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Snake venom is highly modified saliva which is usually yellowish in color. Some venoms are cloudy, some are clear. In some rear fanged snakes, venom is produced in Duvernoy’s gland which is colorless.
Composition of snake venom differs from species to species, even it may differ in the same species at different locations, and in different age groups. But one common thing is that all snake venoms are complex mixtures containing lots of compounds having different toxic and lethal properties.
Toxic compounds found in different snakes are mainly
1) NEUROTOXIN
2) HEMOTOXIN and
3) MYOTOXIN .
In some snakes venom contains CYTOTOXIN which causes local tissue destruction.
A snake may have different combinations of these toxins in its venom.
Neurotoxin–
Snake venom NEUROTOXINS are chemical substances that are poisonous to the nervous system. They affect neuromuscular transmission and subsequent paralysis of different muscles. Paralysis of respiratory muscles is the most common cause of death in Neurotoxic snake bites.
There are so many Neurotoxins found in different snake species, which act on the nervous system in different ways. Some of these Neurotoxins are
1) Presynaptic beta Neurotoxins- such as beta Bungarotoxin, found in venom of Krait ( Bungarus caeruleus & B. multicinctus), Taipoxin (found in Australian taipan),
Viperotoxin (found in Taiwan viper),
Notexin (found in Australian Tiger snakes),
Crotoxin (found in American rattlesnakes).
At first these Neurotoxins cause an augmentation of release of Acetylcholine at the neuromuscular junction and damage the nerve endings causing irreversible block and preventing further release of Acetylcholine.
As a result of deficiency of Acetylcholine there is paralysis of different muscles. Respiratory paralysis caused by these Neurotoxins can not be reverted by administration of neostigmine and death may occur due to respiratory paralysis.
2) Postsynaptic alpha Neurotoxins- Cobratoxin (found in cobra),
alpha Bungarotoxin ( found in Krait B. caeruleus & B. multicinctus).
Sea snakes ( Enhydrina schistosa, Hydrophis cyanocinctus, Lepesis hardwickii ) neurotoxins are mainly postsynaptic alpha Neurotoxins.
Some Coral snakes have postsynaptic alpha Neurotoxins.
These postsynaptic Neurotoxins bind with nicotinic acetylcholine receptors at motor end plate of neuromuscular junctions like curare, competitively inhibiting acetylcholine. As a result, paralysis of muscles occurs. In this type of toxicity administration of neostigmine ( an Acetylcholinesterase inhibitor which increases the level of Acetylcholine ) can prevent paralysis.
3) Fasciculin- found in venom of eastern green mamba ( Dendroaspis spp.) and in some rattlesnakes ( Crotalus spp.) This neurotoxin inhibits acetylcholinesterase function, therefore acetylcholine cannot be broken down producing uncontrollable muscle movements, convulsion subsequently breathing paralysis.
4) Dendrotoxin- found in venom of some mamba. These toxins block voltage gated potassium channels and prevent potassium from traveling in and out of the nerve. As a result there is increased presynaptic release of acetylcholine which in turn causes severe muscle spasm, convulsion & breathing paralysis.
5 Calciseptine- Found in venom of black mamba ( Dendroaspis polylepsis ). It blocks L type calcium channels and inhibits smooth muscle contraction & cardiac function. As a result there is respiratory failure, cardiovascular collapse and death.
Black mamba venom also contains postsynaptic alpha neurotoxin, fasciculin, dendrotoxin, that’s why it is one of the deadliest snakes in the world. Fatalities may occur within as little as 20 minutes. It is also one of the fastest snakes & can run with a speed of 12.5 miles/hour.
HEMOTOXINS–
Viper venom contains mainly hemotoxins. But there are some elapid snakes whose venom contains hemotoxin in addition to neurotoxin. The word Hemotoxin is a misnomer. Because hemotoxins not only destroy blood cells but also interfere with blood coagulation system, destroy blood vessels, increase capillary permeability of blood vessels, interfere with platelet function, interfere with blood pressure regulatory system, interfere with cardiac activities and also they can damage other type of cells and tissues causing profound tissue damage.
Haemorrhage from different sites, shock due to hemorrhage. Organ failure and death may occur.
There are several types of hemotoxins in snake venom of different species of snakes each of them having one or more deleterious effects. A few of these toxins are
1) Snake venom metalloproteinases (SVMP)- there may be several SVMP in a single species of snake venom each having distinct function i) SVMP activate blood clotting factors like factor x & factor II ( Prothrombin) as a result thrombin is released which acts on fibrinogen to produce fibrin clot. This causes depletion of blood clotting factors causing venom induced consumption coagulopathy ( VICC ) ii) Some svmp are capable of inducing platelet aggregation ( by von willebrand factor or collagen mediated activation). Some svmp can inhibit aggregation ( by Potentially blocking integrin receptors found on surface of platelets). Both activation and inhibition ultimately cause thrombocytopenia and VICC. iii) some svmps are fibrinogenolytic causing deficiency of fibrin which causes hemorrhage. iv) Some svmp may affect the integrity of blood vessels causing them to swell and burst and cause spontaneous hemorrhage, this may cause shock or death, may cause hemorrhagic cerebrovascular accident. v) svmp also increase vascular permeability via degradation of capillary basement membrane resulting in capillary leakage and hypotension.
2) Disintegrins bind with fibrinogen receptors in platelet so fibrinogen cannot bind with these receptors in platelets as a result there is inhibition of platelet aggregation resulting in bleeding manifestation
3) Snake venom serine proteases ( SVSP )– They have Fibrinogenolytic activity causing deficiency of fibrin. Some work as plasminogen activators causing release of plasmin that degrade fibrin. Some svsp cause release of bradykinin from plasma kininogen. Bradykinin causes vasodilation, hypotension and shock. some svsp activates factor x and factor v which causes activation of Prothrombin resulting in production of thrombin and there is consumption of clotting factors and venom induced consumption coagulopathy.
4) Factor v activator and factor x activator- they cause activation of Prothrombin, as a result venom induced consumption coagulopathy occurs.
5) Certain Kunitz-type serine protease inhibitors cause inhibition of thrombin and some causes inhibition of plasmin.
6) C type lectins interact with platelet receptors.
7) Bradykinin potentiating peptide ( BPP ) of snake venom causes vasodilatation, hypotension and shock
8) Snake venom phospholipase A2 (PLA2)- Some of them inhibits platelet aggression and some causes hypotension.
MYOTOXINS-
These toxins cause destruction of muscle cells. Venom induced myotoxicity occurs in two clinical pictures.
Local myotoxicity is the characteristic of viperidae snake bites which predominantly affect the muscles located in the vicinity of the snake bite site causing destruction of local muscle cells.
On the other hand in systemic myotoxicity there is widespread muscle damage and necrosis in the body therefore there is severe myalgia, liberation of muscle enzymes causing increased blood levels of muscle enzymes such as creatine kinase ( CK ) and SGOT (Serum glutamic oxaloacetic transaminase ), destruction of muscles cause liberation of myoglobin (which supplies oxygen to muscle cells) and myoglobinuria occurs ( elimination of myoglobin through urine). Hyperkalemia, which is an increased level of potassium in blood, occurs.
As a result patients may die due to acute renal failure, bulbar and respiratory muscles weakness or hyperkalemia. Some MYOTOXINS are
1) MYOTOXIC PLA2- Sea snake myotoxins are mainly myotoxic PLA2. There may not be any local symptom. Even the victim may not be able to understand the bite. Generalised muscle ache and pain may occur as early as 5 minutes but usually within 2 hours. There may be stiffness of neck, face, trunk, arm and thigh. Myoglobinuria may occur within 3 to 6 hours. Mulgotoxin A is also a myotoxic pla2 found in Australian king brown snake ( Pseudechis australis ). Bothrops venom also contains myotoxic PLA2 ).
2) MYOTOXIN A- Found in the Venom of Western diamondback rattlesnake ( Crotalus atrox ) causes extensive muscle fibre damage . Muscle necrosis occurs in patches after 3 days.
3) CROTAMIN- found in South American rattlesnakes.
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