Amanita Phalloides – The Fatality of Consuming this Mushroom

Amanita Phalloides is known as the death cap mushroom and is usually found in the wild and closely resembles other edible varieties. This then follows that you should never consume any mushroom from the wild unless it has been certified by an expert as safe. These deadly varieties of mushroom can cause asphyxiation in humans and lead to nervous breakdown coupled with vomiting, stomach ache and hemorrhage. There are reports that have it that a whole linage of family members have been wiped out after consuming these poisonous variety of mushroom during their dinner meal.

However, there are delicious and nutritious varieties of mushrooms that grow in the dark forests and in thick vegetation where they grow by saprophytism converting organic materials into organic compounds and nutrients which they feed on. They have over the years formed part of the delicacy of most homes across the world and are increasingly becoming a popular food even among people who know very little about it.

The medicinal value of mushroom is also a key factor in its popularity because extracts from mushroom have been used in medicinal treatments where over 2000 varieties of edible mushroom extracts have been deployed in pharmaceutical preparations in combating hepatitis, Alzheimer’s disease and in reducing high cholesterol.

Amanita phalloides is responsible for most mushroom related deaths around the world. It forms ectomycorrhizas with introduced broadleaved trees. It is known in Vancouver and Victoria with Hornbeam (Fagus sylvatica) street and park trees but has also been found growing with native Garry oak on Galiano Island.

Production Of Amatoxins

The deadly mushrooms known as death caps produce amatoxins, a family of bicyclic octapeptides that inhibit nuclear RNA polymerase II. Inhibition of RNA polymerase II leads to decreased protein synthesis and ultimately cell death. The toxins cause severe liver damage, which can be fatal. Amatoxins are also lethal when inhaled, causing respiratory failure and cardiac arrest. They are not destroyed by cooking or drying, and can be spread to other people through direct contact.

Amanita phalloides



Several antidotes exist, but they must be administered as soon as possible after ingestion of death cap mushrooms. Symptoms of poisoning are typically mild to moderate, but can progress to shock, confusion, paralysis, seizures, coma and death. Acetylcysteine is the most effective antidote for ingested amatoxins, but only if it is given within three hours of ingestion. Other drugs that may be used include sodium thiopental, diazepam and haemodialysis.

Amanita phalloides produces two main groups of toxins, the amatoxins and phallotoxins, which are multicyclic peptides spread throughout mushroom tissue. The amatoxins have been shown to exhibit cytotoxic and hemolytic activities in experimental animals. The phallotoxins are believed to have been responsible for the deaths of many people who mistakenly identified Amanita phalloides with the edible paddy straw mushroom, Volvariella volvacea. Misidentification is a leading cause of mushroom poisoning in the United States and Australia, with East- and Southeast Asian immigrants being particularly at risk of fatal overdoses.

The toxicity of Amanita phalloides is not affected by cooking or freezing, but does decrease with age. It is therefore important to gather and store mushrooms in a cool, dry place to ensure their freshness.

Amanita phalloides may be found in urban and rural settings and is common in North America, where it grows in association with oaks and birch. It also forms ectomycorrhizas with other broad-leafed trees, including pine. The fruiting bodies (mushrooms) of Amanita phalloides appear in summer and fall, growing from mycelium near roots or bark of the host tree. The caps of the mushrooms are greenish or white in color and often have a skirt around the base.

Amanita Phalloides Causes Renal Failure

Amanita phalloides, is the most toxic species in the order Agaricales and the cause of the majority of mushroom poisonings worldwide. This deadly basidiomycete fungus is native to Europe and was brought to North America by the roots of imported trees. It forms ectomycorrhizas with a variety of broadleaved hosts, including oak and birch, producing large fruiting bodies in summer and autumn.

The mushroom contains two groups of thermostable cyclic oligopeptide toxins, the amatoxins and the phallotoxins. The main lethal toxin, a-amatoxin, produces hepatocellular damage by binding to eukaryotic RNA polymerase II and causing transcription arrest in metabolically highly active cells such as hepatocytes and kidneys. The toxic effects of a-amatoxin are generally more rapid in the liver than in the kidney, and symptoms progress rapidly to multiorgan failure and death within a week if untreated.

Initial GI upset, typically accompanied by nausea and vomiting is common in most cases of mushroom poisoning, including deaths from Amanita phalloides. This may be confused with other gastrointestinal tract disorders, and thus early recognition and referral to poison control is crucial.

Following the onset of GI signs, clinical progression can be divided into four phases. In the first phase, a 6–40 hour lag period is observed before the onset of severe gastrointestinal symptoms.

During this period, a-amatoxin is excreted by the kidney in fecal matter. Depending on the patient’s age, gender and ingestion amount, this excretion can reach toxic levels.

The second phase begins 6 to 24 hours after mushroom ingestion and is characterized by rapid progression of hepatocellular injury leading to liver failure. Acute renal failure is also seen, especially in patients with preexisting renal disease or in those who ingested a large quantity of mushrooms.

In the third and fourth phases, liver and renal failure progress to end-stage organ failure, often with death within a week if not treated. Therapy consists of supportive measures, gastric decontamination and drugs intended to increase the likelihood of a successful liver transplant. Extracorporeal albumin dialysis is reported to improve patients’ outcomes and facilitate bridging to transplantation.

Amanita Phalloides Causes Severe Liver Injuries

Amanita phalloides produces toxins that cause severe liver injury. This mushroom, which is commonly called death cap or destroying angel, belongs to the lethal amanita group along with Amanita venenata and Amanita pantherina. These mushrooms produce a deadly compound known as a-amanitin or AMA, which causes hepatocellular damage by interfering with the synthesis of proteins in cells. The toxins also bind to RNA polymerase II and interfere with its normal function, causing protein synthesis to slow down. The hepatocellular membranes of the liver are destroyed by the toxin, which ultimately leads to hepatic failure.

The most common symptom of Amanita phalloides poisoning is nausea and vomiting, which begin shortly after the mushroom ingestion. Typically, the nausea and vomiting quickly progress to abdominal pain and then to severe liver dysfunction. This can lead to hepatic failure, which may be fatal if not treated with supportive care.

This mushroom contains two principal toxin groups, heptapeptide phallotoxins and octapeptide amatoxins. These toxins are thermostable, which means they resist heat and low pH, and they are soluble in alcohol and water. The hepatotoxic mechanism of the amatoxins is the binding of the toxin to nuclear RNA polymerase II and preventing its normal function. The phallotoxins are similar to the amatoxins but are more potent, which is why they have a higher mortality rate.

Amanita phalloides is also known to affect the kidneys and brain, resulting in encephalopathy. It is also excreted in the milk of nursing mothers, so breastfeeding should be stopped if this mushroom has been ingested by the mother.

The antidote for a-amanitin is Picroliv, an immunosuppressive drug that has been shown to reduce the severity of symptoms caused by this mushroom. It has been used in cases of severe Amanita phalloides hepatotoxicity, which is often fatal without treatment. The drug can be given intravenously or orally. In a study of 27 patients treated with Picroliv, Escudie et al. found that a prothrombin index below 10% of normal and diarrhea occurring 4 days after ingestion of Amanita phalloides should prompt consideration for urgent liver transplantation.

Inhibition of RNA Polymerase II

Amanita phalloides produces alpha-amanitin, a potent toxin that inhibits RNA polymerase II. This compound has been found to block cellular transcription and halt the production of new genetic material in tumor cells. The toxin works by binding to the bridging helix of the polymerase complex and preventing it from moving away from the DNA template. This binds the helix to a point that prevents the entry and exit of NTPs into the active site. The toxin also interferes with the movement of RNA into and out of the helix, which slows transcription by over 1000 fold.

Amanitin has been shown to have a strong affinity for the nucleoplasmic form of RNA polymerase II from sea urchin, rat liver, and calf thymus cells. However, it has no effect on pol II activity in human cell lines and has little or no affinity for eukaryotic polymerase I or prokaryotic RNA polymerases. The toxin is thought to bind to the bridge helix of RNA polymerase II, which is a central component of the RNA synthesis complex. It is also a key player in the process of protein synthesis, and it interacts with the helix to inhibit its movement.

Researchers have recently made significant progress in dissecting the molecular steps that terminate transcription of protein-encoding genes. The prevailing theory is that the polyadenylation-coupled termination process occurs when Pol II transcribing the 3′ end of a gene pauses to transcribe a polyadenylation signal into nascent RNA before completing the gene transcription. The upstream portion of the nascent RNA is then endonucleolytically cut to produce mature mRNA. The downstream fragment is then ribosomally cleaved and processed to become a functional protein.

This sequence of events is accelerated by the fact that Pol II binds to both the DNA and the RNA transcript. An important step in the termination sequence is a nucleophilic attack by Pol II on the NTP, which is catalyzed by an enzyme called exoribonuclease. This nucleophile attacks the 3′ OH group on the NTP with an activation barrier of 7 kcal/mol. In the recent chemistry simulations, water molecules clustered around this OH site, and the deprotonation energy was sufficient to overcome the barrier.

Some Very Important Mushroom Tips

Mushrooms must be stored in a paper bag or a cloth material and refrigerated. Since they can absorb odor easily, refrain from placing them near materials with a strong or pungent smell.

Use a soft brush to gently remove any surface dirt in Mushrooms and avoid peeling the skin which is also nutritious and tasty!

If you choose to eat mushroom raw which is not advisable, make sure you wipe it clean with a damp cloth or you can rinse it quickly in warm water and pat them dry. Do not soak mushrooms in water.

Above all, seek expert advice on the variety of a mushroom you come in contact with if you are in doubt if it is edible or not. Never consume the deadly Amanita phaloides.