MUSHROOM NEWSLETTER. 15 February 2014 DEATH CAPS

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1 MUSHROOM NEWSLETTER 15 February 2014 DEATH CAPS We are in the depths of winter and fungi are thin on the ground (although not entirely absent try looking for Jew s ears on the few remaining elders that are poking their trunks above the floodwaters). Jew s ears don t mind cool weather and positively love damp they almost always grow on elder Normally I d have left my next newsletter to the emergence of morels next month, but then my wonderful Irish foraging buddy, Bill O Dea ( sent me an interesting link to a quasiscientific paper on death caps by Cat Adams ( 14/02/most_dangerous_mushroom_death_cap_is_spreading_but_poisoni ng_can_be_treated.html). Her paper is too long and sometimes too technical for a newsletter, but it contains some really interesting ideas. I ve based the following on her piece and am hoping the ghoulish nature of the material makes for interesting reading, but do have a look at the original.

2 PART ONE: TOXICITY AND TREATMENT Death caps are common and responsible for 80% of fatalities worldwide (Photo: Charles Pottiger) The death cap (Amanita phalloides) undoubtedly kills more people than any other mushroom. Indeed a study by Copenhagen University suggests it accounts for about 80% of all fatalities around the globe. Death caps kill because they contain high levels of amatoxins. After ingestion, about 60% these travel directly to the liver where they are spat out into the gall bladder. This releases bile into the gut but at the end of the small intestine, most is reabsorbed and returns to the liver to repeat the cycle. Each time it re-enters this vital organ, the amatoxins bind to and disable an enzyme vital to the production of proteins. Without these cells can t function, resulting in liver and organ failure, coma and death. The remaining 40% of the amatoxins concentrate in the kidneys. Unlike the liver, healthy kidneys can extract these and expel them as urine, but until the last bit of poison has left the body, the toxins continue to damage the liver. Even the kidneys can only function if continually flushed out, so victims need aggressive hydration or else the process slows and the amatoxins begin to destroy the kidneys as well. If this happens, rapid organ failure is not far behind.

3 Death caps vary in colour, but are generally white to olive/green (second picture Charles Pottiger) Until recently it was believed to be effectively untreatable that as the victim succumbed to massive liver failure, all the doctors could do was to fire-fight each symptom on a case-by-case basis. Now it seems there may be an effective treatment in the form of silibinin, which is a drug derived from the plant milk thistle, Silybum marianum. This reduces the flow of amatoxins to the liver, giving the kidneys more time to expel them. But even this wonder-drug relies on rapid identification of the cause of the poisoning and this is usually very difficult. To start with, poisonings are thankfully very rare (there have only been two adult fatalities in Britain in the last 100 years). This means the chances that your A&E registrar will be familiar with the signs are very small. Worse, it generally takes 6-24 hours for symptoms to appear. These are unpleasant but infuriatingly vague from a medical perspective. They generally begin with abdominal cramps, vomiting, and severe diarrhoea. Linking these to fungal poisoning is often complicated because many victims claim the mushroom they ate three meals ago was delicious. And to make things more obscure, if the patient is re hydrated, the symptoms may lessen to produce the dreaded honeymoon phase.

4 Milk thistles may offer a chance of a reprieve for the unlucky Even when correctly diagnosed, the three conventional treatments are now suspected to be largely useless or even harmful. The first is pumping activated charcoal into the digestive tract to absorb the poisons. But these have normally long-since been absorbed into the bloodstream. And for the same reasons, stomach pumping is far also far too late. The third treatment of acetylcysteine, works well with some liver-destroying toxins, but has no effect on amatoxins and thins the blood which gives misleading liver-function test results. The latest research suggests the best treatments are aggressive rehydration and silibinin. Unfortunately or perhaps fortunately a shortage of patients means the last has yet to pass scientific scrutiny. Patients go into renal failure for two reasons, says Dr Todd Mitchell of Dominican Hospital in Santa Cruz. One, they just present so late that their kidneys have already shut down. Or two, more commonly, they re just not aggressively hydrated enough. He has treated more than 60 amatoxin patients and has saved all who still had kidney function and started quickly on the drug. His research has yet to be published 60 patients isn t a big enough sample but he is confident: When we present to FDA, it will be a slam dunk for approval, he says. The drug has virtually no side effects, it s very well tolerated, and it can be awesomely effective. So, in the extremely unlikely event that you accidentally consume a death cap, ask your doctors to call Dr Mitchell to request enrolment in his milk thistle study he promises to ship silibinin to anywhere in the world.

5 PART TWO: GLOBAL SPREAD Death caps are ectomycorrhizal. This means they live symbiotically wrapped around the roots of trees as a mycelium stretching out into the soil to funnel nutrients such as nitrogen and phosphorous to their host. In return they receive sugars manufactured by the tree. The mycelium wraps itself around the root and spreads out into the soil Until recently it was believed the death cap had, over countless millennia, spread to every continent (apart from Antarctica) via spore dispersal, but more recently detailed DNA research has thrown this into doubt. Anne Pringle sequenced the DNA of old, dried specimens from across the USA, She found that all specimens before 1938 were actually different Amanitas, while the real McCoy made a sudden appearance in 1938 and rapidly became increasingly common. She also sequenced and compared the DNA of death caps from Europe with those from the USA. She found much less genetic variation in the latter, indicating it had started in Europe and that American mushrooms stemmed from a handful of individuals. It seems the spread may be linked to settlers to the New World and British colonies introducing their favourite trees. Seeds were planted but quickly died. Nothing seemed to help until someone had the bright idea to bring seedlings in pots with their native soil and hey presto! Success in North America, Australia and Asia! Unbeknown to the nurserymen, the answer lay in the vital symbiotic relationship between plant and fungus.

6 Structure of a typical Amanita (although death caps normally lack the flecks on the cap) Now at this point I believe Cat Adams makes an error when she claims that after transplanting in the New World, the death cap became invasive by making a quantum leap. She says that in Europe its only natural host is the European oak. In the USA it transferred first to native oaks, then to other broadleafs and from these to conifers. Superficially at least this seems to be bunkum. I find most of my death caps in conifer plantations and certainly this is backed up by mycological encyclopaedias such as Roger Phillips Mushrooms. Also in the same article Adams claims poisoning in America often occurs because death caps can grow among the entirely pastoral field mushroom, Agaricus campestris. Nevertheless, the basic thesis that death caps have undergone a dramatic expansion of range by leaping species is still possible. Just supposing it was originally largely confined to deciduous woodland in Europe, but at some point in the early 20 th century it became more versatile in its choice of hosts? This species leap could even have happened in Britain after all in 1900 we had only 5% tree cover, but thanks to the Forestry Commission s massive planting of non-native sitka and spruce, this figure has more than doubled to 11%. It is tempting to speculate that presented with what was effectively a vacant habitat niche, the species exploited a minor mutation to become more catholic in its tastes. If so, this might explain its apparent colonisation of new territories in the New World and Australasia.

7 A warning sign in an Australian Park Finally, just in case any of you like this sort of thing, there are now facebook and twitter buttons on my website. I don t tweet much in the quiet months, but will get into gear after Easter. Happy (and safe) foraging! Daniel Butler / P.S. As always, let me know if you want to be removed from the list and I will do it forthwith.