Cobra Envenomation

Updated: Jun 15, 2018
  • Author: Robert L Norris, MD; Chief Editor: Joe Alcock, MD, MS  more...
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To many people, the cobra is the quintessential venomous snake. Cobras discussed in this article include species in the genus Naja and other similar venomous snakes, such as Ophiophagus hannah (king cobra), Hemachatus haemachatus (ringhals), Walterinnesia aegyptia (desert black snake), Boulengerina species (water cobras), and Pseudohaje species (tree cobras).

Most cobras are large snakes, 1.2-2.5 m in length. The king cobra, which may reach 5.2 m, is the largest venomous snake in the world. Cobras live throughout most of Africa and southern Asia. Their habitats vary, and some species adapt readily to life in cultivated areas and around villages.

When encountered, cobras usually try to escape but occasionally defend themselves boldly and may appear aggressive. Most of these snakes elevate the head and spread the neck as a threat gesture. However, a number of other snakes, venomous and nonvenomous, use this defense as well.

Most snakebites are inflicted on body extremities. Because cobras are popular as show snakes, bites on the hands and fingers are common.

By far, rural agricultural workers and other people in Asia and Africa receive most bites while working outdoors without protective footwear or when cutting tall grass with a hand blade. In North America and Europe, captive cobras may cause bites to zookeepers or amateur collectors. [1, 2]

Not all snakebites result in envenomation. In the case of cobras, the percentage of dry bites may be quite high, 45% in one series of 47 cases from Malaysia. In another series, 1 of 3 snake charmers bitten by large king cobras showed no signs of envenomation.

In addition to biting, some cobra species have a unique defense; they eject or spit jets of venom toward an aggressor, usually and accurately directly at the eyes. The fangs of these species are specially modified with the discharge orifice on the anterior face rather than at the tip. The effective discharge range of a large snake is at least 3 m. The ringhals and certain African species of Naja are the most effective spitters, but the spitting behavior also is observed among some Asian Naja species.



Cobra envenomation is an extremely variable process. The envenomations of some species cause profound neurological abnormalities (eg, cranial nerve dysfunction, abnormal mental status, muscle weakness, paralysis, and respiratory arrest). With other cobras, local tissue damage is of primary concern.

Necrosis is typical of bites by the African spitting cobras (Naja nigricollis, Naja mossambica, Naja pallida, and Naja katiensis), the Chinese cobra (Naja atra), the Monocellate cobra (Naja kaouthia), and the Sumatran spitting cobra (Naja sumatrana). Although the venoms of these cobras contain neurotoxins, necrosis often is the chief or only manifestation of envenoming in humans. Occasionally, a combination of neurologic dysfunction and tissue necrosis may occur as with the Indian cobra (Naja naja). The images below depict several species.

Naja atra (Chinese cobra). Photo by Sherman Minto Naja atra (Chinese cobra). Photo by Sherman Minton, MD.

Naja kaouthia (Monocellate cobra). Photo by Sherm Naja kaouthia (Monocellate cobra). Photo by Sherman Minton, MD.

Naja naja (Indian Cobra). Photo by Robert Norris, Naja naja (Indian Cobra). Photo by Robert Norris, MD.

Cobra venoms have been studied extensively. As with all snake venoms, they are multicomponent products whose toxins are mostly proteins and polypeptides.

Venoms can be divided into the following categories:

  • With most species, excluding some of the African spitting cobras, the most clinically significant toxins are postsynaptic neurotoxins that competitively bind to nicotinic acetylcholine receptors to produce depolarizing neuromuscular blockade. One group in this category has 60-62 amino acids and 4 disulfide bridges. Another has 71-74 amino acids and 5 disulfide bridges.

  • The second venom category comprises so-called cardiotoxins, which are actually generalized cell-membrane poisons that produce irreversible cell depolarization. Such depolarization may cause dysrhythmia, hypotension, and death.

  • Toxins in the third category activate complement via the alternative pathway (C3-C9 sequence).

  • The fourth category is composed of enzyme toxins, such as phospholipase A2 (variable toxicity), hyaluronidase (facilitates tissue dispersion of other toxins), L -amino acid oxidase (gives many venoms a characteristic yellow coloration), and acetylcholine acetylhydrolase (unknown toxicity). Other proteolytic enzymes are found in the venom of the king cobra.

Naja philippinensis (Philippine cobra) venom is the most toxic, with a subcutaneous median lethal dose (LD50) of 0.14 mg/kg in mice. In comparison, the corresponding LD50 for Naja naja (Indian cobra) venom is 0.29 mg/kg, for Naja haje (Egyptian cobra) venom is 1.75 mg/kg, for king cobra venom is 1.73 mg/kg, and for Naja nigricollis (black-necked spitting cobra) venom is 3.05 mg/kg.

An additional, unique form of toxicity with some Asian and African species is acute ophthalmia, which occurs when venom is spit into the eyes. Spitting cobras can spit venom into a person's eyes from up to 3 m away. Immediate and intense pain results, with blepharospasm, tearing, and blurring of vision. Systemic toxicity does not occur with eye exposure, but corneal ulcerations, uveitis, and permanent blindness have been reported in untreated cases. Occasionally, ocular exposure occurs when a person has venom on their hands (as following laboratory venom extraction from a snake) and rubs his or her eyes. [3]

About half of the cases ascribed to the African spitting cobras (N nigricollis, N mossambica, N pallida, N katiensis) showed corneal ulceration, and some patients experienced permanent visual impairment or blindness. Cases ascribed to the Asian spitting cobras and the African ringhals are usually less severe.




United States

Envenomations result from human interaction with cobras in zoos, research laboratories, and private collections in the United States and other countries where cobras lack natural habitat. In a series of 54 consultations regarding bites by non-native snakes in the United States, 23 involved cobras. One fatality occurred, and 7 other cases involved serious envenoming. In Russell's 1980 series, cobras inflicted 18 of the 85 bites by non-native snakes. [4] No comparable data are available for other nations, though it was reported that only 3 cobra bites among 32 bites inflicted by non-native venomous snakes occurred in Britain (rattlesnakes were implicated most often in this series).


Snakebites are a significant medical problem in parts of Africa and Asia. In West Africa, the annual bite incidence is 40-120 bites per 100,000 population. Two rural Congolese regions report an annual incidence of 430 bites per 100,000 population. In a 7-year survey, the Natalese incidence was 24 bites per 100,000 population.


Because of increased exposure to snakes, men are bitten more often than women.



In India, the annual mortality incidence is 5.6-12.6 per 100,000 population. At one time, Burma listed snakebite as its fifth leading cause of death. More recently, the annual mortality incidence was 3.3 per 100,000 population. [5] Data from Thailand and Malaysia in the 1980s demonstrate an annual mortality incidence of 0.1 per 100,000 population. [6, 7]

Determining the exact contribution of cobras to overall snakebite morbidity and mortality is difficult. In most cases, bitten individuals are unable to identify the snake. In India, the tendency is to ascribe all fatal or serious bites to cobras. Physicians are also likely to attribute all bites with neurotoxic symptoms to cobras.

In a Thai survey, cobras made up 17% of the 1145 snakes identified in bites and were responsible for 25% of the fatalities associated with those bites. [8] In northern Malaysia, cobras accounted for 23 of 854 bites in which the snake was identified. In a survey in Taiwan, cobras were blamed for 100 of 851 bites in which the snake was identified; none was fatal. [9] Cobras accounted for 2 of 95 bites on a Liberian rubber plantation. [10] The ringhals was responsible for 18 of 314 envenomations in Natal. Based on patients' symptoms alone, 18 other bites in this series were ascribed to cobras.

King cobra bites are considered more serious than bites from other cobra species because of the greater volumes of injected venom and the more rapid onset of neurotoxic symptoms. Mortality is also higher. In a series of 35 cases, 10 deaths occurred. Ringhals bites are similar to other cobra bites but are less serious both locally and systemically. Deaths are rare. A medical report of 4 bites by the desert black snake described relatively mild symptoms and reported recovery without specific treatment. Anecdotal reports of fatal bites exist. No medical accounts of bites by water cobras or tree cobras exist. Anecdotal evidence suggests both are dangerous. [11]



Many patients recover with no specific treatment.

The neurotoxic effects of cobra venom are completely reversible, though recovery may take up to 6 days.

Reports of death within 1 hour of cobra bite exist, but a timeframe of 2-6 hours is more typical of fatal cases.

With sound supportive care (eg, prevention of aspiration and respiratory support) and appropriate, prompt antivenom administration, anticipate recovery from cobra envenomation.


Patient Education

Advise amateur herpetoculturists bitten by a venomous snake in their collection to not keep such animals. If they previously have received antivenom, their risk for an allergic reaction may be increased should antivenom use be required again in the future.

For patient education resources, visit the First Aid and Injuries Center. Also, see the patient education article Snakebite.