- General characteristics
- Taxonomy
- Phylogeny
- Habitat and distribution
- Reproduction
- Toxicity
- Symptoms of intoxication
- Phases of intoxication
- Treatment
- Gastric lavage
- Antidote
- Dialysis
- Symptomatic treatments
- References
Amanita phalloides is a species of mycorrhizal fungus of the order Agaricales, highly toxic due to the presence of amatoxins. It is a particular fungus that is usually confused with the edible species of the genera Agaricus, Tricholoma, Russula and Volvariella.
It is a lethal fungus when ingested accidentally; it causes damage to the liver and kidney, leading to death. It is known as the mushroom of death, green cap, deadly cap, green hemlock, death hat or devil's mushroom.
Amanita phalloides. Source: pixabay.com
It is characterized by a white cylindrical foot covered by a membranous cuticle with greenish-yellow veins. The stem is crowned by a fleshy, oval olive green hat with multiple lamellae radiating across the underside.
Along the foot, at the level of the middle zone, it presents a ring formed by a white membranous layer. In addition, the presence of a volva at the base of the stem is particular in this species.
It usually grows on the leaf litter of deciduous and coniferous trees, preferring acid soils with a high content of organic matter. It emerges during the autumn months in various forest ecosystems with high humidity and medium temperatures.
It contains the toxins amatoxin and phallotoxin that cause liver damage in lethal doses of 5 mg / kg, causing the so-called phalloid syndrome. This disease manifests itself with gastrointestinal pain, vomiting, diarrhea, tachycardia and seizures, leading to death after 15 days.
Treatment depends on the clinical phase of intoxication and the time elapsed after ingesting the mushrooms. Since there is no specific antidote, it is necessary to initiate preventive measures when accidental use is suspected.
General characteristics
- The fruiting body -sporocarp- is a structure in the shape of a curved hat of 5-15 cm in diameter.
- The predominant coloration of the sporocarp is olive green, with light to dark tones, sometimes whitish.
- Generally it is whitish at the edges, becoming white as a result of the rains.
- One of the characteristics that confuses it with edible mushrooms is that the hat is easily peeled.
- The slightly firm pulp, soft color, pleasant smell and sweet taste is extremely toxic.
- The cuticle of the fruiting body is made up of fibrils of dark tones and the upper surface has a completely smooth surface.
- The bottom of the sporocarp has numerous lamellae very close together, broad and whitish tones.
- The stem or peduncle is tubular and elongated, white with slightly yellow-green areas that provide a spotted appearance.
- The foot is about 8-15 cm and has a diameter of 1-3 cm.
- In the central area of the peduncle it has a layer or white ring, slightly furrowed.
- At the base of the stem, foot or peduncle there is a cup-shaped structure called volva, white in color and fibrous in appearance.
- The volva is a characteristic structure of the species, it must be checked under the mantle of leaves at the foot to identify it.
- When the fungus emerges to the surface it is covered by a veil taking on the appearance of an egg.
Initial phase of Amanita phalloides. Source: commons.wikimedia.org
- During growth, this structure breaks giving rise to the volva.
- The spores of the species are globular, 8-10 mm and white.
- It is a very dangerous mushroom that causes more than 90% of poisonings due to the ingestion of amatoxin.
Taxonomy
- Fungi kingdom
- Division: Basidiomycota
- Subdivision: Basidiomycotina
- Class: Homobasidiomycetes
- Subclass: Agaricomycetidae
- Order: Agaricales
- Family: Amanitaceae
- Genre: Amanita
- Species: A. phalloides
- Binomial name: Amanita phalloides (Vaill. Ex Fr.) Link (1833)
- Common name: green hemlock, green cap, deadly cap.
Phylogeny
The genus Amanita is a group of agaricaceous fungi made up of various edible species and others that are extremely toxic. The term phalloides derives from the Greek "pallos" penis and "leidos" form, that is, in the shape of a phallus or penis.
The species was initially reported as Agaricus phalloides (Fries, 1821), subsequent descriptions allowed it to be named Amanita viridis (Persoon). Later reviews managed to define the name of this particular mushroom due to its high toxicity as Amanita phalloides (Link, 1833).
In this regard, Amanita phalloides is the representative species of toxic amanitas, including Amanita bisporigera, Amanita verna and Amanita virosa. In fact, Amanita verna is cataloged by some authors as a subspecies of A. phalloides, differing by color, time of development and toxins.
Habitat and distribution
The Amanita phalloides is a very abundant species in lush, broad-leaved flat-leafy forests and coniferous forests. Likewise, the vegetative structures of this fungus are part of the mycorrhiza of various oak species.
It generally emerges in the cool months, at the end of summer and during the fall, however, it does not adapt to the cold winter. The reproductive structures developed from the subterranean hyphae arise in a localized and individual way.
Natural habitat of Amanita phalloides. Source: H. creativecommons.org
In times of high rainfall it emerges in large groups under the shade of large leafy trees. It prefers sandy and sandy-loam soils, and is located at heights from the coast to the high mountains.
The species develops in temperate climate ecosystems in both the northern and southern hemispheres. It is native to temperate European regions, found in North America, South America and Australia as an introduced species due to the importation of wood.
Reproduction
The Amanita phalloides fungus is a basidiomycete that reproduces by reproductive spores called basidiospores. Each basidiospore is attached to the carpophor through a hymenophore.
Basidiospores are tiny, lightweight structures that are easily dispersed by the movement of wind, insects, or small animals. Upon reaching the ground, under optimal conditions of humidity, temperature and nutritional elements, it develops an underground primary-monokaryotic mycelium.
Growth phases of Amanita phalloides. Source: Justin Pierce (JPierce) creativecommons.org
Each cell of the mycelium has a nucleus differentiated as positive or negative; the survival of the fungus requires the union of opposite nuclei. Through a fibula the micellar cells unite ensuring the presence of two nuclei of the opposite sign per cell.
The process of joining the two haploid nuclei allows the creation of the secondary dikaryotic mycelium or zygote. This secondary mycelium develops and grows underground for a long time as part of the soil mycorrhiza.
Later, through successive divisions and transformations, the seta or basidiocarp - tertiary mycelium - is formed that protrudes from the ground. Finally, at the level of the lamellae, two haploid nuclei fuse, giving rise to diploid basidiospores.
This species can also reproduce vegetatively by fragmentation or cleavage. In this case, a part of the thallus or mycelium is separated or broken from which a new individual is formed.
Toxicity
The mushrooms of the Amanita phalloides fungus contain toxic agents causing acute liver disease or hepatotoxicity, including functional or anatomical damage. The fungus contains the toxins amatoxin (amanitins α, β and γ), falotoxin and virotoxin derived from cyclopeptides.
These toxins are not inactivated by culinary processes such as cooking, drying, or marinating. 40 gr of the fungus contains 5-15 mg of α-amanitin, the lethal dose being 0.1-0.3 mg / kg, hence its high degree of toxicity.
Α-Amanitin (amatoxin) is a toxin that causes damage to the liver and kidney. The damage is caused by the inactivation of RNA polymerase II and the inhibition of protein synthesis leading to cell death.
Falotoxin is a natural metabolite or alkaloid located at the foot of the Amanita phalloides fungus. It intervenes at the level of the intestine causing gastrointestinal toxicity due to the alteration of the cell membrane of the mucosa.
The mechanism of action occurs at the intestinal level, causing the disintegration of the mucosa and facilitating the absorption of amatoxins. As for virotoxins, they are heptapeptide compounds that do not act as toxic agents when ingested by man.
Symptoms of intoxication
The pleasant taste of the Amanita phalloides mushroom and the late manifestation of the first symptoms make it a lethal fungus. The manifestation of symptoms usually occurs after the asymptomatic phase from 10-14 hours after ingestion.
After 24 hours, the action of the Amanita fungus phalotoxins produces acute gastroenteritis. Symptoms begin with severe pain, nausea, vomiting, and diarrhea, leading to vital dehydration and electrolyte variations.
Typical structure of Amanita phalloides. Source: Archenzoderivative work creativecommons.org
From the 2nd to 3rd day the patient enters a phase of transitory improvement or latency. However, after the 4th-5th day it may relapse, developing lesions in the liver and kidneys.
In the case of very strong poisonings, liver symptoms occur suddenly in the early stage (1-2 days). The diagnosis of intoxication is determined based on the anamnesis, either consumption of mushrooms or collection of unidentified mushrooms.
Once the type of poisoning has been determined, a mycological analysis of gastric lavage, vomit and feces is recommended. The objective of this analysis is to determine the presence of Amanita phalloides spores in the analyzed samples.
Furthermore, the determination of amanitin levels in urine samples is recommended. In fact, the toxin remains in the urine for up to 36 hours after ingesting the fungus.
Reductions of less than 70% in prothrombin activity between 16-24 h indicate a high risk of liver failure. Values greater than 1000 IU / I AST and ALT at 24-36 h also indicate liver problems in patients with symptoms of intoxication.
Phases of intoxication
The clinical picture of the disease is manifested by a short asymptomatic period (12-16 h). Followed by a gastrointestinal phase, a latency or recovery phase, and the hepatorenal phase, which can end with the death of the patient.
- Gastrointestinal phase (12-36 hours): pain in the intestine, nausea, vomiting and diarrhea. Dehydration and hydrolytic disorders.
- Recovery phase (12-24 hours): manifests as an apparent improvement. However, liver damage continues due to the presence of toxins.
- Hepatorenal phase (2-4 days): symptoms of liver toxicity, increased bilirubin and transaminases occur. Likewise, alterations in kidney functions occur, the patient can die from liver and kidney failure.
Treatment
At the moment of detecting the poisoning, a gastric lavage should be applied immediately, preferably before the first hour of the event. After this decontamination process, it is advisable to apply activated charcoal through a probe and keep it in the stomach.
Gastric lavage
Gastric lavage should be performed at the time of discovering the poisoning, it is not recommended at the onset of gastrointestinal symptoms. A wash at this stage allows only to identify the cause of the poisoning.
Antidote
At present, no precise antidote has been discovered for the symptomatic treatment of Amanita phalloides poisoning. The use of the natural antioxidant silymarin, high doses of penicillin or the mucolytic N-acetylcysteine (NAC) have reported uncertain results.
Silibinime is one of the active components of silymarin, it must be administered within 24 hours of poisoning. A dose of 5-20 mg / kg is administered intravenously or 50-100 mg / kg orally for 5-6 days until recovery is achieved.
In the case of the mucolytic N-acetylcysteine (NAC), treatment should also be started within 24 hours of detection of poisoning. Three continuous doses are applied for 21 h of 50-100-150 mg / kg diluted in glucose or NaCl until INR normalization.
The use of this antibiotic is disputed; the utility is limited to stopping the passage of amanitin through the cell membrane. The effectiveness of this treatment is restricted to the asymptomatic stage in doses of 0.3-1 million DU / kg / d.
Dialysis
Treatments based on hemodialysis, hemoperfusion or liver dialysis processes have made it possible to eliminate the active agent in initial treatments. Hemodialysis is recommended in the initial stages of poisoning as well as forced diuresis (300-400 ml / h).
Symptomatic treatments
Symptomatic treatments such as the regulation of metabolic changes, acid-base balance or water balance report satisfactory results. However, only liver transplantation is effective when acute liver failure has been diagnosed allowing the patient's life to be saved.
References
- Amanita phalloides (2018) Catalog of Mushrooms and Fungi. Fungipedia Mycological Association. Recovered at: fungipedia.org
- Amanita phalloides (2018) Empendium. Portal for doctors. Recovered at: empendium.com
- Chasco Ganuza Maite (2016) Management of Amanita phalloides poisoning. Newsletter. Faculty of Medicine, University of Navarra.
- Cortese, S., Risso, M., & Trapassi, JH (2013). Amanita phalloides poisoning: series of three cases. Acta toxicológica Argentina, 21 (2), 110-117.
- Espinoza Georgelin (2018) Amanita phalloides or green marjoram, a deadly mushroom. Biologist - ISSN 2529-895X
- Nogué, S., Simón, J., Blanché, C., & Piqueras, J. (2009). Plant and mushroom poisoning. MENARINI scientific area. Badalona.
- Soto B. Eusebio, Sanz G. María and Martínez J. Francisco (2010) Micetisms or intoxication by mushrooms. Clinical Toxicology. Navarre Health Service Osasunbidea. 7 p.
- Talamoni, M., Cabrerizo, S., Cari, C., Diaz, M., Ortiz de Rozas, M., & Sager, I. (2006). Amanita phalloides poisoning, diagnosis and treatment. Argentinian Archives of Pediatrics, 104 (4), 372-374.
- Taxonomy - Amanita phalloides (Death cap) (2018) UniProt. Recovered at: uniprot.org
- Wikipedia contributors (2019) Amanita phalloides. In Wikipedia, The Free Encyclopedia. Recovered at: wikipedia.org