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One of the most poisonous mushrooms known to mycologists is the pale toadstool (Amanita phalloides), and toadstool poisoning, a non-bacterial foodborne toxicity infection, causes the majority of mushroom-related deaths worldwide.
All over the world, mushroom poisoning annually leads to a significant number of deaths, and in almost nine cases out of ten, it is a poisoning with a pale toadstool. 
Over a year, more than fifty fatal poisonings are recorded in Western Europe, in the United States - much less.
According to official figures, 500-1000 cases of mushroom poisoning are recorded in Poland every year, and 90-95% of all fatal poisonings are attributed to Amanita phalloides. 
Toadstool poisoning accounts for more than 9% of the total number of patients with mushroom poisoning admitted to clinics in Bulgaria.
Between 1990 and 2008, there were 93 patients with mushroom poisoning in ten hospitals in Portugal: more than 63% of them were poisoned by mushrooms containing amatoxins; almost 12% of the victims died. 
Approximately 3% of all acute poisoning in Turkey is poisoning with white toadstool.
Statistics show that in Ukraine there are up to a thousand mushroom poisoning every year, and almost 10% of them are fatal; the most common cause is the consumption of poisonous mushrooms, in particular toadstools.
Causes of the poisoning with toadstools
As in all cases of poisoning with poisonous mushrooms , the cause of the toxic effects of the pale toadstool on the body lies in the poisonous substances that Amanita phalloides contains. These are compounds of a pentacyclic structure with hydroxylated amino acid residues and sulfur atoms, and these include amatoxins (amanitins - alpha, beta and gamma, amanin, amaninamide, amanullin, amanullinic acid), as well as bicyclic heptapeptides - phallotoxins (phallidolysin, toxophallin.). 
The most dangerous, resistant to high temperatures, are amatoxins, and among them is alpha-amanitin. The lethal dose determined by toxicologists is 0.1 mg per kilogram of body weight (5-7 mg of total amatoxins), and one mushroom can contain up to 15 mg of deadly toxins. Given the lower body weight, poisoning by toadstools in children is especially dangerous.
Poisoning by the white toadstool - the spring toadstool (Amanita verna), which also belongs to the Amanitaceae family and is a species of the pale toadstool, is also at risk for life.
Risk factors for pale toadstool poisoning are errors in the collection of wild mushrooms. Even an experienced mushroom picker, not to mention those who do not understand mushrooms, can cut and put in a basket a young pale toadstool, which - until a filmy ring appears on its leg - resembles a russula (forked and greenish), as well as talkers (clubfoot and odorous), yellowish-white hygrophor and ryadovka. 
In addition, when buying forest mushrooms on the spontaneous market, you can buy mushrooms cut close to the cap, which makes it difficult to correctly identify their type (the mushroom should be cut near the ground - with a stem).
The mechanism of toxicity of Amanita phalloides, that is, the pathogenesis of toadstool poisoning, is due to the fact that amatoxins are protoplasmic poisons - powerful selective inhibitors of nuclear RNA polymerase II - the most important enzyme in the synthesis of matrix ribonucleic acid (mRNA). 
First, not adsorbed from the intestine and rapidly acting phallotoxins, binding to the globular protein of the cytoplasm of cells actin, block the ion channels of the membranes of the cells of the gastrointestinal mucosa and damage them. And toxofallin causes cell damage by increasing the production of free radicals and the development of oxidative stress.
Amatoxins entering the gastrointestinal tract act more slowly, but they are absorbed into the bloodstream, spread into the portal vascular system of the liver and penetrate the hepatocytes through cell membranes. This leads to inhibition of energy metabolism in cells (a decrease in the synthesis of adenosine triphosphate - ATP); interruption of intracellular protein synthesis; destruction of nuclei and other organelles of liver cells and their death. 
Since amatoxins are excreted mainly by the kidneys - by glomerular filtration, hyaline dystrophy of the renal tubules occurs, and as a result of alpha-amanitin reabsorption, their acute necrosis can develop.
Also, toxins of the pale toadstool (phallolysin) destroy red blood cells - erythrocytes. 
Symptoms of the poisoning with toadstools
The clinical symptoms of poisoning appear depending on the stages or phases of the toxic effects of amatoxins and phallotoxins of the toadstool.
The asymptomatic incubation period, or latency phase, usually lasts six to ten hours after eating pale toadstool.
This is followed by the gastrointestinal phase, the first signs of which are vomiting, watery diarrhea (often bloody) and cramping abdominal pain. The temperature in case of poisoning with a white toadstool can rise to + 38 ° C.
Within 24-48 hours, against the background of acute gastroenteritis due to dehydration of the body, water-electrolyte balance is disturbed, blood pressure falls, and heart rate increases.
Unexpectedly for patients, the listed symptoms disappear for some time: this is how the phase of clinical remission manifests itself, during which amatoxins damage liver cells. Therefore, a short improvement in the general condition - three to four days after eating mushrooms - is followed by a stage of liver and kidney damage in the form of acute hepatic and renal failure with the development of multiple organ failure . 
Acute liver failure with an increase in serum transaminases (liver enzymes) and coagulopathy leads to toxic hepatitis and jaundice.
In severe cases, fulminant hepatitis develops with hepatic coma, bleeding and cessation of urine output (anuria).
Due to impaired liver and kidney function - due to an increase in the level of ammonia in the blood (a by-product of protein metabolism) - neurological symptoms develop in the form of hepatic encephalopathy .
Complications and consequences
The following consequences and complications of toxic infection caused by toadstool are noted:
- a significant decrease in the activity of the blood coagulation system (prothrombin index);
- increased serum creatinine levels ;
- violation of glycogen synthesis;
- metabolic acidosis ;
- liver necrosis and hepatic coma;
- acute tubular renal necrosis;
- encephalopathy with persistent neurological impairment;
- disseminated intravascular coagulation and mesenteric vein thrombosis .
Approximately 20% of survivors develop chronic hepatitis mediated by the immune complex, and 60% develop chronic liver disease with fatty degeneration of its parenchyma. 
Diagnostics of the poisoning with toadstools
Diagnosis of acute poisoning is based on an assessment of the history data, examination and questioning of the patient, the isolation of specific symptoms. White toadstool poisoning is a clinical diagnosis.
Necessary tests: biochemical blood test, for the level of transaminases, for bilirubin, for electrolytes; general urine analysis and for the presence of toxic components.
Instrumental diagnostics includes ECG and liver scintigraphy. 
Differential diagnosis is carried out with other food intoxication, bacterial intestinal infections and acute gastroenteritis of inflammatory etiology.
Treatment of the poisoning with toadstools
First aid for poisoning with pale toadstool: gastric lavage and repeated intake (every two to four hours) 22-50 g of activated carbon (in the form of an aqueous suspension); children - 0.5-1 g / kg.
Activated charcoal can reduce absorption of amatoxins if taken early after ingestion, and it can also prevent reabsorption of toxins after a few hours, as amatoxins undergo enterohepatic recirculation. A dose of 1 g / kg can be administered every 2–4 hours.
All patients with suspected death cap poisoning should be immediately hospitalized in the intensive care unit, where poisoning is treated and symptomatic intensive care for poisoning is carried out .
A direct antidote to toadstool poisoning has not yet been found, but drugs such as Silibinin (a drug based on the biologically active substance of silymarin spotted milk thistle), N-acetylcysteine and Benzylpenicillin (Penicillin G) have been successfully used.
Silibinin is administered by continuous infusion for two to four days (20-50 mg / kg per day). Silymarin in the literature has mostly used both a pharmaceutical form available in Europe as an intravenous preparation and an over-the-counter raw milk thistle extract used in North America. Its mechanism of action is believed to be an inhibitor of the OAT-P transporter, which slows down the penetration of amatoxin into the liver. Doses are 1 g orally four times a day or its purified alkaloid silibinin intravenously 5 mg / kg intravenously for one hour, followed by 20 mg / kg / day as a continuous infusion.
N-acetylcysteine is injected intravenously (within 20 hours with a change in dosage) and benzylpenicillin - 500,000-1,000,000 IU / kg for two days.
With liver necrosis, Western medicine can save a patient with mushroom poisoning from the Amanitaceae family by transplanting a donor organ.
With the development of acute kidney failure, hemodialysis is performed. It may be necessary to maintain respiratory function by artificial ventilation of the lungs.
Neurological symptoms are treated with sedatives of the benzodiazepine group, and barbiturates are used for poorly controlled seizures. 
What is the prevention of toadstool poisoning? Refusal to eat wild mushrooms.
Going into the forest for mushrooms, you cannot pick mushrooms, the safety of which you are not sure.
At the beginning of the 20th century, death after poisoning with a pale toadstool occurred in 70% of cases. In the 1980s, thanks to more effective medical care, the overall mortality rate dropped to 15-20%. According to foreign toxicologists, in 2000, deaths did not exceed 5%, and in 2007 - 1.8%.
The prognosis is worse with a large number of eaten mushrooms, a short latent phase of poisoning, severe coagulopathy, under 10 years of age, or admission to a hospital 36 hours after eating toadstool.