Snake

INDEX Sr.no.ContentsPage no.1Introduction022Venomous snakes033Snake venom114chemistry125Types of snake venom136Interaction with human167Antivenom228Mechanism of antivenom269Venom application3010Reference41 Venomous snake Introduction Venomous snake is a snake that uses modified saliva, snake venom, usually delivered through highly specialized teeth such as hollow fangs, for the purpose of prey immobilization and self-defense. In contrast, non-venomous species either constrict their prey, or simply overpower it with their jaws. Venomous snakes include several families of snakes and do not form a single taxonomic group. This has been interpreted to mean that venom in snakes originated more than once as the result of convergent evolution. Evidence has recently been presented for the Toxicofera hypothesis however; venom was present (in small amounts) in the ancestor of all snakes (as well as several lizard families) as 'toxic saliva' and evolved to extremes in those snake families normally classified as venomous by parallel evolution. The Toxicofera hypothesis further implies that 'non venomous' snake lineages have either lost the ability to produce venom (but may still have lingering venom pseudogenes), or actually do produce venom in small quantities, likely sufficient to assist in small prey capture, but cause no harm to humans if bitten. Venomous snakes are often said to be poisonous, although this is not the correct term, as venoms and poisons are different. Poisons can be absorbed by the body, such as through the skin or digestive system, while venoms must first be introduced directly into tissues or the blood stream (envenomated) through mechanical means. It is, for example, therefore harmless to drink snake venom as long as there are no lacerations inside the mouth or digestive tract. There are however two exceptions: the Rhabdophis snakes (keelback snales) secrete poison from glands that it gets from the poisonous toads that it preys on; similarly certain garter snakes from Oregon retain toxins in their liver from the newts they eat.[1] Families of venomous snakes Over 600 species are known to be venomous—about a quarter of all snake species. The following groups of snakes can be aggressive and inflict dangerous, even potentially lethal bites: FamilyDescriptionAtractaspididae (atractaspidids)Burrowing asps, mole vipers, stiletto snakes.Colubridae (colubrids)Most are harmless, but others have toxic saliva and at least five species, including the boomslang (Dispholidus typus), have caused human fatalities.Elapidae (elapids)Cobras, coral snakes, kraits, mambas, sea snakes, sea kraits and Australian elapids.Viperidae (viperids)True vipers and pit vipers, including rattlesnakes. Big Four (Indian snakes) The Big Four are the four venomous snake species considered[who?] to be responsible for the greatest number of human deaths caused by snakebite in South Asia. The Big Four:[1] Indian cobra, Naja naja, probably the most famous of all Indian snakes. Common krait, Bungarus caeruleus Russell's viper, Daboia russelii. Saw-scaled viper, Echis carinatus. Naja naja, the binocellate cobra.Bungarus caeruleus, the common krait.Daboia russelii, Russel's viper.Echis carinatus, the saw-scaled viper. Another famous species, the king cobra, Ophiophagus hannah, is not a member of the Big Four. This species may have a potent venom of which it can inject enormous quantities and is deadlier when compared to the smaller species listed above, but it is actually shy, living mostly in dense jungle where it rarely comes into contact with humans. It also feeds only on other snakes not mice which may not be found in high population regions (hence its scientific name, which means \"
snake-eater king\"
) and is even listed as a threatened species. The members of the Big Four, on the other hand, are all quite common and bite readily. They are often found in proximity to human habitation, as they are attracted to the associated rodent populations on which they feed. These species are all primarily nocturnal and most victims are bitten at night when walking barefoot and accidentally stepping on them. Thus it is these snakes' feeding behavior, combined with their density in populated areas, which causes these snakes to account for the majority of snakebite incidents in India. Polyvalent serum has been developed in India specifically for treatment of snake bite by any of the Big Four cases. The serum is widely available in India and is used to save the lives of people bitten by any of these snakes. Antivenom for the king cobra is not available in India, but is available in Thailand where, presumably, the likelihood of encounter with this snake is gre Indian Cobra Naja fasciata\"
redirects here. That taxon as described by Bocage in 1895 refers to the Black-necked Spitting Cobra (N. nigricollis). Common names: Cobra, Indian Cobra, Spectacled Cobra, (more...) Naja naja is a species of venomous snake native to the Indian subcontinent which includes present day Pakistan, India, Bangladesh and Sri Lanka. It is the most dangerous of the Big Four, the four snake species responsible for most fatal snakebites in India for which a single polyvalent antivenom has been created. Like other cobras, N. naja is famous for its threat display involving raising the front part of its body and spreading its hood. This snake is revered in Indian mythology and culture and is often seen with snake charmers. It is now protected in India under the Indian Wildlife Protection Act (1972). Venom Binocellate Cobra The Indian cobra's venom contains a powerful post-synaptic neurotoxin. The venom acts on the synaptic gaps of the nerves, thereby paralyzing muscles, and possibly leading to respiratory failure or cardiac arrest. The venom components include enzymes such as hyaluronidase that cause lysis and increase the spread of the venom.[9] Symptoms of cobra envenomation can begin from 15 minutes to two hours after the bite, and can be fatal in less than an hour.[10] The Indian Cobra is one of the Big four (most famous venomous snakes of India) and a polyvalent serum is available for treating snakebites by these snakes. Zedoary, a local spice, is said to be an effective antidote.[11] Common Krait The Common Krait (Bungarus caeruleus) is a type of krait that is found in the jungles of the Indian sub-continent. This snake is highly venomous, and is one of the \"
big four\"
snakes in India. Description The body colour varies from a dark steely blue-black to a pale faded bluish grey. The average length is 1 meter. Subcaudal scales after the anal scales are not divided. It has large hexagonal scales running down its spine. The white cross bands are more prominent near the tail region. The male is larger than the female and also has a longer tail. Common names Hindi - Karait. Urdu - Kala gandait. Kannada - Kattige haavu. Telugu - Katla paamu. Marathi - Manyar, kanadar. Venom Krait venom is extremely neurotoxic and quickly induces muscle paralysis. Clinically, their venom contains pre-synaptic neurotoxins. And it is many times more venomous than that of the common cobras.These neurotoxins generally affect the nerve endings near the synaptic gap of the brain. Fortunately, since kraits are nocturnal they seldom encounter humans during daylight hours, so incidents are rare. Note that there is frequently little or no pain from a krait bite and this can provide false reassurance to the victim. Typically, victims complain of severe abdominal cramps, accompanied by progressive paralysis. As there are no local symptoms, a patient should be carefully observed for signs of paralysis (eg the onset of ptosis) and treated urgently with antivenin. Note that it is also possible to support bite victims via mechanical ventilation, using equipment of the type generally available at hospitals. Such support should be provided until the venom is metabolised and the victim can breathe unaided. If death occurs it takes place approximately 6-8 hours after the krait bite. Cause of death is general respiratory failure i.e. suffocation Daboia Common names: Russell's viper,[2][3] chain viper,[4][5] Indian Russell's viper,[6][7] (more). Daboia is a monotypic genus[8] created for a venomous viper species, D. russelii, which is found in Asia throughout the Indian subcontinent, much of Southeast Asia, southern China and Taiwan.[1] Due largely to its irritable nature, it is responsible for more human fatalities than any other venomous snake.[9] Within much of its range, this species is easily the most dangerous viperid snake and a major cause of snakebite injury and mortality.[2] It is a member of the big four venomous snakes in India, which are together responsible for nearly all Indian snakebite fatalities.[10] The species was named in honor of Dr. Patrick Russell (1726–1805), who had earlier described this animal, and the genus after the Hindi name for it, which means \"
that lies hid\"
, or \"
the lurker.\"
[11] Two subspecies are currently recognized, including the nominate subspecies described here.[12] Common names English – Russell's viper,[2] chain viper,[4][5] Indian Russell's viper,[6][7] common Russell's viper,[16] seven pacer,[17] chain snake, scissors snake.[18] Previously, another common name was used to described a subspecies that is now part of the synonymy of this form: Sri Lankan Russell's viper for D. r. pulchella.[16] Urdu, Hindi, Hindustani, Punjabi – daboia.[19][15] Marathi – ghonas.[15] Telugu – katuka rekula poda.[15] or raktha penjara/penjari. Kannada – mandaladha haavu[20] or mandalata havu,[15] kolakumandala.[15] Taxonomy In the future, more species may be added to Daboia. Obst (1983) reviewed the genus and suggested that it be extended to include Macrovipera lebetina, Vipera palaestinae and V. xanthina. Groombridge (1980, 1986) united V. palaestinae and Daboia as a clade based on a number of shared apomorphies, including snout shape and head color pattern. Lenk et al. (2001) found support for this idea based on molecular evidence, suggesting that Daboia not only include V. palaestinae, but also M. mauritanica and M. deserti.[2] Echis carinatus Common names: saw-scaled viper,[2] Indian saw-scaled viper, little Indian viper, [3] more. Echis carinatus is a venomous viper species found in parts of the Middle East and Central Asia, and especially the Indian subcontinent. It is the smallest of the Big Four dangerous snakes of India.[4] Five subspecies are currently recognized, including the nominate subspecies described here.[5] Common names English - saw-scaled viper,[2] Indian saw-scaled viper, little Indian viper.[3] Tamil - surattai pambu.[7] viriyan pamboo, surutai vireyan[8] Marathi - phoorsa.[8] Kannada - kallu have.[8] Hindi - afai.[8] Venom This species produces on the average of about 18 mg of dry venom by weight, with a recorded maximum of 72 mg. It may inject as much as 12 mg, whereas the lethal dose for an adult is estimated to be only 5 mg.[8] Envenomation results in local symptoms as well as severe systemic symptoms that may prove fatal. Local symptoms include swelling and pain, which appear within minutes of a bite. In very bad cases the swelling may extend up the entire affected limb within 12-24 hours and blisters form on the skin.[13] The venom yield from individual specimens varies considerably, as does the quantity injected per bite. About 20% of all bites are fatal.[8] Of the more dangerous systemic symptoms, hemorrhage and coagulation defects are the most striking. Hematemesis, melena, hemoptysis, hematuria and epistaxis also occur and may lead to hypovolemic shock. Almost all patients develop oliguria or anuria within a few hours to as late as 6 days post bite. In some cases, kidney dialysis is necessary due to acute renal failure (ARF), but this is not often caused by hypotension. It is more often the result of intravascular hemolysis, which occurs in about half of all cases. In other cases, ARF is often caused by disseminated intravascular coagulation.[13] In any case, antivenin therapy and intravenous hydration within hours of the bite are vital for survival.[13] At least eight different polyvalent and monovalent antivenins are available against bites from this species.[3] The venom from this species is used in the manufacture of several drugs. One is called echistatin, which is an anticoagulant. Even though many other snake venoms contain similar toxins, echistatin is not only especially potent, but also simplistic in structure, which makes it easier to replicate. Indeed, it is obtained not only through the purification of whole venom,[14] but also as a product of chemical synthesis.[15][16] Another drug made from E. carinatus venom is called ecarin and is the primary reagent in the ecarin clotting time (ECT) test, which is used to monitor anticoagulation during treatment with hirudin.[17][18] Yet another drug produced from E. carinatus venom is Aggrastat (Tirofiban). Difference Between Venomous and Non-venomous Snakes? Common Krait Bungarus caeruleus Often, during my lectures on `snakes and snakebite’, or on the street or by guests at home, I am confronted by this commonly asked question `how to identify a snake’ or `how to differentiate between a venomous or non-venomous snake’. I think most of them expect me to give them a `quick fix’ answer – snakes those are black or hissing are venomous etc. Its not true, there is no short cut to know about which one is venomous, other than learning by practice – seeing them time and again, all snakes of one particular species look alike. So, all cobras will look alike, when confronted by a human being’s sudden appearance, they raise their hood, all Russell’s Vipers have the same kind of markings and hiss loud, all common kraits are black with twin bands on their body, all rat-snakes are alike, etc. So, you can learn about how to identify a snake, under trained eyes of an expert who is good at handling snakes or anyone who knows about snakes well. CAUTION: As a common man, you must not even try to identify a snake, it solves no purpose. Just follow one rule of thumb: maintain a safe distance from a snake and stay away from its striking range, which is approximately one third of the total body length of the snake in your proximity. For a common man, snake is a snake! In the past, I have seen, with poor knowledge of snakes, many snake handlers have got into trouble – mistaken identity ! Often a Russell’s Viper is mistaken for python baby, saw-scaled viper as common cat snake, common krait as wolf snake, etc. This can be a seriously dangerous and fatal mistake. Such incidents have occurred but not recorded so far. Whenever there is a Russell’s Viper sighted in my town, people often call and say that they have spotted a python baby. And I know that its Russell’s Viper and caution them to stay away at a safe distance and keep an eye till I reach. On the lighter side: the Indian politicians, who have red or blue beacons and flags on their cars as VIPs, are the most dangerous `animals’ and can be identified with those signs, they are the `venomous snakes’ (synonym to evil) in real terms, attack others unprovoked. Sadly, these two-legged animals are out of synch on this planet. No other animal lives outside the rules of our eco-system, to cause anykind of destruction. There is no other animal which is so arrogant, as humans. And not surprised, now humans have started paying the price, most of us are affected by disease. And may be on the brink of self-annihilation. Snake venom Snake venom is highly modified saliva[citation needed] that is produced by special glands of certain species of snakes. The gland which secretes the zootoxin is a modification of the parotid salivary gland of other vertebrates, and is usually situated on each side of the head below and behind the eye, invested in a muscular sheath. It is provided with a large alveoli in which the venom is stored before being conveyed by a duct to the base of the channelled or tubular fang through which it is ejected. Snake venom is a combination of many different proteins and enzymes. Many of these proteins are harmless to humans, but some are toxins. Note that snake venoms are generally not dangerous when ingested, and are therefore not technically poisons. Chemistry Snake venom consists of proteins, enzymes, substances with a cytotoxic effect, neurotoxins and coagulants. Phosphodiesterases are used to interfere with the prey's cardiac system, mainly to lower the blood pressure. Phospholipase A2 causes hemolysis through esterolysis of red cell membranes and promotes muscle necrosis.[1] Snake venom inhibits cholinesterase to make the prey lose muscle control. Hyaluronidase increases tissue permeability to increase the rate that other enzymes are absorbed into the prey's tissues. Amino acid oxidases and proteases are used for digestion. Amino acid oxidase also triggers some other enzymes and is responsible for the yellow color of the venom of some species. Snake venom often contains ATPases which are used for breaking down ATP to disrupt the prey's energy fuel use. Evolution The presence of enzymes in snake venom has led to the belief that it was an adaptation to assist in the digestion of prey, but, studies of the western diamondback rattlesnake, a snake with highly proteolytic venom, show that envenomation has no impact on the time food takes to pass through the gut. More research is needed to determine the selective pressures that have armed snakes in this way.[2] Injection Acetylcholine receptor blocked by cobra venom (PDB code: 1yi5). A similar effect can be achieved by high doses of curare or nicotine [3] Types of Snake Venom Snake venom, interesting! I never thought that snake venom was a topic that would make me dig up some unbelievable facts about it. I urge the people with snake phobias to unwind their coiled, tense, spring-like postures and gain some interesting snake venom information from my article. Things you did not know; things you could never have imagined. Out of the 2950 known snake species in the world (2007 figures), only 450 are venomous, making it just about 15.25 percent from their entire population. Out of the 7000 Americans that are annually reported with snake bites, less than 15 die of the toxic poison. Yet, people go after snakes, trying to kill them at sight, as just the mere sight of one sends everyone into a panicked frenzy. Why? Can you guess by looking at a man, if he's a terrorist? Can you guess from the appearance of someone, if he/she is a psychopathic murderer? And yet both of these are more of a threat to America, and indeed the world, than snakes ever were. Most snakes are not venomous and even from those that are, only about 250 are capable of killing humans.Snakes are dangerous because of their venom. My crash course in organic chemistry hence starts with venom. Venom is essentially highly modified saliva that is made up of 90 percent proteins and about 20 percent enzymes. Most of these enzymes are harmless to humans and are generally not dangerous when ingested. Hence, technically, venom is not really poison. These scientists really do come up with amazing findings, no? Anyways, there are about 20 toxic enzymes known to man and unique mixtures of these zootoxins and proteins, form the lethal weapons of snakes. The venom contains phosphodiesterases (attacks the cardiac system), cholinesterase (loss of muscle control), hyaluronidase (increased tissue permeability), ATPases (disrupt energy fuel use) and various amino acid oxidates and proteases. The venom is stored in a large sac-like structure, known as the aveoli and it is injected through a set of tubular fangs.Snake venom can be broadly categorized into many types, but I will be explaining the most fascinating four:HemotoxicVenomsThese venoms attack the cardiovascular system, circulatory system and muscle tissues, thus directly leading to heart failures. The 'crotalus adamanteus', notoriously known as the western diamondback rattlesnake, uses this deadly venom to make it's prey more pliable. I meant like kill it, duh! 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, no 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. NeurotoxicVenomsThese venoms go after the central nervous system and brain. 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.CytotoxicVenomsThis is a 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.MyotoxicVenomsThis 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.Snake venom is not dangerous if medical treatment is speedily provided. Where it is not possible to get medical aid quickly, it is always advisable to be aware of the first aid measures. Some far out places in South Africa, that do not even speak English, actually ensure that first aid in case of snake bites, is a subject tackled in schools. They know that a snake will not bite when the hospital is near. They also know that there are many killer snakes in South Africa. These animal loving people have devised a way to live with the snakes, by simply being aware and taking care. They try to live in harmony, where no man kills the snake and the snakes return the favor. No wonder then, that Africa is a part of the few remaining wildlife havens. Interactions with humans Most common symptoms of any kind of snake bite poisoning.[61][62][63] Furthermore, there is vast variation in symptoms between bites from different types of snakes.[61] Vipera berus, one fang in glove with a small venom stain, the other still in place. Snakes do not ordinarily prey on humans and most will not attack humans unless the snake is startled or injured, preferring instead to avoid contact. With the exception of large constrictors, non-venomous snakes are not a threat to humans. The bite of non-venomous snakes is usually harmless because their teeth are designed for grabbing and holding, rather than tearing or inflicting a deep puncture wound. Although the possibility of an infection and tissue damage is present in the bite of a non-venomous snake, venomous snakes present far greater hazard to humans.[7]:209 Documented deaths resulting from snake bites are uncommon. Non-fatal bites from venomous snakes may result in the need for amputation of a limb or part thereof. Of the roughly 725 species of venomous snakes worldwide, only 250 are able to kill a human with one bite. Although Australia is home to the largest number of venomous snakes in the world,[citation needed] it averages only one fatal snake bite per year. In India, 250,000 snakebites are recorded in a single year, with as many as 50,000 recorded initial deaths.[64] The treatment for a snakebite is as variable as the bite itself. The most common and effective method is through antivenom, a serum made from the venom of the snake. Some antivenom is species specific (monovalent) while some is made for use with multiple species in mind (polyvalent). In the United States for example, all species of venomous snakes are pit vipers, with the exception of the coral snake. To produce antivenom, a mixture of the venoms of the different species of rattlesnakes, copperheads, and cottonmouths is injected into the body of a horse in ever-increasing dosages until the horse is immunized. Blood is then extracted from the immunized horse and freeze-dried. It is reconstituted with sterile water and becomes antivenom. For this reason, people who are allergic to horses cannot be treated using antivenom. Antivenom for the more dangerous species (such as mambas, taipans, and cobras) is made in a similar manner in India, South Africa, and Australia, although these antivenoms are species-specific. Snake bites Causes Poisonous snake bites include bites by any of the following: Cobra Copperhead Coral snake Cottonmouth (water moccasin) Rattlesnake Various snakes found at zoos All snakes will bite when threatened or surprised, but most will usually avoid people if possible and only bite as a last resort. Snakes found in and near water are often mistaken as being poisonous. Most species of snake are harmless and many bites are not life-threatening, but unless you are absolutely sure that you know the species, treat it seriously. Symptoms Symptoms depend on the type of snake, but may include: Bleeding from wound Blurred vision Burning of the skin Convulsions Diarrhea Dizziness Excessive sweating Fainting Fang marks in the skin Fever Increased thirst Loss of muscle coordination Nausea and vomiting Numbness and tingling Rapid pulse Tissue death Severe pain Skin discoloration Swelling at the site of the bite Weakness KNOW ABOUT SNAKEBITE FIRST AID AND TREATMENT Snake venom is actually a kind of highly evolved salivary secretion which is used to both kill and digest prey. Venom was not made against man. There are two basic types of snake venom. One affects the nerves (venom of cobra and common krait); the other one blood (that of vipers). Polyvalent anti-venom serum is effective against the bites of the Big Four – cobra, saw-scaled viper, common krait, Russell’s viper. If a venomous snake bites someone, just remember two things: don’t panic; go to a hospital and get anti-venom serum. Don’t waste precious time on quack’s remedies, tantra-mantras, jhar-phoons, herbal preparations, etc. In case of snakebite, a well-administered first-aid is vital. Mostly, in case of Russell’s viper bite, a rare complication in very swollen limbs is `compartment syndrome‘. Limbs are divided into compartments of muscles, blood vessels, and nerves. Severe swelling can cut off the blood circulation to a compartment. When the circulation is cut off, the victim usually has severe pain and numbness. Later, the limb may get white and cold. If not treated in time, the limb may need to be amputated. The following activities are important: 1. Keep the victim calm, restrict movement.2. The limb, which has been affected by the bite, should be immobilized with splint and be kept below the level of the heart. A compression bandage (not tight) should cover the entire limb with the splint.3. Assure the victim and do not let him panic. When under panic, it will enhance heart rate and would circulate the venom faster in the body.4. Remove any rings or constricting items; the affected area may swell.5. A snakebite victim is under tremendous psychological stress. It is necessary to keep the patient warm. However, no alcohol/hot beverages should be given. The patient should not be allowed to exert himself in any manner.6. DO NOT COVER THE BITE AREA AND PUNCTURE MARKS. The wound should be gently cleaned with antiseptic.7. Try to aspirate the venom out of the puncture marks with standard suction devices. It has been identified that a suction more than 270 mmHg can initiate the flow from the puncture marks. Suction instruments often are included in commercial snakebite kits. But, the suction should be applied within 5 minutes of the bite.8. The only remedy for venomous snakebite is the anti-venom serum, which is available at most government hospitals and public health centers. Some private nursing homes have also started stocking it and treat snakebite cases. . Antivenom . Milking a snake for the production of antivenom. Antivenom (or antivenin or antivenene) is a biological product used in the treatment of venomous bites or stings. Antivenom is created by injecting a small amount of the targeted venom into an animal such as a horse, sheep, goat, or rabbit; the subject animal will undergo an immune response to the venom, producing antibodies against the venom's active molecule which can then be harvested from the animal's blood and used to treat envenomation. Internationally, antivenoms must conform to the standards of Pharmacopoeia and the World Health Organization (WHO).[1] Terminology The name antivenin comes from the French word venin, meaning venom, and historically antivenin was predominant around the world; however, this usage is archaic in English. In 1981, the World Health Organization decided that the preferred terminology in the English language would be \"
venom\"
and \"
antivenom\"
rather than \"
venin/antivenin\"
or \"
venen/antivenene\"
.[2] Therapeutic use The principle of antivenom is based on that of vaccines, developed by Louis Pasteur; however, instead of inducing immunity in the patient directly, it is induced in a host animal and the hyperimmunized serum is transfused into the patient. Antivenoms can be classified into monovalent (when they are effective against a given species' venom) or polyvalent (when they are effective against a range of species, or several different species at the same time). The first antivenom for snakes (called an anti-ophidic serum) was developed by Albert Calmette, a French scientist of the Pasteur Institute working at its Indochine branch in 1895, against the Indian Cobra (Naja naja). Vital Brazil, a Brazilian scientist, developed in 1901 the first monovalent and polyvalent antivenoms for Central and South American Crotalus, Bothrops and Elaps genera, as well as for certain species of venomous spiders, scorpions, and frogs. They were all developed in a Brazilian institution, the Instituto Butantan, located in São Paulo, Brazil. Antivenoms for therapeutic use are often preserved as freeze-dried ampoules, but some are available only in liquid form and must be kept refrigerated. (They are not immediately inactivated by heat, so a minor gap in the cold chain is not disastrous.) The majority of antivenoms (including all snake antivenoms) are administered intravenously; however, stonefish and redback spider antivenoms are given intramuscularly. The intramuscular route has been questioned in some situations as not uniformly effective.[3] Antivenoms bind to and neutralize the venom, halting further damage, but do not reverse damage already done. Thus, they should be administered as soon as possible after the venom has been injected, but are of some benefit as long as venom is present in the body. Since the advent of antivenoms, some bites which were previously inevitably fatal have become only rarely fatal provided that the antivenom is administered soon enough. Antivenoms are purified by several processes but will still contain other serum proteins that can act as antigens. Some individuals may react to the antivenom with an immediate hypersensitivity reaction (anaphylaxis) or a delayed hypersensitivity (serum sickness) reaction and antivenom should, therefore, be used with caution. Despite this caution, antivenom is typically the sole effective treatment for a life-threatening condition, and once the precautions for managing these reactions are in place, an anaphylactoid reaction is not grounds to refuse to give antivenom if otherwise indicated. Although it is a popular myth that a person allergic to horses \"
cannot\"
be given antivenom, the side effects are manageable, and antivenom should be given as rapidly as the side effects can be managed.[4] Sheep are generally used in preference over horses now, however, as the potential for adverse immunological responses in humans from sheep-derived antibodies is generally somewhat less than that from horse-derived antibodies. The use of horses to raise antibodies - in Australia at least, where much antivenom research has been undertaken (by Sutherland and others for example) - has been attributed to the research base originally having been a large number of veterinary officers. These vets had, in many cases, returned from taking part in the Boer and First World Wars and were generally experienced with horses due to working with cavalry. The large animal vets were similarly oriented given the use of horses as a prime source of motive power and transport, especially in the rural setting. The overall experience with horses naturally made them the preferred subject in which to raise antibodies. It was not until later that the immuno-reactivity of certain horse serum proteins was assessed to be sufficiently problematic that alternatives in which to raise antibodies were investigated.[citation needed] In the U.S. the only approved antivenom for pit viper (rattlesnake, copperhead and water moccasin) snakebite is based on a purified product made in sheep known as Cro-Fab. It was approved by the FDA in October, 2000. U.S. coral snake antivenom is no longer manufactured, and remaining stocks of in-date antivenom for coral snakebite will expire in the Fall of 2009 leaving the U.S. without a Coral snake antivenom at this time (January, 2009). Efforts are being made to obtain approval for a coral snake antivenom produced in Mexico which would work against U.S. coral snakebite, but such approval remains speculative. In the absence of antivenom, all coral snakebite should be treated in a hospital by elective endotracheal intubation and mechanical ventilation until the effects of coral snake neurotoxins abate. It is important to remember that respiratory paralysis in coral snakebite can occur suddenly, often up to 12 or more hours after the bite, so intubation and ventilation should be employed in anticipation of respiratory failure and not after it occurs, when it may be too late. Poultry Eggs May Yield Snake Antivenin, Experts Say How Eggs Yield Antivenin Very young chickens are immunized with small doses of the target-snake venom and as these animals grow older they develop in their blood special proteins which act as antidotes against the toxin, according to the researchers. As the chickens become hens and start egg production, it has been found that the antivenin proteins are passed on, accumulating in the yolk. The eggs are then harvested for extraction of the proteins used to make the antidote. Maneka Gandhi, ardent animal rights activist and until recently a minister in the federal government of India, has greeted the announcement of the antivenin research with enthusiasm. \"
Production of diagnostic and therapeutic products in chicken represents a refinement and reduction in animal use, and the collection of blood is replaced by extraction of antibody from egg yolk. As chickens produce larger amounts of antibodies, there is a reduction in the number of animals we need to use,\"
Gandhi said. The scientists feel the egg-based antivenin should cost much less than its counterpart made from horses. By comparison, the amount of the antidote yielded from a liter (2 pints) of horse blood could be extracted from just 50 eggs, and a single immunized hen could lay over 240 eggs in a year, according to the researchers. \"
My optimistic aim is to develop the technology to get enough [antivenin] from one egg to treat one bite,\"
said Subbarao. Subbarao and co-workers Kusum Paul and J. Manjula have been working on this project for the past three years. It is expected that it will take another year or two to fine-tune the technology and complete safety studies before the antivenin from poultry eggs could go for human clinical trials and subsequent approval for treatment of snakebite victims. Sandip Basu, director of the National Institute of Immunology, New Delhi, describes the breakthrough as a \"
fine new technique having great potential.\"
 Mechanism of Antivenom * Antivenom acts to neutralize the poisonous venom of the cobra and causes the venom to be released from the receptor site. Thus, the receptor sites that were previously blocked by venom are now free to interact with the acetylcholine molecule, and normal respiration resumes. The spent antivenom and the neutralized venom are then excreted from the body. Venom composition (and its corresponding toxicity) can vary among cobras from the same species and even from the same litter--it can also vary for an individual cobra during its lifetime--and all of this makes each cobra bite truly unique. In order to insure correct treatment, antibodies specific to each form of cobra venom must be developed. The correct antibodies may be synthesized by injecting horses with a small amount of cobra venom, and then collecting the antibodies produced by the horses' immune systems. Of course, large samples of cobra venom must be collected for this process, and many snake farms around the world make significant amounts of money by harvesting the deadly snake toxin. Careful execution of the injection of the antivenom is necessary to avoid any complications that may result from improper treatment. If the amount of antivenom is not sufficient to neutralize all of the venom, a portion of the receptor sites will remain blocked and the person would require the use of artificial respiration machines and electrical impulses to have complete respiration. Due to the size of the antivenom molecule, if given in great excess it may act to shield the receptor site from interaction with the acetylcholine molecule. Thus, the victim would develop symptoms similar to that of being bitten by a snake. Unlike cobra venom; however, the antivenom will eventually be released from the body. The rate of release is very slow, and although there are no proven cases of excess antivenom causing death, severe problems such as paralysis have occurred. Cobra Venom Reactions The interaction of the venom and the antivenom with the receptor sites can be modeled as a reaction engineering catalysis problem. Examples of the reactions are given below. Adsorption of venom onto site: Adsorption of antivenom onto site: Reaction of venom with antivenom on site: Reaction of antivenom with venom on site: Reaction of venom and antivenom in blood: Removal of product and reactants from system: where:V = venomA = antivenomS = unoccupied receptor siteVS = site occupied by venomAS = site occupied by antivenomAV = neutralized product from venom/antivenom reaction Venom application’s Value of snake toxins in science and medicine In spite of the harmful effects of snake venom, it has an important place in scientific discovery and medicine. In science, venom toxins provide highly specific research tools. The discovery of -bungarotoxin led directly to the characterisation of acetylcholine receptors, and is still used for receptor studies. Other toxins have proved useful as ion channel probes, and in the study of inflammation: phospholipase A2 (PLA2) peptides are involved in many inflammatory disorders such as asthma, allergic rhinitis, acute pancreatitis and autoimmune diseases; venom PLA2 offers an opportunity to investigate the mechanism of PLA2 action. Venom toxins as a natural resource are of medical importance: the myriad of proteins found in venoms has an important place in the treatment of thrombosis, arthritis, cancer and many other diseases. The usefulness of venom toxins lies in their ability to evade regular control mechanisms through their independence from co-factors and their non-recognition by inhibitors. Venom toxins have developed highly specific molecular targets, which make them valuable for drug usage in terms of limiting potential side effects. The considerable divergence of snake toxins has made them a valuable resource for potential lead compounds. Molecular graphics: application to the structure determination of a snake venom neurotoxin D Tsernoglou, GA Petsko, JE McQueen Jr, and J Hermans Atomic coordinates have been determined for a snake venom alpha-neurotoxic protein by fitting a molecular model to a crystallographically derived 2.2-angstrom electron density map. The fitting was carried out entirely on a computer-operated molecular, graphics system without going through any mechanical model stage SNAKE VENOM COMPOSITIONS AND METHODS OF USE Lachesis Venom-Containing Compositions Used as Adjuvants Lachesis venom and Lachesis venom-containing compositions and formulations as described herein can also be used as adjuvants for other pharmaceutical products or therapeutic methods, increasing the effectiveness of the pharmaceutical products or therapeutic methods, reducing dosage of the pharmaceutical products, and/or reducing the time of administration/application of the specific pharmaceutical products or therapeutic methods (radiotherapy for instance, among others). Biomedical Application of Snake Venom Neurotoxins: Acetylcholine receptor and myasthenia gravis The venom of many of the snakes of the Elapidae and Hydrophiidae is highly toxic, producing flaccid paralysis and respiratory failure in animals. These effects mainly are attributable to postsynaptic neurotoxins known to bind specifically and tightly to the nicotinic acetylcholine receptor (AChR). Sequence analyses findings for postsynaptic neurotoxins from many snake species show they can be classified into short (61-62 amino acid residues) and long (71-74 amino acid residues) neurotoxins. Short-chain neurotoxins bind specifically, but weakly to AChRs, and the binding is slowly reversible. This property makes them particularly useful for the purification of AChRs. Long-chain neurotoxons, such as -Bungarotoxin (-BuTx), bind specifically and tightly to AChRs and are useful as probes to measure the number of AChRs in the bound radioiodinated neurotoxin contents. The most common clinical application of neurotoxin is in the detection of nicotinic AChRs and their antibodies in research related to the pathogenesis of myasthenia gravis (MG). We have developed new assay systems for detecting antibodies that recognize different antigenic determinants in AChR protein. Using them, we detected a markedly high prevalence of anti-AChR antibodies in MG. This determination now allows for a definite diagnosis of MG. We also show that the blocking effect of the anti-AChR antibodies in MG sera is due to stenc hindrance caused by their binding to a region other than that for -BuTx. Snake Venom L-Amino Acid Oxidases and Their Potential Biomedical Applications L-amino acid oxidase (LAAO) occurs widely in snake venoms. The enzyme is highly specific for L-amino acids, and generally hydrophobic amino acids are the best substrates. LAAO is a flavoprotein consisting of two identical subunits, each with a molecular mass of approximately 60 kDa. The purified enzymes are glycoproteins with 3-4% carbohydrate. Deglycosylation of the enzyme did not alter the enzymatic activity but appeared to alter its pharmacological activities. The amino acid sequences of snake venom LAAOs showed a high degree of homology. X-ray structural analysis of LAAO revealed a dynamic active site and the presence of 3 domains: a FAD-binding domain, a substrate-binding domain and a helical domain. LAAOs were reported to exhibit moderate lethal toxicity. Recent studies showed that LAAOs are multifunctional enzymes exhibiting edema-inducing, platelet aggregation inducing or inhibiting, apoptotic inducing as well as anti-bacterial, anti-coagulant and anti-HIV effects. These effects are mostly mediated by the H2O2 liberated in the oxidation process but direct interactions between LAAO and the target cells may play an important role. High resolution X-ray structure of the enzyme revealed the presence of a channel that would direct the H2O2 product to the exterior surface of the protein, near the glycan moiety at Asn 172. The glycan moiety was thought to be involved with LAAO-target cell interaction. This may explain the ability of LAAO to localize H2O2 to the targeted cells. A better understanding of the pharmacological actions of LAAOs will facilitate the application of snake venom LAAOs in the design of anti-cancer and anti-HIV drugs as well as drugs for the treatment of infectious diseases caused by parasites such as leishmaniasis. The use of snake venom derived fibrin glue in hysterorrhaphy of ovine caesarean surgery INTRODUCTION Ovine caesarean sections on healthy animals are performed routinely with excellent results. The most common reasons for ovine caesarean sections include: relative fetal oversize, most commonly in the primiparous animals with a single fetus; incomplete cervical dilation; fetal abnormalities; vaginal prolapse; and the presence of an emphysematous lamb in the uterus Caesarean sections are usually performed to treat dystocia, to obtain gnotobiotic products for research, and in caprine to obtain arthritis-encephalitis (CAE) free kids Significant advances in anesthesia and surgical sepsis made laparohysterotomy a usual obstetric procedure in veterinary medicine. A perfect uterine healing following a caesarean section is pivotal for a future pregnancy According to Schlenger et al. the suboptimal healing of uterotomy following caesarean section in women may result in early suture dehiscence or late uterine rupture at the scar site in cases of pregnancy subsequent to vaginal delivery. Despite its clinical importance, studies on the biology of wound healing in uterotomy are rare. Most surgical wounds require a constant and efficient mechanical support to keep the wound edges together during healing, and suture is the method of choice for the synthesis of surgical wounds .In the last 25 years, fibrin glue, a biological adhesive made mainly by mixing fibrinogen and thrombin, has been used more frequently to help sealing of surgical wounds. Fibrin glue is used in combination with suturing to seal needle and suture thread orifices, strengthen the wound site, and improve overall healing . Aside from its hemostatic properties, fibrin glue may have a role in promoting wound healing. Fibrin is essential for wound healing because the network in the wound acts as a scaffold for migrating fibroblasts and a hemostatic barrier Wheaton et al. reported the efficacy of fibrin glue as a hemostatic agent when applied locally in dog liver after biopsy. Hemorrhage control, absence of inflammatory and toxic responses, absence of adherence, and healing stimulation led to the conclusion that this product may be widely used in veterinary surgery. Schlenger et al. looking for new information about uterine wound, developed a model of uterotomy in rats. Ten mm-incisions were made in the uterus of non-pregnant animals and commercially available fibrin glue (Tissucol Duo) was used. The authors concluded that this proposed model is useful in the investigation of uterine wound and that fibrin associated with tissue necrosis factor  (TNF ) has an important effect only during the initial phase of wound healing. The only report in literature about the use of snake venom derived fibrin glue in ovine was by Sartori Filho et al. in 1998. They applied this fibrin glue on the surgical wound on scrotal skin following testicular biopsy with excellent results in relation to hemostasis and scar formation. The objective of this experiment was to evaluate the use of snake venom derived fibrin glue as an alternative to conventional suture in ovine caesarean surgery. uterus required three to four separated stitches, which were made with nonabsorbable cotton suture material. These stitches were alternated equidistantly in relation to the wound edges in order to diminish tension on the surgical wound so that the edges could be satisfactorily bonded with the glue. Snake venom derived fibrin glue (0.3 - 0.4 ml) was applied along the incision (Figure 1). The components were mixed at the time of application to the site. Two syringes were simultaneously used for the application of calcium chloride/snake venom fraction and fibrinogen. The bond sites were manually kept held for three minutes to permit formation of the fibrin network. The other four animals were submitted to conventional hysterorrhaphy using 2-0 chromic catgut (Brasmedica Ind. Brasil S/A). Conventional laparorrhaphy and skin suturing were then performed on all the animals. Snake Venom Face Cream For A Young Impression People everywhere continually seek ways to prolong a youthful appearance. Botox injections have typically been the most effective means. Snake venom face creams are a new instrument that have recently been introduced for this purpose. Muscles build and change in strength and size with repeated use. The overlying skin adapts and stretches to cover the changing shapes and volumes of the musculature underneath. When we are young, skin is very elastic and rebounds well from the many stretches and pulls it is subject to. As we grow older skin loses this ability. Venom creams rely on the synthetic Syn-ake chemical which acts to relax muscles. This chemical was developed by scientists to replicate the Waglerin 1 tri-petpitde found in the fangs of the tropidolaemus wagleri snake, aka Malaysian Temple Viper. The bite of this animal immobilizes it’s prey by paralyzing the nervous system. Creams contain dilute amounts of the serum at around three to five percent. This small amount allows for a sufficient amount of relaxation of the muscles to relieve skin of undue tension, while still allowing for regular facial expressions. Naturally occurring amino acids in the peptide, block the nicotinic acetylcholine receptor (mnAChR) neurotransmitters in the musculature system. By blocking these receptors, the ion canals stay closed off to sodium ion (Na+) uptake into the post-synaptic membrane and signal contractions of the muscle. The synthetic peptide was developed by a Swiss pharmaceutical company and won the 2006 Swiss Technology Award. It is distributed to various cosmetic companies who incorporate it into their products which are then marketed as their own proprietary versions. The serum was originally developed as a topical alternative to Botox. While Botox has proven to be extremely effective, the required injections are costly, invasive and require the expertise of a physician. By contrast, however, the twice annual injections are longer lasting than the daily application required by venom creams. If daily moisturizer use is already in your regiment, then it might not be a problem. Human skin is designed to keep out external material. It effectively filters out foreign proteins that would come into contact with the inner musculature. This has led scientists to question the effectiveness of the topical creams ability to reach the muscle through layers of subcutaneous fat and muscle, and is a primary reason Botox is injected. Companies that market venom creams are usually upscale. With their name and unique qualities of the creams come a higher price. One to two ounce bottles range from thirty to two hundred dollars. Amount used per application depends on the proprietary concentration of the serum. With regular use, most purchases last one to three months. This can make for an expensive addition to a cosmetic routine. If you’re searching for a way to preserve a youthful appearance while avoiding invasive procedures, snake venom face creams offer a new means. The cost may be a challenge, but your skin is important and the better you take care of it the longer it will last. With any health product, consult a physician if adverse effects occur. New Snake Venom Face Cream is being used to give softer skin and providing an alternative to popular Botox injections. We’ve got the ultimate inside info now at http://www.wrinklecreamdirect.com/snakevenomcream Grab a totally unique version of this article from the Uber Article Directory The Application of a Snake Venom Anticoagulant Enzyme in Burn Therapy. 1978 Abstract : Crotalase, the thrombin-like enzyme from Eastern diamondback rattlesnake (Crotalus adamanteus), has been purified to homogeneity. This was shown by chromatographic and electrophoretic patterns of the enzyme. A single band was observed on SDS polyacrylamide gel electrophoresis. The molecular weight was estimated to be about 33,000 by gel filtration on Sephadex G-100 and SDS polyacrylamide gel electrophoresis. The molecular weight determined from amino acid composition was shown to be 30,334. However, the estimated molecular weight contributed by carbohydrates (2013) gave us an overall value of 32,347. Analytical isoelectric focusing of crotalase showed five bands. This heterogeneity of enzyme may be due to differences in sialic acid content of the different forms of the enzyme. Upon treatment of the enzyme with neuraminidase to remove the sialic acid a single band was obtained by isoelectric focusing, supporting our contention that the enzyme is homogeneous and that the five bands represent different levels of sialylation of the enzyme. This heterogeneity may have been an artifact of preparation. Fibrinolytic activity of crotalase was shown to be an inherent property since the ratio of fibrinogenolytic activity to that of fibrinolytic activity remained constant throughout the purification procedure. Crotalase hydrolysed a chromogenic substrate (S-2238) used for thrombin assay; this activity could be used as a method for estimation of crotalase. Snake Venom As Medication? A chemist at the Vienna University of Technology (TU Vienna) is looking for unusual structures in snake venom and plans to prove their medical effectiveness. What in the 1950s led to the development of Captopril, a drug for the treatment of hypertension, is being continued in an interesting new chapter with the analysis of venom from South American pit vipers and tropical rattlesnakes.Vienna (TU). \"
We receive the snake venom as a yellow crystalline powder in ampules directly from the 'Instituto Butantan' (http://www.butantan.gov.br) in São Paulo, Brazil. That is a well-known scientific institution, also popular with tourists, which studies some of the most poisonous snake species in the world,\"
explains Martina Marchetti, assistant professor at the Institute for Chemical Technologies and Analytics at the Vienna University of Technology (TU Vienna). Her investigations focus on the venoms of four different pit vipers (Bothrops) as well as a tropical rattlesnake (Crotalus durissus terrificus). All five species are native to South America. They are among the most aggressive snake varieties there. Every year in South America, 2.5 million people are bitten by snakes. About 100,000 die as a result.Marchetti analyzes the snake venoms by various methods. She and her coworkers use lab-on-a-chip technology to determine the composition of the toxins and analyze peptide chains (linear sequences of amino acids). The structures of individual members of these chains are then analyzed using tandem mass spectrometry. Two-dimensional gel electrophoresis offers another option for separating samples by molecular weight and pH. According to Marchetti, \"
Not every snake venom is the same. Time and again we encounter unusual new structures. The goal of our research is to find out why individual components of the venom act in a particular way and what they may have to offer to the pharmaceutical industry.\"
A deliberately administered toxic effect in the right amount can actually be beneficial to human health. Snake toxins have a very broad field of potential use, including antibacterial applications, cell growth inhibition, nerve stimulation, blood thinning and clotting. Their effects are also being tested for the treatment of Alzheimer'sdisease.As a result of proteome research, which has become popular in recent years, a number of new analytical methods have been developed. Combinations of these methods allow to uncover clues in order to solve the riddle of the medical effectiveness of snake venom. Of course, another goal is to develop effective antivenoms, which, according to Marchetti, \"
might some day be available to take along in tablet form.\"
Her investigations have been conducted in collaboration with Walter Welz at the Johannes Kepler University in Linz. Researchers first noticed the pharmacological effectiveness of snake venoms in the process of developing antisera. Such investigations in the 1950s resulted in the development of the hypertension drug Captopril, for which the structural information from a peptide (protein) isolated from snake venom served as an archetype. Therapeutic removal of thrombus Fibrinolytic enzymes isolated from venom can directly break down a fibrin clot. Current medical research seeks to find such an enzyme to remove clots causing heart attacks and strokes. The role of snake venom: 1,Cure for cancer: Cancer is one of the three biggest diseases, which is harmful to human health. There is no effective treatment, the research on snake venom is seen to be a new field to overcome this difficulty by scientists from various countries. Laboratory of China Medical University conducted a drug testing which compared the original viper venom and pure venom’s role in inhibiting tumor. The 9 different concentrations of snake venom have different roles to inhibit mouse’s sarcoma, the efficient is up to 87.1%. 2,Theanticoagulant effects of snake venom: The “DEFIBRASE” which is extracted from five-step snake passed technical appraisal in 1981 for the treatment of vascular thrombosis 333 cases, of which 242 cases are cerebral thrombosis. The efficient is up to 86.4%. 3,Hemostatic effect: Procoagulant component extracted from the viper is used in clinical surgery, internal medicine, ENT, obstetrics and other bleeding disorders. This drug called “Reptile Enzyme Injection”. 4,Manufacture of anti-venom serum: Scientists have successfully developed the blood serums of anti-Snake venom, anti-five-step snake venom, anti-Bungarus multicinctus venom and anti-cobra venom. 5, Analgesia: Ketongling extracted from cobra venom has an excellent analgesic effect on the pain induced by a variety of diseases. As the higher analgesic activity and no addiction, snake venom in medicine has been used instead of morphine to therapy the pain caused by advanced cancer. The biggest roles of snake venom: 1, the treatment of cancer; 2, hemostasis and anti-coagulation; 3, analgesic; 4, manufacture of anti-venom serum; 5, scientific research; 6, lower blood pressure; 7, treatment of headache cause by blood stasis; 8, application on the nerve growth factor. References ^ Klauber LM. 1997. Rattlesnakes: Their Habitats, Life Histories, and Influence on Mankind. Second Edition. First published in 1956, 1972. University of California Press, Berkeley. ISBN 0-520-21056-5. ^ a b Fry, Bryan Grieg. \"
Snake LD50 - discussion\"
. Australian Venom & Toxin Database. http://www.kingsnake.com/toxinology/LD50/LD50men.html. Retrieved 2009-09-28. \"
Subcutaneous is the most applicable to actual bites. Only large Bitis or extremely large Bothrops or Crotalus specimens wouls be able to deliver a bite that is truly intramuscular. IV injections are extremly rare in actual bites.\"
 ^ Chippaux, J.P. (1998). \"
Snake-bites: appraisal of the global situation\"
. Bulletin of the World Health Organization 76 (5): 515–24. http://www.kingsnake.com/aho/pdf/menu6/chippaux1998.pdf. Retrieved 2009-07-03. ^ Mackessy, Stephen P. (June 2002). \"
Biochemistry and pharmacology of colubrid snake venoms\"
. Journal of Toxicology: Toxin Reviews 21 (1–2): 43–83. doi:10.1081/TXR-120004741. http://www.unco.edu/nhs/biology/faculty_staff/mackessy/colubrid.pdf. Retrieved 2009-09-26. ^ \"
Venom variability\"
. Women's & Children's Hospital - Clinical Toxinology Resources. University of Adelaide. http://www.toxinology.com/fusebox.cfm?staticaction=snakes/ns-venom02.htm. Retrieved 28 September 2009. \"
The rough scaled snake, Tropidechis carinatus has a much less potent venom than the tiger snake, Notechis scutatus, on LD50 testing in mice. Yet clinically, the two venoms are virtually identical in the type and severity of effects on envenomed humans.\"

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