Mushroom poisoning
| Classification according to ICD-10 | |
|---|---|
| T62 | Toxic effect of other harmful substances ingested with food |
| T62.0 | Eat mushrooms |
| ICD-10 online (WHO version 2019) | |
A mushroom poisoning ( Latin mycetism , from the Greek μύκης mykes "mushroom") is a poisoning caused by the consumption of mushrooms . In a narrower sense, it means “real mushroom poisoning” caused by the consumption of poisonous mushrooms . Toadstools contain certain fungal toxins . Depending on the type and amount of mushrooms consumed, mushroom poisoning can lead to death. In the case of highly poisonous mushrooms, the smallest amounts are sufficient.
The so-called spurious or secondary mushroom poisoning mainly includes food poisoning caused by rotten edible mushrooms or by reheating mushroom dishes after a long storage time.
A distinction must be made between intolerance symptoms , allergic reactions and imaginary mushroom poisoning, which can also be triggered by the consumption of mushrooms. No toxic substances are consumed in these cases, but symptoms are often similar to those of mushroom poisoning. That is why these cases are sometimes referred to as "fake mushroom poisoning".
causes
Poison mushrooms
Real mushroom poisoning with characteristic poisoning syndromes occurs after consuming poison mushrooms . The symptoms usually show up in every consumer and also when the fruiting bodies have not been spoiled and have been cooked for a long time. The most common cause of real mushroom poisoning is confusion with edible mushrooms. In addition, the deliberate consumption of hallucinogenic mushrooms is known as a narcotic drug, which on the one hand can trigger the (poisonous) effects intended by the consumer, on the other hand it can also trigger undesired symptoms.
Raw edible mushrooms or, under certain conditions, poisonous mushrooms
While some edible mushrooms, such as many types of mushrooms, can be eaten raw, mushroom poisoning can occur when eating numerous other edible mushrooms if they have not been heated or only insufficiently heated beforehand. Because many edible mushroom types contain toxins that are only destroyed by heating. The cooking time should be at least 15 minutes.
Some mushrooms contain substances that only have a toxic effect in connection with other substances, for example in the case of tintlings (with the exception of the crested tintling ) in connection with alcohol.
Food poisoning from rotten edible mushrooms
Spoiled mushrooms are the main cause of "fake mushroom poisoning". These can be mushrooms that you have collected yourself, that have already been harvested rotten or that have been insufficiently transported or stored for too long. You can also get mushrooms that have been incorrectly stored when shopping. Examples of improper storage can be: an interruption in the cold chain, poor packaging, storage that is too long or too warm. So it's food poisoning .
Food poisoning from warmed up mushroom dishes
Basically, mushroom dishes can be warmed up a second time for consumption. As with other relatively easily perishable dishes, the prerequisite for safe enjoyment is that it is kept cool and stored for not too long in the meantime. Otherwise there is a risk of bacterial decomposition with the consequences and dangers of food poisoning.
Similar phenomena
The following phenomena are not due to poisoning because they are not caused by poisons. Nevertheless, they are sometimes classified as "fake mushroom poisoning", like the above-mentioned food poisoning.
Mushroom tolerance
Occasionally, mushrooms are apparently intolerable, especially after insufficient cooking or when eaten in large quantities . The symptoms that arise in the short term are often similar to the "gastrointestinal syndrome" with a short latency period .
In addition, there are individual intolerances to all or only to certain fungi. Clearly edible and healthy mushroom specimens are not well tolerated by some people, which usually results in general malaise, digestive problems or a feeling of fullness in those affected. Sometimes it helps to chop the mushrooms mechanically in the mixer before the meal, as the indigestible chitin of the mushroom hyphae may be the cause of this problem.
Allergies
In rare cases, allergic reactions can occur after eating mushrooms, which are harmless in themselves . Typical of this type of apparent "poisoning" is that only a few people are affected, while the majority of people can eat the fungus without harm. In addition to gastrointestinal problems, the skin reactions and asthmatic complaints typical of allergic reactions can occur. In extreme cases, anaphylactic shock can cause a life-threatening condition.
Often there is also an innate hypersensitivity ( idiosyncrasy ) in the endangered group of people , which is often associated with an extreme aversion to fungi.
Imaginary mushroom poisoning
It's a type of nocebo effect . The symptoms are only triggered by the psyche, but externally can correspond to real mushroom poisoning. Therefore, a differential diagnosis to real mushroom poisoning is very difficult. Those affected firmly believe that they have eaten poisonous mushrooms and, out of their conviction, develop symptoms that even an expert helper cannot distinguish from those of real poisoning. That is why such cases as real poisoning should also be treated.
Precautions
As a preventive measure, a few rules should be observed when collecting the mushrooms:
- Only take known mushrooms with you. If there is the slightest uncertainty about the determination of the mushroom species, it is better to leave the mushrooms standing.
- If unknown species are picked for later identification, they must not be placed in the same container with those intended for consumption.
- Collect healthy specimens. Never take mushy, eaten or even moldy mushrooms with you.
- They should be transported in airy baskets or similarly breathable containers. Plastic bags , in which mushrooms can decompose quickly, should be avoided.
- At home, the mushrooms should be prepared on the same day if possible.
- Photograph the result of the collection before cutting.
First aid
In the case of complaints that suggest fungal poisoning, immediate medical help from an emergency doctor or the emergency services is required. The poison control centers have been set up to provide support, and specialist doctors provide instructions on appropriate first aid measures around the clock . Classic first aid measures such as calming down the affected person and using the stable side position in the event of unconsciousness are mandatory. Further measures such as the administration of home remedies, however, can be harmful.
The following measures are important to limit the type of poisoning and to coordinate further treatment:
- Save leftovers from mushroom cleaning, meal and vomit
- Note the length of time between ingesting the mushrooms and the onset of symptoms
- Information on the collection, preparation and condition of the mushrooms consumed, their transport and storage
If necessary, a certified mushroom expert is called in to determine the type of mushrooms consumed.
diagnosis
The time at which the first symptoms appear is important for the diagnosis of suspected mushroom poisoning.
- During the meal up to approx. 4 hours afterwards: Here it can be assumed that the poisoning does not pose a threat to life, unless larger quantities of poisonous mushrooms have been consumed. To be on the safe side, the patient should always be observed and the symptoms treated accordingly. The symptoms can vary greatly depending on the fungus causing it. Gastroinestinal complaints, nausea and vomiting, mental confusion and hallucinations , sweats, restlessness, drowsiness. As a rule, the patients recover completely and there is no permanent damage.
- Delayed appearance of the symptoms (6 to 72 hours later): There is almost always mortal danger here. The main triggers for such poisoning are the spring lobster , cap mushrooms or veils . Even if the poisoning is survived, chronic damage to the liver or kidneys may remain.
However, it must be taken into account: If symptoms occur within the first few hours, more dangerous mushrooms may still have been eaten, which release significant amounts of, for example, Amanitin to the body within the first 4 hours . As a result, further diagnostic measures, such as determining the amanitin in the urine, may be necessary.
Classical classification according to the symptoms
Different mushrooms or groups of mushrooms have different manifestations of poisoning symptoms depending on their toxins. Hence, different syndromes can be described. Food poisoning from rotten edible mushrooms or rotten mushroom dishes as well as mushroom intolerance and allergies are not dealt with in this system.
Mushroom poisoning with a latency period of over four hours
This category includes the most dangerous poisonings. Since the mushroom meal has usually already passed through the stomach, a quick removal of the toxins by vomiting is usually no longer useful. To make matters worse, due to the delayed appearance of the symptoms, the toxins had already had some time to spread in the body and develop their fatal effect.
Phalloides syndrome, amatoxin syndrome
Latency period: 6 to 24 hours, usually 8 to 12 hours, up to a maximum of 48 hours after the mushroom meal.
Signs: Violent vomiting, persistent watery diarrhea with threatening fluid and electrolyte losses, calf cramps, severe abdominal pain. The symptoms subside on the second and third day, which creates an apparent recovery effect. However, it is at this stage that the liver begins to decompose. If the intoxication is severe, jaundice-like changes in skin color can occur.
Duration of illness: 4 to 10 days, even with optimal medical emergency care in approx. 5% of the adult poisoned with fatal outcome. The mortality rate is higher in children, an estimated 10–20%. Of all fatal mushroom poisonings, more than 90% of these are caused by the green death cap mushroom and the two white species of spring cap mushroom and cone cap mushroom.
Causing toxins: The α- amanitin contained in the above-mentioned cape mushrooms is the main active ingredient and one of the most dangerous natural poisons. In addition, the β- and γ-amanitins are also highly toxic. The phallotoxins also contained in the tuberous mushrooms play no role in the severity of the poisoning, as they are already partially broken down in the digestive tract. The lethal dose for α-Amanitin in adults is around 0.1 mg / kg body mass, i.e. ingestion of 20 to 40 grams of amanitin (which contains between 0.02 and 0.04% α-Amanitin) can be lethal. For children, 1/20 of this value applies, i.e. 1 to 2 grams. The poison effect is based on an inhibition of the RNA polymerase and thus prevents the transcription of DNA to mRNA . The liver cells in particular die when the internal mRNA supply is used up. The toxin concentration necessary for the inhibiting effect is reached just one hour after the mushroom meal.
Therapy: Due to the late appearance of the symptoms, it is usually no longer sensible to induce vomiting yourself through mechanical irritation. The patient must be treated as quickly as possible in a clinic under constant medical supervision. Because of the severe diarrhea, fluids and electrolytes must be balanced. Activated charcoal must be administered regularly in order to reduce the enterohepatic poison circulation as much as possible and to induce the excretion of toxins from the body. Excretion via the kidneys should be promoted by means of diuretics. As a further measure, infusions with Silibinin (an ingredient in milk thistle , Silybum marianum ) must be given as early as possible . The previously usual treatment with penicillin is only recommended if no silibinin is available; a combination of both means does not make sense. Since the introduction of silibilin into therapy, the mortality rate has decreased to 5 to 12% with timely treatment, previously it was 20 to 30%. Where drug treatment is inadequate, liver transplantation can save lives. The dialysis is in severe cases used.
A distinction is made between various degrees of severity of poisoning in amatoxin intoxication:
- Severity 1 (slight poisoning): typical gastrointestinal symptoms without liver or kidney damage.
- Severity grade 2 (moderate poisoning): typical gastrointestinal symptoms with slight liver damage, low transaminase concentration.
- Severity 3 (severe poisoning): typical gastrointestinal symptoms with severe liver damage, high transaminase concentration, disorders of the ability to clot.
- Severity 4 (very severe poisoning): liver disintegration and kidney damage, very high transaminase concentration and increased bilirubin values, severe disruption of the ability to clot.
From severity grade 3, the patient should be treated in a clinic with options for a liver transplant .
Causing fungi: Amanita phalloides ( Amanita phalloides ), Spring amanita ( Amanita verna ), Amanita virosa ( Amanita virosa ), galerina marginata ( Galerina marginata ), more galerina ( Galerina sp.), Meat Red poison Schirmling ( Lepiota brunneo-incarnata ), flesh pink poison Schirmling ( Lepiota helveola ), greenhouse umbrella ( Lepiota citrophylla ), other small umbrella ( Lepiota spec.)
Orellanus Syndrome
also Orellana syndrome (see Lexicon of Medicine, Thomas: Labor und Diagnose).
Latency period: The symptoms of poisoning often only appear 36 hours after the mushroom meal, in extreme cases only after 14 days. Even a lethal dose of orellanin shows the first symptoms in animal experiments only after 48 hours.
Signs: After a long, often completely symptom-free latency period, the first unspecific signs such as nausea and vomiting appear. The incipient kidney damage initially manifests itself as pain in the lumbar vertebra area. The patient can also suffer from headache, joint or muscle pain, feeling cold or chills without the body temperature changing significantly. Finally, there are symptoms of excessive thirst, increased urine secretion and even polyuria .
Duration of illness: Depending on the intensity of the illness, the symptoms appear early (36 hours) or much later. In the latter case, a milder course of the poisoning can be expected from the ninth day after the onset of symptoms. The duration of the illness depends heavily on the damage to the kidneys and, in extreme cases, is associated with a kidney transplant. Treatment and convalescence can thus extend over a very long period of time.
Causing toxins: In addition to the main toxin orellanin, there is also the less toxic toxin orellinin. The cyclopeptidic cortinarines A, B, and C, previously described as toxins, do not exist, however, as studies by Hartmut Laatsch (University of Göttingen) have shown. Cortinarius orellanus. contains approx. 1.5 to 2% orellanine in the dry matter. The LD 50 dose fluctuates between 4.9 and 8.3 mg / kg in animal experiments, with 20 to 30% of the test rats being resistant to the poison. Applied to humans, this would mean that there is a life-threatening dose of around 50 to 100 grams of fresh mushroom, and significantly less in children and particularly sensitive people. Orellanin cannot be destroyed by drying and cooking. The lethality in orellanin poisoning is 10 to 15%.
Therapy: If the consumption of poisonous Cortinarius species is suspected, an emergency medical service must be informed immediately and the patient admitted to the hospital. By vomiting, gastric lavage and administration of activated charcoal and lactulose , attempts must be made to excrete the poison that has not yet been absorbed. Since no symptoms have occurred yet, if possible, the poisonous fungus from fungal cleaning residues, leftovers from the meal or the stomach contents should be analyzed in detail in order to determine the further therapy. If there is no kidney damage within the first week, consider hemoperfusion to remove the toxin still present in the body. A hemodialysis is indicated only in case of imminent kidney failure. Since poisoning is often recognized as such relatively late, only symptomatic treatment remains after the start of treatment if the signs of poisoning appear.
Causing fungi: Orange veil ( Cortinarius orellanus ), pointed-humped orange veil ( Cortinarius rubellus ). Other veils ( Cortinarius spec. ), Above all from the rough heads ( Leprocybe ) and skin heads ( Dermocybe ) sections , were also suspected of containing orellanin, but new studies could not confirm this.
The beautiful yellow clubfoot ( Cortinarius splendens ) - with similar symptoms but without orellanin - contains another strong, as yet unknown kidney toxin.
Kidney damage from various types of amanita
Latency period: it takes an average of 12 hours for the first symptoms to appear; in the case of poisoning with Amanita smithsonia , however, much shorter latencies were also observed.
Signs: Initially, non-specific gastrointestinal symptoms (nausea, vomiting and diarrhea) appear. Kidney failure with anuria occurs two to five days after eating the mushrooms .
Duration of illness: With appropriate treatment, patients usually recover completely within a few weeks. Permanent kidney damage cannot be ruled out.
Causing Toxins :?
Therapy: Symptomatic treatment, if necessary dialysis .
Causing fungi: Ocher ring eggplant ( Amanita proxima ), Amanita smithiana (North American species).
Gyromitra syndrome
Latency period: 4 to 24 hours, usually 6 to 8 hours after the mushroom meal, in extreme cases even after 2 hours.
In Russia and Sweden, the spring laurel is still popular. The mushrooms are thoroughly boiled at least twice and the cooking water is then discarded. Despite this cooking procedure, poisoning with the spring lobster is widespread there and accounts for about 45% of all mushroom poisoning in Russia. Toxic vapors are released when cooking, which can lead to poisoning if inhaled.
Signs: After the latency period, symptoms of poisoning such as nausea, headache and abdominal pain, fatigue, abdominal colic appear. Eventually prolonged vomiting and watery diarrhea occur. In terms of symptoms, gyromitrin poisoning is strikingly similar to intoxication with Amanitin (Phalloides syndrome). Here, too, life-threatening fluid loss (= desiccosis) with the risk of circulatory shock can occur. Blood pressure drops, pulse rises, calf cramps occur.
After this phase there is often an apparent improvement in the condition, but liver and kidney problems soon appear (on the second or third day), which can manifest themselves in anuria, hepatic coma with organ bleeding, respiratory failure, circulatory and kidney failure.
Duration of the illness: The acute course of the poisoning extends over two to three days. Treatment and convalescence can take significantly longer.
Causing toxins: The toxin of the spring salmon is gyromitrin , which is broken down into water-soluble monomethyl hydrazine during preparation or at the latest in the gastrointestinal tract . Due to its boiling point at 87 ° C, this can normally escape during the cooking process, which can lead to poisoning through mere inhalation of the cooking vapors. Furthermore, there seem to be great individual differences in the tolerance of the poison. So some eaters survive the poison completely harmless, while others suffer severe poisoning with the same dose. The effect of the poison is based on an inhibition of pyridoxine in the central nervous system. The resulting deficiency in γ-aminobutyric acid leads to coma and cramps. The possible liver damage can also be attributed to the inhibition of pyridoxine, which is also involved in the amino acid metabolism.
The lethal amount of gyromitrin for an adult is around 20 to 50 mg / kg body weight, in children the dose is around half lower. The poison content of the spring lilac is 0.1 to 0.3% in the fresh mushroom and also in the dried mushroom. The drying process also seems to decrease toxins.
In addition, gyromitrin and its breakdown product monomethylhydrazine are suspected of being able to trigger the development of tumors.
Therapy: If the poisoning is recognized early on, attempts can be made to remove any remaining fungus from the digestive tract through artificial vomiting and gastric lavage. As with Phalloides syndrome, activated charcoal and lactulose are administered. As an antidote, pyridoxine is injected intravenously. However, a total dose of 15 to 20 grams per day must not be exceeded. Correspondingly lower values apply to children.
Causing fungi: morel ( Gyromitra esculenta ), Riesenlorchel ( Gyromitra gigas ), miter ( Gyromitra infula ), Helmet Circle Ling ( Cudonia circinans ). Lorelels from the genus Helvella and gelatinous caps ( Leotia sp. ) Are also suspected of being poisonous .
Rhabdomyolysis
In 2001, the green mushroom (Tricholoma equestre) , which had previously been listed in all mushroom books as edible and approved as a market mushroom, was identified as the likely cause of a number of poisonings in France. Of the total of twelve people poisoned, three deaths from rhabdomyolysis were recorded. In 2002 two more cases were reported in Poland.
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Latency period: 30 minutes after the first meal (for Russula subnigricans ), or 24 to 72 hours after multiple meals (e.g. for green animals, Tricholoma equestre ).
Signs: In Russula subnigricans, poisoning begins with dizziness and diarrhea and can either be comparatively harmless or be associated with severe complications from the onset of rhabdomyolysis. In the green body, poisoning begins with fatigue, which is compounded by muscle weakness and pain, especially in the thighs. The breakdown of muscle tissue causes myoglobin to be excreted in the urine, which in more severe cases can be recognized by the dark color of the urine. Laboratory medicine also shows an increased level of creatine kinase in the serum. Muscle damage can also affect the heart and diaphragm muscles, which explains the sometimes fatal outcome of the poisoning. Other symptoms include reddening of the skin, sweating and nausea.
Duration of illness: The symptoms initially increase over three to four days. Even if the poisoning is not fatal, it takes several weeks for the patient to recover.
Causing toxins: The substances responsible for the occurrence of life-threatening muscle weakness in the green body are not yet known. Since the consumption of green vegetables does not always lead to symptoms of poisoning, it is assumed that the concentration of the toxin in the mushrooms fluctuates. The main active ingredient in Russula subnigricans is cycloprop-2-ene-carboxylic acid .
Therapy: Only symptomatic treatment is possible.
Causing fungi: Greenling (Tricholoma equestre) and Nisekurohatsu (Russula subnigricans) . The latter is the only pigeon that has been identified as the cause of fatal poisoning. In contrast to the green compact, which only triggers rhabdomyolysis after repeated consumption, the first effect occurs around 30 minutes after the first meal.
Acromelalga Syndrome
Latency: 1 to 2 days, sometimes longer.
Signs: pain, abnormal sensation and reddening of the skin on legs and arms. Occasionally, there is also swelling, paralysis, and cramps. Symptoms are made worse by warmth (for example, under a duvet).
Duration of illness: days to several weeks; poisonings lasting several months have been reported from Japan.
Causing toxins: acromelic acid.
Therapy: cooling the painful parts of the body, painkillers. The pain can only be relieved poorly with medication.
Causing fungi: Perfumed funnel ( Paralepistopsis amoenolens ), bamboo funnel ( Paralepistopsis acromelalga )
Mushroom poisoning with a latency period of less than four hours
Muscarinic syndrome
Latency: Within a few minutes to 2 hours.
Signs: Muscarin acts as a parasympathomimetic . Typical symptoms are visual disturbances due to constriction of the pupil, tearing and salivation, and excessive sweat secretion. In addition, possible symptoms include vomiting, diarrhea, gastrointestinal disorders, tremors ( tremors ) and headaches. In the case of severe poisoning, the pulse slows down ( bradycardia ) and blood pressure falls, sometimes there is difficulty breathing due to narrowing of the airways and feelings of fear.
Duration of the illness: weak poisoning subsides quickly and is often overcome after two hours without special therapy. Severe poisoning lasts longer (up to 24 hours) and can take on life-threatening forms.
Causing toxins: The toxin was isolated from the fly agaric ( Amanita muscaria ) for the first time and therefore named after this muscarin (German "muscarin"). Curiously, muscarine is not responsible for the poisonous effects of the fly agaric, in which it occurs only in extremely small quantities. It occurs in considerably higher - toxic - effective - concentrations in some types of crack fungi and funnel-shaped mushrooms.
Due to its molecular similarity to acetylcholine , it is able to reversibly occupy the same receptors ( muscarinic acetylcholine receptors ) of the parasympathetic nervous system. Since it can not be broken down by the enzyme acetylcholinesterase , the affected nerves are permanently irritated with the consequences mentioned under signs . The antidote atropine displaces the muscarine from these receptors without triggering any excitement.
The lethal dose of muscarin is around 180 mg per kg of body weight.
Therapy: gastric lavage, activated charcoal, very effective antidote: atropine , of which 0.5–2 mg are administered intravenously.
Causing fungi: Field funnel ( Clitocybe dealbata ) and other funnel-shaped fungi ( Clitocybe spec. ), Brick-red crack fungus ( Inosperma erubescens ) and other crack fungi ( Inocybe spec. ).
Pantherina Syndrome
Latency period: is very short, within a few minutes to two hours, in rare cases symptoms can only appear after up to four hours.
Signs: The first signs of poisoning are dizziness and tiredness. This leads to a state of intoxication, which can include hallucinations, coordination disorders, loss of sense of time and overconfidence. Eventually the poisoned person falls into a deep sleep. Single deaths from shock or respiratory failure have been reported.
To some extent, fly or panther mushrooms also cause nausea, stomach ache and vomiting, and it is rare that their consumption is completely without consequences.
Duration of the illness: The acute symptoms usually last up to about ten hours. A rapid recovery then occurs.
Causing Toxins: Known as toxins are ibotenic acid and muscimol . In addition, there are presumably other, as yet undiscovered substances. Muscarin , which was originally thought to be the effective toxin, occurs only in small, barely effective amounts in toadstools and not at all in panther mushrooms. The lethal dose of muscimol is 45 mg per kilogram of body weight and that of ibotenic acid is 38 mg per kilogram of body weight.
6.6% of all mushroom poisoning is caused by the panther mushroom. The mortality rate is 1 to 2%. Fly agaric poisoning accounts for 1 to 2% of all mushroom poisoning. The mortality is 5%.
Therapy: Only symptomatic treatment is possible.
Causing fungi: Pantherpilz ( Amanita pantherina ), fly agaric ( Amanita muscaria ), King mushroom ( Amanita regalis ), Daffodil Yellow Amanita ( Amanita gemmata ).
Similar edible mushrooms: The pearl mushroom ( Amanita rubescens ) can easily be confused with the panther mushroom by inexperienced collectors.
Gastrointestinal Syndrome
Also called resinoid syndrome .
Latency period: Sometimes the first symptoms appear during the mushroom meal, sometimes only after up to four hours. The latency period is always relatively short. Since usually a mixed mushroom dish is the trigger, which could also have been made of cap mushrooms or rock heads with a long latency period, liver and kidney function should always be monitored over the next few days.
Signs: nausea, vomiting, diarrhea, abdominal pain, as a result of damage to the gastric mucosa. Even when eating mushrooms that are harmless in themselves, fear can lead to the signs just mentioned. These “imagined” symptoms should not be dismissed, but the patient should be treated as in the case of real poisoning.
Duration of the illness: As a rule, the symptoms disappear after one to two days without causing any late effects. However, the consequences of damage to the gastric mucosa can last up to 7 days.
Causing toxins: Gastrointestinal complaints can be triggered by very different poisons, which have in common that they are absorbed through the stomach or intestinal mucosa. Terpenoid substances are considered a common poison . The mutagenic alkaloid necatorone occurs in the Milchling Lactarius necator .
Therapy: Induce vomiting if necessary, gastric lavage and administration of activated charcoal if necessary. As with other diarrheal diseases, it is also important to compensate for the loss of fluids and salts.
Causing fungi:
- Mushrooms : Karbolegerling , poison Egerling ( Agaricus xanthoderma ), guinea fowl gerling ( Agaricus placomyces ) ...
- Boletus : rubroboletus satanas ( Boletus satanas ), boletus calopus ( Boletus calopus ) ...
- Milklings : Bruchreizker , Maggi mushroom ( Lactarius helvus ), Grubiger Milchling ( Lactarius scrobiculatus ), Birch irritant ( Lactarius torminosus ) ...
- Knights : Tiger knight ( Tricholoma pardinum ), burning knight ( Tricholoma virgatum ), possibly sulfur knight ( Tricholoma sulfureum ) ...
- Mullet : entoloma sinuatum ( Enteloma sinuatum ) ...
- Juices : conical juices ( Hygrocybe conica ) ...
- Relatives of the veil : blood-red skin head ( Cortinarius sanguineus , syn. Dermocybe sanguinea ), pale fawn ( Hebeloma crustuliniforme ) ...
- Marasmiaceae : Broadleaf wood Rübling ( Megacollybia platyphylla ), o'lantern mushroom ( Omphalotus olearius ) ...
- Russulas : Russula Emetica ( Russula emetica ), Russula Foetens ( Russula foetens ), change color Täubling ( Russula fragilis ) ...
- Trümmling relatives : Green-leaved sulfur head ( Hypholoma fasciculare ) ...
Psilocybin Syndrome
Latency: A few minutes to an hour.
Signs: state of intoxication with visual illusions , dizziness and euphoria , the severity of which depends on the amount taken. With larger doses, the dizziness increases to nausea with vomiting. Depending on the individual, euphoria can also turn into anxiety states and latent psychoses .
Duration of illness: a few hours.
Causing Toxins: Psilocybin
Therapy: reassuring persuasion , if necessary administration of benzodiazepines .
Causing fungi: various fungi among others in the genera Baldheads ( Psilocybe spec. ), Panaeolus , Gymnopilus , Pluteus , Conocybe .
Accidental poisoning with psilocybin-containing mushrooms due to a mix-up rarely occurs, as these mushrooms are rather small and seem uninteresting to the edible mushroom collector. The mushrooms are more likely to be consumed intentionally as an intoxicant, which can also lead to undesirable effects. It should also be noted that inexperienced collectors can confuse mushrooms containing psilocybin with much more dangerous poisonous mushrooms (including Galerina and Conocybe spp.).
Other symptoms of intoxication
Coprinus Syndrome
The consumption of some actually edible types of mushrooms triggers this syndrome if alcohol is consumed at the same time or afterwards. The second step in the breakdown of ethanol (potable alcohol) is disrupted. Coprin blocks the enzyme acetaldehyde dehydrogenase , which converts the toxic acetaldehyde into harmless acetate. As a result, acetaldehyde accumulates in the body and causes the characteristic symptoms of poisoning.
Latency: The actual latency after consuming mushrooms and alcohol is short. However, drinking alcohol can trigger poisoning for several days after eating the mushrooms.
Signs: flushing of the face, sweating, palpitations, circulatory disorders. The symptoms can be very uncomfortable, but they are usually not dangerous.
Duration of illness: a few hours
Causing Toxins: Coprin
Therapy: Usually not required
Causing fungi: Wrinkled ink ( Coprinus atramentarius ), the occurrence of the poison coprin in club -footed funnels ( Clitocybe clavipes ) and in ox boletus ( Boletus torosus ) is not certain
Paxillus Syndrome
The Paxillus syndrome is probably not a mushroom poisoning in the narrower sense, but an allergic reaction that occurs very rarely (usually only after repeated consumption), but is often difficult. Accordingly, its trigger, the bald curl ( Paxillus involutus ), is often consumed without consequences. In Eastern Europe in particular, it is a common market mushroom.
Latency: 1 to 2 hours
Signs: nausea, vomiting, colic, hemolysis, kidney failure
Duration of illness:
Causing toxins: The trigger is not toxins, but antigens contained in the fungus
Therapy:
Causing fungi: Bald Krempling ( Paxillus involutus )
Others
Causing fungi:
- White tuft rasp ( Lyophyllum connatum ) (toxin: lyophylline)
- Different types of mushrooms (toxins: agaritin, nitroamines)
- Porphyry brown amanita ( Amanita porphyria )
- Albatrellus species
- Potato bovist : leopard skin hard bovist ( Scleroderma areolatum ), brown and black hard bovist ( Scleroderma verrucosum ), thick-skinned potato bovist ( Scleroderma citrinum ). In addition to gastrointestinal complaints, the focus here is on a drop in blood pressure with dizziness and collapse.
Modern layout
Differentiating the gastrointestinal syndrome from other syndromes such as B. Phalloides syndrome does not necessarily make sense, since the former also occurs as a partial syndrome in the latter. Therefore, a different division into 6 main groups and partly further sub-groups has recently been proposed:
Group 1: Cytotoxic mushroom poisoning
Syndromes with a specific pathogenic effect on organs
- 1A primarily hepatotoxic poisoning (e.g. by amatoxins)
- 1B early onset, primarily nephrotoxic poisoning (e.g. due to amino-hexadieno-acid AHDA)
- 1C late onset, primarily nephrotoxic poisoning (e.g. due to orellanin)
Group 2: Primary neurotoxic mushroom poisoning:
- 2A purely hallucinogenic mushroom poisoning (e.g. from psilocybin)
- 2B fungal poisoning primarily affecting the vegetative nervous system (e.g. from muscarin)
- 2C primary central nervous fungal poisoning (e.g. ibotenic acid / muscimol)
- 2D unclear, neurotoxic fungal poisoning, e.g. B. Morchella syndrome
Group 3: Myotoxic mushroom poisoning (rhabdomyolysis)
- 3A rapid onset of rhabdomyolysis (e.g. by cycloprop-2-ene-carboxylic acid, Russula subnigricans )
- 3B late onset of rhabdomyolysis (e.g. by the green body, Tricholoma equestre )
Group 4: Mushroom poisoning affecting metabolic and endocrine processes
- 4A GABA-blocking mushroom poisoning (e.g. from gyromitrin)
- 4B disuliram-like mushroom poisoning (e.g. from Coprin)
- 4C poisoning by polyporic acid (e.g. cinnamon-colored soft pork , Hapalopilus nidulans )
- 4D thrichothecene mushroom poisoning (e.g. by Trichoderma cornu-damae = Podostroma cornu-damae )
- 4E hypoglycemic mushroom poisoning (e.g. from trogia venenata )
- 4F hypercalcitoninemische mushroom poisoning (for. Example, by the Satanspilz , rubroboletus satana )
- 4G pancytopenic mushroom poisoning (e.g. from Ganoderma neojaponicum )
Group 5: Purely gastrointestinal irritation causing fungal poisoning
Group 6: Various other syndromes that do not fit into the grid of groups 1 to 5
- 6A Shiitake dermatitis
- 6B Acromelalga Syndrome
- 6C Paxillus Syndrome
- 6D encephalopathy syndrome (due to Pleurocybella porrigens )
literature
- Lutz Roth, Hanns Frank, Kurt Kormann: Poisonous mushrooms, mushroom poisons. Molds - Mycotoxins - Occurrence - Ingredients - Fungal allergies - Food poisoning . Reprint of the 1989 edition. 1st edition. Nikol, Hamburg 1990, ISBN 3-933203-42-2 .
- René Flammer, Egon Horak: Poison mushrooms - mushroom poisons. Mushroom poisoning. A reference work for doctors, pharmacists, biologists, mycologists, mushroom experts and mushroom pickers . Schwabe, Basel 2003, ISBN 3-7965-2008-1 .
Web links
- Information on mushroom poisoning from the German Society for Mycology
- Information on mushroom poisoning at www.gifte.de
Individual evidence
- ↑ Renate Wahrig-Burfeind (Ed.): True. Illustrated dictionary of the German language . ADAC-Verlag, Munich 2004, ISBN 3-577-10051-6 , pp. 590 .
- ^ A b Andreas Bresinsky, Helmut Besl: Poison mushrooms. A handbook for pharmacists, doctors and biologists . Wissenschaftliche Verlagsgesellschaft, Stuttgart 1985, ISBN 3-8047-0680-0 , p. 2 .
- ↑ Mushroom poisoning . In: Duden online; “Poisoning from the consumption of mushrooms, especially poison mushrooms ” (emphasis added).
- ↑ Mushroom poisoning . In: Pschyrembel . 258th edition, 1998; "The diseases caused by eating poisonous or spoiled mushrooms (formation of toxic protein decomposition products, e.g. by storing mushrooms in plastic bags or reheating mushroom dishes)" (emphasis added).
- ↑ Information on consumer protection of the German Society for Mycology (DGfM): In this text, "diseases caused by rotten but otherwise edible mushrooms" are referred to as "fake mushroom or food poisoning".
- ↑ J. Stein, K.-W. Jauch: Practical Guide to Clinical Nutrition and Infusion Therapy. 2003, Springer-Verlag Berlin Heidelberg, ISBN 978-3-642-62625-8 , p. 830
- ^ Gerhard Eisenbrand, Peter Schreier: RÖMPP Lexikon Lebensmittelchemie. 2nd edition, 2006, ISBN 978-3-13-179282-2 , p. 444
- ↑ See mushroom poisoning , section "The most common causes of mushroom poisoning". The German Society for Mycology (DGfM) names "old mushrooms" as well as too long or incorrect storage as the most important causes of mushroom poisoning.
- ↑ Entry on secondary mushroom poisoning in Flexikon , a Wiki of the DocCheck company , accessed on November 25, 2015. Allergies, intolerances and psychosomatic symptoms of poisoning are also treated here as secondary (fake) mushroom poisoning.
- ↑ Cf. mushroom poisoning , section “The most common causes of mushroom poisoning”: The German Society for Mycology (DGfM) also counts “allergy-like diseases” and “general intolerance reactions”, which only occur in a few consumers, as mushroom poisoning.
- ↑ DGfM mushroom experts. In: dgfm-ev.de. German Society for Mycology, accessed June 5, 2014 .
- ↑ L. Matthies, H. Laatsch, W. Pätzold: Fluoreszenzstoffe aus Cortinarius rubellus Cke. - Steroids instead of nephrotoxic cyclopeptides. In: Z. Mycology. Volume 57, 1991, pp. 273-280.
- ↑ pers. Communication by Wolfgang Steglich, Munich or Lit: P. Spiteller, M. Spiteller, W. Steglich. On the occurrence of the fungal poison orellanin as diglucoside and studies on its biosynthesis. Angewandte Chemie 2003, 115, 2971-2974; Applied Chemistry Int. Ed. 2003, 42, 2864-2867
- ↑ a b c Regis BeDry, Isabelle Baudrimont, Gerard Deffieux, Edmond E. Creppy, Jean P. Pomies: Wild Mushroom poisoning as a cause of rhabdomyolysis . In: New England Journal of Medicine . tape 345 , no. 11 , September 13, 2001, ISSN 0028-4793 , p. 798-802 , doi : 10.1056 / NEJMoa010581 .
- ↑ a b c Masanori Matsuura, Yoko Saikawa, Kosei Inui, Koichi Nakae, Masayuki Igarashi: Identification of the toxic trigger in mushroom poisoning . In: Nature Chemical Biology . tape 5 , no. 7 , July 2009, ISSN 1552-4450 , p. 465-467 , doi : 10.1038 / nchembio.179 .
- ↑ giftpilze.ch: Tricholoma ( page no longer available , search in web archives ) Info: The link was automatically marked as defective. Please check the link according to the instructions and then remove this notice.
- ^ University of Adelaide : Russula subnigricans.
- ↑ Linda Gail Price: Milkcaps. California Academy of Sciences , October 29, 2014
- ↑ Gabija Laubner, Gabija Mikulevičienė: A series of cases of rhabdomyolysis after ingestion of Tricholoma equestre . In: Acta medica Lituanica . tape 23 , no. 3 , 2016, p. 193-197 .
- ↑ Roth, Frank, Kormann. 1990.
- ↑ B. Fugmann, B. Steffan, W. Steglich. In: Tetrahedron Lett. Volume 25, 1984, pp. 3575-3578.
- ↑ "Severe agitation may respond to diazepam (20 mg orally). “Talking down” by reassurance is also effective and is the management of first choice. Antipsychotic medications may intensify the experience and thus are not indicated. ”In: Laurence Brunton, Bruce A. Chabner, Bjorn Knollman: Goodman and Gilman's Manual of Pharmacology and Therapeutics 12th edition. McGraw-Hill 2011, ISBN 978-0-07-175352-4 , p. 1537.
- ^ M. Winkelmann, W. Stangel, I. Schedel, B. Grabensee: Severe hemolysis caused by antibodies against the mushroom Paxillus involutus and its therapy by plasma exchange . In: Clinical weekly . tape 64 , no. 19 , October 1, 1986, ISSN 0023-2173 , pp. 935-938 , doi : 10.1007 / bf01728620 .
- ↑ Common potato bovist . In: Mushroom database of the Munich poison emergency call. Retrieved January 13, 2014.
- ↑ a b Julian White, Scott A. Weinstein, Luc De Haro, Regis Bédry, Andreas Schaper: Mushroom poisoning: A proposed new clinical classification . In: Toxicon . tape 157 , January 2019, p. 53-65 , doi : 10.1016 / j.toxicon.2018.11.007 .
