Edible mushrooms have become a popular protein source in today’s cuisines, and as soon as things go mainstream, we want to up the status quo. As such, foraging for edible wild mushrooms is now trending. The problem is, how does the novice tell the difference between what’s edible and what’s poisonous? Even experts can mistake one mushroom for another, as the morphologies can overlap in similarity. Just recently in California, Death Cap mushroom intoxication has made the news, and in this case it didn’t lead to death, but ingesting this fungus can be very lethal.

Death Cap Mushroom

Amanita Phalloides commonly known as Death Cap mushroom is on of the most poisonous mushrooms, accounting for about 95% of mushroom poisonings in humans. It has a smooth white stalk with a bulbous cup at the base. The cap is a greenish yellow color with gills underneath. It has a sweet smell and pleasant taste. It is generally as tall as the width of its cap, and grows symbiotically with a variety of trees. It’s appearance can vary by season, region, climate, and soil. Toxicity is also influenced by these factors, as-well-as age; toxicity being highest in early development.

Amanita Phalloides Toxicity

A. Phalloides contains three groups of toxins: Amatoxins, phallotoxins, and virotoxins. Amatoxins are the main cause of fatality. Phallotoxins are easily degraded by heat and digestion, and not readily absorbed in the gastrointestinal tract (G.I). Virotoxins are NOT easily degrade by heat or digestion, but they are also poorly absorbed in the G.I. and therefore don’t pose any risks to human through ingestion.

 

Amatoxins. Amanitins are highly toxic cyclopeptide compounds; the primary human toxin being alpha-amanitin. This mushroom toxin is not inactivated by drying, cooking or digestion, and can cause death in just 2 days. As little as 0.1mg/kg body weight is enough to kill a human, and this amount can be found in a single mushroom. The toxin targets the Liver, but the kidney is usually also involved.

 

 

Mechanism of Toxicity. Alpha-amanitin works by binding to and inhibiting the enzyme RNA polymerase II in the cell nucleus. This results in the inhibition of messenger RNA (mRNA), from which proteins are translated. The resultant protein deficiency leads to cell death. Alpha-amanitin may also trigger cell death through inducing oxidative stress, signaling a cellular response involving a cascade of cytokine release, leading to apoptosis.

Signs & Symptoms. Gastrointestinal disorders are the beginning of toxic response. This phase consists of, nausea, vomiting, diarrhea, and abdominal pain. It may be accompanied by fever and tachycardia (rapid heart beat). A latent phase follows, in which symptoms stop. During this time, hepatic and renal function starts to decline. Finally, due to liver necrosis, jaundice, hypoglycemia (low blood sugar), and oliguria (no urine) develop. Central nervous system damage, secondary to hemorrhagic hepato-renal failure and hypotension, causes delirium and confusion, coma, and death.

Treatment and Therapy. There is no antidote for Death Cap mushroom toxicity. The only true resolution is liver transplantation. However, G.I decontamination with gastric lavage and activated charcoal has been used to try to rid the body of the toxin. This however is mostly useful only within the early stages of ingestion, as the toxin is rapidly absorbed, circulated in the liver’s enteric cirulation, and excreted via the kidneys into the urine. The problem is that it is not metabolized and therefore concentrates in the nephrons of the kidney where is is reabsorbed and recirculated, causing repeated harm.

N. Acetylcysteine. The antioxidant n-acetylcysteine, which is a known liver protectant, used also in acetaminophen overdose (for the same reason), is used to ameliorate liver damage, and helps reduce oxidative injury by reactive oxygen species.

Silybin. Another antioxidant and liver detoxifing agent, Silybin, has been successfully used to treat amanitin toxicity. Silybin is the major active compound of a group of Silymarin compounds found in Silybum Marianum also-known-as, the plant Milk thistle.

Benzylpenicillin. The antibiotic benzylpenicillin has also to been used as an effective treatment. Although it is not known exactly how or why this compound helps, it is thought to help prevent the toxin from binding to its transporter proteins and receptors.

All of these therapies still cary a significantly high death rate. The earlier treatment begins the better, and the longer it takes for symtoms to develop the worse the prognosis. Many of those who survive develop Chronic Liver Disease. The degree of liver necrosis determine the ability of the Liver to regenerate.

Summary

So, we see that this is a very serious situation, as one can find themselves in a dire predicament over the ingestion of as few as one or two “wrong” mushrooms. You have to ask yourself if it is worth the risk, but if you ask me, the risk to benefit ratio of foraging for wild edible mushrooms is too high.