Snake Bites
&
Venom
Made by www.thesnake.org
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 .
Treatments
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 . The pressure is maintained until no
more venom is discharged . In electrical stimulation , electrodes are touched to
the opposite sides of the snake’s head , causing the muscles around the venom
gland to contract , expelling venom into a collection container . The venom is
freeze-dried (the preferred method) , or dried with the help of a drying agent
or a vacuum .
Healthy horses , usually seven to eight years old , are injected at regular
intervals with non-lethal doses of a solution prepared from the freeze-dried
venom until they build up an immunity to the venom . The dosage can then be
slowly increased over time to create greater immunity . The horse’s immune
system neutralizes the venom by producing antibodies (specialized proteins) .
These horse antibodies in turn neutralize the same venom when injected into
humans .
To obtain the antibodies , a small amount of blood (6 to 8 liters) is regularly
removed from the horse’s jugular vein . The blood is combined with a
sodium-citrate solution , to prevent coagulation and degradation , and the
globulin to which the antibodies are attached is separated out and purified .
About twenty-five laboratories throughout the world produce antivenoms for the
venomous snakes in their regions .
Can Venom Be Used As Medicine ?
Snake venoms have great potential for medical use because of the wide variety of
compounds they contain and the specific action of each compound . Although no
medical preparation derived directly from snake venom is used now in the United
States , a few such compounds are used in Asia , Europe , and Latin America for
treatment of blood disorders . Nowhere is a whole venom used as a medicine ;
instead , specific components are extracted .
Beat-blockers-drugs widely used in the treatment of cardiovascular diseases-owe
their discovery to research on Bothrops venoms . These venoms contain a peptide
that interrupts the activity of an enzyme involved in hypertension (high blood
pressure) . Two analgesics derive from cobra venom : Cobroxin is used like
morphine to block nerve transmission , and Nyloxin reduces severe arthritis pain
. Arvin , an extract of the Malayan pitviper (Calloselasma) , is an effective
anticoagulant (it inhibits the formation of blood cloths) .
Venom components are also used in basic research in physiology , biochemistry ,
and immunology . By retarding or speeding up biochemical and cellular process ,
such nerve-impulse transfer and blood clotting , venom components allow
researchers to examine the operation of the process and to develop drugs to
correct malfunctions due to disease . For example , venoms are currently being
investigated for their potential as antiviral and antibacterial agents (tetanus
, hepatitis , trachoma , scarlet fewer , malaria , botulism) and
anticarcinogenic agents (cancer and nonmalignant tumors) . Other diseases for
which snake venoms have been used in research include nerve disesases , such as
epilepsy , multiple sclerosis , myasthenia gravis (Lou Gehrig’s disease) ,
Parkinson’s disease , and poliomyelitis ; musculoskeletal disease , including
arthritis and rheumatism ; cardiovascular diseases , such as hypotension ,
hypertension , angina , and cardiac arrhythmias , and visual disorders ,
including neuritis , conjunctivitis , and cataracts .
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