Three feet. Three feet of red sand and clay the hunter-gatherer Bushmen of the Kalahari Desert dig through to find the poison which they use to fall their prey. Do they search for the venom of snakes, spiders, or scorpions? No, they dig for the larvae of a lowly leaf beetle.
Beetles of the genus Diamphidia lay their eggs on the stems of shrubs from the Commiphora genus – commonly known as frankincense and myrrh.* The doting mothers then coat their precious eggs with their own feces (that’s faeces for my UK friends), which harden into a protective armor. As the eggs develop through the instar and grub phases, the larvae will shed their poo protection and burrow up to (down to?) three feet, where they make a cocoon from sand and take a needed break. They may lay dormant for several years before molting into pupae, and continue their life cycle. This long dormancy period means that the Bushmen can find the cocoons and larvae year-round and have a ready supply of poison, especially important since mature beetles are not poisonous.
* Remember that part in The Matrix where Neo sees the tracking device “bug” extracted from his navel, and shouts “Jesus Christ, that thing’s real?” That’s me when I found out frankincense and myrrh were real things, and not just a belated baby shower gift delivered by three wise men.
The Bushmen, also known as the San people, dig beside Commiphora host plants, such as Commiphora angolensis, in search of Diamphidia nigroornata, or Commiphora africana for Diamphidia vittatipennis. Once collected, the Bushmen will squeeze the fluid from the larvae and pupae, otherwise known as hemolymph, onto the shaft of their arrows, but not the tip, to avoid “accidents.” Up to ten larvae could be applied to one arrow, which is then dried over hot coals to bond the poison, which maintains its lethal potential for up to a year.
Their bows and arrows are not powerful – which is one reason why they use poisoned arrows – so the Bushmen hunters must stalk their prey and get close before taking a shot. Death comes slowly to the animals – ostrich, zebra, giraffe, eland, springbok, or wildebeest to name a few – and depending upon the size, takes from hours to days. The Bushmen, therefore, track the wounded and poisoned animals up to several miles before the prey becomes disorientated and finally immobilized. If not already dead when found, a piercing blow from a Bushman’s spear finishes the job.
Chemical studies on this particular arrow poison started in the late 1800’s, with simple, yet important, observations that the toxin can be extracted with water or precipitated with alcohol, and is unstable in aqueous solutions and completely deactivated with boiling. Fast forward one hundred years to the 1980’s, and we have the isolation of a 60,000 molecular weight protein named diamphotoxin.
For many years, the primary mechanism of action was thought to be neurotoxicity with a pinch of cardiotoxicity, as the toxin appeared to block neuromuscular function, like the South American arrow poison curare (also like curare, diamphotoxin has no oral activity, and eating poisoned meat has no effect whatsoever). Symptoms of diamphotoxin in test animals include partial paralysis and labored breathing, followed by cyanosis and respiration ceasing. These symptoms certainly could be interpreted as a result of a neuromuscular blocking agent, in which paralysis of the diaphragm occurs. A lack of oxygen ensues, which is consistent with the partial paralysis and cyanosis, which is simply a blueish coloration of the skin due to low oxygen saturation.
Today though, the mechanism of toxicity is generally regarded to be that of hemolysis, in which red blood cells burst, or lyse. The effects are two-fold. First, a loss of red blood cells means a reduction of hemoglobin, which carries oxygen from our lungs to every tissue in our body. Second, the burst cells spill their contents into the surrounding fluid creating an electrolyte imbalance, such as an increase in serum potassium and magnesium.
The first is fairly self-explanatory, without oxygen you die, plain and simple. Administration of diamphotoxin has a dramatic hemolytic effect, and can reduce hemoglobin levels by 75%. It would be a slow suffocation, and a slow death, as each cell in your body is robbed and starved of vital oxygen. Hemoglobin, not solely confined within red blood cells now, is increased in the plasma and then filtered by the kidneys, with eventual excretion into the urine. This all sounds benign, but the excess hemoglobin in the urine, called hemoglobinuria, gives the urine a dark, almost black color. So I suppose the Bushmen can track their poisoned prey by following the inky pee.
The second, an increase in electrolytes causing an imbalance, is where things get interesting. Researchers of diamphotoxin do not directly mention this, but massive hemolysis, such as that associated with diamphotoxin, can result in hyperkalemia, an increase in serum potassium. Symptoms are general weakness and malaise, but in extreme situations arrhythmia and sudden cardiac death can occur. If that sounds familiar, it’s a similar mechanism of death associated with cardiac glycosides like those in oleander and the suicide tree.
An increase in magnesium is called hypermagnesemia, and is relatively rare as the kidneys are efficient in removing magnesium. However, in severe cases of hemolysis, plasma magnesium increases to concentrations high enough to cause weakness, labored breathing, low heart rate, and dizziness.
All together, diamphotoxin is a wonderful poison. The massive hemolysis with cumulative effects of reducing oxygen transport, hyperkalemia, and hypermagnesemia is a thing of beauty. Slow and labored, yes, but beautiful nonetheless. Of equal beauty is the tradition of the Bushmen. I imagine they have the ability to make more powerful bows and stronger arrows, but sticking to tradition and digging for poisonous larvae, right up to tracking their poisoned meals, is a romantic vision for me. Who would have though beauty and romance could come from lowly leaf beetle larvae.
- Schapera, Isaac. “Bushman Arrow Poisons.” Bantu Studies 2.1 (1923): 199-214.
- Woollard, John Mck.r., Frederick A. Fuhrman, and Harry S. Mosher. “The Bushman Arrow Toxin, Diamphidia Toxin: Isolation from Pupae of Diamphidia Nigro-ornata.” Toxicon 22.6 (1984): 937-46.
- Kao, C.y., M.j. Salwen, S.l. Hu, H.m. Pitter, and J.m.r. Woollard. “Diamphidia Toxin, the Bushmen’s Arrow Poison: Possible Mechanism of Prey-killing.” Toxicon 27.12 (1989): 1351-366.
- De la Harpe, J., Reich, E., Reich, K.A., Dowdle, E.B. “Diamphotoxin. The arrow poison of the !Kung Bushmen.” The Journal of Biological Chemistry 258.19 (1983): 11924-31.
Is there an antidote?
Good question, and one I should have addressed….Nope, no “antidote,” just supportive care.
have you ever done an article on Phyllobates? Haven’t seen one on your site….
Thanks! I’m getting back to my normal routine. No, I haven’t yet, but it’s on the list!
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Thank you for a really clear, vivid article. What kind of tests do you need to do postmortem to diagnosis this kind of diamphotoxin poisoning? Is it possible to see the red blood cell damage microscopically?
That’s a great question! From a toxicology, or specifically postmortem toxicology viewpoint, I don’t believe you’d have a good chance of detecting, and conforming, diamphotoxin in blood. For a normal lab, it’s too large a molecule and too esoteric to even bother with. The better assay would be vitreous (eyeball fluid) electrolytes, looking for increased potassium (hyperkalemia), and other electrolytes. Hemolysis of the blood could definitely be seen as well, though this also occurs naturally after death. What it would come down to is the history and circumstances, clinical findings, pathology (autopsy) findings, and toxicology – essentially what every medico-legal death investigation entails, though this would be a bit more challenging.
Thanks for reading!
I just want to know how the bushmen discovered this. Was it accidental or research or some encounter with death themselves