Snake venom
The venom is stored in large glands called alveoli before being conveyed by a duct to the base of channeled or tubular fangs through which it is ejected.
[2] Enzymes (molecular weight 13-150 KDa) make up 80-90% of viperid and 25-70% of elapid venoms, including digestive hydrolases, L-amino-acid oxidase, phospholipases, thrombin-like pro-coagulant, and kallikrein-like serine proteases and metalloproteinases (hemorrhagins), which damage vascular endothelium.
Polypeptide toxins (molecular weight 5-10 KDa) include cytotoxins, cardiotoxins, and postsynaptic neurotoxins (such as α-bungarotoxin and α-Cobratoxin), which bind to acetylcholine receptors at neuromuscular junctions.
Compounds with low molecular weight (up to 1.5 KDa) include metals, peptides, lipids, nucleosides, carbohydrates, amines, and oligopeptides, which inhibit angiotensin-converting enzyme (ACE) and potentiate bradykinin (BPP).
Some snake venoms carry fasciculins, like the mambas (Dendroaspis), which inhibit cholinesterase to make the prey lose muscle control.
However, exceptions occur – the venom of the black-necked spitting cobra (Naja nigricollis), an elapid, consists mainly of cytotoxins, while that of the Mojave rattlesnake (Crotalus scutulatus), a viperid, is primarily neurotoxic.
The first myotoxin to be identified and isolated was crotamine, discovered in the 1950s by Brazilian scientist José Moura Gonçalves from the venom of tropical South American rattlesnake Crotalus durissus terrificus.
[19] Fraction V is structurally stable because it has seventeen disulfide bonds; it's unique in that it has the highest solubility and lowest isoelectric point of major plasma proteins.
[21] The Cohn Process exploits differences in plasma proteins properties, specifically, the high solubility and low pI of albumin.
Several variations to this process exist, including an adapted method by Nitschmann and Kistler that uses fewer steps, and replaces centrifugation and bulk freezing with filtration and diafiltration.
Scientists performed experiments on the opossums and found that multiple trials showed replacement to silent substitutions in the von Willebrand factor (vWf) gene that encodes for a venom-targeted hemostatic blood protein.
These substitutions are thought to weaken the connection between vWf and a toxic snake venom ligand (botrocetin), which changes the net charge and hydrophobicity.
From the anterior extremity of the gland, the duct passes below the eye and above the maxillary bone, to the basal orifice of the venom fang, which is ensheathed in a thick fold of mucous membrane.
When the snake bites, the jaws close and the muscles surrounding the gland contract, causing venom to be ejected via the fangs.
When biting, viperid snakes often strike quickly, discharging venom as the fangs penetrate the skin, and then immediately release.
Although usually no serious symptoms result if the venom is washed away immediately with plenty of water, blindness can become permanent if left untreated.
In from twelve to twenty-four hours these severe constitutional symptoms usually pass off; but in the meantime, the swelling and discoloration have spread enormously.
That cases of death, in adults as well as in children, are not infrequent in some parts of the Continent is mentioned in the last chapter of this Introduction.The Viperidae differ much among themselves in the toxicity of their venoms.
The bite of the larger European vipers may be very dangerous, and followed by fatal results, especially in children, at least in the hotter parts of the Continent; whilst the small meadow viper (Vipera ursinii), which hardly ever bites unless roughly handled, does not seem to be possessed of a very virulent venom, and although very common in some parts of Austria and Hungary, is not known to have ever caused a serious accident.
The deaths of two prominent herpetologists, Robert Mertens and Karl Schmidt, from African colubrid bites, changed that assessment, and recent events reveal that several other species of rear-fanged snakes have venoms that are potentially lethal to large vertebrates.
Early symptoms include headaches, nausea, diarrhea, lethargy, mental disorientation, bruising, and bleeding at the site and all body openings.
Symptoms of a bite from these snakes include nausea and internal bleeding, and one could die from a brain hemorrhage and respiratory collapse.
The question whether individual snakes are immune to their own venom has not yet been definitively settled, though an example is known of a cobra that self-envenomated, resulting in a large abscess requiring surgical intervention, but showing none of the other effects that would have proven rapidly lethal in prey species or humans.
The hedgehog (Erinaceidae), the mongoose (Herpestidae), the honey badger (Mellivora capensis) and the opossum are known to be immune to a dose of snake venom.
[citation needed] Recently, the honey badger and domestic pig were found to have convergently evolved amino-acid replacements in their nicotinic acetylcholine receptor, which are known to confer resistance to alpha-neurotoxins in hedgehogs.
Emergency snake medicines are obtained by chewing a three-inch piece of the root of bois canôt (Cecropia peltata) and administering this chewed-root solution to the bitten subject (usually a hunting dog).
Another native plant used is mardi gras (Renealmia alpinia) (berries), which are crushed together with the juice of wild cane (Costus scaber) and given to the bitten.
[note 1] Both adaptive immunity and serotherapy are specific to the type of snake; venom with identical physiological action do not cross-neutralize.
Boulenger 1913 describes the following cases: A European in Australia who had become immune to the venom of the deadly Australian tiger snake (Notechis scutatus), manipulating these snakes with impunity, and was under the impression that his immunity extended also to other species, when bitten by a lowland copperhead (Austrelaps superbus), an allied elapine, died the following day.
The situation is even more complex in countries such as India, with its rich mix of vipers (Viperidae) and highly neurotoxic cobras and kraits of the Elapidae.
