Snake venom

Snake venom is a highly modified saliva. There are more than 2000 species of snakes living at the present time, and at least 10 % of these are are venomous (see discussion page). Possessing venom is a survival advantage for "poisonous" snakes. Unlike most other predators, snakes swallow prey whole, and are thereby particularly subject to injury from animals taken alive. Most snake venoms contain specific proteins that act to (1) paralyze the prey so that it no longer moves (2) block the prey animals ability to clot blood so that it rapidly bleeds to death and (3) begin the digestive process by breaking down the tissues of the prey animal. Venom also acts to deter predators from harming the snake and is an important defense mechanism for those who possess it.

The process of introducing venom into a victim is called "envenoming". Envenoming by snakes is most often done through the wound of their bite, but, in some species of snake, like the 'spitting cobra', is accomplished by squirting venom onto the mucous membranes of prey animals; including eyes, nose, and mouth.

Venoms differ from snake species to snake species, and appear to be specialized for the prey that make up the individual species diet. The great majority of the many biological toxins in snake venom are proteins, generally either with enzymatic activity, or the ability to blockade nerve or muscle cell receptors. With advances in molecular biology over the last few decades, a general schema for the expression of such proteins by genes in the specialized salivary gland that secretes venom is apparent. There is evidence that the exact components of the venom may even change over the course of a snakes lifespan, in species(for example, certain rattlesnakes of the genus Crotalus) who rely on one set of prey animals as juveniles (cold-blooded lizards and other small exotherms) , and a different set of prey animals (warm-blooded rodents and other small endotherms) as adults.(Ontogenetic Variation in Venom Composition and Diet of Crotalus oreganus concolor: A Case of Venom Paedomorphosis? Stephen P. Mackessy, Kwame Williams, Kyle G. Ashton Copeia Volume 2003, Issue 4 (December 2003) pp. 769–782 DOI: 10.1643/HA03-037.1)

The danger to a human presented by any particular species of venomous snake depends on many factors. First, there is the toxicity of that species venom, which can vary from mildly harmful to highly lethal. Secondly, there is the actual dose of venom the snake is capable of effectively delivering. Finally, there is the liklihood that the snake will attack if confronted, rather than withdraw.

Toxicity: LD50

Toxicity of venoms is usually expressed by the LD50: the lowest dose that kills 50% of a group of experimental animals (most often rodents). That dose varies not just between the venoms tested, but also depends on which species of prey animals chosen to receive the venom. Generally, the most toxic venom is the one with the lowest LD50. However, some snakes have venoms that are quite specialized for certain types of prey animals. The venom of the eastern copperhead (I have to look up scientific name) is more lethal to fish and amphibians than to mammals (I have to check reference to make sure I have right species. will be coming). Human susceptibility to a snake venom is generally estimated from the LD50 for rodents. The next factor in assessing the danger of a particular species of venomous snakes' bite is the dose of venom that is actually introduced into the tissues with a bite. As will be discussed, some types of snakes have an extremely efficient mechanism of injecting venom, others have markedly less success in doing so. The amount of venom produced by venomous snakes that is available for secretion with a bite also varies between kinds of snakes, and between individuals (usually by size) of any one species.

Delivery of Venom

The venomous snakes are represented in only five families. These are the Colubridae (colubrids), Elapidae (elapids), Hydrophiidae (sea-snakes), Viperidae (true vipers), and Crotalidae (pit vipers). There are variations in the methods of envenomation according to family.

Colubridae (colubrids)

In some of the proteroglyphous colubrids, the venom fangs are not tubular, but only channelled and open along the anterior surface; and as the maxillary bone in these snakes is more or less elongate, and not or but slightly movable vertically, the venom duct runs above the latter, making a bend only at its anterior extremity, and the tranverse bone has not the same action on the erection of the fangs. Otherwise the mechanism is the same.

In the opisthoglyphous colubrids, with grooved teeth situated at the posterior extremity of the maxilla, a small posterior portion of the upper labial or salivary gland is converted into a venom-secreting organ, distinguished by a light yellow colour, provided with a duct larger than any of those of the labial gland, and proceeding inward and downward to the base of the grooved fang; the duct is not in direct connection with the groove, but the two communicate through the mediation of the cavity enclosed by the folds of mucous membrane surrounding the tooth, and united in front.

Viperidae (true vipers)

In the vipers, which furnish examples of the most highly developed venom delivery apparatus, although inferior to some in its toxic effects, the venom gland is very large and in intimate relation with the masseter or temporal muscle, consisting of two bands, the superior arising from behind the eye, the inferior extending from the gland to the mandible. A groove or duct can be located traveling from the modified salivary glands where venom is produced down the length of the fang and out to the tip. In some species, notably the vipers and cobras, this groove is completely closed over. In other species, such as the adders and mambas, this groove is not covered, or only covered partially. From the anterior extremity of the gland the duct passes below the eye and above the maxillary bone, where it makes a bend, to the basal orifice of the venom fang, which is ensheathed in a thick fold of mucous membrane, the vagina dentis. By means of the movable maxillary bone hinged to the prefrontal, and connected with the tranverse bone which is pushed forward by muscles set in action by the opening of the mouth, the tubular fang is erected and the venom discharged through the distal orifice in which it terminates. When the snake bites, the jaws close up, causing the gland to be powerfully wrung, and the venom pressed out into the duct.

Effects of Venom

Paralysis

Most neurotoxins in snake venoms are proteins that are too large to cross the blood-brain barrier. This means that the venoms usually exert their effects on the peripheral nervous system rather than directly on the brain and spinal cord. Many of these neurotoxins cause paralysis by blocking the neuromuscular junction.

The Neuromuscular Junction

The neuromuscular junction is the microscopic connection between a motor nerve fiber and a muscle fiber. It is a type of synapse. A chemical neurotransmitter, acetylcholine, is released by the axons of the motor nerve, diffuses across the synapse of the neuromuscular junction, to be taken up by the muscle fiber on the other side of the tiny space between the nerve ending and the muscle cell membrane. The acetylcholine stimulates receptors on the muscle cell which then depolarizes and moves (contracts). This effect of acetylcholine is quickly stopped by acetylcholinesterase, an enzyme that specifically breaks down the acetylcholine molecule. Once acetylcholinesterase removes aceytlcholine from the receptor switch on the muscle cell membrane, the receptor is again clear and the process can repeat. Should there be a problem with the activity of acetylcholinesterase, the neurotransmitter acetylcholine will stay on the muscle cell receptor and keep the muscle cell in contraction, in a form of tetany.

Neurotoxins in snake venom can block transmission of acetylcholine from nerve to muscle at the side of the nerve ending (pre-synaptic literally, before the synapse) or affect the activity of the muscle fiber past the synapse (post-synaptic literally after the synapse). Most commonly, the postsynaptic method of producing paralysis is anti-cholinesterase. Most snake venoms contain toxins that do both (ref: Lewis RL. Gutmann L. Snake venoms and the neuromuscular junction. [Review] [26 refs] [Journal Article. Review] Seminars in Neurology. 24(2):175-9, 2004 Jun. UI: 15257514). Presynaptic neurotoxins are commonly called [beta]-neurotoxins and have been isolated from venoms of snakes of families Elapidae, Viperidae, Crotalidae, and Hydrophiidae. [beta]-Bungarotoxin was the first presynaptically active toxin to be isolated from Bungarus multicinctus (Banded Krait) of the Elapidae family.

Blood clotting

Many components in snake venom act to disrupt normal blood flow and normal blood clotting. When many tiny blood clots form in the bloodstream there is a pathological condition known as disseminated intravascular coagulation (DIC). Some enzymes in snake venom set off DIC in the bloodstream of their envenomated prey by XXXX.

Other components of many snake venoms increase bleeding in prey animals by breaking down established clots. An additional mechanism that increases bleeding are components that inhibit the aggregation of platelets, those small odd-shaped blood cells that collect at the site of a tear in a blood vessel and form a plug to close it.

Immunity

Antivenom

Antivenoms are antibodies made by injecting partially denatured proteins from snake venoms into large host animals, such as horses or sheep, in low enough doses so that the animal is not harmed, but produces serum antibodies to the active components of the venom. Early forms of antivenoms were problematic because whole horse serum eas used, and many people suffered reactions to the plasma of horses. As refinements have been made in the purification of the antibody fractions of the serum, allergic and other reactions have been reduced.

Since antivenoms are specific antidotes that neutralize the particular active toxins of venoms, the type of antivenom must be properly matched to the snake responsible for the bite. Antivenoms have revolutionized the treatment for the more deadly snake enovamtions. For example, a recent report of the first manufacture of a horse antivenom for the Bungarus canida snake in Vietnam changed the course of a group of patients from an 80% mortality to 100% recovery. (Trinh, Kiem Xuan; Trinh, Long Xuan; et al. The Production Of bungarus Candidus Antivenom From Horses Immunized With Venom & it's Application For The Treatment Of Snake Bite Patients In Vietnam: 75. Therapeutic Drug Monitoring. 27(2):230, April 2005.)

Regional considerations

Even in those areas where laws against the keeping venomous snakes in captivity exist, enforcement is not strict enough to prevent this practice entirely. Additionally, although rare in occurance, snakes can be introduced into distant locations through importation of goods. Therefore, snake bite by a a venomous snake that is not native to a particular geographic region is possible. However, statistically, the number and type of snake bites in the general population occurs in geographic distribution that reflects the native habitat of these snakes, and, sometimes, occupations and recreational practices by residents and travellers that are higher risk for snake bite. Most envenomations from snakes occur in tropical countries.