Grebe poisoning

One of the most poisonous mushrooms known to mycologists is the death cap (Amanita phalloides), and death cap poisoning, a nonbacterial foodborne illness, accounts for the majority of mushroom-related deaths worldwide.

Epidemiology

Mushroom poisoning causes a significant number of deaths worldwide each year, and nearly nine out of ten cases are caused by death cap poisoning. [ 1 ]

Over the course of a year, more than fifty cases of poisoning with fatal outcomes are recorded in Western Europe; in the USA, there are much fewer.

According to official data, 500-1000 cases of mushroom poisoning are registered in Poland every year, and 90-95% of all fatal poisonings are caused by Amanita phalloides. [ 2 ]

Death cap poisoning accounts for more than 9% of the total number of patients with mushroom poisoning admitted to clinics in Bulgaria.

Between 1990 and 2008, ten hospitals in Portugal treated 93 patients with mushroom poisoning: more than 63% of them were poisoned by mushrooms containing amatoxins; almost 12% of the victims died. [ 3 ]

Approximately 3% of all acute poisonings in Turkey are caused by death cap mushrooms.

Statistics show that up to a thousand mushroom poisonings are reported in Ukraine every year, and almost 10% of them are fatal; most often the cause is the consumption of poisonous mushrooms, in particular toadstools.

Causes grebe poisoning

As in all cases of poisoning by poisonous mushrooms, the cause of the toxic effect of the death cap on the body lies in the toxic substances that Amanita phalloides contains. These are compounds of a pentacyclic structure with hydroxylated amino acid residues and sulfur atoms, and they include amatoxins (amanitins - alpha, beta and gamma, amanin, amaninamide, amanullin, amanullinic acid), as well as bicyclic heptapeptides - phallotoxins (phallolizin, phalloidin, toxophallin, etc.).

The most dangerous, resistant to high temperatures, are considered to be amatoxins, and among them is alpha-amanitin. [ 4 ] 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 is especially dangerous for children.

Poisoning by the white death cap (Amanita verna), which also belongs to the Amanitaceae family and is a variety of death cap, also poses a risk to life.

Risk factors

Risk factors for poisoning with death cap are mistakes made when picking 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 death cap, which - until a filmy ring appears on its stem - is similar to the russula (forked and greenish), as well as talkers (club-footed and fragrant), yellowish-white hygrophorus and rowan.

In addition, when buying wild mushrooms at a spontaneous market, you can buy mushrooms cut close to the cap, which makes it difficult to correctly identify their species (the mushroom should be cut at the very ground - with the stem).

Pathogenesis

The mechanism of toxicity of Amanita phalloides, that is, the pathogenesis of poisoning by the toadstool, 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). [ 5 ]

At first, non-absorbable from the intestine and fast-acting phallotoxins, binding to the globular protein of the cell cytoplasm actin, block the ion channels of the membranes of the cells of the gastrointestinal mucosa and damage them. And toxophallin causes cell damage by increasing the production of free radicals and the development of oxidative stress.

Amatoxins that enter the gastrointestinal tract act more slowly, but they are absorbed into the blood, spread into the portal vascular system of the liver and penetrate hepatocytes through cell membranes. This leads to inhibition of energy metabolism in cells (reduction of adenosine triphosphate – ATP synthesis); interruption of intracellular protein synthesis; destruction of nuclei and other organelles of liver cells and their death. [ 6 ]

Since amatoxins are excreted mainly by the kidneys – through glomerular filtration, hyaline dystrophy of the renal tubules occurs, and as a result of the reabsorption of alpha-amanitin, their acute necrosis may develop.

Also, the toxins of the death cap (phallolysin) destroy red blood cells – erythrocytes.

Symptoms grebe poisoning

Clinical symptoms of poisoning appear depending on the stages or phases of toxic effects of amatoxins and phallotoxins of the toadstool.

The asymptomatic incubation period, or latent phase, typically lasts six to ten hours after ingestion of death cap.

Then comes 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 white death cap can rise to +38°C.

Within 24-48 hours, against the background of acute gastroenteritis, due to dehydration of the body, a disturbance in the water-electrolyte balance occurs, blood pressure drops, and an increase in heart rate is observed.

Unexpectedly for patients, the listed symptoms disappear for a while: 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 liver and kidney failure with the development of multiple organ failure.

Acute liver failure with increased serum transaminase (liver enzyme) levels and coagulopathy leads to toxic hepatitis and jaundice.

In severe cases, fulminant hepatitis develops with hepatic coma, bleeding and cessation of urine excretion (anuria).

Due to impaired liver and kidney function – in connection with an increase in the blood level of ammonia (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:

• significant decrease in the activity of the blood coagulation system (prothrombin index);
• increased serum creatinine levels;
• disruption of glycogen synthesis;
• metabolic acidosis;
• liver necrosis and hepatic coma;
• acute tubular necrosis of the kidney;
• encephalopathy with permanent neurological disorders;
• disseminated intravascular coagulation and mesenteric vein thrombosis.

Approximately 20% of survivors develop immune complex-mediated chronic hepatitis, and 60% develop chronic liver disease with fatty degeneration of its parenchyma.

Diagnostics grebe poisoning

Diagnosis of acute poisoning is based on anamnesis data assessment, examination and questioning of the patient, and identification of specific symptoms. Poisoning with white toadstool is a clinical diagnosis.

Necessary tests: biochemical blood test, transaminase level, bilirubin, electrolytes; general urine test and urine test for toxic components.

Instrumental diagnostics include ECG and liver scintigraphy. [ 7 ]

Differential diagnosis

Differential diagnosis is carried out with other food intoxications, bacterial intestinal infections and acute gastroenteritis of inflammatory etiology.

Treatment grebe poisoning

First aid for death cap poisoning: gastric lavage and repeated administration (every two to four hours) of 22-50 g of activated charcoal (in the form of an aqueous suspension); for children – 0.5-1 g/kg.

Activated charcoal may reduce the absorption of amatoxins if given early after ingestion and may also prevent reabsorption of toxins several hours later because amatoxins undergo enterohepatic recirculation. A dose of 1 g/kg may be given every 2–4 hours.

All patients with suspected death cap poisoning should be immediately hospitalized in an intensive care unit, where treatment for poisoning and symptomatic intensive care for poisoning are carried out.

A direct antidote for poisoning by toadstool has not yet been found, but drugs such as Silibinin (a drug based on the biologically active substance of milk thistle silymarin), N-acetylcysteine and Benzylpenicillin (Penicillin G) are successfully used.

Silibinin is administered by continuous infusion for two to four days (20-50 mg/kg per day). Silymarin has been used in most cases in the literature both as a pharmaceutical form available in Europe as an intravenous preparation and as an over-the-counter crude milk thistle extract used in North America. Its mechanism of action is thought to be an inhibitor of the OAT-P transporter, which slows the uptake of amatoxin into the liver. Doses are 1 g orally four times daily or its purified alkaloid silibinin intravenously 5 mg/kg intravenously over one hour, then 20 mg/kg/day as a continuous infusion.

N-acetylcysteine is administered intravenously (within 20 hours with a change in dosage) and Benzylpenicillin - 500,000-1,000,000 IU/kg for two days.

In case of liver necrosis, Western medicine can save a patient with poisoning by mushrooms of the Amanitaceae family by transplanting a donor organ.

In the event of acute renal failure, hemodialysis is performed. It may be necessary to support respiratory function with artificial ventilation.

Neurological symptoms are treated with sedatives from the benzodiazepine group, and barbiturates are used for poorly controlled seizures. [ 8 ]

Prevention

What is the prevention of poisoning by toadstool? Refusing to eat wild mushrooms.

When going into the forest to pick mushrooms, you should not pick mushrooms that you are not sure are safe.

Forecast

At the beginning of the 20th century, death after poisoning with death cap occurred in 70% of cases. In the 80s, thanks to more effective medical care, the overall mortality rate dropped to 15-20%. According to foreign toxicologists, in 2000, the fatality rate did not exceed 5%, and in 2007 – 1.8%.

The prognosis is worse if a large number of mushrooms are eaten, the latent phase of poisoning is short, there is severe coagulopathy, the patient is under 10 years of age, or the patient is admitted to a medical facility 36 hours after eating the toadstool.