The black mamba (Dendroaspis polylepis) is a species of extremely venomous snake, a member of the family Elapidae native to parts of Sub-Saharan Africa.
First formally described by Albert Günther in 1864, it is the second-longest venomous snake after the king cobra; mature specimens generally exceed 2 metres (6.6 feet) and commonly grow to 3 m (10 ft). Specimens of 4.3 to 4.5 m (14.1 to 14.8 ft) have been reported. Its skin colour varies from grey to dark brown. Juvenile black mambas tend to be paler than adults and darken with age.
The species is both terrestrial (ground-living) and arboreal (tree-living); it inhabits savannah, woodland, rocky slopes and in some regions, dense forest. It is diurnal and is known to prey on birds and small mammals. Over suitable surfaces, it can move at speeds up to 16 km/h (10 mph) for short distances. Adult black mambas have few natural predators.
Did you know: An adult black mamba can grow up to 14 feet in length.
Did you know: All mambas are highly venomous.
The black mamba is a long, slender, cylindrical snake. It has a “coffin-shaped” head with a somewhat pronounced brow ridge and a medium-sized eye. The adult snake’s length typically ranges from 2 to 3 m (6 ft 7 in to 9 ft 10 in) but specimens have grown to lengths of 4.3 to 4.5 m (14.1 to 14.8 ft).
It is the second-longest venomous snake species, exceeded in length only by the king cobra. The black mamba is a proteroglyphous (front-fanged) snake, with fangs up to 6.5 mm (0.26 in) in length, located at the front of the maxilla.
The tail of the species is long and thin, the caudal vertebrae making up 17–25% of its body length.
Black mambas weigh about 1.6 kg (3.5 lb) on average.
Specimens vary considerably in colour, including olive, yellowish-brown, khaki and gunmetal but are rarely black. The scales of some individuals may have a purplish glow. Individuals occasionally display dark mottling towards the posterior, which may appear in the form of diagonal crossbands. Black mambas have greyish-white underbellies and the inside of the mouth is dark bluish-grey to nearly black. Mamba eyes range between greyish-brown and shades of black; the pupil is surrounded by a silvery-white or yellow colour. Juvenile snakes are lighter in colour than adults; these are typically grey or olive green and darken as they age
The black mamba is the most feared snake in Africa because of its size, aggression, toxicity and speed of onset of symptoms, and is classified as a snake of medical importance by the World Health Organization.
A survey in South Africa from 1957 to 1979 recorded 2553 venomous snakebites, 75 of which were confirmed as being from black mambas. Of these 75 cases, 63 had symptoms of systemic envenomation and 21 died.
Those bitten before 1962 received a polyvalent antivenom that had no effect on black mamba venom, and 15 people out of 35 who received the antivenom died. A mamba-specific antivenom was introduced in 1962, followed by a fully polyvalent antivenom in 1971. Over this period, 5 people out of 38 bitten by black mambas and given antivenom died.[b][A census in rural Zimbabwe in 1991 and 1992 revealed 274 cases of snakebite, of which 5 died. Black mambas were confirmed in 15 cases, of which 2 died.
The peak period for deaths is the species’ breeding season from September to February, during which black mambas are most irritable. Bites are very rare outside Africa; snake handlers and enthusiasts are the usual victims.
Unlike many venomous snake species, black mamba venom does not contain protease enzymes. Its bites do not generally cause local swelling or necrosis, and a tingling sensation in the bitten area might be the only initial symptom. The snake tends to bite repeatedly and let go, so there might be multiple puncture wounds.
Its bite can deliver about 100–120 mg of venom on average; the maximum recorded dose is 400 mg. The murine median lethal dose (LD50) when administered intravenously has been calculated at 0.32 and 0.33 mg/kg. Bites were often fatal before antivenom was widely available.
The venom is predominantly neurotoxic; symptoms often become apparent within ten minutes. Early neurological signs that indicate severe envenoming include metallic taste, drooping eyelids (ptosis) and gradual symptoms of bulbar palsy. Other neurological symptoms include miosis, blurred or diminished vision, paresthesia, dysarthria, dysphagia, dyspnea, difficulty handling oral secretions, an absent gag reflex, fasciculations, ataxia, vertigo, drowsiness and loss of consciousness, and respiratory paralysis. Other more general symptoms include nausea and vomiting, abdominal pain, diarrhoea, sweating, salivation, goosebumps and red eyes. The bite of a black mamba can cause collapse in humans within 45 minutes or less.
Without appropriate antivenom treatment, symptoms typically progress to respiratory failure, which leads to cardiovascular collapse and death. This typically occurs in 7 to 15 hours.
In 2015, the proteome (complete protein profile) of black mamba venom was assessed and published, revealing 41 distinct proteins and one nucleoside.
The venom is composed of two main families of toxic agents, dendrotoxins (I and K) and (at a slightly lower proportion) three-finger toxins. Dendrotoxins are akin to kunitz-type protease inhibitors that interact with voltage-dependent potassium channels, stimulating acetylcholine and causing an excitatory effect, and are thought to cause symptoms such as sweating. Member of the three-finger family include alpha-neurotoxin, cardiotoxins, fasciculins and mambalgins. The most toxic components are the alpha-neurotoxin, which bind nicotinic acetylcholine receptors and hence block the action of acetylcholine at the postsynaptic membrane and cause neuromuscular blockade and hence paralysis.
Fasciculins are anticholinesterase inhibitors that cause muscle fasciculation. The venom has little or no haemolytic, haemorrhagic or procoagulant activity. Mambalgins act as inhibitors for acid-sensing ion channels in the central and peripheral nervous system, causing a pain-inhibiting effect. There is research interest in their analgesic potential