Snake krait

The similarity of the primary structure of different sea snake venoms has already been discussed. Postsynaptic neurotoxins from Elapidae venom have been extensively studied. Elapidae include well-known snakes such as cobra, krait, mambas, coral snakes, and all Australian snakes. Like sea snake toxins, Elapidae toxins can also be grouped into short-chain (Type I) and long-chain (Type II) toxins. Moreover, two types of neurotoxins are also similar to cardiotoxins, especially in the positions of disulfide bonds. However, amino acid sequences between cardiotoxins and sea snake and Elapidae neurotoxins are quite different. In comparing the sequence of sea snake and Elapidae neurotoxins, there is a considerable conservation in amino acid sequence, but the difference is greater than among the various sea snake toxins. 

Elapidae Cobras Kraits Coral snakes Neurotoxin (some very potent) Fixed fangs, usually low dose Nervous system effects, paralysis, numbness, respiratory failure... 

The clinical features depend upon the type of snake bite. There are three main patterns neurotoxic, as with elapidae such as cobras and kraits vasculotoxic with alteration in blood coagulation as with vipers and myotoxic as with sea snakes although they are all often complicated by local tissue damage. The severity of poisoning will depend on the amount and potency of venom injected and the patient s general health. 

Where the snake has been identified and specific antivenom is available, then this should be used. However, since treatment is urgent, and identification of snakes is difficult, in many Asian countries polyvalent antivenom is used. The Indian anti-snake venom (ASV), manufactured by Serum Institute India, Pune, and Haffkine Bio Pharmaceutical Corporation, Mumbai, consists of hyperimmune horse serum against four common snakes - cobra, common krait, Russell s viper and saw-scale viper. 

Vipers, Cobras and Kraits are the common poisonous snakes and in India 40,000 to 50,000 deaths recorded per year due to snake bite. 

The venom of the elapid snake Bungarus multicinctus (Southeast Asian banded krait) contains a-bungarotoxin, a protein composed fo 74 amino acids (about 8000 daltons) having five disulfide bridges. The LD50 in mice is 0.21 mg/g (s.c.)... 

This family includes coral snakes, cobras, mambas, and kraits. In the United States, Elapidae are responsible for 1-2% of poisonous snakebites. The incidence of envenomations is greater in some other parts of the world. Examples of coral snakes commonly found in the United States are the eastern coral snake, the Sonoran coral snake, and the Texas coral snake. Coral snakes are smaller than pit vipers. They do not have facial pits, and the head is rounded, as are the pupils. Eangs are 2mm and fixed to the jaw. Coral snakes are also more brightly colored, with bands of black and red, separated by yellow and white bands. Coral snakes are timid, nocturnal creatures. 

Acetylcholine receptors provide another target for chemicals with neurotoxic potential most of these act as antagonists. o-Tubocurarine is the classical nicotinic receptor antagonist, and curare-like substances are found in elapid and hydrophid snakes (a-neuro-toxins) such as cobra (a-cobratoxin) and krait... 

There are roughly fifty species of true sea snakes and five species of Sea Kraits. The biggest difference between the two is that kraits return to the land to lay their eggs. 

Both kraits and sea snakes have adapted to marine life. Their tails are flattened for swimming. They have glands in their mouths that remove and excrete salt from the seawater that they happen to swallow. Their nostrils close when they... 

Not only the Kraits produce a-neurotoxins. The Indian Cobra Cobra naja naja) also utilises one of fhe mosf pofenf of all fhe snake toxins, cobratoxin, which is also an a-neurotoxin. Cobratoxin is phenomenally toxic only 4.5 mg is needed to kill a human. In fact, a single Cobra can produce sufficient toxin to kill ten men. The Sea Kraits (e.g. Laticauda semifasciata from Malaysia) are the most toxic of all snakes they produce erabutoxin which is an a-neurotoxin of unbelievable potency, but fortunately, as discussed earlier, they have small jaws, which makes it difficult for them to bite a human. 

Elapidae Micrurus Naja Bungarus Dendroaspis Coral snake Cobra Krait Mamba Human envenomation difficult because of small mouth and small fixed fangs in rear of mouth. Neurotoxicity usually predominates. 

Bungarotoxins. Toxins of the very poisonous southeast Asian snake Bungarus multicinctus (striped krait, Elapidae). Crude extract of venom LD50 (mouse s.c.) 0.019 to 0.33 mg/kg. The postsynaptic neurotoxin a-B. is a polypeptide (Mr ca. 8000) of 74 amino acids and 5 disulfide bridges exhibiting curare-like activity. jS-B. contains different polypeptides and is a pre-synaptic neurotoxin. 

Snake venom is modified saliva that is stored in a specialized structure and has been augmented with a series of toxic proteins. Despite the wide array of proteins that may contribute to the toxicity of snake venom (no fewer than twenty-five), the impacts of venom fall loosely into two categories venoms that impair the circulation of blood, and venoms that impair the electrical connections between locomotor nerves and muscles. The pit vipers of the Americas—the ratdesnakes, for example—generally employ venoms that target circulation, while the kraits of Asia and the mambas of Africa employ neurotoxic venom. 

As noted above, ACh produces an electrical impulse at the post-junctional membrane of the chohnergic synapse which is either transmitted on to another neurone or to smooth or skeletal muscle causing contraction. This occurs by binding of the ACh molecules at special receptor sites which control entiy of ions into a channel. At the NMJ, there are two such sites at the entrance of an ion channel in the post-junctional membrane. When ACh combines with these, the channel is opened and there is an ion flow through it leading to depolarisation of the membrane. In the case of NMJ, this causes the associated muscle fibre to contract. The action of the ACh is terminated by AChE. If, however, the ACh receptor sites are blocked, the transmitter cannot attach to them and depolarisation cannot take place. Toxic substances such as curare, alpha-bungarotoxin from krait snakes and black widow spider venom can do this. The overall main chnical effect is the same as for BoTx, namely a paralysis which leads to respiratory failure and arrest. However, the timescale of a post-junctional block is shorter than a pre-junctional ACh release block and the... 

Snake neurotoxins are the main toxic proteins of cobra, krait, tiger snake and sea snake venoms which block neuromuscular transmission and cause animals death of respiratory paralysis. Snake neurotoxins are classified into two distinct types, postsynaptic and presynaptic neurotoxins, in relation to the neuromuscular junction. Postsynaptic neurotoxins bind specifically to nicotinic acetylcholine receptor (AChR) at the motor endplate and produce a nondepolarizing block of neuromuscular transmission. Presynaptic neurotoxins block the release of acetylcholine from the presynaptic motor nerve terminals. 

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