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Snake Bites


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Animal Bites
Each year in the United States, between 1 and 2 million animal-bite wounds are sustained; the vast majority are inflicted by pet dogs and cats, which number more than 100 million. Other bite wounds are a consequence of encounters with animals in the wild or in occupational settings. While many of these wounds require minimal or no therapy, a significant number result in infection, which may be life-threatening. The microbiology of bite-wound infections in general reflects the oropharyngeal flora of the biting animal, although organisms from the soil, the skin of the animal and victim, and the animal's feces may also be involved.

Venomous Or Poisonous : What Is The Difference?
Poison is a broad term for any substance that irritates or kills . It is also used in a restricted sense for any harmful substance that enters the body by absorption through the skin or through eating or breathing . Poison ivy , for instance , irritates the skin ; poison dartfrogs kill predators that swallow them. Such plants and animals are called poisonous . Venom is a poison that one animal-whether a spider , a snake , or a bee-injects into another animal . Thus a snake or scorpion that injects a poison by biting or stinging is called venomous .

What Is Venom?
In snakes , venom is an evolutionary adaptation to immobilize prey , secondarily used in defense . Venoms are highly toxic secretions produced in special oral glands . Because these oral glands are related to the salivary glands of other vertebrates , venom can be considered a modified saliva . Venom immobilizes the prey when injected into its body , and in some cases initiates the digestive process by beginning the breakdown of the prey’s tissues .

Each species has a unique venom with different components and different amounts of toxic and nontoxic compounds . The more closely related two species of snakes , the more similar their venoms . It is probable that venoms and venom mechanisms evolved several times among snakes , increasing the diversity of venom chemistry and of the venom apparatus .

The chemistry of snake venoms is complicated . Venoms are at least 90% protein (by dry weight) , and most of the proteins in venoms are enzymes . About twenty-five different enzymes have been isolated from snake venoms , ten of which occur in the venoms of most snakes . Proteolytic enzymes , phospholipases , and hyaluronidases are the most common types . Proteolytic enzymes catalyze the breakdown of tissue proteins . Phospholipases , which occur in almost all snakes , vary from mildly toxic to highly destructive of musculature and nerves . The hyaluronidases dissolve intercellular materials and speed the spread of venom through the prey’s tissue . Other enzymes include collagenases , which occur in the venom of vipers and pitvipers and promote the breakdown of a key structural componenet of connective tissues (the protein collagen) ; ribonucleases , deoxyribonucleases , nucleotidases , amino acid oxidases , lactate dehydrogenases , and acidic and basic phosphatases all disrupt normal cellular function , causing the collapse of cell metabolism , shock , and death .

Not all toxic chemical compounds in snake venoms are enzymes . Polypeptide toxins , glycoproteins , and low-molecular-weight compounds are also present in mambas and colubrids . The roles of the other components of venom are largely unknown .

Every snake’s venom contains more than one toxin , and in combination the toxins have a more potent effect than the sum of their individual effects . In general , venoms are described as either neurotoxic (affecting the nervous system) or hemotoxic (affecting the circulatory system) , although the venoms of many snakes contain both neurotoxic and hemotoxic components .

Venom componenets are broadly categorized by how they work to disrupt normal function .

Enxymes - found in all snake venoms-spur on physiologically disruptive or destructive process .
Proteolysins - found mostly in viper and pitviper venom-dissolve cells and tissue at the bite site , causing local pain and swelling .
Cardiotoxins - associated mostly with elapids ad vipers-have variable effects ; some depolarize cardiac muscles and alter heart contraction , causing heart failure .
Hemorrhagins - occurring in the venom of vipers , pitvipers , and the king cobra-destroy capillary walls , causing hemorrhages near and distant from the bite .
Coagulation - retarding compounds-found in some elapids-prevent blood clotting .
Thromboses - which some vipers have-coagulate blood and foster clot formation throughout the circulatory system .
Hemolysis - which are in the venom of elapids , vipers and pitvipers-destroy red blood cells .
Cytolysins - components of viper and pitviper venom-destroy white blood cells .
Neurotoxins - found in elapids , vipers , tropical rattlesnakes , and some North American Mojave rattlesnakes-block the transmission of nerve impulses to muscles , especially those associated with the diaphragm and breathing .

Venom composition can vary among individuals of the same species , and even in the same litter , but variation is greater among geographically different populations . For example , Mojave rattlesnakes (Crotalus scutulatus) from eastern Arizona and adjacent New Mexico have a special neurotoxin known as Mojave toxin , but their venom lacks hemorrhagic and some proteolytic properties . Venom from Mojave rattlesnakes of central Arizona lacks the Mojave but has strong hemorrhagic and proteolytic properties . Where the two populations overlap , individual rattlesnakes have a venom with intermediate properties .

Venom toxicity may also vary over time in the same individual . Generally speaking , the venom of newborn and small juvenile snakes appears to be more potent than that adults of the same species . Also , a bite from a snake that has not fed recently , such as one that has just emerged from hibernation , is more dangerous than that of one that has recently fed , because it has more venom to inject . Venom glands must replace venom lost with each strike-bite , and full replacement takes time .

Chemical Components Of Snake Venoms

A . Organic Components with Role , or Potential Role , in Toxicity

Toxic high-molecular-weight compounds

Compound : Peptide bradykinin potentiators .
Action : Greatly enhance one of the body’s natural responses to injury (dilation and increased permeabilty of blood vessels , stimulation of pain receptors , and contraction of some smooth muscles) , thereby enhancing diffusion of venom in the bloodstream , increasing bleeding , and thwarting the ability to flee . Taxon with the compound in its venom : Bothrops , Crotalus .

Compound : Polypeptide toxins .
Action : Directly disrupt nerve-impulse transmission , usually causing heart or respiratory failure Taxon with the compound in its venom : Mambas and colubrids : Naja (cobratoxin) , Hydrophis ( Hydrophitoxin) , Laticauda (lactocotoxin) , Pelamis (pelamitoxin) , Naja (cardiotoxin) , Crotalus scutulatus (Mojavetoxin) , Bungarus (bungarotoxin) , Crotalus (crotactin) , Vipera (viperptoxin) .

Compound : Proteolytic enzymes .
Action : Catalyze the breakdown of structural components of tissues . Taxon with the compound in its venom : All venomous species .

Compound : Hyluronidases .
Action : Catalyze reactions that break mucopolysaccharide links in connective tissues , thereby enhancing diffusion of venom . Taxon with the compound in its venom : Several genera .

Compound : Proteases .
Action : Catalyze reactions that disrupt protein peptide bonds in tissues , causing blood-vessel wall damage and hemorrhaging and muscle-fiber deterioration . Taxon with the compound in its venom : Vipers , pitvipers .

Compound : Phospholipases .
Action : Catalyzes reactions that harm musculature and nerves . Taxon with the compound in its venom : Almost all venomous species (e . g . , phospholipase A , in Agkistrodon , Bothrops , Crotalus , Naja , Vipera)

Compound : Thrombinlike enzymes .
Action : Inhibit blood clotting . Taxon with the compound in its venom : Vipers , pitvipers , a few elapids (but rare)

Compound : Nerve growth factor (an enzyme) .
Action : Stimulates the growth of nerve cells . Taxon with the compound in its venom : Agkistrodon , Crotalus .

Compound : Other enzymes : ribonucleases , deoxyribonucleases , nucleotidases , amino acid oxidases , lactate dehydrogenases , acidic and basic phosphatases .
Action : Disrupt normal cellular function , causing death of the affected cells . Taxon with the compound in its venom : Vipers and elapids (occurrences vary) .

Compound : Glycoproteins .
Action : Suppress normal immune response of tissues through anticomplementary reactions . Taxon with the compound in its venom : Some vipers .

Potentially toxic low-molecular-weight compounds

Compound : Nucleotides (amino acids) .
Action : Not known . Taxon with the compound in its venom : Bitis , Dendroaspis , Notechis (adenosine) , Bungarus (guanosine) .

Compound : Biogenic amines .
Action : Disrupt normal transmission of nerve impulses and other types of signalling between cells . Taxon with the compound in its venom : Agkistrodon , Crotalus (catecholamine) , Trimeresurus (histamine) Agkistrodon , Crotalus (seratonin) , Trimeresurus (spermine) .

Compound : Acectylcholine .
Action : Disrupts normal transmission of nerve impulses , causing heart and respiratory failure . Taxon with the compound in its venom : Several genera .

B . Other Components (Organic and Ignorganic)

Nontoxic organic components and organic components with unclear roles :
Carbohydrates : Neutral sugars , Amino sugars , Sialic acid .
Lipids : Cholesterol , Monoglycerides , Diglycerides , Triglycerides , Phospholipids .

Inorganic ions (which activate and deactivate enzymes) :
Macrocomponents : Calcium , Chlorine , Copper, Iron , Magnesium , Manganese , Nickel , Phosphate , Potassium , Sodium , Sulfate , Zinc .
Microcomponents : Bismuth , Gold , Molybdnum , Palladium , Platinum , Selenium , Silver . Water .

How Many Snakes Are Venomous ?
Four families of snakes (Atractaspididae , Colubridae , Elapidae , and Viperidae) include species dangerous to humans , a total of roughly 450 species or about 19% of all snake species . In none of these families are all species lethal to humans , although all atractaspidine , elapid , and viperid snakes are venomous . Generally speaking , the venoms most dangerous to humans are those of snakes that specialize on warm-blooded prey . Because human physiology is similar to that of prey , the venoms react similarly in humans .But humans are also sensitive to snake venoms adapted to kill prey other than birds or mammals .

Danger may vary with the volume of venom injected . Even a mildly toxic venom is lethal if the snake injects enough of it . Conversely , a snake with a highly toxic venom is not dangerous if it is small and incapable of breaking the skin , or if it does not bite in defense . The Sonoran coralsnakes (Micruroides euryxantus) have small mouths and usually do not break the skin when they bite . Some species have venom-delivery systems that do not permit them to deliver venom efficiently to large animals . Other species rarely come in contact with humans .

In the large family Colubridae , about one-quarter of the species (over 600 species) have fangs , or at least enlarged and grooved maxillary teeth . But only four have caused human fatalities : the African boomslang (Dispholidus typus) , Oriental tigersnake (Rhabdophis tigrina) , African birdsnake (Thelotornis kirtlandii) , and Peruvian gray falseviper (Tachymenis peruviana) . In the other three families , all species have fangs and should be considered potentially dangerous , though some are small or have venoms with weak effects on humans .

The salivas of some non-venomous colubrids have , in rare instances , caused mild to moderate poisoning in humans . In the United States , people have had reactions to bites of the black-striped snake (Coniophanes imperialis) , ringneck snake (Diadophis punctatus) , western hognose snake (Heterodon nasicus) , cat-eyed snake (Leptodeira septentrionalis) , Mexican vinesnake (Oxybelis aeneus) , western terrestrial gartersnake ( Thamnophis elegans) , common gartersnake (T . sirtalis) , and lyre snake (Trimorphodon biscutatus) . None of these snakes’ venom-delivery systems operates efficiently on humans ; most must chew for the venom to enter the wound . Symptoms of envenomation appear in fewer than 1% of gartersnake bites , though such bites are common among people who handle these snakes . It is possible that the salivas of all colubrids have a toxic component , and that some susceptible than others .

Proportions of venomous and nonvenomous snakes worldwide . Venomous snakes are here defined as those dangerous animals :

Nonvenomous snakes:
Nonvenomous colubrids : 64%
Blindsnakes : 12%
Boas and related species : 5%

Venomous snakes:
Vipers : 8%
Cobras and related species : 10%
Venomous colubrids : 1%

Where Are Venomous Snakes Found ?
Venomous snakes inhabit all the continents except Antarctica . They also live on islands off the coasts of these continents and even on some remote oceanic islands . The snake fauna of each continent is different , and different venomous groups are dominant in each region .

In the Americas , pitvipers (Crotalinae) predominate ; many coralsnakes (Elapinae) are present in the tropical areas , but true vipers (Viperinae) are absent . The Unites States has fifteen species of rattlesnakes (Crotalus , Sistrurus) ; two moccasins , the copperhead and cottonmouth (Akistrodon) ; two coralsnakes (Micruroides , Micrurus) ; and the yellow-bellied seasnake (Pelamis , Hydrophiinae) , a rare visitor to the southern California coast and the Hawaiian Islands . Venomous snakes have been recorded in every state except Alaska .

The venomous snake fauna of Latin America is dominated by pitvipers and coralsnakes ; a seasnake and one potentially dangerous colubrid , the Peruvian falseviper (Tachymenis peruviana) , are also present .

Europe and Middle East have the fewest species of venomous snakes , the majority of which are true vipers (Viperinae) . One species , the common European viper (Vipera berus) , has a range extending from southern England eastward all the way to the Pacific coast of Russia .

Africa’s rich venomous snake fauna is dominated by true vipers (ncluding arboreal vipers , desert vipers , nightadders , puffadders , and saw-scaled vipers) , terrestrial elapids , (cobras and mambas) , molevipers (Atractaspidinae) , and two of the world’s four deadliest colubrids , the boomslang (Dispholidus typus) and the African birdsnake (Thelotornis kirtlandii) .

Asia is home to many pitvipers , including more than thirty species of Trimeresurus , abundant terrestrial elapids (cobras , the king cobra , kraits and others) , several marine elapids (seasnakes , Hydrophiinae , and sea kraits , Laticaudinae) , a few true vipers ,and Fea’s viper (Azemiopinae : Azemiops feac ) . One colubrid capable of fatal bites , the oriental tigersnake (Rhabdophis tigrina) , occurs in Japan and much of China . The red-necked keelback (Rhabdopis subminiatus) is also potentially dangerous .

Occurrences of venomous snake species , by the world’s major geographic regions

Family or Subfamily :
Colubridae : Latin America - 1 , Africa - 2 , Asia - 1
Atractaspidinae : Europe and the Middle East - 2 , Africa - 16
Acanthophiinae : Australia and New Guinea - 94 , Pacific oceanic islands - 4
Elapinae : North America - 2 , Latin America - 54 , Europe and the Middle East - 3 , Asia - 34
Hydrophiinae : North America - 1 , Latin America - 1 , Europe and the Middle East - 6 , Africa - 1 , Asia - 33 , Australia and New Guinea - 31 , Pacific oceanic islands - 4
Laticaudinae : Asia - 9 , Australia and New Guinea - 2 , Pacific oceanic islands - 3
Azemiopinae : Asia - 1
Viperinae : Europe and the Middle East - 16 , Africa - 31 , Asia - 6
Crotalinae : North America - 17 , Latin America - 89 , Europe and the Middle East - 1 , Asia - 44
Total : North America - 20 , Latin America - 145 , Europe and the Middle East - 28 , Africa - 75 , Asia - 128 , Australia and New Guinea - 127 , Pacific oceanic islands - 11

Which Snakes Have The Most Potent Venom ?
This question can be answered in two ways , yielding different answers . One way estimates lethality based on the potential amount of venom that a snake might deliver with a single bite . However , no snake empties its venom glands with a single bite , and occasionally a snake delivers a “dry” bite . The other way of estimating lethality is to rest a venom’s killing power on mice .

The mouse-test produce estimates the strength of a venom by injecting measured amounts into a large sample of mice and recording the dosage of venom that kills 50% of the mice within twenty-four hours .This dosage , called the LD50 (LD standing for “lethal dose”) , is measured in milligrams of venom per kilogram of mouse . The venoms of many species of snakes have been characterized in this way . For obvious reasons , the lethal dose for humans have not been determined .

Assuming that mice and humans have similar susceptibilities to the venom of each species , that of the hook-nosed seasnake (Enhydrina schistosa) is the most lethal venom tested so far ; it is estimated that only 1.5 milligrams of its venom will kill a human being . The hook-nosed seasnake ranges from the Persian Gulf and the waters of southern Asia to the northern coast of Australia . Russel’s viper (Vipera russelii) of southern Asia and the inland taipan (Oxyuranus microlepidotus) of Australia are nearly as deadly . Of course , these comparisons are only estimates of the venom’s toxity in humans . Also the LD50 values are mixed data , derived from different studies using different sites of venom injection (intramuscular , intraperitoneal , subcutaneous) . Subcunateus injections are typically less lethal than intraperitoneal ones , and may require two to five times the venom dosage to obtain the same kill rate .

Estimates of yield require forcibly draining (milking) all venom from a snake’s venom glands , drying the sample , and then weighing the powdery residue . This milking procedure is performed on a sample of adult snakes of a single species , and the average yield is determined . King cobras (Ophiophagus hannah) , Gaboon vipers (Bitis Gabonica) , eastern diamondback rattlesnakes (Crotalus adamanteus) , and bushmasters (Lachesis muta) have the capacity to deliver the largest volume of venom in a single bite . The toxicity of their venoms differs , but the bites of all four are highly dangerous even if they inject only one-quarter of their venom supply . Approximately 100 milligrams of venom from an eastern diamondback rattlesnake kills an adult man , and large diamondbacks store as much as 850 milligrams in their venom glands !

The deadliness of a venom varies with the prey . Even if we confine our attention to humans-though humans are not the prey of any snake-many factors besides yield and LD50 values influence the seriousness of a bite . In humans , the factors include the individual’s health , size , age , and psychological state . Factors associated with the nature of the bite include penetration of one or both fangs , amount of venom injected , location of the bite , and proximity to major blood vessels . The health of the snake and the interval since it last used its venom mechanism also enter in . These multiple variables make every bite unique . Depending on circumstances , the bite of a “mildly” venomous snake may be life-threatening and that of a “strongly” venomous snake may not

Toxicity of Selected Snake Venoms

Species : Hook-nosed seasnake (Enhydrina schistosa) Mouse LD50 (mg/kg) : 0.02 Venom yield per snake (mg) : 7.79.0

Species : Russel’s viper (Vipera russelii) Mouse LD50 (mg/kg) : 0.03 Venom yield per snake (mg) : 130.0-250.0

Species : Inland taipan (Oxyuranus microlepidotus) Mouse LD50 (mg/kg) : 0.03 Venom yield per snake (mg) : 44.0-110.0

Species : Dubois’s reef saesnake (Aipysurus duboisii) Mouse LD50 (mg/kg) : 0.04 Venom yield per snake (mg) : 0.07

Species : Eastern brownsnake (Pseudechis textilis) Mouse LD50 (mg/kg) : 0.05 Venom yield per snake (mg) : 2.0-67.0

Species : Black mamba (Dendroaspis polylepis) Mouse LD50 (mg/kg) : 0.05 Venom yield per snake (mg) : 50.0-100.0

Species : Tiger rattlesnake (Crotalus tigris) Mouse LD50 (mg/kg) : 0.06 Venom yield per snake (mg) : 6.0-11.0

Species : Boomslang (Dispholidus typus) Mouse LD50 (mg/kg) : 0.07 Venom yield per snake (mg) : 1.6-8.0

Species : Yellow-bellied seasnake (Pelamis platurus) Mouse LD50 (mg/kg) : 0.07 Venom yield per snake (mg) : 1.0-4.0

Species : Common Indian krait (Bungarus caeruleus) Mouse LD50 (mg/kg) : 0.09 Venom yield per snake (mg) : 8.0-20.0

Species : Desert horned viper (Cerastes cerastes) Mouse LD50 (mg/kg) : 0.10 Venom yield per snake (mg) : 20.0-45.0

Species : Common taipan (Oxyuranus scutellatus) Mouse LD50 (mg/kg) : 0.10 Venom yield per snake (mg) : 120.0-400.0

Species : Common European viper (Vipera berus) Mouse LD50 (mg/kg) : 0.11 Venom yield per snake (mg) : 10.0-18.0

Species : Tigersnake (Notechis scutatus) Mouse LD50 (mg/kg) : 0.12 Venom yield per snake (mg) : 35.0-189.0

Species : Forest cobra (Naja melanoleuca) Mouse LD50 (mg/kg) : 0.12 Venom yield per snake (mg) : ?

Species : Puffadder (Bitis arietans) Mouse LD50 (mg/kg) : 0.14 Venom yield per snake (mg) : 100.0-300.0

Species : Gaboon viper (Bitis gabonica) Mouse LD50 (mg/kg) : 0.14 Venom yield per snake (mg) : 350.0-600.0

Species : Seakrait (Laticauda laticaudata) Mouse LD50 (mg/kg) : 0.16 Venom yield per snake (mg) : ?

Species : Neotropical rattlesnake (Crotalus durissus) Mouse LD50 (mg/kg) : 0.17 Venom yield per snake (mg) : 20.0-100.0

Species : Mojave rattlesnake (Crotalus sculutulus) Mouse LD50 (mg/kg) : 0.18 Venom yield per snake (mg) : 50.0-150

Species : Egyptian cobra (Naja haje) Mouse LD50 (mg/kg) : 0.19 Venom yield per snake (mg) : 175.0-300.0

Species : Harlequin coralsnake (Micrurus fulvius) Mouse LD50 (mg/kg) : 0.20 Venom yield per snake (mg) : 3.0-5.0

Species : Ottoman viper (Vipera xanthina) Mouse LD50 (mg/kg) : 0.20 Venom yield per snake (mg) : 8.0-18.0

Species : Erabu seakrait (Laticauda semifasciata) Mouse LD50 (mg/kg) : 0.21 Venom yield per snake (mg) : 2.0-14.0

Species : African birdsnake (Thelotornis kirtlandii) Mouse LD50 (mg/kg) : 0.21 Venom yield per snake (mg) : ?

Species : Ringhal (Hemachatus haemachatus) Mouse LD50 (mg/kg) : 0.22 Venom yield per snake (mg) : 80.0-120.0

Species : Olive seasnake (Aipysurus laevis) Mouse LD50 (mg/kg) : 0.22 Venom yield per snake (mg) : 10.0-33.0

Species : Black-necked cobra (Naja nigricollis) Mouse LD50 (mg/kg) : 0.23 Venom yield per snake (mg) : 150.0-350.0

Species : Saw-scaled viper (Echis carinatus) Mouse LD50 (mg/kg) : 0.24 Venom yield per snake (mg) : 5.0-48.0

Species : Common mamba (Dendroaspis angusticeps) Mouse LD50 (mg/kg) : 0.26 Venom yield per snake (mg) : 60.0-95.0

Species : Bar-beelied seasnake (Hydrophis elegans) Mouse LD50 (mg/kg) : 0.27 Venom yield per snake (mg) : 9.0-24.0

Species : Spectacled cobra (Naja naja) Mouse LD50 (mg/kg) : 0.28 Venom yield per snake (mg) : 150.0-600.0

Species : Annulated seasnake (Hydrophis cyanocinctus) Mouse LD50 (mg/kg) : 0.35 Venom yield per snake (mg) : 5.0-8.0

Species : Fer-de-lance (Bothrops atrox) Mouse LD50 (mg/kg) : 0.35 Venom yield per snake (mg) : 100.0-200.0

Species : White-lipped tree pitviper (Trimeresurus albolabris) Mouse LD50 (mg/kg) : 0.37 Venom yield per snake (mg) : 8.0-15.0

Species : Hundred-pace pitviper (Deinagkistrodon acutus) Mouse LD50 (mg/kg) : 0.38 Venom yield per snake (mg) : ?

Species : Central American coralsnake (Micrurus nigrocinctus) Mouse LD50 (mg/kg) : 0.40 Venom yield per snake (mg) : 5.0-8.0

Species : Northern moleviper (Atractaspis microlepidota) Mouse LD50 (mg/kg) : ? Venom yield per snake (mg) : 5.0-10.0

Species : Yellow-lipped seakrait (Laticauda colubrina) Mouse LD50 (mg/kg) : 0.40 Venom yield per snake (mg) : ?

Species : Jararacussu (Bothrobs jararacussu) Mouse LD50 (mg/kg) : 0.46 Venom yield per snake (mg) : 200.0-321.0

Species : Nose-horned viper (Vipera ammodytes) Mouse LD50 (mg/kg) : 0.48 Venom yield per snake (mg) : ?

Species : Common blacksnake (Pseudechis porphyriacus) Mouse LD50 (mg/kg) : 0.50 Venom yield per snake (mg) : 30.0-50.0

Species : Deathadder (Acanthophis antarcticus) Mouse LD50 (mg/kg) : 0.60 Venom yield per snake (mg) : 70.0-236.0

Species : Hardwicke’s seasnake (Lapemis curtus) Mouse LD50 (mg/kg) : 0.62 Venom yield per snake (mg) : 2.4-15.0

Species : Southern coralsnake (Micrurus frontalis) Mouse LD50 (mg/kg) : 0.63 Venom yield per snake (mg) : 20.0-30.0

Species : Blunt-nosed viper (Viperina lebetina) Mouse LD50 (mg/kg) : 0.64 Venom yield per snake (mg) : 12.0-150.0

Species : Wagler’s pitviper (Tropidolaemus wagleri) Mouse LD50 (mg/kg) : 0.75 Venom yield per snake (mg) : 65.0-90.0

Species : Cantil (Agkistrodon bilineatus) Mouse LD50 (mg/kg) : 0.80 Venom yield per snake (mg) : 50.0-95.0

Species : King cobra (Ophiophagus hannah) Mouse LD50 (mg/kg) : 0.90 Venom yield per snake (mg) : 350.0-500.0

Species : Twin-spoted rattlesnake (Crotalus pricei) Mouse LD50 (mg/kg) : 0.95 Venom yield per snake (mg) : 4.0-8.0

Species : European asp (Vipera aspis) Mouse LD50 (mg/kg) : 1.00 Venom yield per snake (mg) : 9.0-10.0

Species : Western rattlesnake (Crotalus viridis) Mouse LD50 (mg/kg) : 1.01 Venom yield per snake (mg) : 35.0-250.0

Species : Terciopelo (Bothrops asper) Mouse LD50 (mg/kg) : 1.10 Venom yield per snake (mg) : 100.0.-310.0

Species : Jararaca (Bothrops jararaca) Mouse LD50 (mg/kg) : 1.10 Venom yield per snake (mg) : 40.0-70.0

Species : Banded krait (Bungarus fasciatus) Mouse LD50 (mg/kg) : 1.20. Venom yield per snake (mg) : 20.0-114.0

Species : Mamushi (Agkistrodon blomhffii) Mouse LD50 (mg/kg) : 1.20 Venom yield per snake (mg) : 1.0-7.0

Species : Eastern diamondback rattlesnake (Crotalus adamentus) Mouse LD50 (mg/kg) : 1.20 Venom yield per snake (mg) : 200.0-850.0

Species : Malayan pitviper (Callosellasma rhodostoma) Mouse LD50 (mg/kg) : 1.24 Venom yield per snake (mg) : 40.0-60.0

Species : Picados pitviper (Porthidium picadoi) Mouse LD50 (mg/kg) : 1.33 Venom yield per snake (mg) : 50.0-70.0

Species : Eyelash palm pitviper (Bothriechis schlegelii) Mouse LD50 (mg/kg) : 1.60 Venom yield per snake (mg) : 10.0-20.0

Species : Timber rattlesnake (Crotalus horridus) Mouse LD50 (mg/kg) : 1.64 Venom yield per snake (mg) : 75.0-210.0

Species : Common nightadder (Causus Rhombeatus) Mouse LD50 (mg/kg) : 1.85 Venom yield per snake (mg) : 20.0-30.0

Species : Lowland copperhead (Austrelaps superbus) Mouse LD50 (mg/kg) : 2.00 Venom yield per snake (mg) : ?

Species : Urutu (Bothrps alternatus) Mouse LD50 (mg/kg) : 2.00 Venom yield per snake (mg) : 60.0-100.0

Species : Cottonmouth ( Agkistrodon piscivorus) Mouse LD50 (mg/kg) : 2.04 Venom yield per snake (mg) : 80.0-170.0

Species : Orsini’s viper (Vipera ursinii) Mouse LD50 (mg/kg) : 2.17 Venom yield per snake (mg) : 1.0-4.0

Species : Western diamondback rattlesnake (Crotalus atrox) Mouse LD50 (mg/kg) : 2.20 Venom yield per snake (mg) : 175.0-600.0

Species : Jumping pitviper (Porthidium nummifer) Mouse LD50 (mg/kg) : 2.40 Venom yield per snake (mg) : 40.0-60.0

Species : Sidewinder (Crotalus cerastes) Mouse LD50 (mg/kg) : 2.60 Venom yield per snake (mg) : 18.0-50.0

Species : Pygmy rattlesnake (Sistrurus miliarius) Mouse LD50 (mg/kg) : 2.80 Venom yield per snake (mg) : 12.0-35.0

Species : Massasauga (Sistrurus catenatus) Mouse LD50 (mg/kg) : 2.90 Venom yield per snake (mg) : 15.0-45.0

Species : Okinawa habu (Trimeresurus flavoviridis) Mouse LD50 (mg/kg) : 3.05 Venom yield per snake (mg) : ?

Species : Red diamond rattlesnake (Crotalus rubber) Mouse LD50 (mg/kg) : 3.70 Venom yield per snake (mg) : 120.0-450.0

Species : Speckled palm pitviper (Bothriechis nigroviridis) Mouse LD50 (mg/kg) : 4.00 Venom yield per snake (mg) : 10.0-20.0

Species : Bushmaster (Lachesis muta) Mouse LD50 (mg/kg) : 4.50 Venom yield per snake (mg) : 200.0-500.0

Species : Rainforest hognosed pitviper (Porthidium nsautum) Mouse LD50 (mg/kg) : 4.60 Venom yield per snake (mg) : 12.0-25.0

Species : Side-stirped palm pitviper (Bothriechis lateralis) Mouse LD50 (mg/kg) : 4.84 Venom yield per snake (mg) : 10.0-20.0

Species : Slender hognosed pitviper (Porthidium ophryomegas) Mouse LD50 (mg/kg) : 6.30 Venom yield per snake (mg) : 10.0-20.0

Species : Godman’s pitviper (Pothidium godmani) Mouse LD50 (mg/kg) : 7.60 Venom yield per snake (mg) : 10.0-20.0

Species : Rock rattlesnake (Crotalus lepidus) Mouse LD50 (mg/kg) : 9.00 Venom yield per snake (mg) : 129.0

Species : Copperhead (Agkistrodon contotrix) Mouse LD50 (mg/kg) : 10.90 Venom yield per snake (mg) : 40.0-75.0

How Do Fangs Work ?
A fang is simply a tooth modified to inject venom into prey . The fangs work in concert with other structures to form a complete venom-delivery apparatus , which functions like a hypodermic syringe and needle .

Venom is produced by a pair of large venom glands . One gland is located on each side of the head , below and behind the eye , above the upper rear corner of the jaw . In some species , the gland extends backward along the neck , and in African nightadders (Causus) the gland can extend to midbody and even beyond . Within these glands , which are typically almond-or pear-shaped , the venom is produced by several (usually four to five) lobes of secretory cells . The secretory cells can make up as much as 80% of the gland’s total cell content . Their secretions drain through small tubules into a hollow space , the lumen of the gland . The lumen in turn joins the venom duct , which carries the venom forward to the base of the fang . To continue the syringe analogy , the venom gland corresponds to the body of the syringe , and the venom duct to its throat . The venom duct is surrounded by small masses of glandular tissue , the accessory glands , which may act as valves to regulate the flow of venom to the fang . Though the accessory glands’ secretions are not toxic , they may activate some venom components : venom drawn from the lumen of the venom gland is less toxic than venom taken from the fang .

The venom duct does not extend into the fang . It opens adjacent to the fang , within a sheath of connective tissue surrounding the fang’s base . This sheath is a seal around the fang , directing the flow of venom into the fang’s canal and outward into the prey .

Fangs are wide at their bases and gradually taper to needlelike points . All snakes’ fangs are curved . The amount of curvature varies among species ; in rattlesnakes (Crotalus) , for instance , the middle of each fang forms an arc of 60 to 70 degrees . The broad base of each fang sits in a socket of the maxillary bone and contains an opening adjacent to the end of the venom duct . The venom flows into the fang’s venom canal , which extends downward through the fang to a discharge orifice on the front surface of the fang , just above its solid tip . The discharge orifice is an elongated slit whose size varies among species .

Both the venom canal and the other outer surface of the fang are covered with enamel . The presence of enamel on both surfaces is a clue to the evolution of fangs . The first change appears to have been the appearance of a groove on the outer surface of one or maxillary teeth . Concurrent with selection for more effective venom , grooved teeth then enlarged and the grooves deepened . Eventually the walls of the groove closed over it , forming a closed canal . Among the evidence for this hypothesis of fang evolution s a faint seam on the face of each fang in some elapid and viperid snakes , indicating the point of contact and fusion of the two sides . Other evidence includes partially closed venom canals , such as in the African nightadders (Causus) .

How Is Venom Injected ?
A snake’s fang correspond s to a syringe’s needle . In fact , the free end of the fang is identical to the tip of a needle . Both have sharp tips to penetrate skin and muscle , and discharge orifices near the tip . Finally , the jaw musculature surrounding the venom gland corresponds to the syringe’s plunger . The contraction of these muscles squeezes the gland , forcing venom from the lumen into the venom duct and outward through the fang .
Among the various venomous snakes , biologists have identified three distinct venom-delivery systems . There is evidence that each system evolved more than once . For instance , the folding fang of vipers and pitvipers is also found in the Australian deathadders and African stilettovipers , three groups that are not closely related . All three systems evolved from the basic snake tooth , which is slightly curved ond cone-shaped . This basic aglyphous (grooveless) tooth (a , without ; glyphe , carving or groove) occurs in all snakes , even those with fangs , and most snakes have only these grooved teeth . Evolution of grooved and , eventually , canaled teeth (fangs) occurred only on the maxillary bone of the upper jaw . The three types of venom-delivery systems differ with regard to the position of the fang on the maxillary , the nature of the venom groove or canal , and the mobility of the fang-maxillary unit .
Ancestral snakes were venomless and had only grooveless teeth . All blindsnakes , boas , pythons , and other henophidian snakes still have exclusively aglyphous teeth . The majority of the colubrid snakes-the largest and most diverse snake family-are also aglyhous , although some species have one or two enlarged rear teeth on each maxillary bone . These enlarged teeth may be separated from the front maxillary teeth by gap known as a diastema . A diastema commonly separates the enlarged rear teeth , whether grooved or not , from the smaller front maxillary teeth .
Snakes with enlarged rear maxillary teeth are termed opisthoglyphous (opiistho , behind) . In some opisthoglyphous colubrids the enlarged teeth are ungrooved , but most others have a groove on the face or the side of the enlarged tooth . Originally these elongated teeth probably served only to hold prey , and this use persists in gartersnakes (Thamnophis) . However , such teeth puncture the prey’s skin , and some saliva inevitably enters the puncture wounds . An adaptive advantage would have resulted from increasing the toxicity , digestive ability , or tranquilizing effects of saliva , and assuring its delivery deep into the wound . Any of these advantages would have driven the evolution of fangs and venom glands , producing a range of venoms and venom-delivery systems .
Evolution of venom-delivery systems proceeded in two main directions : toward fixed proteroglyhous (Protero , earlier) and toward hinged solenoglyphous fangs (soleno , pipe) . In both instances , the grooved tooth became a fang by virtue of closure of the groove and a shifting forward of the enlarged tooth to the front of the mouth .
In proteroglyphous snakes , the fangs are short because large fixed fangs would require a deepening of the mouth cavity to prevent the fangs from perforating the floor of the mouth . The proteroglyphous condition is typical of the elapid snakes (cobras , taipan , coralsnakes , seasnakes , and their relatives) . In many species , particularly the seasnakes , the fang is barely longer than the teeth behind it . Proteroglyphous snakes typically bite and hold their prey , and then chew to inject venom deep in the wound . This behaviour is virtually universal among seasnakes , whose fish prey would otherwise swim or drift away before being incapacitated an envenomating strike-bite and withdraw . The largest elapid , the king cobra (Ophiophagus hannah) , has fangs only 8 to 10 millimeters long ; fangs are less than 8 millimeters long in mambas (Dendroaspis) , less than 7 millimeters in Indian cobras (Naja naja) , and less 3 millimeters long in adult harlequin coralsnakes (Micrurus fulvius) and yellow-bellied seasnakes (Pelamis platurus) .
The hinged fangs of the vipers and pitvipers (Viperidae) represent a more intricate system that allows a snake to strike , envenomate , and withdraw from the struggling prey , thereby avoiding injury . The hinged fang sits at the front of the mouth on a short maxillary bone that can rotate forward and backward . When not in use , the fang folds backward and upward against the roof of the mouth , where it lies enclosed in a membranous sheath . During a strike , the maxilla rotates forward , erecting the fang , and the mouth opens nearly 180 degrees . AS the mouth strikes the prey , the jaws close , propelling the fangs into the prey ; the venom is injected at the time of penetration . The right and left fangs can be rotated independently , although they erect jointly . A viper often works its fangs back into their resting sheaths one at a time after swallowing its prey .
The advantage of folding fangs is that long fangs can be housed in the mouth without perforating the floor of the mouth . Viperids have significantly longer fangs than the proteroglyphous elapids , and some viperids seem to have taken the evolutionary opportunity of lengthening their fangs to the extreme . Bitis , a group of African vipers , have the longest fangs known : up to 28 millimeters in the puffadder (B . arietans) , and over 30 millimeters in large Gaboon vipers (B . gabonica) . Even in the smaller copperhead (Agkistrodon contortrix) and common European viper (Vipera berus) , fangs are 7 millimeters or longer .
Folding fangs occur in two other groups of snakes . The Australian deathadders (Acantophis) , though they are elapids , are solenoglyphous . Their folding-fang mechanism is very similar in appearance and operation to that of the vipers and pitvipers . The deathadders also have the body shape and ambush-hunting habits of many viperids , an excellent example of convergent evolution .
The African molevipers (Atractaspidinae) are also solenoglyphous . Their short maxillary bones rotate and bear long fangs , but their strike-bite differs from that of the viperids and deathadders . They are burrowers , and the confines of narrow burrows make a typical rearing strike impossible . Instead they crawl along side their prey , open their mouths slightly , and shift the lower jaw away from the prey , freeing the fang nearest the prey . With a backward and sideward stab , they embed the fang , and inject venom into their prey (typically newborn rodents and burrowing lizards) . Because they stab backward , rather than biting forward , a snake handler who grabs one behind the head often ends up with a fang embedded in a finger or thumb ; this accounts for the snake’s common name , stilettoviper .
Newborn venomous snakes are fully operational . They have fangs and inject venom when bite . Throughout the lives of all snakes , however , teeth and fangs are shed and replaced regularly . An ordinary tooth is replaced by one that form beneath it , eventually loosening and then pushing it out of its socket . Proteroglyphous and solenoglyphous fangs are replaced an a somewhat different fashion . A series of five to seven replacement fangs lies in the gums of behind and above the functional fang . these replacement fangs are arranged in a graduated series , the largest adjacent to the functional fang . AS the functional fang wears down , it is replaced by the next fang . The reserve-fang series than shifts forward , so that a replacement fang is always available to replace a damaged functional fang .
The replacement fangs do not develop fully formed but in miniature ; instead , the growth process forms the tip first and then builds up the base , thus enlarging the fang and pushing the tip outward . The hollow-needle shape is apparent early in development . Functional fangs are shed in cycles as short as ten days and as long as six to ten weeks , depending on the species and the health of the individual snake . During the replacement phase , a snake may briefly have two fangs on each side of its head .

Do Snakes Spit Their Venom ?
Some cobras can spray their venom for a distance of up to 2.5 meters . This action is called spitting , but it does not evolve puckering the lips and blowing the venom outward . Spitting is a defensive behaviour that has nothing to do with killing prey . Spitting cobras bite and envenomate their prey just as do other venomous snakes .

Venom-spitting apparently evolved at three separate times in the family Elapidae but in no other snake families . Two of the spitting-cobra groups are African ; one group is the African ringhal cobra (Hemachatus haemachatus) , and the second includes the black-necked cobra (Naja nigricollis) , the Mozambique spitting cobra (N . mossambica) , the Mozambique red spitting cobra (N . pallida) , and the wEst African spitting cobra (N . katiensis) . The third group of spitters is from eastern Asia and includes the golden spitting cobra (Naja sumatrana) of the Malay Peninsula and Sumatra , the Indonesian spitting cobra (N . sputatrix) of southern Indonesia , the common spiting cobra (N . philippinensis) and Samar spitting cobra (N . samarensis) of the Philippines , the Chinese and Indochinese populations of the Asian black cobra (N . atra) , and some populations of the widespread Asian monocled cobra (N . kaouthia) . These snakes live in areas inhabited by large herbivores that might trample them or large carnivores that might eat them , and thus use their venom defensively .

Spitting or spraying of venom involves no major evolutionary structural modification . The fangs of spitting cobras resemble those of their nonspitting relatives , except that the discharge orifice of the fang is greatly reduced in size and pointed more forward . When compression of the venom gland forces its secretion through the venom duct and hollow fang , the venom is not discharged from the fang as quickly as in a snake with a normal-sized discharge orifice . The venom thus backs up in the fang , creating greater pressure at the discharge opening than in a normal fang , and the venom sprays from the fang in tiny droplets instead of large drops . The snake aids expulsion of venom by forcibly collapsing its lung and blowing air out of its mouth . The air carries the venom in a pair of fine sprays aimed at the eyes of the intruder .

At close quarters , the spitting cobras have very accurate aim . If the neurotoxic venom reaches the eyes , it is quickly absorbed by the capillaries of the conjunctiva . The venom may cause temporary blindness by irritating the cornea ; extensive damage of the cornea can lead to permanenr blindness . The venom should be rinsed out of the eye as soon as possible .

Reports occasionally surface of venom-spitting by vipers or pitvipers (Viperidae) , some of which may sling venom around if agitated and striking violently . Some small West Indian boas of the genus Tropidophis are said to spit blood when disturbed ; these reports may be faulty observations of these snakes’ defensive behaviour of dripping blood from their eyes . The only true venom-spitting snakes are cobras .

How Dangerous Is A Snakebite ?
A snakebite is usually not dangerous , unless it involves one of the more than two hundred species that produce a potent venom . Every day , people are bitten by nonvenomous snakes and experience only the slight discomfort caused by the snake’s teeth puncturing or scratching the skin .Of course , such wounds may be painful if the snake has long teeth , such as those of a python or large ratsnake , but serious effects are rare . Bites by nonvenomous species can be treated by washing the wound and applying an antiseptic to the punctures or scratches . Bites by venomous snakes require medical treatment . If untreated , a venomous bite may result in serious tissue or organ damage and even death . Serious secondary bacterial infections , such as gas gangrene and tetanus , may also follow venomous snakebites , and loss of a limb , finger , or toe is not uncommon . A nonvenomous snakebite usually involves several puncture marks of equal depth ; that of a venomous snake is characterized by one or two larger and deeper punctures among more shallow marks . However , tooth marks are not a reliable method for identifying the potential danger of a snakebite .

If the snake is venomous , discomfort is usually felt within a few minutes . a burning sensation or pulsating pain is often accompanied by swelling or discoloration of the tissues surrounding the wound . Such localized discomfort is particularly particularly characteristic of hemotoxic envenomation by pitvipers and true vipers , but moderate to severe local pain may also accompany neurotoxic bites of some elapids .

Medical treatment should be obtained for all elapid bites , even when there is no pain . Serious elapid bites are not usually apparent , since immediate pain does not always occur . A characteristic early sign of a serious neurotoxic elapid bite is drooping eyelids , followed by difficulty in swallowing , slurred speech , severe thirst , vertigo , and difficulty in breathing . Later , blood pressure often drops , and cardiac arrest may occur .

The most extensive study , published nearly fifty years ago , estimated that 300,000 venomous snakebites occurred throughout the world each year , almost 40,000 of which resulted death . More recent coordinated data is unavailable . The rate of death from snakebite is highest in developing nations with extensive natural snake habitat and scarce medical facilities , and lowest in developed nations with plentiful medical facilities .

The more natural the habitat , the greater the chance of encountering a venomous snake . On the Indian subcontinent , about 7,000 to 15,000 people died annually of snakebite from 1940 to 1949 , a probable mortality rate of about four deaths per 100,000 people . The most frequent culprits were the various kraits (Bungarus) , cobras (Naja , Ophiophagus) , saw-scaled vipers (Echis) , and the Russel’s viper (Vipera russelii) . In Brazil 2,000 to 4,800 persons died annually of snakebite between1929 and 1949 , mostly due to the bites of the tropical rattlesnake (Crotalus durissus) and various large species of lanceheads (Bothrops) . In the United States , by contrast , only 10 to 20 persons died of snakebite each year from 1944 to 1950 , or fewer than 0.2 per 100,000 people . Over 90% of these fatal bites were attributed to the cottonmouth (Agkistrodon piscivrus) , western rattlesnake (Crotalus viridis) , and eastern and western diamondback rattlesnakes (C . adamanteus , C .atrox) . In 1957 and 1966 , H . M . Parrish reported 6,000 to 7,000 annual envenomations by snakes in the United States , causing 14 to 15 deaths . In Canada fewer than fifteen people died of snakebite during the period 1944-1948 , and in Europe the death rate from all venomous animal bites was less than 0.5 per 100,000 people .

Today , snakebite mortality worldwide is probably about 50% of what it was when the preceding data were compiled . Modern medical treatment has improved survivorship , and treatment is more widely available . Between 1965 and 1971 , for instance , only 18 of 5,387 venomous snakebites in Malaysia and 191 of 14,578 in Thailand were fatal .

How Do You Avoid Snakebites?
Do not handle venomous snakes . In Europe and North America , most snakebites occur when the victim is either holding a snake or attempting to pick up or kill it .

Never play with venomous snakes . Remain at a safe distance-no nearer than two snake body lengths-from the snake .

Do not pick up a “dead” snake ! It may only be injured , stunned , or playing dead . Even with a truly dead snake , reflex action can cause the jaws to open and close .A fatal envenomation from the decapitated head of a canebrake rattlesnake (Crotalus horridus atricaudatus) has been reported .

Bites from unseen snakes in the wild may be prevented by common sense and proper dress . Boots and coarse long trousers should be worn in such areas . Most bites that occur in the wild are on the extremities . Do not put your hands or feet in places that you have not visually examined first . At night , one’s path should always be lighted to make snakes visible , since many venomous snakes are nocturnal .

If Bitten What Next?
A person bitten by a venomous snake should be taken to a hospital immediately . The traditional cut-and suck first-aid methods for snakebite are now subject to serious doubt . Because they involve cutting and constriction of blood flow , they can do more harm than good . Self-treatment is likely to worsen an already serious condition .

Before arriving at the hospital , (1) keep the patient as calm and still as possible ; (2) immobilize the bitten limb , using a splint if possible and positioning below the level of the heart ; (3) do not perform such traditional measures as cooling with ice , applying a tourniquet , cutting and sucking , giving alcohol or aspirin , pouring turpentine onto the wound , and the like ; and (4) if the bite is that of a neurotoxic snake , wrap the limb in a pressure bandage to localize the venom (a measure that has proven effective for bites of Australian elapids) . Whenever possible , the snake responsible for the bite should be brought to the medical facility for purposes of identification . It is better to avoid a second bite , however , if the snake is difficult to capture . And neither capture nor first-aid measures should delay transport of the patient to a hospital .

At the hospital , encourage the medical staff to call a poison-control center for expert advice on snakebite treatment . Because snakebites are uncommon in the United States , few medical personnel have experience in treating them . Generally speaking , the recommended course of action is to observe the patient to determine the extent of envenomation . Venomous snakes can strike and bite entirely in defense without injecting venom . Such “dry” bites account for 20 to 40% of all snakebites .

The patient is typically observed for at least eight hours , because the onset of some symptoms (particularly those of neurotoxic venom) may occur hours after the bite . Like all puncture wounds , bites must be thoroughly cleaned , and antitetanus serum and a broad-spectrum antibiotic are often recommended .

Antivenom is the only specific treatment for envenomation , and it should be given only to persons with symptoms or signs of envenomation . Antivenom should be administered only in a medical facility and only by a health-care specialist . The patient must first be tested for hypersensivity to horse serum , since antivenom derives from purified horse blood .In the United States , an anti-crotalid antivenom produced by Wyeth-Ayerst Laboratories is used for patients exhibiting hemotixic effects .

Antivenoms are developed for specific venomous snakes . Thus a European antivenom would not neutralize the toxin of North American pitvipers , because it was developed for different vipers . The Wyeth-Ayerst anti-crotalid polyvalent antivenom also includes antibodies to the neurotoxic rattlesnakes , and may be used for bites by the Mojave rattlesnake (Crotlaus scutulatus) . Symptomatic coralsnake (Micruroides , Micrurus) envenomation should be treated with North American coralsnake antivenom , also produced by Wyeth-Ayerst Laboratories .


Venoms And Clinical Manifestations : Snake venoms are complex mixtures of enzymes, low-molecular-weight polypeptides, glycoproteins, and metal ions. The enzymes and polypeptides affect the human body in a multisystem fashion. Among the deleterious components are hemorrhagins that render the vasculature leaky and thus cause both local and systemic bleeding; various proteolytic enzymes that cause local tissue necrosis, affect the coagulation pathway at various steps, or impair organ function; myocardial depressant factors that reduce cardiac output; and neurotoxins that act either pre- or postsynaptically to inhibit peripheral nerve impulses. Most snake venoms can adversely affect multiple organs.

Treatment (Field Management) : First-aid or "field" measures to be used in the management of venomous snakebite should focus on delivery of the victim to definitive medical care as quickly as possible; the victim should be as inactive as is feasible to limit systemic spread of the venom. Beyond this, any measure employed should at least do no further harm.

After viperid bites, local mechanical suction may be beneficial if applied to the puncture wounds within 3 to 5 min. A useful device is the Extractor (Sawyer Products, Safety Harbor, FL), which delivers one atmosphere of negative pressure to the wound. Suction should be continued for at least 30 min. Mouth suction should be avoided as it inoculates the wound with oral flora and theoretically can also result in the absorption of venom by the rescuer through lesions of the upper digestive tract. A proximal lymphatic-occlusive constriction band may limit the spread of venom if applied within 30 min. To avoid compounding of tissue necrosis, however, the band should not be allowed to interrupt arterial flow. A bitten extremity should be splinted if possible and kept at approximately heart level. Incisions into the bite site should never be made, and no form of cooling or electric shock is advantageous.

For elapid or sea snake bites, the Australian pressure-immobilization technique, in which the entire bitten extremity is wrapped with an elastic or crepe bandage and then splinted, is highly beneficial. The bandage is applied as tightly as it would be to treat a sprained ankle. This technique greatly restricts the absorption and circulation of venom from the bite site. However, an assessment of the potential utility of this method in viperid poisoning requires further research, as it may compound local tissue damage following these bites.

Treatment (Hospital Management) : Once in the hospital, the victim should be closely monitored (vital signs, cardiac rhythm, and oxygen saturation) while a history is quickly obtained and a brief but thorough physical examination is performed. The level of erythema/swelling in a bitten extremity should be marked and the circumferences measured in several locations every 15 min until swelling has stabilized. Large-bore intravenous access in unaffected extremities should be obtained in the event that hypotension develops. Early hypotension is due to pooling of blood in the pulmonary and splanchnic vascular beds; hours later, hemolysis and loss of intravascular volume into soft tissues may play important roles. Fluid resuscitation with normal saline or Ringer's lactate should be initiated for clinical shock. If the blood pressure response is inadequate after the administration of 20 to 40 mL/kg body weight, then a trial of 5% albumin (10 to 20 mL/kg) is in order. If volume resuscitation fails to improve tissue perfusion, vasopressors (e.g., dopamine) should be administered. Invasive hemodynamic monitoring (central venous and/or pulmonary arterial pressures) can be helpful in such cases. Central access must be obtained with extra caution if coagulopathy is evident.

Blood should be drawn for laboratory evaluation (including determination of blood type and cross-matching) as soon as possible, before the effects of circulating venom interfere with typing. Also important are a complete blood count to evaluate the degree of hemorrhage or hemolysis, studies of renal and hepatic function, coagulation studies to identify signs of consumptive coagulopathy, and testing of urine for blood or myoglobin. In severe cases or in the face of significant comorbidity, arterial blood gas studies, electrocardiography, and chest radiography may be necessary.

Attempts to locate a source of appropriate antivenin should begin early in all cases of known venomous snakebite, regardless of symptoms. If signs or symptoms develop, they may progress rapidly, making any delay in the administration of antivenin dangerous for the victim. Antivenins rarely offer cross-protection against snake species other than those used in their production unless the species are closely related. An example of good cross-protection is in the use of Australian tiger snake (Notechis scutatus) antivenin for sea snake bites (see below). The package insert accompanying a particular antivenin should be consulted for information regarding the spectrum of coverage. In the United States, assistance in finding antivenin can be obtained 24 hours a day from the University of Arizona Poison and Drug Information Center (520-626-6016).

Rapidly progressive and severe local findings (soft tissue swelling, ecchymosis, petechiae, etc.) or manifestations of systemic toxicity (signs and symptoms or laboratory abnormalities), are indications for the administration of intravenous antivenin. The package insert outlines techniques for reconstitution of antivenin (when necessary), skin-testing procedures (for potential allergy), and appropriate starting doses. Most antivenins are of equine origin and carry a risk of anaphylactic, anaphylactoid, and delayed-hypersensitivity reactions. Skin testing does not always reliably predict which patients will have an allergic reaction to equine antivenin; a skin test can be either false negative or false positive. Before antivenin infusion, the patient should receive appropriate loading doses of intravenous antihistamines (e.g., diphenhydramine, 1 mg/kg to a maximum of 100 mg; and cimetidine, 5 to 10 mg/kg to a maximum of 300 mg) in an effort to limit acute reactions. Expanding the patient's intravascular volume with crystalloids may also be beneficial in this regard (unless contraindicated by the patient's cardiac status). Epinephrine should be immediately available, and the antivenin dose to be administered should be diluted (e.g., in 1000 mL of normal saline, Ringer's lactate, or 5% dextrose in water for adults or in 20 mL/kg for children). This volume can be decreased if necessary for the treatment of patients with compromised cardiovascular reserve. The antivenin infusion should be started slowly, with the physician at the bedside to intervene in the event of an acute reaction. The rate of infusion can be increased gradually in the absence of allergic phenomena until the total starting dose has been administered (over a period of 1 to 4 h). Further antivenin may be necessary if clinical abnormalities worsen. Laboratory values should be rechecked hourly, particularly if abnormal, until stability is ensured.

The management of a life-threatening envenomation in a victim with an apparent allergy to antivenin requires significant expertise. Consultation with a poison specialist, an intensive care specialist, or an allergist is recommended. Often, antivenin can still be administered in these situations under closely controlled conditions and with intensive premedication (e.g., with epinephrine, antihistamines, and steroids).

Care of the bite wound should include application of a dry sterile dressing and splinting of the extremity with padding between the digits. Because of the risk of central spread of venom, an extremity should be elevated only when antivenin is available. Tetanus immunization should be updated as appropriate. The use of prophylactic antibiotics is controversial, as the incidence of secondary infection following venomous snakebite appears to be low. Many authorities, however, prescribe a broad-spectrum antibiotic (such as ampicillin or a cephalosporin) for the first few days.

If swelling in the bitten extremity raises concern that subfascial muscle edema may be impeding tissue perfusion (muscle-compartment syndrome), intracompartmental pressures should be checked watched for at least 6 to 8 h before discharge. An occasional viperid "dry" bite progresses to significant toxicity after a delay of several hours, and the onset of systemic symptoms is commonly delayed for a number of hours after bites by several of the elapids (especially the coral snakes) and sea snakes. Patients bitten by these reptiles should be observed in the hospital for 24 h.

Morbidity And Mortality : The overall mortality rates for venomous snakebite are low in areas of the world with rapid access to medical care and appropriate antivenin. In the United States, for example, the mortality rate is 1 percent for victims who receive antivenin. Eastern and western diamondback rattlesnakes (Crotalus adamanteus and Crotalus atrox, respectively) are responsible for most snakebite deaths in the United States. Snakes responsible for large numbers of deaths in other regions of the world include the cobras (Naja species) of Asia and Africa, the carpet and saw-scaled vipers of the Middle East and Africa (Echis species), Russell's viper (Vipera russelli) of the Middle East and Asia, the large African vipers (Bitis species), and the lancehead pit vipers of Central and South America (Bothrops species).

The incidence of morbidity in terms of permanent functional loss in a bitten extremity is difficult to estimate but is probably substantial. Such loss may be due to muscle, nerve, or vascular injury or to scar contracture. In the United States, such loss due to snakebite tends to be much more common and severe after rattlesnake bites than after bites by copperheads or water moccasins.

What Is Antivenom ?
Antivenom is a serum that is commercially produced to neutralize the effects of envenomation by venomous snakes . The fresh snake venom used to produce antivenom is obtained either by manually milking a sinkae or by electrical stimulation . Venom is extracted from captive snakes every twenty or thirty days . In manual milking , the snake is held behind its head and induced to bite a thin rubber diaphragm covering a collecting vessel while the handler applies pressure to the snake’s venom glands.