 20 to 30 minutes redness and swelling will occur. This bite can affect the whole leg or arm within hours. When the rattlesnake bites, it causes feeling of tingling and numbness in fingers or toes or around the mouth, also it causes metallic taste in the mouth.

There are other symptoms including: Fever, chills, sweating, general weakness, confusion, anxiety, nausea and vomiting. Terror rather than venom itself causes some of these symptoms. After Mojave rattlesnake bites breathing difficulties can be developed. Also people could get a dry mouth, a headache, blurred vision, and drooping eyelids.

In case of moderate or severe pit viper poisoning usually leads to bruise of the skin after 3 to 6 hours of the bite. The area surrounding the bite appears discolored, tight and it may contain bloody blisters. Unless treatment occurs, tissue of the bite could be destroyed. Bleeding gums may occur, and blood may be present in the person's vomit, stools, and urine.

Coral Snakes: its bite may cause little or no rapidly pain and swelling. Severe symptoms may occur after several hours. The skin surrounding the bite could be tingle, and muscles almost become weak. Sometimes severe general weakness and Muscle incoordination occur. Other symptoms may include drowsinss, confusion, increase saliva production, blurred vision, double vision, and difficulties in swallowing & speech. Also breathing problems may be present.

Coral Snake

Management of snake venom toxicity:

Self-Care at Home:

The patient needs tetanus shot if he has not had one within 5 years.

Examine the wound for dirt or broken teeth.

Person must get away from the snake to stop a second bite as snakes can continue biting and inject venom with continuous bites until they finish venom

Remove squeezing items from the victim (like rings or other jewelry) which could take away blood flow if the bite spot swells.

Using mechanical suction is not recommended as it does not remove any considerable amount of venom, and it increase damage of the tissue.


Victim must not cut into the bite spot can cause damage underlying tissues, also increase infection risk, and does not remove venom.

Victim must not use ice because ice does not disable the venom effect and can result in frostbite.

Victim must not use alcohol as alcohol can decrease the pain; however it dilates the local blood vessels that increase absorption of venom.

Victim must not use bandages or narrowing bands these may increase damage of tissue. (Snakebite Treatment)

The lymphatic system is responsible for spread of venoms. This spread can be reduced by the use of a safe bandage over a crumpled pad located over the bitten area. The firm should not be constricted that it stops blood flow. Bandage immediately over the bite area. A pressure bandage should be applied on bite area if it anywhere in body such as trunk.

Special bites as in the head, neck, and back should apply a firm pressure locally if achievable.

Medical treatment:

Aid breathing, airway and circulation

If respiration failed ventilate with 100% Oxygen

Antivenom is given immediately

Adrenaline intravenous should be given only for serious hypotension or anaphylaxis and cerebral hemorrhage

the patient must be well hydrated to decrease the threat of acute renal failure

Repeat blood tests, ECG, at clinically related breaks

Abnormal coagulation must be corrected; watch for spread intravascular coagulation, heparin contra-indicated in DIC from snake bite

Hypotension must be monitored

Recommended for Tetanus prophylaxis


Antivenin (Crotalidae) Polyvalent (ACP) equine (horse)-derived antivenin was the standard treatment in emergency departments. (Snakebite Treatment)

Antivenoms are set from horse serum. The anaphylaxis risk is low but is increased in people who exposure to horses, horsey tetanus vaccines, and allergic history.

It is recommended to pre-treatment with non-sedating anti-histamine (promethazine), subcutaneous, and intravenous steroids (hydrocortisone). (Chris Thompson)

Antivenin is administered either through the veins or injected into muscle and works by neutralizing snake venom that has entered the body (Vincent Iannelli)


Crotalidae polyvalent immune FAB (ovine):

Mixed monospecific used as Crotalid bites antivenom. Accustomed to neutralize snakebite toxins it decrease tissue damage and need for fasciotomy deprived of allergic effects. (Brian James Daley)


Antibiotics are given in hospital for severe conditions. Though, antibiotic prophylaxis is suggested such as Ceftriaxone (Rocephin) a Third-generation cephalosporin has wide-spectrum gram-negative action, it hinders bacterial growth by binding to penicillin-binding proteins. (Brian James Daley)

Emergency Department Care:

1-Treatment consists of revising the ABCs and assessing the patient for marks of shock such as:

Tachypnea Tachycardia

Dry pale skin Mental status changes


2-To decide the need for antivenin in victims envenomation grading is classified as:

Mild envenomation:

Characterized by there is no systemic toxicity signs, edema, local pain and laboratory values are normal.

Moderate envenomation:

Characterized by:

Serious local pain

Edema more than 12 inches nearby the wound

Systemic toxicity involving nausea and vomiting

Alterations in laboratory values such as the decrease in hematocrit and platelet count

Severe envenomation:

Characterized by: generalized petechiae

Ecchymosis (subcutaneous purpura larger than 1 centimeter or a hematoma)

Sputum with blood, hypotension, renal dysfunction, and abnormal results significant for consumptive coagulopathy.

3- Antivenin is given for patient that exhibits within 12 hours of the bite in spite of local or systemic symptoms. Neurotoxicity may progress unexpectedly and causes respiratory failure. (Brian James Daley)

4- antigen-binding fragment antivenom (FabAV) aids regulate local tissue effects and hemotoxicity, insistent antivenom treatment does not usually improve effects of neurotoxicity such as myokymia (which is impulsive, sufficient fascicular contractions of muscle without atrophy. The physician must keep continuous checking of myokymia patients mainly of the chest, diaphragm and shoulders to avoid progress of respiratory failure. (Brian James Daley)

5- Surgical treatment aims on the site of injury:

Fasciotomy is specified only for patients with raised partition pressure.

Liberal checking of compartment pressure is necessary. If not accessible, apply the physical seal of compartment hypertension, accompanied by distal pallor, paresthesia, or for the clinical valuation. Injury of tissue after compartment condition is not revocable but can be prevented. (Brian James Daley)