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Snake Venoms

Snake venoms are generally produced in specific venom glands, derived from salivary glands, the exception being Duvernoy’s glands in some Colubrid species. The venom, once produced, is delivered by a duct to the fang base, where it is transported into the victim either by a groove in the fang, or through a fang duct. Contraction of muscles around the gland producing intra-glandular pressure are the usual mode of venom transport, often allowing the snake to “fine-tune” how much venom is expended in a given bite. This may explain, in part, why many venomous snakes exhibit the “dry bite” phenomenon, whereby a bite fails to inject enough venom to cause medically significant envenoming.

Snake venoms generally consist of a complex mixture of substances, each of which may exhibit one or more distinct toxic actions. Many of the most potent snake toxins have evolved highly specific targets, such as the neuromuscular junction or components of the haemostatic system. It is likely all snake venoms fulfil multiple functions for the snake, principally:

  • Prey acquisition
  • Prey digestion
  • Defense against predators

There are many ways of classifying snake venoms; some still frequently used in medical texts are misleading or inaccurate. Foremost amongst these is the old aphorism that Elapids are neurotoxic and Viperids are haemorrhagic, a classification that is quite inaccurate and should be abandoned. Some of the most potent toxins active against human haemostasis are found in some Elapid venoms, while some other Elapid species cause major local tissue injury at the bite site. Conversely, there are a number of Viperid species whose principal clinical effect is neurotoxic paralysis and which produce no or minimal effect on either local tissues at the bite site or on the haemostatic system. From a medical perspective, a classification based on clinical effects is generally useful and will be adopted widely on this site, but the user should be aware that more biochemically based classifications of venoms yield a quite different picture and that some medically important toxins from snake venoms have several physiologically distinct actions, each caused by separate regions of the toxin structure.

Broad medical classification of snake venom activities.

Toxin activity type Clinical effects
Flaccid paralysis
Resistant to late antivenom therapy
Often reversal with antivenom therapy
Myotoxin Systemic skeletal muscle damage
Haemostatic system toxins Interfere with normal haemostasis, causing either bleeding or thrombosis
Haemorrhagins Damage vascular wall, causing bleeding
Nephrotoxins Direct renal damage
Cardiotoxins Direct cardiotoxicity
Necrotoxins Direct tissue injury at the bite site/bitten limb

Broad biochemical classification of snake venom activities.

Toxin class Clinical effects
Polypeptide toxins Various; autonomic, neurotoxic, cardiotoxic, myotoxic

Phospholipase toxins

Various; presynaptic neurotoxic, myolytic, procoagulant, cardiotoxic, necrotic
Enzyme toxins Various; interfere with haemostasis, necrotic, haemolytic
Carbon-nitrogen lyases
Other toxins Various; autonomic etc
Nerve growth factors
Phospholipase inhibitors
Proteinase inhibitors
Complement inhibitors
Other components Various or ill-defined
Amino acids  
Biogenic amines  
Nucleosides & nucleotides  
Organic acids  

It is also important to understand that there may be considerable variability in venom composition even within a species, let alone between closely related species, and even within an individual animal over time.

It is also important to understand that there are several different ways of measuring venom toxicity that may yield quite different comparitive results. Also, choice of animal for lethality studies can be crucial, as can route of injection, again making comparisons between species difficult.

Go To General Overview of Clinical Effects