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

(www.mushroomstuff.com) sent me an interesting link to a quasi-scientific paper on death caps by Cat Adams

(http://www.slate.com/articles/health_and_science/medical_examiner/2014/02/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.

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.

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’.

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 re-hydration 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.

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.

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 20th 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.

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

www.fungiforays.co.uk

01597 811168 / 0779 429 4221

P.S. As always, let me know if you want to be removed from the list and I will do it forthwith.