Death Cap (Amanita phalloide) Photo by By Archenzo – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=329999

Dear Readers, I have been following the Australian Death Cap Poisoning case (where three people died after being fed Beef Wellington with a Death Cap duxelle) with some interest. For a start, I always thought of Death Cap as being a European fungus rather than an international one. Plus, why is this fungus so deadly? Well, an interesting article in New Scientist last week describes both how its poison works, why it evolved, and how the toxin changes from place to place.

For a start, Death Cap looks like a number of other mushrooms which are very edible, so it’s easy to make a mistake – over 90 percent of mushroom-related deaths are caused by Death Cap. But why? The active ingredient is alpha-amantin, which inhibits the action of the enzyme RNA Polymerase II. Anyone who is just recovering from their biology studies will remember that this enzyme is absolutely crucial to the manufacture of proteins, and hence to the survival of practically all the cells in the body. When ingested (as a mushroom risotto for example) the poison enters the bloodstream, migrates to the liver and then hides out in the gall bladder. Once this has happened, the person poisoned might start to feel better, but as soon as they eat, the poison is secreted along with the bile used to digest the food, and the cycle starts again. Eventually, if not treated, the person dies from liver and kidney damage.

Interestingly, the fatality rate from Death Cap is ‘only’ about 10 to 30 percent. If diagnosed correctly, the patient can be treated with fluids, activated charcoal to soak up the toxins and benzyl penicillin to prevent the toxin being taken into the liver. However there is no antidote to the poison, and those affected may require a liver transplant.

But why did the poison evolve in the first place?

Clearly, it wasn’t to poison humans – as it takes 6-12 hours for the toxin to affect us, it wouldn’t prevent the fungus from being eaten. The consensus seems to be that Death Cap developed alpha-amantin to deter insects, which are presumably more susceptible to instant death from ingesting it. Death Cap is also an ectomycorrhizal fungus, which means that it forms a symbiotic relationship with tree roots, swapping nutrients such as nitrogen and phosphorous for carbohydrates – another theory is that the toxins help the fungus to out-compete other fungi. One problem for scientists is that Death Cap can’t be grown ‘in captivity’, and so it can only be studied in situ. However, we are discovering some fascinating things about how Death Cap is changing as it spreads around the world.

Death Cap originated in Europe, but was originally taken to North America on the roots of imported trees, and has subsequently spread to every continent except Antarctica. What is fascinating is that the fungus is associating with different trees in each place, and that the chemical structure of the toxins that it contains are changing, depending on the micro-organisms and other life forms that it encounters.

Even more interestingly, Death Cap has changed how it reproduces. Reproduction in fungi is complex, but normally two individuals are involved. However, Death Cap has taken to reproducing unisexually, which means that a single individual fungus can produce masses of viable spores on its own, all of which can grow up to found a new colony. No wonder the fungus is doing so well, and spreading so widely.

This does, of course, represent a problem for the unwary. In particular, it appears that the fungus strongly resembles Paddy Straw Mushroom (popular in Chinese cuisine) and the White Caesar Mushroom, beloved by the Hmong and people of Laotian origin. When Death Cap is found in places like Australia and North America, by people with a culture that includes foraging for food, mistakes may happen, with terrible consequences. All the more reason to be extremely careful when skipping through the woods looking for mushrooms.