|Classification and external resources|
A bite on a finger from a Montpellier snake
|ICD-10||T63.0, T14.1, W59 (nonvenomous), X20 (venomous)|
|ICD-9||989.5, E905.0, E906.2|
A snakebite is an injury caused by a bite from a snake, often resulting in puncture wounds inflicted by the animal's fangs and sometimes resulting in envenomation. Although the majority of snake species are non-venomous and typically kill their prey with constriction rather than venom, venomous snakes can be found on every continent except Antarctica. Snakes often bite their prey as a method of hunting, but also for defensive purposes against predators. Since the physical appearance of snakes may differ, there is often no practical way to identify a species and professional medical attention should be sought.
The outcome of snake bites depends on numerous factors, including the species of snake, the area of the body bitten, the amount of venom injected, and the health conditions of the person. Feelings of terror and panic are common after a snakebite and can produce a characteristic set of symptoms mediated by the autonomic nervous system, such as a racing heart and nausea. Bites from non-venomous snakes can also cause injury, often due to lacerations caused by the snake's teeth, or from a resulting infection. A bite may also trigger an anaphylactic reaction, which is potentially fatal. First aid recommendations for bites depend on the snakes inhabiting the region, as effective treatments for bites inflicted by some species can be ineffective for others.
The number of fatalities attributed to snake bites varies greatly by geographical area. Although deaths are relatively rare in Australia, Europe and North America, the morbidity and mortality associated with snake bites is a serious public health problem in many regions of the world, particularly in rural areas lacking medical facilities. Further, while South Asia, Southeast Asia, and sub-Saharan Africa report the highest number of bites, there is also a high incidence in the Neotropics and other equatorial and subtropical regions. Each year tens of thousands of people die from snake bites, yet the risk of being bitten can be lowered with preventive measures, such as wearing protective footwear and avoiding areas known to be inhabited by dangerous snakes.
- 1 Signs and symptoms
- 2 Pathophysiology
- 3 Prevention
- 4 Treatment
- 5 Epidemiology
- 6 Cause
- 6.1 Most venomous
- 6.2 Extremely dangerous
- 6.3 Highly dangerous
- 6.3.1 The Big Four
- 6.3.2 Many-banded krait
- 6.3.3 Inland taipan
- 6.3.4 Eastern brown snake
- 6.3.5 Common death adder
- 6.3.6 Tiger snake
- 6.3.7 Gaboon viper
- 6.3.8 Green mambas
- 6.4 Considerably dangerous
- 6.4.1 Terciopelo
- 6.4.2 Jararaca
- 6.4.3 South American bushmaster or Atlantic bushmaster
- 6.4.4 King cobra
- 6.4.5 True cobras
- 6.4.6 Spitting cobras
- 6.4.7 African vipers
- 6.4.8 Australian black snakes
- 6.4.9 Australian brown snakes
- 6.4.10 Rattlesnakes
- 6.4.11 Pit vipers
- 7 Society and culture
- 8 References
- 9 Further reading
- 10 External links
Signs and symptoms
The most common symptoms of all snakebites are overwhelming fear, panic, and emotional instability, which may cause symptoms such as nausea and vomiting, diarrhea, vertigo, fainting, tachycardia, and cold, clammy skin. Television, literature, and folklore are in part responsible for the hype surrounding snakebites, and people may have unwarranted thoughts of imminent death.
Dry snakebites, and those inflicted by a non-venomous species, can still cause severe injury. There are several reasons for this: a snakebite may become infected with the snake's saliva and fangs sometimes harboring pathogenic microbial organisms, including Clostridium tetani. Infection is often reported with viper bites whose fangs are capable of deep puncture wounds. Bites may cause anaphylaxis in certain people.
Most snakebites, whether by a venomous snake or not, will have some type of local effect. There is minor pain and redness in over 90% of cases, although this varies depending on the site. Bites by vipers and some cobras may be extremely painful, with the local tissue sometimes becoming tender and severely swollen within 5 minutes. This area may also bleed and blister and can eventually lead to tissue necrosis. Other common initial symptoms of pitviper and viper bites include lethargy, bleeding, weakness, nausea, and vomiting. Symptoms may become more life-threatening over time, developing into hypotension, tachypnea, severe tachycardia, severe internal bleeding, altered sensorium, kidney failure, and respiratory failure.
Interestingly, bites caused by the Mojave rattlesnake, kraits, coral snake, and the speckled rattlesnake reportedly cause little or no pain despite being serious injuries. Those bitten may also describe a "rubbery," "minty," or "metallic" taste if bitten by certain species of rattlesnake. Spitting cobras and rinkhalses can spit venom in a persons eyes. This results in immediate pain, ophthalmoparesis, and sometimes blindness.
Some Australian elapids and most viper envenomations will cause coagulopathy, sometimes so severe that a person may bleed spontaneously from the mouth, nose, and even old, seemingly healed wounds. Internal organs may bleed, including the brain and intestines and will cause ecchymosis (bruising) of the skin.
Venom emitted from elapids, including sea snakes, kraits, cobras, king cobra, mambas, and many Australian species, contain toxins which attack the nervous system, causing neurotoxicity. The person may present with strange disturbances to their vision, including blurriness. Paresthesia throughout the body, as well as difficulty in speaking and breathing, may be reported. Nervous system problems will cause a huge array of symptoms, and those provided here are not exhaustive. If not treated immediately they may die from respiratory failure.
Venom emitted from some types of cobras, almost all vipers, some Australian elapids and some sea snakes causes necrosis of muscle tissue. Muscle tissue will begin to die throughout the body, a condition known as rhabdomyolysis. Rhabdomyolysis can result in damage to the kidneys as a result of myoglobin accumulation in the renal tubules. This, coupled with hypotension, can lead to acute renal failure, and, if left untreated, eventually death.
Since envenomation is completely voluntary, all venomous snakes are capable of biting without injecting venom into a person. Snakes may deliver such a "dry bite" rather than waste their venom on a creature too large for them to eat, a behaviour called venom metering. However, the percentage of dry bites varies between species: 80% of bites inflicted by sea snakes, which are normally timid, do not result in envenomation, whereas only 25% of pitviper bites are dry. Furthermore, some snake genera, such as rattlesnakes, significantly increase the amount of venom injected in defensive bites compared to predatory strikes.
Some dry bites may also be the result of imprecise timing on the snake's part, as venom may be prematurely released before the fangs have penetrated the person. Even without venom, some snakes, particularly large constrictors such as those belonging to the Boidae and Pythonidae families, can deliver damaging bites; large specimens often cause severe lacerations, or the snake itself pulls away, causing the flesh to be torn by the needle-sharp recurved teeth embedded in the person. While not as life-threatening as a bite from a venomous species, the bite can be at least temporarily debilitating and could lead to dangerous infections if improperly dealt with.
While most snakes must open their mouths before biting, African and Middle Eastern snakes belonging to the family Atractaspididae are able to fold their fangs to the side of their head without opening their mouth and jab a person.
It has been suggested that snakes evolved the mechanisms necessary for venom formation and delivery sometime during the Miocene epoch. During the mid-Tertiary, most snakes were large ambush predators belonging to the superfamily Henophidia, which use constriction to kill their prey. As open grasslands replaced forested areas in parts of the world, some snake families evolved to become smaller and thus more agile. However, subduing and killing prey became more difficult for the smaller snakes, leading to the evolution of snake venom. Other research on Toxicofera, a hypothetical clade thought to be ancestral to most living reptiles, suggests an earlier time frame for the evolution of snake venom, possibly to the order of tens of millions of years, during the Late Cretaceous.
Snake venom is produced in modified parotid glands normally responsible for secreting saliva. It is stored in structures called alveoli behind the animal's eyes, and ejected voluntarily through its hollow tubular fangs. Venom is composed of hundreds to thousands of different proteins and enzymes, all serving a variety of purposes, such as interfering with a prey's cardiac system or increasing tissue permeability so that venom is absorbed faster.
Venom in many snakes, such as pitvipers, affects virtually every organ system in the human body and can be a combination of many toxins, including cytotoxins, hemotoxins, neurotoxins, and myotoxins, allowing for an enormous variety of symptoms. Earlier, the venom of a particular snake was considered to be one kind only i.e. either hemotoxic or neurotoxic, and this erroneous belief may still persist wherever the updated literature is hard to access. Although there is much known about the protein compositions of venoms from Asian and American snakes, comparatively little is known of Australian snakes.
The strength of venom differs markedly between species and even more so between families, as measured by median lethal dose (LD50) in mice. Subcutaneous LD50 varies by over 140-fold within elapids and by more than 100-fold in vipers. The amount of venom produced also differs among species, with the Gaboon viper able to potentially deliver from 450–600 milligrams of venom in a single bite, the most of any snake. Opisthoglyphous colubrids have venom ranging from life-threatening (in the case of the boomslang) to barely noticeable (as in Tantilla).
Snakes are most likely to bite when they feel threatened, are startled, are provoked, or have no means of escape when cornered. Encountering a snake is potentially dangerous and it is recommended to leave the vicinity. It is difficult to safely identify many snake species as appearances may vary dramatically.
Snakes are likely to approach residential areas when attracted by prey, such as rodents. Practising regular pest control can reduce the threat of snakes considerably. It is beneficial to know the species of snake that are common in local areas, or while travelling or hiking. Areas of the world such as Africa, Australia, the Neotropics, and southern Asia are inhabited by many highly dangerous species. Being wary of snake presence and ultimately avoiding it when known is strongly recommended.
When in the wilderness, treading heavily creates ground vibrations and noise, which will often cause snakes to flee from the area. However, this generally only applies to vipers as some larger and more aggressive snakes in other parts of the world, such as the forest cobra and black mambas, will respond more aggressively. When dealing with direct encounters it is best to remain silent and motionless. If the snake has not yet fled it is important to step away slowly and cautiously.
The use of a flashlight when engaged in camping activities, such as gathering firewood at night, can be helpful. Snakes may also be unusually active during especially warm nights when ambient temperatures exceed 21 °C (70 °F). It is advised not to reach blindly into hollow logs, flip over large rocks, and enter old cabins or other potential snake hiding-places. When rock climbing, it is not safe to grab ledges or crevices without examining them first, as snakes are cold-blooded and often sunbathe atop rock ledges.
In the United States more than 40% of people bitten by snake intentionally put themselves in harm's way by attempting to capture wild snakes or by carelessly handling their dangerous pets—40% of that number had a blood alcohol level of 0.1% or more.
It is also important to avoid snakes that appear to be dead, as some species will actually roll over on their backs and stick out their tongue to fool potential threats. A snake's detached head can immediately act by reflex and potentially bite. The induced bite can be just as severe as that of a live snake. Dead snakes are also incapable of regulating the venom they inject, so a bite from a dead snake can often contain large amounts of venom.
It is not an easy task determining whether or not a bite by any species of snake is life-threatening. A bite by a North American copperhead on the ankle is usually a moderate injury to a healthy adult, but a bite to a child's abdomen or face by the same snake may be fatal. The outcome of all snakebites depends on a multitude of factors: the size, physical condition, and temperature of the snake, the age and physical condition of the person, the area and tissue bitten (e.g., foot, torso, vein or muscle), the amount of venom injected, the time it takes for the person to find treatment, and finally the quality of that treatment.
Identification of the snake is important in planning treatment in certain areas of the world, but is not always possible. Ideally the dead snake would be brought in with the person, but in areas where snake bite is more common, local knowledge may be sufficient to recognize the snake. However, in regions where polyvalent antivenoms are available, such as North America, identification of snake is not a high priority item. Attempting to catch or kill the offending snake also puts one at risk for re-envenomation or creating a second person bitten, and generally is not recommended.
The three types of venomous snakes that cause the majority of major clinical problems are vipers, kraits, and cobras. Knowledge of what species are present locally can be crucial, as is knowledge of typical signs and symptoms of envenomation by each type of snake. A scoring system can be used to try to determine the biting snake based on clinical features, but these scoring systems are extremely specific to particular geographical areas.
Snakebite first aid recommendations vary, in part because different snakes have different types of venom. Some have little local effect, but life-threatening systemic effects, in which case containing the venom in the region of the bite by pressure immobilization is desirable. Other venoms instigate localized tissue damage around the bitten area, and immobilization may increase the severity of the damage in this area, but also reduce the total area affected; whether this trade-off is desirable remains a point of controversy. Because snakes vary from one country to another, first aid methods also vary.
However, most first aid guidelines agree on the following:
- Protect the person and others from further bites. While identifying the species is desirable in certain regions, risking further bites or delaying proper medical treatment by attempting to capture or kill the snake is not recommended.
- Keep the person calm. Acute stress reaction increases blood flow and endangers the person.
- Call for help to arrange for transport to the nearest hospital emergency room, where antivenom for snakes common to the area will often be available.
- Make sure to keep the bitten limb in a functional position and below the person's heart level so as to minimize blood returning to the heart and other organs of the body.
- Do not give the person anything to eat or drink. This is especially important with consumable alcohol, a known vasodilator which will speed up the absorption of venom. Do not administer stimulants or pain medications, unless specifically directed to do so by a physician.
- Remove any items or clothing which may constrict the bitten limb if it swells (rings, bracelets, watches, footwear, etc.)
- Keep the person as still as possible.
- Do not incise the bitten site.
Many organizations, including the American Medical Association and American Red Cross, recommend washing the bite with soap and water. Australian recommendations for snake bite treatment recommend against cleaning the wound. Traces of venom left on the skin/bandages from the strike can be used in combination with a snake bite identification kit to identify the species of snake. This speeds determination of which antivenom to administer in the emergency room.
India developed a national snake-bite protocol in 2007 which includes advice to:
- Reassure the patient. 70% of all snakebites are from non-venomous species. Only 50% of bites from vemomous species actually envenomate the patient
- Immobilise in the same way as a fractured limb. Use bandages or cloth to hold the splints, with care taken not to apply pressure or block the blood supply (such as with ligatures).
- Get to Hospital Immediately. Traditional remedies have no proven benefit in treating snakebite.
- Tell the doctor of any systemic symptoms, such as droopiness of a body part, that manifest on the way to hospital.
As of 2008, clinical evidence for pressure immobilization via the use of an elastic bandage is limited. It is recommended for snakebite that have occurred in Australia (due to elapids which are neurotoxic). It is not recommended for bites from non neurotoxic snakes such as found in North America and other regions of the world. The British military recommends pressure immobilization in all cases where the type of snake is unknown.
The object of pressure immobilization is to contain venom within a bitten limb and prevent it from moving through the lymphatic system to the vital organs. This therapy has two components: pressure to prevent lymphatic drainage, and immobilization of the bitten limb to prevent the pumping action of the skeletal muscles.
Until the advent of antivenom, bites from some species of snake were almost universally fatal. Despite huge advances in emergency therapy, antivenom is often still the only effective treatment for envenomation. The first antivenom was developed in 1895 by French physician Albert Calmette for the treatment of Indian cobra bites. Antivenom is made by injecting a small amount of venom into an animal (usually a horse or sheep) to initiate an immune system response. The resulting antibodies are then harvested from the animal's blood.
Antivenom is injected into the person intravenously, and works by binding to and neutralizing venom enzymes. It cannot undo damage already caused by venom, so antivenom treatment should be sought as soon as possible. Modern antivenoms are usually polyvalent, making them effective against the venom of numerous snake species. Pharmaceutical companies which produce antivenom target their products against the species native to a particular area. Although some people may develop serious adverse reactions to antivenom, such as anaphylaxis, in emergency situations this is usually treatable and hence the benefit outweighs the potential consequences of not using antivenom. Giving adrenaline (epinephrine) to prevent adverse effect to antivenom before they occur might be reasonable where they occur commonly. Antihistamines do not appear to provide any benefit in preventing adverse reactions.
The following treatments while once recommended are considered of no use or harmful including: tourniquets, incisions, suction, application of cold, and application of electricity. Cases in which these treatments appear to work may be the result of dry bites.
- Application of a tourniquet to the bitten limb is generally not recommended. There is no convincing evidence that it is an effective first aid tool as ordinarily applied. Tourniquets have been found to be completely ineffective in the treatment of Crotalus durissus bites, but some positive results have been seen with properly applied tourniquets for cobra venom in the Philippines. Uninformed tourniquet use is dangerous, since reducing or cutting off circulation can lead to gangrene, which can be fatal. The use of a compression bandage is generally as effective, and much safer.
- Cutting open the bitten area, an action often taken prior to suction, is not recommended since it causes further damage and increases the risk of infection.
- Sucking out venom, either by mouth or with a pump, does not work and may harm the affected area directly. Suction started after 3 minutes removes a clinically insignificant quantity—less than one thousandth of the venom injected—as shown in a human study. In a study with pigs, suction not only caused no improvement but led to necrosis in the suctioned area. Suctioning by mouth presents a risk of further poisoning through the mouth's mucous tissues. The well-meaning family member or friend may also release bacteria into the persons wound, leading to infection.
- Immersion in warm water or sour milk, followed by the application of snake-stones (also known as la Pierre Noire), which are believed to draw off the poison in much the way a sponge soaks up water.
- Application of potassium permanganate.
- Use of electroshock therapy in animal tests has shown this treatment to be useless and potentially dangerous.
In extreme cases, in remote areas, all of these misguided attempts at treatment have resulted in injuries far worse than an otherwise mild to moderate snakebite. In worst case scenarios, thoroughly constricting tourniquets have been applied to bitten limbs, completely shutting off blood flow to the area. By the time the person finally reached appropriate medical facilities their limbs had to be amputated.
Most snakebites are caused by non-venomous snakes. Of the roughly 3,000 known species of snake found worldwide, only 15% are considered dangerous to humans. Snakes are found on every continent except Antarctica. The most diverse and widely distributed snake family, the colubrids, has approximately 700 venomous species, but only five genera—boomslangs, twig snakes, keelback snakes, green snakes, and slender snakes—have caused human fatalities.
Since reporting is not mandatory in many regions of the world, snakebites often go unreported. Consequently, no accurate study has ever been conducted to determine the frequency of snakebites on the international level. However, some estimates put the number at 5.4 million snakebites, 2.5 million envenomings, resulting in perhaps 125,000 deaths. Others estimate 1.2 to 5.5 million snakebites, 421,000 to 1.8 million envenomings, and 20,000 to 94,000 deaths. Many people who survive bites nevertheless suffer from permanent tissue damage caused by venom, leading to disability. Most snake envenomings and fatalities occur in South Asia, Southeast Asia, and sub-Saharan Africa, with India reporting the most snakebite deaths of any country.
Worldwide, snakebites occur most frequently in the summer season when snakes are active and humans are outdoors. Agricultural and tropical regions report more snakebites than anywhere else. In the USA, those bitten are typically male and between 17 and 27 years of age. Children and the elderly are the most likely to die.
|The most venomous snakes of the world by Ernst and Zug et al. (1996)|
|The most venomous snakes of the world by Australian Venom and Toxins database (1999)|
Mortality rate (often determined by measured toxicity on mice) is a commonly used indicator to determine the danger of any given venomous snake, but important too are its efficiency of venom delivery, its venom yield and its behavior when it encounters humans. Experts invariably name the black mamba and coastal taipan as the deadliest venomous snake species in the world. Of all the venomous snake species in the world, the black mamba and the coastal taipan are considered to be the biggest threats to humans in case of a bite. Both species are elapids and they're very similar to each other. In fact, in several aspects of morphology, ecology and behaviour, the coastal taipan is strongly convergent with the black mamba. Black mamba and coastal taipan bites require very rapid and vigorous antivenom therapy as they are almost always fatal. The venoms of both species are exceptionally quick acting and both can cause human fatality in as little as 30 minutes. Black mambas in particular have been known to cause death in as little as 20 minutes post-envenomation. Many snake experts have cited the black mamba and the coastal taipan as the world's most dangerous snakes (Hunter, 1998).
|Inland taipan (O. microlepidotus)||0.01 mg/kg||110 mg||1,085,000||289|
|Black mamba (D. polylepis)||0.05 mg/kg||400 mg||400,000||107|
|Forest cobra (N. melanoleuca)||0.225 mg/kg||1102 mg||244,889||65|
|Eastern brown snake (P. textilis)||0.03 mg/kg||155 mg||212,329||58|
|Coastal taipan (O. s. scutellatus)||0.106 mg/kg||400 mg||208,019||56|
|Caspian cobra (N. oxiana)||0.18 mg/kg||590 mg||162,165||42|
|Russell's viper (D. russelli)||0.162 mg/kg||268 mg||88,211||22|
|King cobra (O. hannah)||1.09 mg/kg||1000 mg||45,830||11|
|Indian cobra (N. naja)||0.80 mg/kg||610 mg||33,689||10|
|Cape cobra (N. nivea)||0.4 mg/kg||250 mg||31,250||9|
|Terciopelo (B. asper)||3.1 mg/kg||1530 mg||24,380||6|
|Gaboon viper (B. gabonica)||5 mg/kg||2400 mg||24,000||6|
|Saw-scaled viper (E. carinatus)||0.151 mg/kg||72 mg||23,841||6|
The African Black mamba (Dendroaspis polylepis) is a large and highly venomous snake species native to much of Sub-Saharan Africa. It is the second longest venomous snake species in the world and is the fastest moving land snake, capable of moving at 4.32 to 5.4 metres per second (16–20 km/h, 10–12 mph). It is by far the most feared snake species in Africa and it has a legendary reputation as a very fierce and territorial snake. Black mambas are well known to have an irascible temperament - they tend to be high-strung, nervous, agile, extremely quick, are highly aggressive and will attack with no provocation. They are among the world's most venomous snake species. When cornered or threatened, the black mamba can put up a fearsome display of defense and aggression. A black mamba will often mimic a cobra by spreading a neck-flap; exposing its black mouth, raising its body off the ground, and hissing. It can rear up around one-third of its body from the ground, which can put it at about four feet high. When warding off a threat, the black mamba delivers multiple strikes, injecting large amounts of virulently toxic venom with each strike, often landing bites on the body or head, unlike other snakes. Their strikes are very quick and extremely accurate and effective. If the attempt to scare away the threat fails, it will strike repeatedly. This species of snake often shows an incredible amount of tenacity, fearlessness, and aggression when cornered or threatened, during breeding season, or when defending its territory. They are also known to have a 100% rate of envenomation. The probability of dry bites (no venom injected) in black mamba strikes is almost non-existent. The venom of the black mamba is a protein of low molecular weight and as a result is able to spread extraordinarily rapidly within the bitten tissue. The venom of this species is the most rapid-acting venom of any snake species and consists mainly of highly potent neurotoxins; it also contains cardiotoxins, fasciculins, and calciseptine. The median lethal dose (LD50) values for this species' venom varies greatly from one toxicological study to the next. Ernst and Zug et al. 1996 listed a value of 0.05 mg/kg for subcutaneous injection (SC). The Australian venom and toxin database provides values of 0.32 mg/kg SC and 0.25 mg/kg for IV. Spawls & Branch and Minton & Minton both listed a value of 0.28 mg/kg SC and Brown lists a SC value of 0.12 mg/kg. It is estimated that only 10 to 15 mg will kill a human adult, and its bites delivers about 120 mg of venom on average. Although they may deliver up to 400 mg of venom in a single bite. To demonstrate just how deadly this species is, an estimate was made on the number of mice and adult human fatalities it is capable of causing in a single bite that yields the maximum dose of 400 mg. Based on the study by Ernst and Zug et al. 1996, which listed the LD50 of the black mamba at 0.05 mg SC, a bite yield of 400 mg, and the estimated lethal adult human dose of 10 mg, this would be sufficient enough to kill 400,000 mice and 107 adult humans in a single bite that delivers 400 mg of venom.
If bitten, severe neurotoxicity often ensues. Neurological, respiratory, and cardiovascular symptoms rapidly begin to manifest, usually within less than ten minutes. Common symptoms are rapid onset of dizziness, drowsiness, headache, coughing or difficulty breathing, convulsions, and an erratic heartbeat. Other common symptoms which come on rapidly include neuromuscular symptoms, shock, loss of consciousness, hypotension, pallor, ataxia, excessive salivation (oral secretions may become profuse and thick), limb paralysis, nausea and vomiting, ptosis, fever, and very severe abdominal pain. Local tissue damage appears to be relatively infrequent and of minor severity in most cases of black mamba envenomation. Edema is typically minimal. Acute renal failure has been reported in a few cases of black mamba bites in humans as well as in animal models. The venom of this species has been known to cause permanent paralysis in some cases. Death is due to suffocation resulting from paralysis of the respiratory muscles. To date there has been no reported case of confirmed and medically treated black mamba bite in children that has ever been successful. Bites to children by this species are fatal, even with proper medical treatment. Untreated black mamba bites have a mortality rate of 100%. Antivenom therapy is the mainstay of treatment for black mamba envenomation. A polyvalent antivenom produced by the South African Institute for Medical Research (SAIMR) is used to treat all black mamba bites from different localities. Due to antivenom, a bite from a black mamba is no longer a certain death sentence. But in order for the antivenom therapy to be successful, vigorous treatment and large doses of antivenom must be administered very rapidly post-envenomation. In case studies of black mamba envenomation, respiratory paralysis has occurred in less than 15 minutes. In a case of 10 envenomations in South Africa all ten received medical treatment but only five lived. One developed respiratory paralysis in ten minutes, and all other patients were showing signs of neurotoxicity upon arrival at the hospital. Symptoms initially included mild swelling at bite site, confusion, excessive sweating, urinary incontinence, fecal incontinence, loss of coordination, ptosis, erratic heartbeat, drowsiness, and breathing difficulties. Out of the 10 patients, five were fatal despite prompt hospitalization and induction of medical treatment. One patient died in just under 30 minutes. The four other patients all died within 3-8 hours post-envenomation. The other five patients survived but all of them required massive amounts of antivenom and assisted mechanical ventilation for a prolonged period. Three of the patients were on mechanical ventilation for 10 days, while the other two required assisted mechanical ventilation for 16 days. Cases of this nature are not at all uncommon among cases of envenomation by the black mamba. Envenomation by this species invariably causes very severe neurotoxicity due to the fact that black mambas often strike repeatedly in a single lunge, biting the victim up to 12 times in extremely rapid succession. Such an attack is very fast, lasting less than one second and so it appears to be a single strike and single bite. With each bite the snake delivers anywhere from 100 to 400 mg of a rapid-acting and virulently toxic venom. As a result, the doses of antivenom required are often massive (10–30+ vials) for bites from this species. Although antivenom saves many lives, mortality due to black mamba envenomation is still at 14%, even with antivenom therapy. In addition to antivenom therapy, endotracheal intubation and mechanical ventilation are required for supportive therapy.
The Coastal taipan (Oxyuranus scutellatus scutellatus) is a large, highly venomous Australian elapid that ranges in an arc along the east coast of Australia from northeastern New South Wales through Queensland and across the northern parts of the Northern Territory to northern Western Australia. It has one subspecies the Papuan taipan (Oxyuranus scutellatus canni). The Papuan taipan is found throughout the southern parts of the island of New Guinea. This snake can be highly aggressive when cornered and will actively defend themselves. They are extremely nervous and alert snakes, and any movement near them is likely to trigger an attack. When threatened, this species adopts a loose striking stance with its head and forebody raised. It inflates and compresses its body laterally (not dorso-ventrally like many other species) and may also spread the back of its jaws to give the head a broader, lance-shaped appearance. In this position the snake will strike without much provocation, inflicting multiple bites with extreme accuracy and efficiency. The muscular lightweight body of the Taipan allows it to hurl itself forwards or sideways and reach high off the ground, and such is the speed of the attack that a person may be bitten several times before realizing the snake is there. This snake is considered to be one of the most venomous in the world. Ernst and Zug et al. 1996 and the Australian venom and toxin databse both list a LD50 value of 0.106 mg/kg for subcutaneous injection. Engelmann and Obst (1981) list a value of 0.12 mg/kg SC, with an average venom yield of 120 mg per bite and a maximum record of 400 mg. To demonstrate just how deadly this species is, an estimate was made on the number of mice and adult human fatalities it is capable of causing in a single bite that yields the maximum dose of 400 mg. Based on the study by Ernst and Zug et al. 1996, which listed the LD50 of the coastal taipan at 0.106 mg SC and a venom yield of 400 mg, this would be sufficient enough to kill 208,019 mice and 56 adult humans in a single bite that delivers 400 mg of venom. The venom apparatus of this species is well developed. The fangs are the longest of any Australian elapid snake, being up to 12 millimetres (1.2 cm; 0.47 in) long, and are able to be brought forward slightly when a strike is contemplated. Coastal taipans can inject large amounts of highly toxic venom deep into tissue. Its venom contains primarily taicatoxin, a highly potent neurotoxin known to cause hemolytic and coagulopathic reactions. The venom affects the nervous system and the blood’s ability to clot, and bite victims may experience headache, nausea and vomiting, collapse, convulsions (especially in children), paralysis, internal bleeding, myolysis (destruction of muscle tissue) and kidney damage. In a single study done in Papua New Guinea, 166 patients with enzyme immunoassay-proven bites by Papuan taipans (Oxyuranus scutellatus canni) were studied in Port Moresby, Papua New Guinea. Of the 166 bite victims, 139 (84%) showed clinical evidence of envenoming: local signs were trivial, but the majority developed hemostatic disorders and neurotoxicity. The blood of 77% of the patients was incoagulable and 35% bled spontaneously, usually from the gums. Microhematuria was observed in 51% of the patients. Neurotoxic symptoms (ptosis, ophthalmoplegia, bulbar paralysis, and peripheral muscular weakness) developed in 85%. Endotracheal intubation was required in 42% and mechanical ventilation in 37%. Electrocardiographic (ECG or EKG) abnormalities were found in 52% of a group of 69 unselected patients. Specific antivenom raised against Australian taipan venom was effective in stopping spontaneous systemic bleeding and restoring blood coagulability but, in most cases, it neither reversed nor prevented the evolution of paralysis even when given within a few hours of the bite. However, early antivenom treatment was associated statistically with decreased incidence and severity of neurotoxic signs. The low case fatality rate of 4.3% is attributable mainly to the use of mechanical ventilation, a technique rarely available in Papua New Guinea. Earlier use of increased doses of antivenoms of improved specificity might prove more effective. The onset of symptoms is often rapid, and a bite from this species is a life threatening medical emergency. Prior to the introduction of specific antivenom by the Commonwealth Serum Laboratories in 1956, a coastal taipan bite was nearly always fatal. In case of severe envenomation, death can occur as early as 30 minutes after being bitten, but average death time after a bite is around 3-6 hours and it is variable, depending on various factors such as the nature of the bite and the health state of the victim. Envenomation rate is very high, over 80% of bites inject venom. The mortality rate among untreated bite victims is nearly 100%.
The Big Four
The Big Four are the four venomous snake species responsible for causing the most snake bite cases in South Asia (mostly in India). The Big Four snakes cause far more snakebites because they are much more abundant in highly populated areas. They are the Indian cobra (Naja naja), common krait (Bungarus caeruleus), Russell's viper (Daboia russelii) and the Saw-scaled viper (Echis carinatus).
The Indian cobra is a moderately venomous species, but has a rapid-acting venom. In mice, the SC LD50 for this species is 0.80 mg/kg and the average venom yield per bite is between 169 and 250 mg. Though it is responsible for many bites, only a small percentage are fatal if proper medical treatment and antivenom are given. Mortality rate for untreated bite victims can vary from case to case, depending upon the quantity of venom delivered by the individual involved. According to one study, it is approximately 15–20%. but in another study, with 1,224 bite cases, the mortality rate was only 6.5%. Estimated fatalities as a result of this species is approximately 15,000 per year, but they are responsible for an estimated 100,000-150,000 non-fatal bites per year.
The common krait (Bungarus caeruleus) is often considered to be the most dangerous Asian snake species. Its venom consists mostly of powerful neurotoxins which induce muscle paralysis. Clinically, its venom contains presynaptic and postsynaptic neurotoxins, which generally affect the nerve endings near the synaptic cleft of the brain. Due to the fact that krait venom contains many presynaptic neurotoxins, patients bitten will often not respond to antivenom because once paralysis has developed it is not reversible. This species causes an estimated 10,000 fatalities per year in India alone. There is a 70-80% mortality rate in cases where there is no treatment or poor and ineffective treatment (e.g., no use of mechanical ventilation, low quantities of antivenom, poor management of possible infection). Average venom yield per bite is 10 mg (Brown, 1973), 8 to 20 mg (dry weight) (U.S. Dept. Navy, 1968), and 8 to 12 mg (dry weight) (Minton, 1974). The lethal adult human dose is 60 mg. In mice, the LD50 values of its venom are 0.365 mg/kg SC, 0.169 mg/kg IV and 0.089 mg/kg IP. Another extremely venomous and dangerous krait species is the Malayan krait (Bungarus candidus). In mice, the IV LD50 for this species is 0.1 mg/kg. Envenomation rate among this species is very high and the untreated mortality is 70%, although even with antivenom and mechanical ventilation the mortality rate is at 50%.
Russell's viper (Daboia russelii) produces one of the most excruciatingly painful bites of all venomous snakes. Internal bleeding is common. Bruising, blistering and necrosis may appear relatively quickly as well. The Russell's viper is irritable, short-tempered and a very aggressive snake by nature and when it gets irritated it coils tightly, hisses, and strikes with a lightning speed. This species is responsible for more human fatalities in India than any other snakes species, causing an estimated 25,000 fatalities annually. The LD50 in mice, which is used as a possible indicator of snake venom toxicity, is as follows: 0.133 mg/kg intravenous, 0.40 mg/kg intraperitoneal, and about 0.75 mg/kg subcutaneous. For most humans, a lethal dose is approximately 40–70 mg. However, the quantity of venom produced by individual specimens is considerable. Reported venom yields for adult specimens range from 130–250 mg to 150–250 mg to 21–268 mg. For 13 juveniles with an average length of 79 cm, the average venom yield was 8–79 mg (mean 45 mg).
The Saw-scaled viper (Echis carinatus) is small, but it's ill-temper, irritability, highly aggressive nature, loud hissing, and lethal venom potency make it very dangerous. This species is one of the fastest striking snakes in the world, and mortality rates for those bitten are very high. In India alone, the saw-scaled viper is responsible for an estimated 5,000 human fatalities annually. However, because it ranges from Pakistan, India (in rocky regions of Maharastra, Rajasthan, Uttar Pradesh and Punjab), Sri Lanka, parts of the Middle East and Africa north of the equator, is believed to cause more human fatalities every year than any other snake species. In drier regions of the African continent, such as sahels and savannas, the saw-scaled vipers inflict up to 90% of all bites. The rate of envenomation is over 80%. The saw-scaled viper also produces a particularly painful bite. 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 human is estimated to be only 5 mg. Envenomation results in local symptoms as well as severe systemic symptoms that may prove fatal. Local symptoms include swelling and intense 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. 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.
The Many-banded krait (Bungarus multicinctus) is the most venomous krait species known based on toxinological studies conducted on mice. The venom of the many-banded krait consists of both pre- and postsynaptic neurotoxins (known as α-bungarotoxins and β-bungarotoxins, among others). Due to poor response to antivenom therapy, mortality rates are very high in cases of envenomation - up to 50% of cases that receive antivenom are fatal. Case fatality rates of the many-banded krait envenoming reach up to 77%–100% without treatment. The average venom yield from specimens kept on snake farms was between 4.6—18.4 mg per bite. In another study, the average venom yield was 11 mg (Sawai, 1976). The venom is the most toxic of any Bungarus (krait) species and the most toxic of any snake species in Asia, with LD50 values of 0.09 mg/kg—0.108 mg/kg SC, 0.113 mg/kg IV and 0.08 mg/kg IP on mice. The lethal dose for an 80 kg adult human is approximately 10-15 mg. Based on several LD50 studies, the many-banded krait is among the most venomous land snake in the world. The Taiwan National Poison Control Center reports that the chief cause of deaths from snakebites during the decade (2002-2012) was respiratory failure, 80% of which was caused by bites from the many-banded krait.
The Inland taipan (Oxyuranus microlepidotus) is considered the most venomous snake in the world with a murine LD50 value of 0.025 mg/kg SC. Ernst and Zug et al. 1996 list a value of 0.01 mg/kg SC, which makes it the most venomous snake in the world in their study too. They have an average venom yield of 44 mg. Bites from this species have a mortality rate of 80% if left untreated, although it is very rare for this species to bite. This species known to be a very shy, reclusive and a laid-back snake that will most always slither away from disturbance. It is not an aggressive species and rarely strikes.
Eastern brown snake
The Eastern brown snake (Pseudonaja textilis) has a venom LD50 value of 0.053 mg SC according to (Brown, 1973) and a value of 0.0365 mg SC according to (Ernst and Zug et al. 1996). According to both studies, it is the second most venomous snake in the world. Average venom yield is 2–6 mg according to (Meier and White, 1995). According to (Minton, 1974) average venom yield (dry weight) is between 5–10 mg. Maximum venom yield for this species is 155 mg. This species is legendary for its bad temper, aggression, and for its speed. This species is responsible for more deaths every year in Australia than any other group of snakes.
Common death adder
The Common death adder (Acanthophis antarcticus) is a highly venomous snake species with a 50-60% untreated mortality rate. It is also the fastest striking venomous snake in the world. It lashes out with the quickest strike of any snake in the world. A death adder can go from a strike position, to strike and envenoming their prey, and back to strike position again, in less than 0.15 seconds. The SC LD50 value is 0.4 mg/kg and the venom yield per bite can range anywhere from 70–236 mg. Unlike other snakes that flee from approaching humans crashing through the undergrowth, common death adders are more likely to sit tight and risk being stepped on, making them more dangerous to the unwary bushwalker. They are said to be reluctant to bite unless actually touched.
Tiger snakes (Notechis spp) are highly venomous. Their venoms possess potent neurotoxins, coagulants, haemolysins and myotoxins and the venom is quick-acting with rapid onset of breathing difficulties and paralysis. The untreated mortality rate from tiger snake bites is reported to be between 40 and 60%. They are a major cause of snakebites and occasional snakebite deaths in Australia.
The most medically important species of snake in Central Asia is the Caspian cobra (Naja oxiana). It is the most venomous species of cobra in the world, slightly ahead of the Philippines cobra based on a toxinological study from 1992 found in the Indian Journal of Experimental Biology, in which this species produced the highest potency venom among cobras. The venom of this species has the most potent composition of toxins found among any cobra species known. It is made up of primarily highly potent neurotoxins but it also has cytotoxic activity (tissue-death, necrosis) and cardiotoxins. Two forms of "cytotoxin II" (cardiotoxin) were found in the venom of this species. The Caspian cobra is the most venomous species of cobra in the world. The crude venom of this species produced the lowest known lethal dose (LCLo) of 0.005 mg/kg, the lowest among all cobra species, derived from an individual case of poisoning by intracerebroventricular injection. A 1992 extensive toxinology study gave a value of 0.18 mg/kg (range of 0.1 mg/kg - 0.26 mg/kg) by subcutaneous injection. According to Brown (1973), the subcutaneous LD50 value is 0.4 mg/kg, while Ernst and Zug et al. list a value of 0.21 mg/kg SC and 0.037 mg/kg IV. Latifi (1984) listed a subcutaneous value of 0.2 mg/kg. In another study, where venom was collected from a number of specimens in Iran, the IV LD50 in lab mice was 0.078 mg/kg. Average venom yield per bite for this species is between 75 and 125 mg (dry weight), but it may yield up to 590 mg (dry weight) in a single bite. The bite of this species may cause severe pain and swelling, along with severe neurotoxicity. Weakness, drowsiness, ataxia, hypotension, and paralysis of throat and limbs may appear in less than one hour after the bite. Without medical treatment, symptoms rapidly worsen and death can occur rapidly after a bite due to respiratory failure. An adult woman bitten by this species in northwestern Pakistan suffered severe neurotoxicity and died while en route to the closest hospital nearly 50 minutes after envenomation. Between 1979 and 1987, 136 confirmed bites were attributed to this species in the former Soviet Union. Of the 136, 121 received antivenom, and only four died. Of the 15 who did not receive antivenom, 11 died. This species is an abundant snake in northeastern Iran and is responsible for a very large number of snakebite mortality. Antivenom is not as effective for envenomation by this species as it is for other Asiatic cobras within the same region, like the Indian cobra (Naja naja) and due to the dangerous toxicity of this species' venom, massive amounts of antivenom are often required for patients. As a result, a monovalent antivenom serum is being developed by the Razi Serum and Vaccine Research Institute in Iran. The untreated mortality rate for this species is 70-75%, which is the highest among all cobra species of the genus Naja.
The Forest cobra (Naja melanoleuca) is the largest true cobra of the Naja species and is a very bad-tempered, aggressive, and irritable snake when cornered or molested. According to Brown (1973) this species has a murine IP LD50 value of 0.324 mg/kg, while the IV LD50 value is 0.6 mg/kg. Ernst and Zug et al. 1996 list a value of 0.225 mg/kg SC. The average venom yield per bite is 571 mg and the maximum venom yield is 1102 mg. The forest cobra is one of the least frequent causes of snake bite among the African cobras, this is largely due to its forest-dwelling habits. It is the largest of the Naja cobras and the venom is considered highly toxic. If the snake becomes cornered or is agitated, it can quickly attack the aggressor, and if a large amount of venom is injected, a rapidly fatal outcome is possible. Clinical experience with forest cobras has been very sparse, and few recorded bites have been documented. However, in 2008, around the area of Friguiagbé in Guinea, there were 375 bites attributed to the forest cobra and of those 79 were fatal. Most of the fatal bites were patients who received no medical treatment. Deaths from respiratory failure have been reported, but most victims will survive if prompt administration of antivenom is undertaken as soon as clinical signs of envenomation have been noted.
The Philippine cobra (Naja philippinensis) is one of the most venomous cobra species in the world based on murine LD50 studies. The average subcutaneous LD50 for this species is 0.20 mg/kg. The lowest LD50 reported value for this snake is 0.14 mg/kg SC, while the highest is 0.48 mg/kg SC. and the average venom yield per bite is 90–100 mg. The venom of the Philippine cobra is a potent postsynaptic neurotoxin which affects respiratory function and can cause neurotoxicity and respiratory paralysis, as the neurotoxins interrupt the transmission of nerve signals by binding to the neuromuscular junctions near the muscles. Research has shown its venom is purely a neurotoxin, with no apparent necrotizing components and no cardiotoxins. These snakes are capable of accurately spitting their venom at a target up to 3 metres (9.8 ft) away. Bites from this species produce prominent neurotoxicity and are considered especially dangerous. A study of 39 patients envenomed by the Philippine cobra was conducted in 1988. Neurotoxicity occurred in 38 cases and was the predominant clinical feature. Complete Respiratory failure developed in 19 patients, and was often rapid in onset; in three cases, apnea occurred within just 30 minutes of the bite. There were two deaths, both in patients who were moribund upon arrival at the hospital. Three patients developed necrosis, and 14 individuals with systemic symptoms had no local swelling at all. Both cardiotoxicity and reliable nonspecific signs of envenoming were absent. Bites by the Philippine cobra produce a distinctive clinical picture characterized by severe neurotoxicity of rapid onset and minimal local tissue damage.
The Gaboon viper (Bitis gabonica), although generally docile and sluggish, have the longest fangs of any venomous snake and their venom glands are enormous and each bite produces the largest quantities of venom of any venomous snake. Yield is probably related to body weight, as opposed to milking interval. Brown (1973) gives a venom yield range of 200–1000 mg (of dried venom), A range of 200–600 mg for specimens 125–155 cm in length has also been reported. Spawls and Branch (1995) state from 5 to 7 ml (450–600 mg) of venom may be injected in a single bite. Based on how sensitive monkeys were to the venom, Whaler (1971) estimated 14 mg of venom would be enough to kill a human being: equivalent to 0.06 ml of venom, or 1/50 to 1/1000 of what can be obtained in a single milking. Marsh and Whaler (1984) wrote that 35 mg (1/30 of the average venom yield) would be enough to kill a man of 70 kilograms (150 lb). A study by Marsh and Whaler (1984) reported a maximum yield of 9.7 ml of wet venom, which translated to 2400 mg of dried venom. They attached "alligator" clip electrodes to the angle of the open jaw of anesthetized specimens (length 133–136 cm, girth 23–25 cm, weight 1.3–3.4 kg), yielding 1.3–7.6 ml (mean 4.4 ml) of venom. Two to three electrical bursts within a space of five seconds apart were enough to empty the venom glands. The snakes used for the study were milked seven to 11 times over a 12-month period, during which they remained in good health and the potency of their venom remained the same. In addition, Gaboon vipers produce the most painful bite of any venomous snake in the world. A bite causes very rapid and conspicuous swelling, intense pain, severe shock and local blistering. Other symptoms may include uncoordinated movements, defecation, urination, swelling of the tongue and eyelids, convulsions and unconsciousness. Blistering, bruising and necrosis is often very extensive. There may be sudden hypotension, heart damage and dyspnoea. The blood may become incoagulable with internal bleeding that may lead to haematuria and haematemesis. Local tissue damage may require surgical excision and possibly amputation. Healing may be slow and fatalities during the recovery period are not uncommon.
Green mambas (Western, Eastern, and Jameson's) are all highly venomous snakes with bad tempers and a tendency to strike repeatedly with little provocation.
The Western green mamba (Dendroaspis viridis) is highly venomous and aggressive with a LD50 of 0.7 mg/kg SC and the average venom yield per bite is approximately 100 mg. The mortality rate of untreated bites is unknown but is thought to be very high (>80%).
The Eastern green mamba (Dendroaspis angusticeps) has an average venom yield per bite of 80 mg according to Engelmann and Obst (1981). The subcutaneous LD50 for this species ranges from 0.40 mg/kg to 3.05 mg/kg depending on different toxicology studies, authority figures and estimates. The mortality rate of untreated bites is unknown but is thought to be very high (70-75%).
The Jameson's mamba (Dendroaspis jamesoni) is known to be quite aggressive and defensive. The average venom yield per bite for this species is 80 mg, but some specimens may yield as much as 120 mg in a single bite. The SC LD50 for this species according to Brown (1973) is 1.0 mg/kg, while the IV LD50 is 0.8 mg/kg. Envenomation by a Jameson's mamba can be deadly in as little as 30 to 120 minutes after being bitten, if proper medical treatment is not attained. The mortality rate of untreated bites is not exactly known, but it's said to be very high (>80%).
The Terciopelo (Bothrops asper) has been described as excitable and unpredictable when disturbed. They can, and often will, move very quickly, usually opting to flee from danger, but are capable of suddenly reversing direction to vigorously defend themselves. Adult specimens, when cornered and fully alert, should be considered dangerous. In a review of bites from this species suffered by field biologists, Hardy (1994) referred to it as the "ultimate pit viper". Venom yield (dry weight) averages 458 mg, with a maximum of 1530 mg (Bolaños, 1984) and an LD50 in mice of 2.844 mg/kg IP. This species is an important cause of snakebite within its range. It is considered the most dangerous snake in Costa Rica, responsible for 46% of all bites and 30% of all hospitalized cases; before 1947, the fatality rate was 7%, but this has since declined to almost 0% (Bolaños, 1984), mostly due to the Clodomiro Picado Research Institute, responsible for the production of antivenom. In the Colombian states of Antioquia and Chocó, it causes 50-70% of all snakebites, with a sequelae rate of 6% and a fatality rate of 5% (Otero et al., 1992). In the state of Lara, Venezuela, it is responsible for 78% of all envenomations and all snakebite fatalities (Dao-L., 1971). One of the reasons so many people are bitten is because of its association with human habitation and many bites actually occur indoors (Sasa & Vázquez, 2003).
The Jararaca (Bothrops jararaca) is a species that is often abundant within its range, where it is an important cause of snakebite. It is the best-known venomous snake in the wealthy and heavily populated areas of southeastern Brazil, where it was responsible for 52% (3,446 cases) of snakebites between 1902 and 1945, with a 0.7% mortality rate (25 deaths). The average venom yield is 25–26 milligrams (0.386–0.401 gr) with a maximum of 300 milligrams (4.6 gr) of dried venom. The venom is slightly more toxic than that of the terciopelo or fer-de-lance (B. asper). In mice, the median lethal dose (LD50) is 1.2-1.3 mg/kg IV, 1.4 mg/kg IP and 3.0 mg/kg SC. For humans, the LD50 is estimated to be 210 milligrams (3.2 gr) subcutaneous.
South American bushmaster or Atlantic bushmaster
The South American bushmaster or Atlantic bushmaster (Lachesis muta) is the longest species of venomous snake in the Western Hemisphere and the longest pit viper in the world. It is native to parts of South America, especially the equatorial forests east of the Andes. They are active at dusk or after dark and so they are very secretive and elusive. This species is large, fast and has a reputation for being particularly aggressive when cornered. Some reports suggest that this species produces a large amount of venom that is weak compared to some other vipers. Others, however, suggest that such conclusions may not be accurate. These animals are badly affected by stress and rarely live long in captivity. This makes it difficult to obtain venom in useful quantities and good condition for study purposes. For example, Bolaños (1972) observed that venom yield from his specimens fell from 233 mg to 64 mg while they remained in his care. As the stress of being milked regularly has this effect on venom yield, it is reasoned that it may also affect venom toxicity. This may explain the disparity described by Hardy and Haad (1998) between the low laboratory toxicity of the venom and the high mortality rate of bite victims. However, wild specimens have an average venom yield per bite of 280-450 mg (dry weight) (U.S. Dept. Navy, 1968). According to (Sanchez et al., 1992), who used wild specimens from Pará, Brazil, the average venom yield per bite was 324 mg, with a range of 168-552 mg (dry weight). Brown (1973) gives the following LD50 values for mice: 1.5 mg/kg IV, 1.6–6.2 mg/kg IP, 6.0 mg/kg SC. He also notes a venom yield of 200–411 mg. Human envenoming by this species, although infrequent, can be rather severe due to the large volumes of venom injected. Envenomation is characterized by pronounced local tissue damage and systemic dysfunctions, including massive internal bleeding.
King cobras (Ophiophagus hannah) are not particularly venomous nor are they aggressive or bad tempered. The venom LD50 is 1.80 mg/kg SC according to Broad et al. (1979). The mean value of subcutaneous LD50 of five wild-caught king cobras in Southeast Asia was determined as 1.93 mg/kg. However, because the king cobra is the longest venomous snake in the world, it can inject very high volumes of venom in a single bite. Between 350 to 500 mg (dry weight) of venom can be injected at once (Minton, 1974). In another study by (Broad et al., 1979), the average venom quantity was 421 mg (dry weight of milked venom). The maximum venom yield is approximately 1000 mg (dry weight). The king cobra has a fearsome reputation. When annoyed, it spreads a narrow hood and growls loudly, but scientists claim that their "legendary aggressiveness" is grossly exaggerated. In most of the local encounters with live, wild king cobras, the snakes appear to be of rather placid disposition, and they usually end up being killed or subdued with hardly any hysterics. These support the view that wild king cobras generally have a mild temperament, and despite their frequent occurrence in disturbed and built-up areas, are adept at avoiding humans. Naturalist Michael Wilmer Forbes Tweedie felt that "this notion is based on the general tendency to dramatise all attributes of snakes with little regard for the truth about them. A moment’s reflection shows that this must be so, for the species is not uncommon, even in populated areas, and consciously or unconsciously, people must encounter king cobras quite frequently. If the snake were really habitually aggressive records of its bite would be frequent; as it is they are extremely rare." Mortality rates vary sharply depending on many factors. Most bites involve non-fatal amounts. Still, despite its mild disposition and reluctance to bite, the king cobra is capable of severely envenoming an adult human. Massive amounts of venom can cause severe neurotoxicity. In cases where envenomation is severe, death can be rapid.
The cobras (Naja spp) are a medically important group of snakes due number of bites and fatalities they cause across to their geographical range. The genus Naja consists of 20 to 22 species, but has undergone several taxonomic revisions in recent years, so sources vary greatly. They range throughout Africa (including some parts of the Sahara where Naja haje can be found), Southwest Asia, Central Asia, South Asia, East Asia, and Southeast Asia. The most recent revison, listed 28 species after the synonymisation of Boulengerina and Paranaja with Naja. But unlike some other members of the Elapidae family (the species of the genus Bungarus, genus Oxyuranus, genus Pseudohaje, and especially genus Dendroaspis), half of the bites by many species of both African and Asian origin of the genus Naja are "dry bites" (a dry bite is a bite by a venomous snake in which no venom is released). Roughly 45-50% of bites by most cobra species are dry bites and thus don't cause envenomation. Some of the species which are known and documented to deliver dry bites in a majority of cases (50% +) include: Naja naja, Naja kaouthia, Naja sputatrix, Naja siamensis, Naja haje, Naja annulifera, Naja anchietae and Naja nigricollis. Some species will inject venom in the majority of their bites, but still deliver high number of dry bites (40-45%) include: Naja sumatrana, Naja melanoleuca, Naja atra, Naja mossambica and Naja katiensis. Within this genus, there are a few species in which dry bites are very rare. Envenoming occurs in at least 75-80% of bite cases involving these species. The species which typically cause envenomation in the majority of their bites include some of the more dangerous and venomous species of this genus: Naja oxiana, Naja philippinensis, Naja nivea, and Naja samarensis. There are many more species within the genus which have not yet been subject to much researched and studies, and as a result, very little is known about their behaviour, venom, diet, habitat and general temperaments. Some of these species include Naja sagittifera, Naja annulata, Naja christyi and many others.
The Chinese cobra (Naja atra) is a highly venomous member of the true cobras (genus Naja). Its venom consists mainly of postsynaptic neurotoxins and cardiotoxins. Four cardiotoxin-analogues I, II, III, and IV, account for about 54% of the dry weight of the crude venom and have cytotoxic properties. The LD50 values of its venom in mice are 0.29 mg/kg IV, and 0.29—0.53 mg/kg SC. The average venom yield from a snake of this species kept at a snake farm was about 250.8 mg (80 mg dry weight). According to Minton (1974), this cobra has a venom yield range of 150 to 200 mg (dry weight). Brown listed a venom yield of 184 mg (dry weight). It is one of the most prevalent venomous snakes in mainland China and Taiwan, which has caused many snakebite incidents to humans.
The Asian Monocled cobra (Naja kaouthia) is a medically important species as it is responsible for a considerable amount of bites throughout its range. The major toxic components in the Monocled cobras venom are postsynaptic neurotoxins, which block the nerve transmission by binding specifically to the nicotinic acetylcholine receptor, leading to flaccid paralysis and even death by respiratory failure. The major α-neurotoxin in Naja kaouthia venom is a long neurotoxin, α-cobratoxin; the minor α-neurotoxin is different from cobrotoxin in one residue. The neurotoxins of this particular species are weak. The venom of this species also contains myotoxins and cardiotoxins. The median lethal dose (LD50) is 0.28-0.33 mg per gram of mouse body weight. In case of IV the LD50 is 0.373 mg/kg, and 0.225 mg/kg in case of IP. The average venom yield per bite is approximately 263 mg (dry weight). The monocled cobra causes the highest fatality due to snake venom poisoning in Thailand. Envenomation usually presents predominantly with extensive local necrosis and systemic manifestations to a lesser degree. Drowsiness, neurological and neuromuscular symptoms will usually manifest earliest; hypotension, flushing of the face, warm skin, and pain around bite site typically manifest within one to four hours following the bite; paralysis, ventilatory failure or death could ensue rapidly, possibly as early as 60 minutes in very severe cases of envenomation. However, the presence of fang marks does not always imply that envenomation actually occurred.
The Egyptian cobra (Naja haje) is another species of cobra which causes a significant amount of bites and human fatalities throughout its range. The venom of the Egyptian cobra consists mainly of neurotoxins and cytotoxins. The average venom yield is 175 to 300 mg in a single bite, and the murine subcutaneous LD50 value is 1.15 mg/kg. This species has large fangs and can produce large quantities of venom. Envenomation by this snake is a very serious medical emergency.
The water cobras found in central and western Africa are the most venomous cobra species (Naja) in the world. These species were formerly under the genus Boulengerina. The Banded water cobra (Naja annulata) and the Congo water cobra (Naja christyi) are dangerously venomous. The banded water cobra has one subspecies which is known as Storms water cobra (Naja annulata stormsi). Their venoms are extremely potent neurotoxins. A toxicological study listed the intraperitoneal (IP) LD50 of N. annulata at 0.143 mg/kg. Brown (1973) listed the intravenous LD50 for N. a. annulata at 0.2 mg/kg. The same study listed the intraperitoneal (IP) LD50 of N. christyi at 0.12 mg/kg. The venoms of these little-known elapids have the lowest intraperitoneal LD50 of any Naja species studied thus far and have high concentrations of potent postsynaptic neurotoxins. Serious and dangerous envenomation can result from a bite from either of these snakes. There is at least one case of human envenomation caused by the Congo water cobra (N. christyi). Symptoms of the envenomation were mild. There is no specific antivenom currently produced for either of these two species.
Black desert cobra
The Black desert cobra (Walterinnesia aegyptia) is a highly venomous snake found in the Middle East. The subcutaneous LD50 for the venom of this species is 0.4 mg/kg. For comparison, the Indian cobra's (naja naja) subcutaneous LD50 is 0.80 mg/kg, while the Cape cobra's (naja nivea) subcutaneous LD50 is 0.72 mg/kg. This makes the black desert cobra a more venomous species than both. The venom is strongly neurotoxic and also has mild hemotoxic factors. Envenomation usually causes some combination of local pain, swelling, fever, general weakness, headache, & vomiting. This is not a typically aggressive snake, but it will strike and hiss loudly when provoked. It can strike at a distance of ⅔ of its body length. It does not usually spread a hood nor hold up its body up off the ground like true cobras do. Envenomation by this species should be considered a serious medical emergency. Reports of human fatalities due to envenomation by this species has been reported.
Spitting cobras are another group of cobras that belong the Naja genus. Spitting cobras can be found in both Africa and Asia. These cobras have the ability to eject venom from their fangs when defending themselves against predators. The sprayed venom is harmless to intact skin. However, it can cause permanent blindness if introduced to the eye and left untreated (causing chemosis and corneal swelling). The venom sprays out in distinctive geometric patterns, using muscular contractions upon the venom glands. These muscles squeeze the glands and force the venom out through forward-facing holes at the tips of the fangs. The explanation that a large gust of air is expelled from the lung to propel the venom forward has been proven wrong. When cornered, some species can "spit" their venom a distance as great as 2 m (6.6 ft). While spitting is typically their primary form of defense, all spitting cobras are capable of delivering venom through a bite as well. Most species' venom exhibit significant hemotoxic effects, along with more typical neurotoxic effects of other cobra species.
The Samar cobra (Naja samarensis) is a highly venomous species of spitting cobra that is found in the southern islands of the Philippines. Although it is a spitting cobra, this species only rarely spits its venom. It is considered to be an extremely aggressive snake that strikes with little provocation. The venom of this species is not well studied, but is known to be an extremely potent postsynaptic neurotoxin that also contains cytotoxic agents. According to Ernst & Zug et al the murine SC LD50 value is 0.23 mg/kg, while Brown lists a LD50 value of 0.36 mg/kg, making it one of the most venomous cobras in the world. Severe envenomation is likely in case of a bite and envenomation rate is high. The untreated mortality rate is not known, but is thought to be high (~60%). Envenomation results in marked local effects such as pain, severe swelling, bruising, blistering, and necrosis. Other effects include headache, nausea, vomiting, abdominal pain, diarrhea, dizziness, collapse or convulsions. There may also be moderate to severe flaccid paralysis and renal damage. Cardiotoxicity is possible, but rare.
Indochinese spitting cobra
The Indochinese spitting cobra (Naja siamensis) is a venomous spitting cobra whose venom consists of postsynaptic neurotoxins, metalloproteinases, powerful cardiotoxins, with cytolytic activity, and Phospholipase A2 with a diversity of activities. The LD50 of its venom is 1.07-1.42 mg/gram of mouse body weight. Cranial palsy and respiratory depression are reported to be more common after bites by Naja siamensis than by Naja kaouthia. Indochinese sptting cobras will use their venom for self-defense with little provocation, and as the name implies, are capable of spitting venom when alarmed, often at the face and eyes of the animal or human threatening them. A case report in the literature describes pain and irritation of the eyes, bilateral redness, excessive tear production and whitish discharge, with superficial corneal opacity but normal acuity.
Black-necked spitting cobra
The Black-necked spitting cobra (Naja nigricollis) is a species of spitting cobra found mostly in Sub-Saharan Africa. They possess medically significant venom, although the mortality rate for untreated bites on humans is relatively low (~5-10%). Like other spitting cobras, this species is known for its ability to project venom at a potential threat. The venom is an irritant to the skin and eyes. If it enters the eyes, symptoms include extreme burning pain, loss of coordination, partial loss of vision and permanent blindness. N. nigricollis is known for its tendency to liberally spit venom with only the slightest provocation. However, this aggressiveness is counterbalanced by it being less prone to bite than other related species. The venom of the black-necked spitting cobra is somewhat unique among elapids in that it consists primarily of cytotoxins, but with other components also. It retains the typical elapid neurotoxic properties while combining these with highly potent cytotoxins (necrotic agents) and cardiotoxins. Bite symptoms include severe external hemorrhaging and tissue necrosis around the bite area and difficulty breathing. Although mortality rate in untreated cases is low (~5-10%), when death occurs it is usually due to asphyxiation by paralysis of the diaphragm. The LD50 of this species is 2 mg/kg SC and 1.15 mg/kg IV. The average venom yield per bite of this species is 200 to 350 mg (dry weight) according to Minton (1974).
Mozambique spitting cobra
Another medically important African spitting cobra is the Mozambique spitting cobra (Naja mossambica). This species is considered irritable and highly aggressive. The Mozambique spitting cobra is responsible for a significant amount of bites throughout its range, but most are not fatal. The venom is both neurotoxic and cytotoxic.
West African spitting cobra
The West African spitting cobra (Naja katiensis) is a venomous species of spitting cobra native to western Africa. The venom of this species consists of postsynaptic neurotoxins and cardiotoxins with cytotoxic (necrotizing) activity. An average wet venom yield of 100 mg has been reported for this species. The average murine LD50 value of this species is 1.15 mg/kg IV, but there is an IV LD50 range of 0.97 mg/kg-1.45 mg/kg. The West African spitting cobra is one of the most common causes of snakebite in Senegal. Over 24 years, from 1976 to 1999, a prospective study was conducted of overall and cause-specific mortality among the population of 42 villages of southeastern Senegal. Of 4228 deaths registered during this period, 26 were caused by snakebite, four by invertebrate stings and eight by other wild or domestic animals. The average annual mortality rate from snakebite was 14 deaths per 100,000 population. Among persons aged one year or over, 0.9% (26/2880) of deaths were caused by snakebite and this cause represented 28% (26/94) of total deaths by accidents. Of 1280 snakes belonging to 34 species collected, one-third were dangerous, and the proportions of Viperidae, Elapidae and Atractaspidae were 23%, 11% and 0.6%, respectively. This species was third, responsible for 5.5% of the snakebites.
The Rinkhals (Hemachatus haemachatus) is a not a true cobra in that it does not belong to the genus Naja. However, it is closely related to the true cobras and is considered to be one of the true spitting cobras. The venom of this species is less viscous than that of other African elapids, naturally, as thinner fluid is naturally easier to spit. However, the venom of the rinkhals is produced in copious amounts. Average venom yield is 80–120 mg and the murine LD50 is 1.1-1.6 mg/kg SC with an estimated lethal dose for humans of 50–60 mg. Actual bites from this species are fairly rare, and deaths in modern times are so far unheard of. Local symptoms of swelling and bruising is reported in about 25% of cases. General symptoms of drowsiness, nausea, vomiting, violent abdominal pain and vertigo often occur, as does a mild pyrexial reaction. Neurotoxic symptoms are however rare and have only included diplopia and dyspnoea. Ophthalmia has been reported, but has not caused as severe complications as in some of the spitters in the genus Naja (especially N. nigricollis and N. mossambica).
The Puff adder (Bitis arietans) is responsible for more fatalities than any other African snake. This is due to a combination of factors, including its wide distribution, common occurrence, large size, potent venom that is produced in large amounts, long fangs, their habit of basking by footpaths and sitting quietly when approached. The venom has cytotoxic effects and is one of the most toxic of any vipers based on LD50 studies. The LD50 values in mice vary: 0.4–2.0 mg/kg IV, 0.9–3.7 mg/kg IP, 4.4–7.7 mg/kg SC. Mallow et al. (2003) gives a LD50 range of 1.0–7.75 mg/kg SC. Venom yield is typically between 100–350 mg, with a maximum of 750 mg. Brown (1973) mentions a venom yield of 180–750 mg. About 100 mg is thought to be enough to kill a healthy adult human male, with death occurring after 25 hours. In humans, bites from this species can produce severe local and systemic symptoms. Based on the degree and type of local effect, bites can be divided into two symptomatic categories: those with little or no surface extravasation, and those with hemorrhages evident as ecchymosis, bleeding and swelling. In both cases there is severe pain and tenderness, but in the latter there is widespread superficial or deep necrosis and compartment syndrome. Serious bites cause limbs to become immovably flexed as a result of significant hemorrhage or coagulation in the affected muscles. Residual induration, however, is rare and usually these areas completely resolve. The fatality rate highly depends on the severity of the bites and some other factors. Deaths can be exceptionally rare and probably occur in less than 10% of all untreated cases (usually in 2–4 days from complications following blood volume deficit and a disseminated intravascular coagulopathy), although some reports show that very severe envenomations have a 52% mortality rate. Most fatalities are associated with bad clinical management and neglect.
The Rhinoceros viper (Bitis nasicornis) is a large species of viper that is similar to the Gaboon viper, but not as venomous, smaller and with a less dangerous bite. They are slow moving, but like other Bitis species, they're capable of striking quickly, forwards or sideways, without coiling first or giving a warning. Holding them by the tail is not safe; as it is somewhat prehensile, they can use it to fling themselves upwards and strike. They have been described as generally placid creatures, not as bad-tempered as the Puff adder. When approached, they often reveal their presence by hissing, said to be the loudest hiss of any African snake—almost a shriek. Relatively little is known about the toxicity and composition of the venom, but it has very minor neurotoxic, as well as hemotoxic venom, as do most other venomous snakes. The hemotoxic venom in rhinoceros vipers is much more dominant. This venom attacks the circulatory system of the snake's victim, destroying tissue and blood vessels. Internal bleeding also occurs. In mice, the intravenous LD50 is 1.1 mg/kg. The venom is supposedly slightly less toxic than those of the Puff adder and the Gaboon viper. The maximum wet venom yield is 200 mg. In only a few detailed reports of human envenomation, massive swelling, which may lead to necrosis, had been described. In 2003, a man in Dayton, Ohio, who was keeping a specimen as a pet, was bitten and subsequently died. At least one antivenom protects specifically against bites from this species: India Antiserum Africa Polyvalent.
Australian black snakes
King brown snake or Mulga snake
The Australian King brown snake or Mulga snake is a the second longest species of venomous snake in Australia. The venom of this snake is relatively weak compared to many other Australian species. The LD50 is 2.38 mg/kg subcutaneous. However, these snakes can deliver large amounts of venom when they bite, compensating for the lower venom potency. Average venom yield is 180 mg and they have a maximum yield of 600 mg. The venom of this species contains potent myotoxins and anticoagulants, that can inhibit blood clotting. The neurotoxic components are weak. This snake can cause severe envenomation of humans. They are a moderately common cause of snakebites and uncommonly to rarely cause snakebite deaths in Australia at present. Envenomation can cause anticoagulation coagulopathy, renal damage or renal failure (kidney failure). They do not cause significant neurotoxic paralysis (muscle weakness, respiratory failure), though rarely they may cause ptosis (drooping of the upper eyelids). Bites can also cause myolysis (rhabdomyolysis, muscle damage) which can be very severe and is the major effect of bites. Rate of envenomation is 40-60%, while untreated mortality rate is 30-40%.
Red-bellied black snake
The Red-bellied black snake (Pseudechis porphyriacus) is a venomous species native to Australia. The venom of the red-bellied black snake consists of myotoxins, coagulants and also has haemolytic and cytotoxic properties. It also contains weak pre-synaptic neurotoxins. The murine LD50 is 2.52 mg/kg SC. Average venom yield per bite is 37 mg and a maximum yield of 97 mg. Bites from red-bellied black snake are rarely life-threatening due to the snake usually choosing to inject little venom toxin, but are still in need of immediate medical attention. Rate of envenomation is 40-60%, but the untreated mortality rate is less than 1%.
Australian brown snakes
The Dugite (Pseudonaja affinis) is a highly venomous Australian brown snake species. The venom of this species contains highly potent presynaptic and postsynaptic neurotoxins and procoagulants. The murine LD50 is 0.66 mg/kg SC. The average venom yield per bite is 18 mg (dry weight of milked venom) according to Meier and White (1995). Rate of envenomation is 20-40% and the untreated mortality rate is 10–20 %by cardiac arrest, renal failure, or cerebral hemorrhage.
Western Brown snake
The Western brown snake (Pseudonaja nuchalis) is a highly venomous species of brown snake common throughout northern Australia. Its venom contains powerful neurotoxins, nephrotoxins and a procoagulant, although humans are not usually affected by the neurotoxins. The bite is usually painless and difficult to see due to their small fangs. Human symptoms of a Western Brown snake bite are headache, nausea/vomiting, abdominal pain, severe coagulopathy and sometimes, kidney damage. The LD50 in mice is 0.47 mg/kg and the average venom yield per bite is 18 mg (dry weight of milked venom) according to Meier and White (1995). The western brown snake can cause rapid death in humans by cardiac arrest, renal failure, or cerebral hemorrhage. The envenomation rate is 20-40% and the untreated mortality rate is 10-20%.
Some rattlesnake species can be quite dangerous to humans.
The Tiger rattlesnake (Crotalus tigris), although it has a comparatively low venom yield, its venom toxicity is considered to be the highest of all rattlesnake venoms, and the highest of all snakes in the Western Hemisphere. Although they're reluctant to bite, tiger rattlensakes are known to be cantankerous and they are an aggressive species. This tendency to stand their ground and aggressively defend themselves along with their highly potent venom, they pose a serious threat to humans. It has a high neurotoxic fraction that is antigenically related to Mojave toxin (see Crotalus scutulatus, venom A), and includes another component immunologically identical to crotamine, which is a myotoxin also found in tropical rattlesnakes (see Crotalus durissus). A low but significant protease activity is in the venom, although there does not seem to be any hemolytic activity. Brown (1973) lists an average venom yield of 11 mg (dried venom) and LD50 values of 0.07 mg/kg IP, 0.056 mg/kg IV, and 0.21 mg/kg SC. Minton and Weinstein (1984) list an average venom yield of 6.4 mg (based on two specimens). Weinstein and Smith (1990) list a venom yield of 10 mg. There is very little information available for bite symptoms. Human bites by the tiger rattlesnake are infrequent, and literature available on bites by this snake is scarce. The several recorded human envenomations by tiger rattlesnakes produced little local pain, swelling, or other reaction following the bite, and despite the toxicity of its venom no significant systemic symptoms. The comparatively low venom yield (6.4–11 mg dried venom) and short 4.0 mm (0.40 cm) to 4.6 mm (0.46 cm) fangs of the tiger rattlesnake possibly prevent severe envenoming in adult humans. However, the clinical picture could be much more serious if the person bitten was a child or an individual with a slight build. The early therapeutic use of antivenom is important if significant envenomation is suspected. Despite the low venom yield, a bite by this rattlesnake should be considered a life-threatening medical emergency. Untreated mortality rate is unknown but this snake has a very high venom toxicity and its bites are capable of producing major envenomation.
The Neotropical rattlesnake or Cascabel (Crotalus durissus) is a medically important species due to its venom toxicity and the human fatalities it is responsible for. The IP LD50 value is 0.17 mg/kg with an average venom yield between between 20–100 mg/kg per bite. Bite symptoms are very different from those of Nearctic species due to the presence of neurotoxins (crotoxin and crotamine) that cause progressive paralysis. Bites from C. d. terrificus in particular can result in impaired vision or complete blindness, auditory disorders, ptosis, paralysis of the peripheral muscles, especially of the neck, which becomes so limp as to appear broken, and eventually life-threatening respiratory paralysis. The ocular disturbances, which according to Alvaro (1939) occur in some 60% of C. d. terrificus cases, are sometimes followed by permanent blindness. Phospholipase A2 neurotoxins also cause damage to skeletal muscles and possibly the heart, causing general aches, pain, and tenderness throughout the body. Myoglobin released into the blood results in dark urine. Other serious complications may result from systemic disorders (incoagulable blood and general spontaneous bleeding), hypotension, and shock. Hemorrhagins may be present in the venom, but any corresponding effects are completely overshadowed by the startling and serious neurotoxic symptoms. Subcutaneous venom LD50 for this species is 0.193 mg/kg. The neotropical rattlesnake in Brazil is of special importance because of the high incidence of envenoming and mortality rates. Clinically, venom of this snake does not usually cause local effects at the bite site and is usually painless. However, the etiology progresses to systemic neurotoxic and myalgic symptoms, with frequent renal failure accompanied by acute tubular necrosis. The huge area of distribution, potent venom in fairly large quantities and a definite willingness to defend themselves are important factors in their dangerousness. In Brazil and probably also in other countries in their area of distribution, this species is probably the most dangerous rattlesnake. After the fer-de-lance (Bothrops asper), it is the most common cause of snake envenoming. In the first half of the 20th century as well as in the 1950s and 1960s, 12% of treated cases ended fatally. Untreated cases apparently had a mortality rate of 72% in the same period, but this was due to the fact that there was no antivenom, poor medical care and neglect (Rosenfeld, 1971). In more recent times, an average of 20,000 snakebites are registered each year in Brazil, almost 10% of them caused by the neotropical rattlesnake. The mortality rate is estimated at 3.3% and is thus much lower than in the past (Ribeiro, 1990b). A study from southeastern Brazil documented only one fatality from 87 treated cases (Silveira and Nishioka, 1992).
The Mojave rattlesnake (Crotalus scutulatus) is another species which is considered to be dangerous. Although they have a reputation for being aggressive towards people, such behavior is not described in the scientific literature. Like other rattlesnakes, they will defend themselves vigorously when disturbed. The IP LD50 value is 0.18 mg/kg with an average venom yield between between 50–150 mg/kg per bite. The most common subspecies of Mohave rattlesnake (type A) has venom that is considered to be one of the most debilitating and potentially deadly of all North American snakes, although chances for survival are very good if medical attention is sought as soon as possible after a bite. Based on median LD50 values in lab mice, venom A from subspecies A Mojave rattlesnakes is more than ten times as toxic as venom B, from type B Mohave green rattlesnakes which lacks Mojave toxin. Medical treatment as soon as possible after a bite is critical to a positive outcome, dramatically increasing chances for survival. However, venom B causes pronounced proteolytic and hemorrhagic effects, similar to the bites of other rattlesnake species; these effects are significantly reduced or absent from bites by venom A snakes. Risk to life and limb is still significant, as with all rattlesnakes, if not treated as soon as possible after a bite. All rattlesnake venoms are complex cocktails of enzymes and other proteins that vary greatly in composition and effects, not only between species, but also between geographic populations within the same species. The Mojave rattlesnake is widely regarded as producing one of the most toxic snake venoms in the New World, based on LD50 studies in laboratory mice. Their potent venom is the result of a presynaptic neurotoxin composed of two distinct peptide subunits. The basic subunit (a phospholipase A2) is mildly toxic and apparently rather common in North American rattlesnake venoms. The less common acidic subunit is not toxic by itself, but in combination with the basic subunit, produces the potent neurotoxin called “Mojave toxin”. Nearly identical neurotoxins have been discovered in five North American rattlesnake species besides the Mojave rattlesnake. However, not all populations express both subunits. The venom of many Mojave rattlesnakes from south-central Arizona lacks the acidic subunit and has been designated “venom B,” while Mojave rattlesnakes tested from all other areas express both subunits and have been designated “venom A” populations.
Malayan pit viper
The Malayan pit viper (Calloselasma rhodostoma) is an Asian species of pitviper that is reputed to be an ill-tempered snake that is quick to strike in defense. This species is one of the main causes of snakebite envenoming in Southeast Asia. However, mortality rate among untreated bite victims is very low (1-10%). Although bites are common, death is very rare. When a victim dies of a bite it is chiefly caused by haemorrhages and secondary infections. Before specific antivenom became available, the mortality rate in hospitalised patients was around 1% (Reid et al. 1963a). In the study of Reid et al. (1963a), of a total of 291 patients with verified C. rhodostoma bites, only 2 patients died, and their deaths could only be indirectly attributed to the snakebites. One patient died of tetanus and one from a combination of an anaphylactic reaction to the antivenom, an intracerebral haemorrhage and severe pre-existing anaemia. In 23 fatalities due to C. rhodostoma bites recorded in northern Malaysia between 1955 and 1960, the average time between the bite and death was 64.6 h (5–240 h), the median time 32 h (Reid et al. 1963a). According to a study of fatal snakebites in rural areas of Thailand, 13 out of 46 were caused by C. rhodostoma (Looareesuwan et al. 1988). The local necrotising effect of the venom is a common cause of morbidity. Gangrene can lead to the loss of toes, fingers or whole extremities; chronic infections (osteomyelitis) can also occur. The intravenous LD50 for Malayan pit viper venom is 6.1 mg/g mouse and the average venom yield per bite is 40-60 mg (dry weight).
Sharp-nosed pit viper
The Sharp-nosed pit viper or hundred pacer (Deinagkistrodon acutus) is another Asian species of pitviper that is medically important. This species is considered dangerous, and fatalities are not unusual. According to the U.S. Armed Forces Pest Management Board, the venom is a potent hemotoxin that is strongly hemorrhagic. Bite symptoms include severe local pain and bleeding that may begin almost immediately. This is followed by considerable swelling, blistering, necrosis, and ulceration. Brown (1973) mentions a venom yield of up to 214 mg (dried) and LD50 values of 0.04 mg/kg IV, 4.0 mg/kg IP and 9.2-10.0 mg/kg SC. The envenomation rate is up to 80% and the untreated mortality rate is very low (1-10%). Antivenom is produced in China and Taiwan.
Society and culture
Snakes were both revered and worshipped and feared by early civilizations. The ancient Egyptians recorded prescribed treatments for snakebites as early as the Thirteenth dynasty in the Brooklyn Papyrus, which includes at least seven venomous species common to the region today, such as the horned vipers. In Judaism, the Nehushtan was a pole with a snake made of copper wrapped around it, similar in appearance to the Rod of Asclepius. The object was considered sacred with the power to heal bites caused by the snakes which had infested the desert, with people merely having to touch it in order to save themselves from imminent death.
Historically, snakebites were seen as a means of execution in some cultures. In medieval Europe, a form of capital punishment was to throw people into snake pits, leaving people to die from multiple venomous bites. A similar form of punishment was common in Southern Han during China's Five Dynasties and Ten Kingdoms period and in India. Snakebites were also used as a form of suicide, most notably by Egyptian queen Cleopatra VII, who reportedly died from the bite of an asp—likely an Egyptian cobra—after hearing of Mark Antony's death.
Snakebite as a surreptitious form of murder has been featured in stories such as Sir Arthur Conan Doyle's The Adventure of the Speckled Band, but actual occurrences are virtually unheard of, with only a few documented cases. It has been suggested that Boris III of Bulgaria, who was allied to Nazi Germany during World War II, may have been killed with snake venom, although there is no definitive evidence. At least one attempted suicide by snakebite has been documented in medical literature involving a puff adder bite to the hand.
- Kasturiratne, A., Wickremasinghe A. R., de Silva N., Gunawardena N. K. et al. (2008). "The Global Burden of Snakebite: A Literature Analysis and Modelling Based on Regional Estimates of Envenoming and Deaths". In Winkel, Ken. PloS Medicine 5 (11): e218. doi:10.1371/journal.pmed.0050218. PMC 2577696. PMID 18986210. Retrieved 2009-06-24.
- Snake Venom Detection Kit: Detection and Identification of Snake Venom. CSL Limited. 2007. Retrieved 2009-11-24. "The physical identification of Australian and Papua New Guinean snakes is notoriously unreliable. There is often marked colour variation between juvenile and adult snakes and wide size, shape and colour variation between snakes of the same species. Reliable snake identification requires expert knowledge of snake anatomy, a snake key and the physical handling of the snake"
- White, Julian (2006). Snakebite & Spiderbite: Management Guidelines. Adelaide: Department of Health, Government of South Australia. pp. 1–71. ISBN 0-7308-9551-3. Retrieved 2009-11-24. "The colour of brown snakes is very variable and misleading for identification purposes. They may be brown, red brown, grey, very dark brown and may be plain in color, have speckling, stripes or bands, or have a dark or black head"
- Gold, Barry S.; Richard C. Dart, Robert A. Barish (1 April 2002). "Bites of venomous snakes". The New England Journal of Medicine 347 (5): 347–56. doi:10.1056/NEJMra013477. PMID 12151473.
- Kitchens C, Van Mierop L (1987). "Envenomation by the Eastern coral snake (Micrurus fulvius fulvius). A study of 39 victims". JAMA 258 (12): 1615–18. doi:10.1001/jama.258.12.1615. PMID 3625968.
- Chippaux, J.P. (1998). "Snake-bites: appraisal of the global situation". Bulletin of the World Health Organization 76 (5): 515–24. PMC 2305789. PMID 9868843. Retrieved 2009-07-03.
- Gutiérrez, José María; Bruno Lomonte, Guillermo León, Alexandra Rucavado, Fernando Chaves, Yamileth Angulo (2007). "Trends in Snakebite Envenomation Therapy: Scientific, Technological and Public Health Considerations". Current Pharmaceutical Design 13 (28): 2935–50. doi:10.2174/138161207782023784. PMID 17979738.
- MedlinePlus - Snake bites From Tintinalli JE, Kelen GD, Stapcynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York, NY: McGraw Hill; 2004. Update Date: 2/27/2008. Updated by: Stephen C. Acosta, MD, Department of Emergency Medicine, Portland VA Medical Center, Portland, OR. Review provided by VeriMed Healthcare Network. Also reviewed by David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc. Retrieved on 19 mars, 2009
- Health-care-clinic.org - Snake Bite First Aid – Snakebite Retrieved on 21 mars, 2009
- Snake bite image example at MDconsult - Patient Education - Wounds, Cuts and Punctures, First Aid for
- Warrell, David A.; L. David Ormerod (1976). "Snake Venom Ophthalmia and Blindness Caused by the Spitting Cobra (Naja Nigricollis) in Nigeria". The American Society of Tropical Medicine and Hygiene 25 (3): 525–9. PMID 1084700. Retrieved 2009-09-05.
- Ismail, Mohammad; Abdullah M. Al-Bekairi, Ayman M. El-Bedaiwy, Mohammad A. Abd-El Salam (1993). "The ocular effects of spitting cobras: I. The ringhals cobra (Hemachatus haemachatus) Venom-Induced corneal opacification syndrome". Clinical Toxicology 31 (1): 31–41. doi:10.3109/15563659309000372. PMID 8433414.
- "Confronting the Neglected Problem of Snake Bite Envenoming: The Need for a Global Partnership". PLoS Medicine. Retrieved 2012-06-06.
- Phillips, Charles M. (2002). "Sea snake envenomation". Dermatologic Therapy 15 (1): 58–61(4). doi:10.1046/j.1529-8019.2002.01504.x. Retrieved 2009-07-24.
- Young, Bruce A.; Cynthia E. Lee, Kylle M. Daley (2002). "Do Snakes Meter Venom?". BioScience 52 (12): 1121–26. doi:10.1641/0006-3568(2002)052[1121:DSMV]2.0.CO;2. "The second major assumption that underlies venom metering is the snake's ability to accurately assess the target"
- Young, Bruce A.; Krista Zahn (2001). "Venom flow in rattlesnakes: mechanics and metering". Journal of Experimental Biology 204 (Pt 24): 4345–4351. PMID 11815658. "With the species and size of target held constant, the duration of venom flow, maximum venom flow rate and total venom volume were all significantly lower in predatory than in defensive strikes"
- Deufel, Alexandra; David Cundall (2003). "Feeding in Atractaspis (Serpentes: Atractaspididae): a study in conflicting functional constraints". Zoology 106 (1): 43–61. doi:10.1078/0944-2006-00088. PMID 16351890. Retrieved 2009-08-25.[dead link]
- Jackson, Kate (2003). "The evolution of venom-delivery systems in snakes". Zoological Journal of the Linnean Society 137 (3): 337–354. doi:10.1046/j.1096-3642.2003.00052.x. Retrieved 2009-07-25.
- Fry, Bryan G.; Nicolas Vidal, Janette A. Norman, Freek J. Vonk, Holger Scheib, S. F. Ryan Ramjan, Sanjaya Kuruppu, Kim Fung, S. Blair Hedges, Michael K. Richardson, Wayne. C. Hodgson, Vera Ignjatovic, Robyn Summerhayes, Elazar Kochva (2006). "Early evolution of the venom system in lizards and snakes". Nature 439 (7076): 584–8. doi:10.1038/nature04328. PMID 16292255. Retrieved 2009-09-18.
- Russell, Findlay E. (1980). "Snake Venom Poisoning in the United States". Annual Review of Medicine 31: 247–59. doi:10.1146/annurev.me.31.020180.001335. PMID 6994610.
- Spawls, Stephen; Bill Branch (1997). The Dangerous Snakes of Africa. Johannesburg: Southern Book Publishers. p. 192. ISBN 1-86812-575-0.
- Haji, R. "Venomous snakes and snake bites". Zoocheck Canada. Retrieved 25 October 2013.
- Kurecki B, Brownlee H (1987). "Venomous snakebites in the United States". Journal of Family Practice 25 (4): 386–92. PMID 3655676.
- Gold B, Barish R (1992). "Venomous snakebites. Current concepts in diagnosis, treatment, and management". Emerg Med Clin North Am 10 (2): 249–67. PMID 1559468.
- Suchard, JR; LoVecchio F. (1999). "Envenomations by Rattlesnakes Thought to Be Dead". The New England Journal of Medicine 340 (24): 1930. doi:10.1056/NEJM199906173402420. PMID 10375322.
- Gold BS, Wingert WA (1994). "Snake venom poisoning in the United States: a review of therapeutic practice". South. Med. J. 87 (6): 579–89. doi:10.1097/00007611-199406000-00001. PMID 8202764.
- Pathmeswaran A, Kasturiratne A, Fonseka M, Nandasena S, Lalloo D, de Silva H (2006). "Identifying the biting species in snakebite by clinical features: an epidemiological tool for community surveys". Trans R Soc Trop Med Hyg 100 (9): 874–8. doi:10.1016/j.trstmh.2005.10.003. PMID 16412486.
- Chris Thompson. "Treatment of Australian Snake Bites". Australian anaesthetists' website.[dead link]
- "Indian National Snakebite Protocols 2007". Indian National Snakebite Protocol Consultation Meeting, 2nd August 2007, Delhi. Retrieved 31 May 2012.
- Currie, Bart J.; Elizabeth Canale, Geoffrey K. Isbister (2008). "Effectiveness of pressure-immobilization first aid for snakebite requires further study". Emergency Medicine Australasia 20 (3): 267–270(4). doi:10.1111/j.1742-6723.2008.01093.x. PMID 18549384.
- Patrick Walker, J; Morrison, R; Stewart, R; Gore, D (2013 Jan). "Venomous bites and stings". Current problems in surgery 50 (1): 9–44. doi:10.1067/j.cpsurg.2012.09.003. PMID 23244230.
- American College of Medical, Toxicology; American Academy of Clinical, Toxicology; American Association of Poison Control, Centers; European Association of Poison Control, Centres; International Society of, Toxinology; Asia Pacific Association of Medical, Toxicology (2011 Dec). "Pressure immobilization after North American Crotalinae snake envenomation". Journal of Medical Toxicology 7 (4): 322–3. doi:10.1007/s13181-011-0174-2. PMC 3550191. PMID 22065370.
- Wall, C (2012 Sep). "British Military snake-bite guidelines: pressure immobilisation". Journal of the Royal Army Medical Corps 158 (3): 194–8. doi:10.1136/jramc-158-03-09. PMID 23472565.
- White, Julian (November 1991). "Oxyuranus microlepidotus". Chemical Safety Information from Intergovernmental Organizations. Retrieved 24 July 2009. "Without appropriate antivenom treatment up to 75% of taipan bites will be fatal. Indeed, in the era prior to specific antivenom therapy, virtually no survivors of taipan bite were recorded."
- Nuchpraryoon, I; Garner, P (2000). "Interventions for preventing reactions to snake antivenom.". The Cochrane database of systematic reviews (2): CD002153. PMID 10796682.
- Theakston RD (1997). "An objective approach to antivenom therapy and assessment of first-aid measures in snake bite" (PDF). Ann. Trop. Med. Parasitol. 91 (7): 857–65. doi:10.1080/00034989760626. PMID 9625943.
- Amaral CF, Campolina D, Dias MB, Bueno CM, Rezende NA (1998). "Tourniquet ineffectiveness to reduce the severity of envenoming after Crotalus durissus snake bite in Belo Horizonte, Minas Gerais, Brazil". Toxicon 36 (5): 805–8. doi:10.1016/S0041-0101(97)00132-3. PMID 9655642.
- Watt G, Padre L, Tuazon ML, Theakston RD, Laughlin LW (1988). "Tourniquet application after cobra bite: delay in the onset of neurotoxicity and the dangers of sudden release". Am. J. Trop. Med. Hyg. 38 (3): 618–22. PMID 3275141.
- Holstege CP, Singletary EM (2006). "Images in emergency medicine. Skin damage following application of suction device for snakebite". Annals of Emergency Medicine 48 (1): 105, 113. doi:10.1016/j.annemergmed.2005.12.019. PMID 16781926.
- Alberts M, Shalit M, LoGalbo F (2004). "Suction for venomous snakebite: a study of "mock venom" extraction in a human model". Annals of Emergency Medicine 43 (2): 181–6. doi:10.1016/S0196-0644(03)00813-8. PMID 14747805.
- Bush SP, Hegewald KG, Green SM, Cardwell MD, Hayes WK (2000). "Effects of a negative pressure venom extraction device (Extractor) on local tissue injury after artificial rattlesnake envenomation in a porcine model". Wilderness & environmental medicine 11 (3): 180–8. doi:10.1580/1080-6032(2000)011[0180:EOANPV]2.3.CO;2. PMID 11055564.
- Riggs BS, Smilkstein MJ, Kulig KW, et al. Rattlesnake envenomation with massive oropharyngeal edema following incision and suction (Abstract). Presented at the AACT/AAPCC/ABMT/CAPCC Annual Scientific Meeting, Vancouver, Canada, September 27 October 2, 1987.
- Russell F (1987). "Another warning about electric shock for snakebite". Postgrad Med 82 (5): 32. PMID 3671201.
- Ryan A (1987). "Don't use electric shock for snakebite". Postgrad Med 82 (2): 42. PMID 3497394.
- Howe N, Meisenheimer J (1988). "Electric shock does not save snakebitten rats". Annals of Emergency Medicine 17 (3): 254–6. doi:10.1016/S0196-0644(88)80118-5. PMID 3257850.
- Johnson E, Kardong K, Mackessy S (1987). "Electric shocks are ineffective in treatment of lethal effects of rattlesnake envenomation in mice". Toxicon 25 (12): 1347–9. doi:10.1016/0041-0101(87)90013-4. PMID 3438923.
- Russell, F. E. (1990). "When a snake strikes". Emerg Med 22 (12): 33–4, 37–40, 43.
- Mackessy, Stephen P. (2002). "Biochemistry and pharmacology of colubrid snake venoms". Journal of Toxicology: Toxin Reviews 21 (1–2): 43–83. doi:10.1081/TXR-120004741. Retrieved 2009-09-26. "Estimates of the number of venomous colubrids approach 700 species. Most may not produce a venom capable of causing serious damage to humans, but at least five species (Dispholidus typus, Thelotornis capensis, Rhabdophis tigrinus, Philodryas olfersii and Tachymenis peruviana) have caused human fatalities"
- Wingert W, Chan L (1 January 1988). "Rattlesnake Bites in Southern California and Rationale for Recommended Treatment". West J Med 148 (1): 37–44. PMC 1026007. PMID 3277335.
- Gutiérrez, José María; R. David G. Theakston, David A. Warrell (6 June 2006). "Confronting the Neglected Problem of Snake Bite Envenoming: The Need for a Global Partnership". PLOS Medicine 3 (6): e150. doi:10.1371/journal.pmed.0030150. PMC 1472552. PMID 16729843. Retrieved 2009-06-30.
- Parrish H (1966). "Incidence of treated snakebites in the United States". Public Health Rep 81 (3): 269–76. doi:10.2307/4592691. PMC 1919692. PMID 4956000.
- Zug, George R. (1996). Snakes in Question: The Smithsonian Answer Book. Washington D.C., USA: Smithsonian Institution Scholarly Press. ISBN 1-56098-648-4.
- Dr. Bryan Grieg Fry. "LD50 menu (Archived)".
- Séan Thomas & Eugene Griessel – Dec 1999. "LD50 (Archived)".
- Venomous Snakes. World's Deadliest Snakes – Ranking scale. Reptile Gardens. Retrieved October 18, 2013.
- Walls, Jerry G. . Deadly Snakes: What are the world's most deadly venomous snakes?. Reptiles (magazine). Retrieved November 5, 2013.
- Shine, Richard; Covacevich, Jeanette. (March 1983). "A Ecology of Highly Venomous Snakes: the Australian Genus Oxyuranus (Elapidae)". Journal of Herpetology 17 (1): 60–69.
- "Black Mamba". National Geographic. National Geographic. Retrieved 20 October 2013.
- White, Nancy (2009). Black Mambas: Susen Death!. Bearport Publishing. ISBN 1-59716-766-5.[page needed]
- Pitman, Charles R.S. (1974). A Guide to the Snakes of Uganda. United Kingdom: Wheldon & Wesley. p. 290. ISBN 0-85486-020-7.
- "Coastal Taipan". Queensland Museum. Queensland Government. Retrieved 21 October 2013.
- White, Julian (November 1991). "Oxyuranus microlepidotus". International Programme on Chemical Safety. Retrieved 6 November 2013.
- Chippaux, Jean-phillipe (2006). Snake Venoms and Envenomations. United States: Krieger Publishing Company. p. 300. ISBN 1-57524-272-9.
- Minton, SA (1967). "Paraspecific protection by elapid and sea snake antivenins". Toxicon 5 (1): 47–55. doi:10.1016/0041-0101(67)90118-3.
- Mirtschin, Peter J.; Nathan Dunstan, Ben Hough, Ewan Hamilton, Sharna Klein, Jonathan Lucas, David Millar, Frank Madaras, Timothy Nias (26). "Venom yields from Australian and some other species of snakes". Ecotoxicology 15 (6): 531–538. doi:10.1007/s10646-006-0089-x. Retrieved 6 November 2013.
- Khare, AD; Khole V, Gade PR (December 1992). "Toxicities, LD50 prediction and in vivo neutralisation of some elapid and viperid venoms". Indian Journal of Experimental Biology 30 (12): 1158–62. PMID 1294479. Retrieved 6 December 2013.
- Latifi, M (1984). "Variation in yield and lethality of venoms from Iranian snakes". Toxicon 22 (3): 373–380. PMID 6474490.
- Mallow D, Ludwig D, Nilson G. 2003. True Vipers: Natural History and Toxinology of Old World Vipers. Malabar, Florida: Krieger Publishing Company. 359 pp. ISBN 0-89464-877-2.
- Pung, Yuh Fen; Peter T. H. Wong, Prakash P. Kumar, Wayne C. Hodgson, R. Manjunatha Kini (24). "Ohanin, a Novel Protein from King Cobra Venom, Induces Hypolocomotion and Hyperalgesia in Mice". Journal of Biological Chemistry 280 (13): 13137–13147. doi:10.1074/jbc.M414137200. Retrieved 6 November 2013.
- Brown JH. 1973. Toxicology and Pharmacology of Venoms from Poisonous Snakes. Springfield, Illinois: Charles C. Thomas. 184 pp. LCCCN 73-229. ISBN 0-398-02808-7.
- Minton, Minton, SA, MR (1969). Venomous Reptiles. USA: New York Charles Scribner's Sons.[page needed]
- Branch, Bill (1998). Field Guide Snakes and Other Reptiles of Southern Africa. Struik Publishers. p. 108. ISBN 1868720403.
- Warrell DA. 2004. Snakebites in Central and South America: Epidemiology, Clinical Features, and Clinical Management. In Campbell JA, Lamar WW. 2004. The Venomous Reptiles of the Western Hemisphere. Comstock Publishing Associates, Ithaca and London. 870 pp. 1500 plates. ISBN 0-8014-4141-2.[page needed]
- Daniels,J. C. (2002) The Book of Indian Reptiles and Amphibians, BNHS & Oxford University Press, Mumbai, pp 151-153. ISBN 0-19-566099-4
- Glenday, Craig (2009). Guinness World Records 2009. Bantam. p. 57. ISBN 0553592564.
- "IMMEDIATE FIRST AID for bites by Black Mamba (Dendroaspis polylepis polylepis)". University of California at San Diego.
- Crisp, NG (1985). "Black mamba envenomation". South African Medical Journal 68 (5): 293–4. PMID 4035489.
- "Sii Polyvalent Anti-Snake Venom Serum (central Africa)". Serum Institute of India. Serum Institute.
- Strydom, Daniel J. (1). "Purification and Properties of Low-Molecular-Weight Polypeptides of Dendroaspis polylepis polylepis (Black Mamba) Venom". European Journal of Biochemistry 69 (1): 169–176. PMID 991854. Retrieved 4 November 2013.
- "Dendroaspis polylepis – General Details, Taxonomy and Biology, Venom, Clinical Effects, Treatment, First Aid, Antivenoms". WCH Clinical Toxinology Resource. University of Adelaide.[dead link]
- Reed, Tim; Eaton, Katie; Peng, Cathy and Doern, BettyLou. Neurotoxins in Snake Venom. California State University Stanislaus. csustan.edu.
- Mitchell, Deborah (September 2009). The Encyclopedia of Poisons and Antidotes. New York, USA: Facts on File, Inc. p. 324. ISBN 0-8160-6401-6.
- Van Aswegen, G.; Van Rooyen, J.M.; Fourie, C.; Oberholzer, G. (1996). "Putative cardiotoxicity of the venoms of three mamba species". Wilderness & Environmental Medicine 7 (2): 115–21. doi:10.1580/1080-6032(1996)007[0115:PCOTVO]2.3.CO;2. PMID 11990104.
- De Weille, J. R.; Schweitz, H.; Maes, P.; Tartar, A.; Lazdunski, M. (1991). "Calciseptine, a peptide isolated from black mamba venom, is a specific blocker of the L-type calcium channel". Proceedings of the National Academy of Sciences 88 (6): 2437–40. Bibcode:1991PNAS...88.2437D. doi:10.1073/pnas.88.6.2437. JSTOR 2356398. PMC 51247. PMID 1848702.
- Spawls S, Branch B. 1995. The Dangerous Snakes of Africa. Ralph Curtis Books. Dubai: Oriental Press. 192 pp. ISBN 0-88359-029-8.
- Hilligan, R (1987). "Black mamba bites. A report of 2 cases". South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde 72 (3): 220–1. PMID 3603321.
- Závada, J.; Valenta J., Kopecký O., Stach Z., Leden P (2011). "Black Mamba Dendroaspis Polylepis Bite: A Case Report". Prague Medical Journal 112 (4): 298–304. PMID 22142525. Retrieved 3 December 2013.
- Visser, Chapman, John, David S (1978). Snakes and Snakebite: Venomous snakes and management of snake bite in Southern Africa. Purnell. ISBN 0-86843-011-0.
- "Venomous and Poisonous Animals Biology & Clinical Management (Dendroaspis sp)". VAPAGuide. Retrieved 3 December 2013.
- "Black Mamba (Dendroaspis polylepis)". The Wildlife Museum.
- Christensen, PA (20 June 1981). "Snakebite and the use of antivenom in southern Africa". South Africn Medical Journal 59 (26): 934–938. PMID 7244896.
- "IMMEDIATE FIRST AID for bites by Australian Taipan or Common Taipan (Oxyuranus scutellatus scutellatus)". University of California at San Diego. Retrieved 4 November 2013.
- "Coastal Taipan". Australian Museum. Retrieved 5 November 2013.
- "Australian Venom Research Unit". University of Melbourne.
- Engelmann, Wolf-Eberhard (1981). Snakes: Biology, Behavior, and Relationship to Man. Leipzig; English version NY, USA: Leipzig Publishing; English version published by Exeter Books (1982). p. 51. ISBN 0-89673-110-3.
- Lalloo, DG; Trevett AJ, Korinhona A, Nwokolo N, Laurenson IF, Paul M, Black J, Naraqi S, Mavo B, Saweri A, et al. (June 1995). "nake bites by the Papuan taipan (Oxyuranus scutellatus canni): paralysis, hemostatic and electrocardiographic abnormalities, and effects of antivenom". American Journal of Tropical Medicine and Hygeine 52 (6): 525–531. PMID 7611559. Retrieved 5 November 2013.
- "Oxyuranus scutellatus". Clinical Toxinology Resource. University of Adelaide. Retrieved 4 November 2013.
- Whitaker Z. 1990. Snakeman. Penguin Books Ltd. 192 pp. ISBN 0-14-014308-4.
- "Naja naja". University of Adelaide.
- Whitaker, Captain, Romulus, Ashok (2004). Snakes of India, The Field Guide. India: Draco Books. p. 372. ISBN 81-901873-0-9.
- World Health Organization. "Zoonotic disease control: baseline epidemiological study on snake-bite treatment and management". Weekly Epidemiological Record (WER) 62 (42): 319–320. ISSN 0049-8114.
- Whitaker, Romulus. "Publicity Notes One Million Snake Bite". IconFilms. Retrieved 21 October 2013.
- "University of Adelaide Clinical Toxinology Resources". "Mortality rate:70-80%"
- Isbister, G K (2005). "Snake antivenom research: the importance of case definition". Emergency Medical Journal 22 (6): 397. doi:10.1136/emj.2004.022251. Retrieved 26 October 2013.
- Tan, Nget Hong. "Toxins from Venoms of Poisonous Snake Indigenous to Malaysia: A Review". Department of Molecular Medicine, Faculty of Medicine. University of Malaya. Retrieved 21 October 2013.
- "University of Adelaide Clinical Toxinology Resources". "Mortality rate:70%"
- Warrell, David A. "Clinical Features of Snakebite". Encyclopedia of Occupational Health and Safety. Encyclopedia of Occupational Health and Safety. Retrieved 21 October 2013.
- Snake of medical importance. Singapore: Venom and toxins research group. ISBN 9971-62-217-3.
- McDiarmid RW, Campbell JA, Touré T. 1999. Snake Species of the World: A Taxonomic and Geographic Reference, vol. 1. Herpetologists' League. 511 pp. ISBN 1-893777-00-6 (series). ISBN 1-893777-01-4 (volume).
- "Saw-scaled viper". Encyclopedia Britannica. Encyclopedia Britannica. Retrieved 20 October 2013.
- Mackessy 2010, p. 456
- "University of Adelaide Clinical Toxinology Resources".
- Ali G, Kak M, Kumar M, Bali SK, Tak SI, Hassan G, Wadhwa MB. 2004. Acute renal failure following echis carinatus (saw–scaled viper) envenomation. Indian Journal of Nephrology 14:177-181. PDF at Indian Medlars Centre. Accessed 27 October 2013.
- White; Meier, Julian; Jurg (1995). "27". In White, MA. Handbook of clinical toxicology of animal venoms and poisons (in English) (First ed.). CRC Press. pp. 493–588. ISBN 978-0-84-934489-3. More than one of
- "Clinical Toxinology-Bungarus multicinctus".
- Chi, Wen Juan (29). "Venomous Snake Bites in Taiwan". Journal of Critical Care and Emergency Medicine 23 (4): 98. Retrieved 22 October 2013.
- "University of Adelaide Clinical Toxinology Resources". "Mortality rate:80%"
- "University of Adelaide Clinical Toxinology Resources".
- "Australia's 10 most dangerous snakes". Australian Geographic. Australian Geographic. Retrieved 20 October 2013.
- "University of Adelaide Clinical Toxinology Resources". "Mortality rate:50-60%"
- Fastest striking snake
- "LD50 of venomous snakes - Ultimate species list". Snake Database. Retrieved 21 October 2013.
- "Common death adder Venom Yield". Retrieved 21 October 2013.
- "Australia's 10 most dangerous snakes". Australian Geographic. Australian Geographic. Retrieved 20 October 2013.
- University of Adelaide Clinical Toxinology Resource
- "Australian Tiger Snakes". Clinical Toxinology Resources. University of Adelaide. Retrieved 22 October 2013.
- Sharonov, George V.; Sharonov, Alexei V.; Astapova, Maria V.; Rodionov, Dmitriy I.; Utkin, Yuriy N.; Arseniev, Alexander S. (2005). "Cancer cell injury by cytotoxins from cobra venom is mediated through lysosomal damage". Biochemical Journal 390 (Pt 1): 11–8. doi:10.1042/BJ20041892. PMC 1184559. PMID 15847607.
- Dementieva, Daria V.; Bocharov, Eduard V.; Arseniev, Alexander. S. (1999). "Two forms of cytotoxin II (cardiotoxin) from Naja naja oxiana in aqueous solution . Spatial structures with tightly bound water molecules". European Journal of Biochemistry 263 (1): 152–62. doi:10.1046/j.1432-1327.1999.00478.x. PMID 10429199.
- Lysz, Thomas W.; Rosenberg, Philip (May 1974). "Convulsant activity of Naja naja oxiana venom and its phospholipase A component". Toxicon 12 (3): 253–265. doi:10.1016/0041-0101(74)90067-1.
- Akbari, A; Rabiei , H., Hedayat, A., Mohammadpour, N., Zolfagharian, H., Teimorzadeh, Sh. (June 2010). "Production of effective antivenin to treat cobra snake (Naja naja oxiana) envenoming". Archives of Razi Institute 65 (1): 33–37. Retrieved 7 December 2013.
- "Naja oxiana". Clinical Toxinology Resource. University of Adelaide.
- Latifi, Mahmoud (1984). Snakes of Iran. Society for the Study of Amphibians & Reptiles. ISBN 978-0-91-698422-9.
- Gopalkrishnakone, Chou, P., LM (1990). Snakes of Medical Importance (Asia-Pacific Region). Singapore: National University of Singapore. ISBN 9971-62-217-3.[page needed]
- Warrell, David A. "Guidelines for the Prevention and Clinical Management of Snakebite in Africa". World Health Organization. Retrieved 23 October 2013.
- "IMMEDIATE FIRST AID for bites by Forest Cobra (Naja melanoleuca)". Retrieved 22 October 2013.
- Watt, G; Theakston RD, Hayes CG, Yambao ML, Sangalang R, et al. (4). "Positive response to edrophonium in patients with neurotoxic envenoming by cobras (Naja naja philippinensis). A placebo-controlled study". New England Journal of Medicine 315 (23): 1444–8. PMID 3537783. Retrieved 6 December 2013.
- Watt, G; Padre, L; Tuazon, L; Theakston, RD; Laughlin, L (1988). "Bites by the Philippine cobra (Naja naja philippinensis): Prominent neurotoxicity with minimal local signs". The American journal of tropical medicine and hygiene 39 (3): 306–11. PMID 3177741.
- Spawls S, Howell K, Drewes R, Ashe J. 2004. A Field Guide To The Reptiles Of East Africa. London: A & C Black Publishers Ltd. 543 pp. ISBN 0-7136-6817-2.
- Brown, John H. (1973). Toxicology and Pharmacology of Venoms from Poisonous Snakes. Springfield, IL USA: Charles C. Thomas. p. 81. ISBN 0-398-02808-7.
- Campbell; Lamar, Jonathan; William (2004). The Venomous Reptiles of the Western Hemisphere. Ithaca and London: Comstock Publishing Associates. ISBN 0-8014-4141-2.[page needed]
- Sierra. "Captive care of B.asper". A collection of captive care notes. www.venomousreptiles.org. Retrieved 6 November 2006.
- O'Shea, Mark (first published in 2005). VENOMOUS SNAKES OF THE WORLD. USA: Princeton University Press (Princeton and Oxford). ISBN 978-0-691-15023-9.
- "Clodomiro Picado Research Institute".
- Fowler, Cubas, ME, ZS (2001). Biology, Medicine, and Surgery of South American Wild Animals (1st ed.). Wiley-Blackwell. p. 42. ISBN 0813828465.
- Bartlett, Bartlett, Richard, Patricia (2003). Reptiles and Amphibians of the Amazon: An Ecotourist's Guide. USA: University Press of Florida. ISBN 0813026237.
- Lachesis muta, The Silent Fate at South American Pictures. Accessed 26 October 2013.
- Ripa, D. 2001. Bushmasters and the Heat Strike at VenomousReptiles.org. Accessed 26 October 2013.
- "University of Adelaide Clinical Toxinology Resources".
- Damico, Daniela C.S.; Nascimento, Juliana Minardi; Lomonte, Bruno; Ponce-Soto, Luis A.; Joazeiro, Paulo P.; Novello, José Camillo; Marangoni, Sérgio; Collares-Buzato, Carla B. (2007). "Cytotoxicity of Lachesis muta muta snake (bushmaster) venom and its purified basic phospholipase A2 (LmTX-I) in cultured cells". Toxicon 49 (5): 678–92. doi:10.1016/j.toxicon.2006.11.014. PMID 17208264.
- University of Adelaide Clinical Toxinology Resource
- Handbook of clinical toxicology of animal venoms and poisons 236. USA: CRC Press. 1995. ISBN 0-8493-4489-1.
- Greene, HW (1997). Snakes: The Evolution of Mystery in Nature. California, USA: University of California Press. ISBN 0520224876.[page needed]
- Tweedie, MWF (1983). The Snakes of Malaya. Singapore: Singapore National Printers Ltd. OCLC 686366097.[page needed]
- Mathew, Gera, JL, T. "http://www.priory.com/mehasophitoxaemia.htm". MEDICINE ON-LINE. Retrieved 20 October 2013.
- "Naja". Integrated Taxonomic Information System. Retrieved 13 April 2008.
- Wallach, Van; Wüster, W; Broadley, Donald G. (2009). "In praise of subgenera: taxonomic status of cobras of the genus Naja Laurenti (Serpentes: Elapidae)". Zootaxa 2236 (1): 26–36.
- Warrell, DA; Theakston RD; Griffiths E (April 2003). "Report of a WHO workshop on the standardization and control of antivenoms". Toxicon 41 (5): 541–57. PMID 12676433. Retrieved 8 December 2013.
- A H Wang; Yang, CC (1981). "Crystallographic studies of snake venom proteins from Taiwan cobra (Naja nana atra). Cardiotoxin-analogue III and phospholipase A2". Journal of Biological Chemistry 256 (17): 9279–82. PMID 7263715.
- Snake of medical importance. Singapore: Venom and toxins research group. ISBN 9971-62-217-3.
- "University of Adelaide Clinical Toxinology Resources".
- Wei, JF; Lü, QM; Jin, Y; Li, DS; Xiong, YL; Wang, WY (2003). "Alpha-neurotoxins of Naja atra and Naja kaouthia snakes in different regions". Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica 35 (8): 683–8. PMID 12897961.
- Ogay, Alexey Ya.; Rzhevsky, Dmitry I.; Murashev, Arkady N.; Tsetlin, Victor I.; Utkin, Yuri N. (2005). "Weak neurotoxin from Naja kaouthia cobra venom affects haemodynamic regulation by acting on acetylcholine receptors". Toxicon 45 (1): 93–9. doi:10.1016/j.toxicon.2004.09.014. PMID 15581687.
- Mahanta, Monimala; Mukherjee, Ashis Kumar (2001). "Neutralisation of lethality, myotoxicity and toxic enzymes of Naja kaouthia venom by Mimosa pudica root extracts". Journal of Ethnopharmacology 75 (1): 55–60. doi:10.1016/S0378-8741(00)00373-1. PMID 11282444.
- Fletcher, Jeffrey E.; Jiang, Ming-Shi; Gong, Qi-Hua; Yudkowsky, Michelle L.; Wieland, Steven J. (1991). "Effects of a cardiotoxin from Naja naja kaouthia venom on skeletal muscle: Involvement of calcium-induced calcium release, sodium ion currents and phospholipases A2 and C". Toxicon 29 (12): 1489–500. doi:10.1016/0041-0101(91)90005-C. PMID 1666202.
- Chanhome, L., Cox, M. J., Vasaruchaponga, T., Chaiyabutra, N. Sitprija, V. (2011). Characterization of venomous snakes of Thailand. Asian Biomedicine 5 (3): 311–328.
- Pratanaphon, Ronachai; Akesowan, Surasak; Khow, Orawan; Sriprapat, Supod; Ratanabanangkoon, Kavi (1997). "Production of highly potent horse antivenom against the Thai cobra (Naja kaouthia)". Vaccine 15 (14): 1523–8. doi:10.1016/S0264-410X(97)00098-4. PMID 9330463.
- Joubert, Francois J.; Taljaard, Nico (1978). "Naja haje haje (Egyptian cobra) Venom. Some Properties and the Complete Primary Structure of Three Toxins (CM-2, CM-11 and CM-12)". European Journal of Biochemistry 90 (2): 359–67. doi:10.1111/j.1432-1033.1978.tb12612.x. PMID 710433.
- Weinstein, Scott A.; Schmidt, James J.; Smith, Leonard A. (1991). "Lethal toxins and cross-neutralization of venoms from the African water cobras, Boulengerina annulata annulata and Boulengerina christyi". Toxicon 29 (11): 1315–27. doi:10.1016/0041-0101(91)90118-B. PMID 1814007.
- "Venomous Animals - Boulengerina annulata and Boulengerina christyi". Armed Forces Pest Management Board. United States Army. Retrieved 24 October 2013.
- "Venomous Animals - Walterinnesia aegyptia". Armed Forces Pest Management Board. United States Army. Retrieved 24 October 2013.
- Young, B. A. (2004). "The buccal buckle: The functional morphology of venom spitting in cobras". Journal of Experimental Biology 207 (20): 3483. doi:10.1242/jeb.01170.
- Rasmussen, Sara; Young, B.; Krimm, Heather (1995). "On the 'spitting' behaviour in cobras (Serpentes: Elapidae)". Journal of Zoology 237: 27. doi:10.1111/j.1469-7998.1995.tb02743.x.
- "Naja samarensis". University of Adelaide.
- Dart, Richard C (2003). Medical Toxicology. USA: Lippincott Williams & Wilkins; 3 edition. p. 1569. ISBN 0-7817-2845-2.
- Wüster, W.; Thorpe, R. S. (1991). "Asiatic cobras: Systematics and snakebite". Experientia 47 (2): 205–9. doi:10.1007/BF01945429. PMID 2001726.
- Williams, Jensen, O'Shea, David J., Simon D., Mark. "Snake Management in Cambodia". Retrieved 23 October 2013.
- Marais, Johan (2004). A Complete Guide to the Snakes of Southern Africa. Cape Town, South Africa: Struik Nature. ISBN 1-86872-932-X.[page needed]
- Fryklund, Linda; Eaker, David (1975). "Complete covalent structure of a cardiotoxin from the venom of Naja nigricollis (African black-necked spitting cobra)". Biochemistry 14 (13): 2865–71. doi:10.1021/bi00684a012. PMID 1148181.
- Warrell, David A (2010). "Snake bite". The Lancet 375 (9708): 77. doi:10.1016/S0140-6736(09)61754-2.
- Tilbury, CR. "Observations on the bite of the Mozambique spitting cobra". Retrieved 23 October 2013.
- "Naja katiensis". Clinical Toxinology Resource. University of Adelaide. Retrieved 24 October 2013.
- Leong, Poh Kuan; Sim, Si Mui; Fung, Shin Yee; Sumana, Khomvilai; Sitprija, Visith; Tan, Nget Hong (2012). "Cross Neutralization of Afro-Asian Cobra and Asian Krait Venoms by a Thai Polyvalent Snake Antivenom (Neuro Polyvalent Snake Antivenom)". In De Silva, Janaka. PLoS Neglected Tropical Diseases 6 (6): e1672. doi:10.1371/journal.pntd.0001672. PMC 3367981. PMID 22679522.
- Trape, J.F.; Pison, G.; Guyavarch, E.; Mane, Y. (2001). "High mortality from snakebite in south-eastern Senegal". Transactions of the Royal Society of Tropical Medicine and Hygiene 95 (4): 420–3. doi:10.1016/S0035-9203(01)90202-0. PMID 11579888.
- S. Hunter (2000). "Venomous Reptiles".
- "The Natural History and Captive Care of the Rinkhals spitting cobra". Retrieved 23 October 2013.
- Widgerow, A.D.; Ritz, M.; Song, C. (1994). "Load cycling closure of fasciotomies following puff adder bite". European Journal of Plastic Surgery 17. doi:10.1007/BF00176504.
- Rainer, PP; Kaufmann, P; Smolle-Juettner, FM; Krejs, GJ (2010). "Case report: Hyperbaric oxygen in the treatment of puff adder (Bitis arietans) bite". Undersea & hyperbaric medicine 37 (6): 395–8. PMID 21226389.
- U.S. Navy. 1991. Venomous Snakes of the World. US Govt. New York: Dover Publications Inc. 203 pp. ISBN 0-486-26629-X.[page needed]
- Firefighter Dies After Bite From Pet Snake at channelcincinnati.com. Accessed 24 October 2013.
- Miami-Dade Fire Rescue Venom Response Unit at VenomousReptiles.org. Accessed 24 October 2013.
- The Australian venom research unit (August 25, 2007). "Which snakes are the most venomous?". University of Melbourne. Retrieved October 24, 2013.
- Shea, GM (1999). "The distribution and identification of dangerously venomous Australian terrestrial snakes". Australian Veterinary Journal 77 (12): 791–8. doi:10.1111/j.1751-0813.1999.tb12947.x. PMID 10685181.
- Sutherland, SK (1983). Australian Animal Toxins. OUP Australia and New Zealand. ISBN 019554367X.
- "Australian Mulga Snakes". Clinical Toxinology Resource. University of Adelaide. Retrieved 24 October 2013.
- "University of Adelaide Clinical Toxinology Resources". "Mortality rate:30-40%"
- "University of Adelaide Clinical Toxinology Resources". "Mortality rate:<1%"
- Cheng, David. "Brown Snake Envenomation". Retrieved 24 October 2013.
- Venom Supplies Pty Ltd. "Brown Snakes".
- Toxinology Department, Women's & Children's Hospital, Adelaide, Australia. "CSL Antivenom Handbook - Brown Snake Antivenom".
- "University of Adelaide Clinical Toxinology Resources". "Mortality rate:10-20%"
- Weinstein and Smith (1990)
- Norris R. 2004. Venom Poisoning in North American Reptiles. In Campbell JA, Lamar WW. 2004. The Venomous Reptiles of the Western Hemisphere. Comstock Publishing Associates, Ithaca and London. 870 pp. 1500 plates. ISBN 0-8014-4141-2.[page needed]
- Calvete, Juan J.; Pérez, Alicia; Lomonte, Bruno; Sánchez, Elda E.; Sanz, Libia (2012). "Snake Venomics ofCrotalus tigris: The Minimalist Toxin Arsenal of the Deadliest Neartic Rattlesnake Venom. Evolutionary Clues for Generating a Pan-Specific Antivenom against Crotalid Type II Venoms". Journal of Proteome Research 11 (2): 1382–90. doi:10.1021/pr201021d. PMC 3272105. PMID 22181673.
- "University of Adelaide Clinical Toxinology Resources".
- Laurence Monroe Klauber (1997). Rattlesnakes: Their Habits, Life Histories, and Influence on Mankind (2nd ed.). University of California Press. ISBN 978-0-520-21056-1.[page needed]
- d'Império Lima, Maria Regina; Dos Santos, Maria; Tambourgi, Denise Vilarinho; Marques, Thaís; Da Silva, Wilmar; Kipnis, Thereza (1991). "Susceptibility of different strains of mice to South American rattlesnake (Crotalus durissus terrificus) venom: Correlation between lethal effect and creatine kinase release". Toxicon 29 (6): 783–6. doi:10.1016/0041-0101(91)90070-8. PMID 1926179.
- Furtado, M. F. D.; Santos, M. C.; Kamiguti, A. S. (2003). "Age-related biological activity of South American rattlesnake (Crotalus durissus terrificus) venom". Journal of Venomous Animals and Toxins including Tropical Diseases 9 (2): 186. doi:10.1590/S1678-91992003000200005.
- "Venomous and Poisonous Animals Biology & Clinical Management". VAPAGuide. Biomedical database. Retrieved 25 October 2013.
- "Mojave Green snake bites 6-year-old California boy, 42 vials of antivenom needed", Jaslow, Ryan, CBS News, July 10th, 2012, http://www.cbsnews.com/8301-504763_162-57469802-10391704/mojave-green-snake-bites-6-year-old-california-boy-42-vials-of-antivenom-needed/
- Hendon, R.A., A.L. Bieber. 1982. Presynaptic toxins from rattlesnake venoms. In: Tu, A. (ed) Rattlesnake Venoms, Their Actions and Treatment. New York: Marcel Dekker, Inc.[page needed]
- Norris RA. 2004. Venom poisoning by North American reptiles. In Campbell JA, Lamar WW. 2004. The Venomous Reptiles of the Western Hemisphere. Comstock Publishing Associates, Ithaca and London. 870 pp. 1500 plates. ISBN 0-8014-4141-2.[page needed]
- Glenn, J.L., R.C.Straight. 1982. The rattlesnakes and their venom yield and lethal toxicity. In: Tu, A. (ed) Rattlesnake Venoms, Their Actions and Treatment. New York: Marcel Dekker, Inc.[page needed]
- Aird, Steven D.; Kaiser, Ivan I.; Lewis, Randolph V.; Kruggel, William G. (1985). "Rattlesnake presynaptic neurotoxins: Primary structure and evolutionary origin of the acidic subunit". Biochemistry 24 (25): 7054–8. doi:10.1021/bi00346a005. PMID 4084559.
- Powell, R.L. 2003. Evolutionary Genetics of Mojave Toxin Among Selected Rattlesnake Species (Squamata: Crotalinae). Unpublished PhD dissertation. El Paso: University of Texas.[page needed]
- Glenn, James L.; Straight, Richard C.; Wolfe, Martha C.; Hardy, David L. (1983). "Geographical variation in Crotalus scutulatus scutulatus (Mojave rattlesnake) venom properties". Toxicon 21 (1): 119–30. doi:10.1016/0041-0101(83)90055-7. PMID 6342208.
- "Calloselasma rhodostoma". Clinical Toxinology Resource. University of Adelaide. Retrieved 3 November 2013.
- Warrell, DA (1986). Natural toxins : animal, plant, and microbial. Clarendon Press; Oxford University Press. pp. 25–45. ISBN 0198541732.
- "Deinagkistrodon acutus". Armed Forces Pest Management Board. United States Army. Retrieved 3 November 2013.
- "Deinagkistrodon acutus". Clinical Toxinology Resource. University of Adelaide. Retrieved 3 November 2013.
- Mehrtens JM. 1987. Living Snakes of the World in Color. New York: Sterling Publishers. 480 pp. ISBN 0-8069-6460-X.
- Schneemann, M.; R. Cathomas, S.T. Laidlaw, A.M. El Nahas, R.D.G. Theakston, and D.A. Warrell (2004). "Life-threatening envenoming by the Saharan horned viper (Cerastes cerastes) causing micro-angiopathic haemolysis, coagulopathy and acute renal failure: clinical cases and review". QJM: an International Journal of Medicine 97 (11): 717–27. doi:10.1093/qjmed/hch118. PMID 15496528. Retrieved 2009-09-04. "This echoed the opinion of the Egyptian physicians who wrote the earliest known account of the treatment of snake bite, the Brooklyn Museum Papyri, dating perhaps from 2200 BC. They regarded bites by horned vipers 'fy' as non-lethal, as the victims could be saved."
- Anil, Aggrawal (2004). "Homicide with snakes: A distinct possibility and its medicolegal ramifications". Anil Aggrawal's Internet Journal of Forensic Medicine and Toxicology 4 (2).
- Crawford, Amy (April 1, 2007). "Who Was Cleopatra? Mythology, propaganda, Liz Taylor and the real Queen of the Nile". Smithsonian.com. Retrieved 4 September 2009.
- Warrell, D.A. (2009). "Commissioned article: management of exotic snakebites". QJM: an International Journal of Medicine 102 (9): 593–601. doi:10.1093/qjmed/hcp075. PMID 19535618.
- Straight, Richard C.; James L. Glenn (1994). "Human fatalities caused by venomous animals in Utah, 1900–90". Great Basin Naturalist 53 (4): 390–4. Retrieved 2009-09-04. "A third unusual death was a tragic fatality (1987), recorded as a homicide, which resulted when a large rattlesnake (G. v. lutosus) bit a 22-month-old girl after the snake had been placed around her neck (Washington County). The child died in approximately 5 h."
- Strubel, T.; A. Birkhofer, F. Eyer, K.D. Werber, H. Förstl (2008). "Suizidversuch durch Schlangenbiss: Kasuistik und Literaturübersicht" [Attempted suicide by snake bite: Case report and literature survey]. Der Nervenarzt (in German) 79 (5): 604–6. doi:10.1007/s00115-008-2431-4. PMID 18365165. "Ein etwa 20-jähriger Arbeiter wurde nach dem Biss seiner Puffotter (Bitis arietans) in die Hand auf die toxikologische Intensivstation aufgenommen. Zunächst berichtet der Patient, dass es beim „Melken“ der Giftschlange zu dem Biss gekommen sei, erst im weiteren Verlauf räumt er einen Suizidversuch ein. Als Gründe werden Einsamkeit angeführt sowie unerträgliche Schmerzen im Penis."
- Greene, Harry W. (1997). Snakes: The Evolution of Mystery in Nature. Berkeley, CA: University of California Press. ISBN 978-0-520-20014-2.
- Stephen P., Mackessy, ed. (2010). Handbook of Venoms and Toxins of Reptiles (2nd ed.). Boca Raton, FL: CRC Press. ISBN 978-0-8493-9165-1.
- Valenta, Jiri (2010). Venomous Snakes: Envenoming, Therapy (2nd ed.). Hauppauge, NY: Nova Science Publishers. ISBN 978-1-60876-618-5.
- Campbell, Jonathan A.; William W. Lamar (2004). The Venomous Reptiles of the Western Hemisphere. Ithaca, NY: Cornell University Press. ISBN 978-0-8014-4141-7
- Spawls, Stephen; Bill Branch (1995). The Dangerous Snakes of Africa: Natural History, Species Directory, Venoms and Snakebite. Sanibel Island, FL: Ralph Curtis Publishing. ISBN 978-0-88359-029-4
- Sullivan JB, Wingert WA, Norris Jr RL. (1995). North American Venomous Reptile Bites. Wilderness Medicine: Management of Wilderness and Environmental Emergencies. 3: 680–709.
- Thorpe, Roger S.; Wolfgang Wüster, Anita Malhotra (1996). Venomous Snakes: Ecology, Evolution, and Snakebite'. Oxford, England: Oxford University Press. ISBN 978-0-19-854986-4