Snake venom is a mixture of dozens of proteins, each with its own job. Most venoms combine several kinds of toxin, which is why a single bite can paralyse, stop blood clotting and destroy tissue at the same time.
The labels below group toxins by what they do to a person, not by their chemistry. One toxin family can fall under several labels: some phospholipase toxins attack nerves, others break down muscle.
| Other terms you will see | What they mean |
|---|---|
| Cardiotoxic | An old name for cobra cytotoxins, from their effect on heart muscle in the lab. Direct effects on the human heart are less common than the name suggests. |
| Nephrotoxic | Kidney damage. Usually a result of bleeding, clotting problems or muscle breakdown rather than a separate toxin. Russell’s viper bites are especially known for it. |
| Spreading factors | Enzymes such as hyaluronidase that help venom move through tissue. They make other toxins act faster but are not very toxic themselves. |
Counted from the venom effects recorded for the 94 species in our dataset. Most rattlesnake and viper venoms fall under haemotoxic; most cobra, krait and sea snake venoms under neurotoxic.
These species are often described with the wrong combination. This is what the evidence supports.
| Species | Main effects | Notes |
|---|
The same snake can cause a dry bite with no venom or a life-threatening one. These factors make the difference.
Snakes control their venom. Many defensive bites are “dry” and inject little or none; others empty the glands.
Venom injected straight into a blood vessel acts far faster than venom under the skin.
The same dose is more concentrated in a smaller body, which is why children are at greater risk.
Walking and a racing heart push venom through the lymph system faster. Keeping still is the most useful first aid.
How quickly someone reaches a hospital that holds the right antivenom often matters more than the venom itself.