Mushroom Poisoning

Background: Poisonous mushrooms are eaten by mushroom hunters out of ignorance, after misidentification as edible mushrooms, or as a psychoactive drug. Mushroom poisoning commonly leads to consultation with a poison information center and to hospitalization.

Methods: This review is based on pertinent publications about the syndromes, toxins, and diagnostic modalities that are presented here, which were retrieved by a selective search in PubMed. It is additionally based on the authors’ longstanding experience in the diagnosis and treatment of mushroom intoxication, expert consultation in suspected cases, macroscopic identification of wild mushrooms, and analytic techniques.

Results: A distinction is usually drawn between mushroom poisoning with a short latency of less than six hours, presenting with a gastrointestinal syndrome whose course is usually relatively harmless, and cases with a longer latency of six to 24 hours or more, whose course can be life-threatening (e.g., phalloides, gyromitra, orellanus, and rhabdomyolysis syndrome). The DRG diagnosis data for Germany over the period 2000–2018 include a total of 4412 hospitalizations and 22 deaths due to the toxic effects of mushroom consumption. 90% of the fatalities were due to the death cap mushroom (amatoxins). Gastrointestinal syndromes due to mushroom consumption can be caused not only by poisonous mushrooms, but also by the eating of microbially spoiled, raw, or inadequately cooked mushrooms, or by excessively copious or frequent mushroom consumption.

Conclusion: There are few analytic techniques available other than the qualitative demonstration of amatoxins. Thus, the diagnosis is generally made on the basis of the clinical manifestations and their latency, along with meticulous history-taking, assisted by a mushroom expert, about the type(s) of mushroom that were consumed and the manner of their preparation.

The incidence of mushroom poisoning varies from region to region, season to season, and depending on the weather. In routine clinical practice mushroom poisoning is rare, so clinicians often lack experience in its diagnosis and treatment. Mushrooms (fungi, μύκης) are heterotropic eukaryotic organisms, the fungi, which form their own kingdom alongside the animals and plants in the biological classification of life.

This article deals particularly with poisoning by the fruiting bodies of higher fungi that occur in Europe and can lead to symptoms that are persistent and non-self-limiting, or at least not quickly self-limiting. Of the approximately 5000 kinds of fungi known worldwide, about 20 are excellent eaters, a few hundred are edible, and in Europe around 150 are known to be poisonous—including a few that are potentially deadly (Table 1).

Table 1

Overview of mushroom poisoning syndromes, their most important causative species, and species with which they may be confused

Mushroom foragers ingest poisonous mushrooms out of ignorance, or after confusing them with another, edible kind (Table 1), or misuse them as intoxicating drugs. Along with medical drugs, household chemicals, and plants, mushrooms are among the noxa that often give rise to enquiries at Poison Centers (Giftinformationszentren, GIZ) (see annual reports of the Munich [1] and Göttingen Poison Centers [2]).

Methods

Using the search terms “mushroom [and] poisoning” and the term “analytic” combined with the individual toxins, the PubMed database was searched for articles published up to January 2020. Also fed into the data analysis were opinions and experience from experts from the Society of Clinical Toxicology (Gesellschaft für Klinische Toxikologie e. V., the professional association of Poison Centers in the German-speaking countries and of clinical toxicologists; www.klinitox.de) and from the Clinical Toxicology Working Group of the Society of Forensic and Toxicological Chemistry (Gesellschaft für Forensische und Toxikologische Chemie; www.gtfch.org). Epidemiological data were collected by searching the databases of the Munich and Göttingen Poison Centers and the Federal Health Reports information system for cases treated in German hospitals that were coded with the ICD-10 diagnosis T62.0 “Toxic effect of ingested mushrooms” (data for the years 2010–2018) (3).

Clinical aspects of mushroom poisoning

Diagnostic clues

Because experience is scarce and the subject only marginally touched on during medical training, there is always a danger that diagnosis and the start of treatment will be delayed. The diagnosis of mushroom poisoning rests on three pillars (in the order given below) (4):

• Identification of the ingested mushroom
• The time interval between mushroom ingestion and the onset of symptoms
• Confirmation by laboratory tests (if available).

The emergency doctor or emergency room clinician can start narrowing down the nature of a poisoning and coordinating the patient’s further treatment by proceeding as follows:

The most reliable means of diagnosis is still macroscopic identification of the ingested mushrooms or uningested leftovers (gills current or decurrent; pores; stem shape; cap color), or microscopic identification of the spores in cooked mushroom remains, vomit, or feces, by a qualified mushroom expert (contact details may be obtained from the relevant Poison Center [5]). Other useful information includes how the mushrooms were cooked or prepared, the condition they were in, where they were collected, and how they were transported and stored, together with the latency period to symptom onset (using an interpreter if required). The checklist in Table 2 can be helpful for structured questioning.

Table 2

Information that is helpful for a diagnosis (checklist)

If the patient has eaten a gilled mushroom with a white or green cap, there is cause for extreme alarm. Nevertheless, caution is still needed if one has only the patient’s description to rely on, and it should always be borne in mind that there may have been other mushrooms in a dish apart from the samples brought in with the patient (4).

Mushroom poisoning can be divided into two major categories depending on the interval (latency) from mushroom ingestion to the onset of the first symptoms of poisoning:

• Latency < 6 hours: functional syndromes, usually with a mild course (the exception is Panthercap poisoning) (Table 3a)
• Latency > 6 hours: organ-damaging syndromes, often with fatal outcome (Table 3b).

It should be noted that in some cases gastrointestinal symptoms caused by mushrooms are due not to mushrooms that are poisonous in themselves, but to mushrooms that are microbially contaminated, or raw or inadequately cooked, or eaten in too large a quantity, or eaten too often at too frequent intervals.

Laboratory tests

Apart from the toxins contained in the Deathcap and the Destroying Angel, there are few mushroom toxins for which laboratory tests have been developed, and laboratory tests are not routinely used in the diagnostic workup. For retrospective confirmation of a diagnosis, it may be possible to request testing for some toxins from a specialist laboratory (overview in Tables 3a and 3b; information regarding these may be obtained through the Poison Centers).

By contrast, many laboratories provide testing for amatoxins, the presence of which can be shown in urine before the onset of symptoms after poisoning by the Deathcap or Destroying Angel. Qualitative evidence of amatoxin in the urine can be valuable, since a confirmed diagnosis allows aggressive treatment to be started early, thus probably reducing mortality rates.

Clinical chemical laboratory tests to determine, e.g., impairment of liver function, may not be very helpful towards obtaining a diagnosis, since often they do not yield pathological results until organ damage has already occurred. Because the analytic options are limited, the suspected diagnosis needs to be made primarily on a clinical basis, to allow intensive medical treatment, if required, to be initiated as early as possible.

Case numbers

To estimate case numbers, data from the Poison Centers relating to cases of suspected mushroom poisoning for Southern and Northern Germany and France were collated (Table 4). Depending on weather conditions, numbers can very greatly from one year to the next. There is no central registry in Germany, although efforts have been made to establish a database for monitoring at a national level (6). For this reason, only a generalized search could be made for the numbers of hospitalizations and deaths reported to the German Federal Statistical Office with the diagnostic code ICD-10 T62.0 “Toxic effect of ingested mushrooms.” All the numbers given in Table 4 have limitations, since the data reflect either emergency call statistics or hospital statistics. The numbers of patients treated at local doctor offices or as hospital outpatients, or whose main or discharge diagnosis was coded as “acute liver or kidney failure,” for example, are not included in these figures. Furthermore, mushroom poisoning is not a notifiable condition, so an unknown number of unrecorded cases must exist.

Table 4

Data on the incidence of mushroom poisoning in Germany and France

Mushroom poisoning syndromes and how to treat them

For quick reference, Tables 3a and 3b list the ten most important poisoning syndromes observed after the ingestion of mushrooms, showing their typical symptoms, latency period, treatment, and antidote if any. The mechanism of action, relevant toxins (if known), and any options for laboratory analysis are also given. Table 1 lists the typical poisonous mushrooms and those they can be confused with. Figure 1 shows the Deathcap mushroom (Amanita phalloides), Figure 2 the Fool’s Webcap (Cortinarius orellanus), and Figure 3 the Frosty Funnel (Clitocybe phyllophila) . To identify other kinds of mushrooms, mushroom identification guides should be referred to (7, 8, 9).

Figure 1

The Deathcap (Amanita phalloides) is one of the most poisonous mushrooms in the world. Photo: Robert Wennig, Luxembourg

Figure 2

The Fool’s Webcap (Cortinarius orellanus) has nephrotoxic properties. Photo: Bernd Fellmann, Munich

Figure 3

The Frosty Funnel (Clitocybe phyllophila) contains the toxin muscarine. Photo: Bernd Fellmann, Munich

In most cases treatment for mushroom poisoning is symptomatic. Depending on the toxin involved, fluid and electrolyte replacement, administration of antiemetics, activated charcoal, atropine, beta blockers, benzodiazepines, or neuroleptics, or hemodialysis/plasmapheresis may be used. To enable a quick overview, the therapeutic options for all except amatoxin poisoning are summarized in Tables 3a and 3b.

The symptoms of many kinds of mushroom poisoning often spontaneously disappear after 2 to 3 days at most. Although mushroom poisoning with a short latency period is usually not life-threatening, it should nevertheless not be underestimated, as often only the rapidly occurring signs of poisoning are paid attention to at first. A short latency period does not always rule out amatoxin poisoning (think mixed mushroom dishes). For this reason, patients with symptoms or who have eaten what were probably poisonous mushrooms should generally be kept under observation in hospital for at least 36 hours. Since many cases of mushroom poisoning occur in multiple persons who have shared the same mushroom dish, the other diners should also be examined and if appropriate admitted to hospital—even if they have not developed any symptoms.

Up until 1990, about a dozen different kinds of mushroom poisoning were known in Germany. After 1990, another half dozen additional types of poisoning were published (overview in 3, 9, 10, 11, 12, 13, 14).

For example, mushroom intolerances can arise on an individual basis in immunosuppressed patients, young children, pregnant women, and older persons—including intolerance to mushrooms generally regarded as good to eat, such as the Clouded Funnel (Clitocybe nebularis).

Poisoning syndromes with a short latency period (<6 hours) include gastrointestinal irritant syndrome, muscarinic poisoning, Panthercap/Fly Agaric poisoning, Psilocybin or Magic Mushroom poisoning (hallucinogenic syndrome), coprine poisoning, and paxillus poisoning (Brown Rollrim) (Table 3a).

Table 3a

Mushroom poisoning syndromes with short latency (<6 h)

Poisoning syndromes with a longer latency period (6 to 24 hours) include amatoxin poisoning (described at greater length below), gyromitrin poisoning, orellanine poisoning, and rhabdomyolysis syndrome (Table 3b).

Table 3b

Mushroom poisoning syndromes with long latency (6 to 24 h)

Amatoxin poisoning

Ninety percent of all fatal cases of mushroom poisoning are caused by Amanita phalloides (15), the symptoms and treatment of which will now be described in detail.

Symptoms

The symptoms go through three stages:

• A gastrointestinal stage with 6 to 24 hour latency: severe stomach pains, nausea, vomiting, cholera-like diarrhea
• A hepatic stage with 12 to 48 hour latency: cytolytic hepatitis with a rise in liver enzyme values, apparent clinical improvement
• Progressive acute liver and kidney failure after 24 to 72 h latency: coagulopathy, encephalopathy, nephropathy, seizures, hepatic coma, brain edema, possibly a fatal outcome.

Mechanism of action

Amatoxins are a group of ten heat-stable bicyclic oligopeptides. The main active substances -amanitin and β-amanitin are resistant to digestive peptidases. They inhibit RNA polymerase II and so prevent transcription of DNA to mRNA, thus blocking the biosynthesis of many proteins (enzymes, structural proteins, peptide hormones, membrane receptors). In addition, the presence of some other, temperature-sensitive and acid-sensitive peptide toxins has been demonstrated.

Toxicity of α-amanitin

In animal trials, -amanitin has proved deadly (LD50, mouse) at doses as low as 0.3 mg/kg body weight. In humans, a fatal dose is assumed to be as low as 0.1 mg/kg body weight: that is, as little as 50 to 100 g mushrooms (containing 0.02% to 0.04% α-amanitin)—that is, roughly the amount of a mature fruit body—can be deadly for an adult; for a child the amount is 5 to 10 g mushrooms.

Treatment

Treatment for amatoxin poisoning rests on four pillars (16, 17, 18, 19, 20, 21):

• Volume replacement therapy (a)
• Toxin binding (b)
• Antidote therapy (c)
• Treatment for liver failure, including liver transplantation (d).

a) On admission to hospital, patients are dehydrated by vomiting and diarrhea. This needs to be compensated by copious fluid replacement including electrolytes. Patients should be monitored for adequate urine production, since the toxin is eliminated primarily through the kidneys.

b) Due to the long latency period before symptoms occur, it is usually too late for primary toxin elimination. Patients who attend hospital during the latency period can receive hemodialysis to remove the toxin. Another option for secondary toxin elimination which interrupts the enterohepatic circulation of the toxin is oral administration of activated charcoal 0.5 to 1 g/kg body weight or up to a maximum of 50 g as a bolus in adults (19).

c) Three medications are available as antidotes: penicillin G, silibinin, and N-acetylcysteine (NAC). Silibinin is derived from the milk thistle and is the pharmacologically active substance in the silymarin complex. No randomized clinical studies have been carried out on these substances, and indeed such studies are hardly possible owing to the low case numbers and ethical difficulties of withholding a plausibly effective treatment from patients. Penicillin G and silibinin act mainly by inhibiting uptake of the amatoxins by hepatocytes, which is mediated by the OATP-1B3 transporter (OATP, organic anion transporting polypeptide) (20). NAC has antioxidant and glutathione-regenerating effects. Mortality rates in a retrospectively studied group of patients were 22% with penicillin therapy alone (46/205) (21), 9% with combined penicillin and silibinin therapy (22/248), and 5% with silibinin monotherapy (6/118) (16). On this basis, silibinin monotherapy seems advisable. NAC can be given either as an alternative (if silibinin is not available) or as an adjunct to silibinin. There is a rationale for combining silibinin and NAC therapy, since these two substances have different mechanisms of action (22).

d) Treatment for liver failure is the same as for liver failure of other etiologies. The Clichy criteria (23) and Munich criteria (24) both provide a suitable basis for decision making on whether a liver transplant is indicated. The Clichy criteria include the latency period, coagulopathy, and encephalopathy, while the Munich criteria are based on coagulopathy and renal function. Combining both scores together could be a reasonable option. Albumin-based dialysis techniques (e.g., MARS, Prometheus, ADVOS) have no significant effect in terms of toxin elimination, but can be a suitable interim measure until liver transplantation can be carried out (25, 26).

Laboratory tests

Various methods based on liquid chromatography–mass spectrometry (LCMS) are available to determine the presence of the main active substance α-amanitin and any other amatoxins that may be present (e.g., β-amanitin), but in Germany most of them are not available 24 hours a day. It is extremely important to note that a reliable result can only be obtained if the urine sample is taken within a window of 6 to, at the outside, 36 hours after the mushrooms have been ingested (27, 28). If there is uncertainty about suspected ingestion of Deathcap or Destroying Angel, an immunoassay can be a good alternative, and these are available almost everywhere in Germany (information from Poison Centers). Recently, the development of a rapid test has been reported, although it is not yet available commercially (29). Blood tests for functional liver impairment only give positive results after a considerable delay—usually after organ damage has already occurred. By contrast, amatoxins can be demonstrated in urine even before the onset of symptoms. However, a negative test result does not indicate with any certainty that poisoning has not occurred, since amatoxins are only detectable in the urine for a short time.

Acknowledgments
Many thanks to colleagues in the “Groupe de recherche mycologique de la Société des Naturalistes Luxembourgeois” work group and to Bernd Fellmann, mushroom expert at the German Mycological Society, Munich, for kindly providing photographs.

We thank Bettina Haberl, Department of Clinical Toxicology and Munich Poison Center, Klinikum rechts der Isar, Munich Technical University, for carefully checking the final manuscript.

Conflict of interest statement
The authors declare that no conflict of interest exists.

Translated from the original German by Kersti Wagstaff.

Manuscript received on 3 March 2020, revised version accepted on 17 September 2020.

Corresponding author:
Prof. Dr. Robert Wennig
143, rue de Trèves, 2630 Luxembourg

Cite this as:
Wennig R, Eyer F, Schaper A, Zilker T, Andresen-Streichert H: Mushroom poisoning. Dtsch Arztebl Int 2020; 117: 701–8. DOI: 10.3238/arztebl.2020.0701

►Supplementary material

For eReferences please refer to:
www.aerzteblatt-international.de/ref4220

References

1. Jahresberichte des Giftnotrufs München. www.toxinfo.med.tum.de/inhalt/jahresberichte (last accessed on 6 July 2020).

2. Jahresberichte des Giftinformationszentrums Nord Göttingen. www.giz-nord.de/cms/index.php/jahresberichte.html (last accessed on 6 July 2020).

3. Informationssystem der Gesundheitsberichterstattung des Bundes. www.gbe-bund.de (last accessed on 24 August 2020)

4. Zilker T: Vergiftungen durch Pilze. In: Klinische Toxikologie für die Notfall- und Intensivmedizin. Bremen: UNI-MED 2008; 247–70

5. Liste der Giftnotrufzentralen. www.bvl.bund.de/DE/Arbeitsbereiche/01_Lebensmittel/03_Verbraucher/09_InfektionenIntoxikationen/02_Giftnotrufzentralen/lm_LMVergiftung_giftnotrufzentralen_node.html (last accessed on 20 July 2020).

6. Feistkorn E, Greiner M, Desel H, et al.: Gesundheitsberichterstattung über Vergiftungen in Deutschland – Wissenschaftliche Untersuchung zur Einrichtung eines nationalen Monitorings von Vergiftungen in Deutschland. Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz 2019; 62: 341–9

7. Bon M: Collins Pocket Guide; Mushrooms and Toadstools of Britain and North-Western Europe, Harper Collins Canada, 2004.

8. Pegler D.N. The Conscise Illustrated Book of Mushrooms and other Fungi, Gallery Books, New York, 1989.

9. Harris JC. Pocket Guide to Mushrooms, Bloomsbury Wildlife, London, 2019.

10. White J, Weinstein SA, De Haro L, et al.: Mushroom poisoning: a proposed new clinical classification. Toxicon 2019; 157: 53–65

11. Diaz JH: Syndromic diagnosis and management of confirmed mushroom poisonings. Crit Care Med 2005; 33: 427–43

12. Saviuc P, Danel V: New syndromes in mushroom poisoning. Toxicol Rev 2006; 25: 199–209

13. Romanek K, Haberl B, Pfab R, Stich R, Eyer F: Pilzvergiftungen: Symptome, Diagnostik und Therapie. Notf Rett Med 2016; 19: 301–14

14. Romanek K, Eyer F: Mushroom poisoning. MMW Fortschr Med 2019; 161: 64–5

15. Sinno-Tellier S, Bruneau C, Daoudi J, Greillet C, Verrier A, Bloch J: National surveillance of food poisoning by mushrooms: cases reported to the network of poison control centres from 2010 to 2017. Bull Epidemiol Hebd (Paris) 2019; 33: 666–78.

16. Ganzert M, Felgenhauer N, Schuster T, Eyer F, Gourdin C, Zilker T: Knollenblätterpilzvergiftung: Silibinin und Kombination von Silibinin und Penicillin im Vergleich. Dtsch Med Wochenschr 2008; 133: 2261–7

17. Enjalbert F, Rapior S, Nouguier-Soulé J, Guillon S, Amouroux N, Cabot C: Treatment of amatoxin poisoning: 20-year retrospective analysis. J Toxicol Clin Toxicol 2002; 40: 715–57

18. Giannini L, Vannacci A, Missanelli A, et al.: Amatoxin poisoning: a 15-year retrospective analysis and follow-up evaluation of 105 patients. Clin Toxicol (Phila) 2007; 45: 539–42

19. Zellner T, Prasa D, Färber E, Hoffmann-Walbeck P, Genser D, Eyer F: The use of activated charcoal to treat intoxications. Dtsch Arztebl Int 2019; 116: 311–7

20. Popp T, Balszuweit F, Schmidt A, Eyer F, Thiermann H, Steinritz D: Assessment of α-amanitin toxicity and effects of silibinin and penicillin in different in vitro models. Toxicol In Vitro 2020; 67:104921

21. Floersheim GL, Weber O, Tschumi P, Ulbrich M: Die klinische Knollenblätterpilzvergiftung: prognostische Faktoren und therapeutische Maßnahmen. Schweiz Med Wochenschr 1982; 112: 1164–77.

22. Liu J, Chen Y, Gao Y, et al.: N-acetylcysteine as a treatment for amatoxin poisoning: a systematic review. Clin Toxicol (Phila) 2020; 1–8.

23. Escudié L, Francoz C, Vinel JP, et al.: Amanita phalloides poisoning: reassessment of prognostic factors and indications for emergency liver transplantation. J Hepatol 2007; 46: 466–73

24. Ganzert M, Felgenhauer N, Zilker T: Indication of liver transplantation following amatoxin intoxication. J Hepatol 2005; 42: 202–9

25. Wittebole X, Hantson P: Use of the molecular adsorbent recirculating system (MARS) for the management of acute poisoning with or without liver failure. Clin Toxicol (Phila) 2011; 49: 782–93

26. Bergis D, Friedrich-Rust M, Zeuzem S, Betz C, Sarrazin C, Bojunga J: Treatment of Amanita phalloides intoxication by fractionated plasma separation and adsorption (Prometheus®). J Gastrointestin Liver Dis 2012; 21: 171–6.

27. Butera R, Locatelli C, Coccini T, Manzo L: Diagnostic accuracy of urinary amanitin in suspected mushroom poisoning: a pilot study. J Toxicol Clin Toxicol 2004; 42: 901–12

28. Michely JA, Helfer AG, Meyer MR, Maurer HH: Is LC-High-Resolution-MS/MS a suitable alternative to ELISA in diagnosis of Amanita phalloides poisonings?— A two years’ experience. Toxichem Krimtech 2015; 82 (Special Issue): 155.

29. Bever CS, Barnych B, Hnasko R, Cheng LW, Stanker LH: A new conjugation method used for the development of an immunoassay for the detection of amanitin, a deadly mushroom toxin. Toxins (Basel) 2018; 10: 265

e1. Merová B, Ondra P, Staňková M, et al.: Determination of muscarine in human urine by electrospray liquid chromatographic-mass spectrometric. J Chromatogr B Analyt Technol Biomed Life Sci 2011; 879: 2549–53

e2. Tomková J, Ondra P, Válka I: Simultaneous determination of mushroom toxins α-amanitin, β-amanitin and muscarine in human urine by solid-phase extraction and ultra-high-performance liquid chromatography coupled with ultra-high-resolution TOF mass spectrometry. Forensic Sci Int 2015; 251: 209–13

e3. Reichl FX (ed.): Taschenatlas Toxikologie. Stuttgart: Georg Thieme Verlag KG 2009

e4. Stříbrný J, Sokol M, Merová B, Ondra P: GC/MS determination of ibotenic acid and muscimol in the urine of patients intoxicated with Amanita pantherina. Int J Legal Med 2012; 126: 519–24

e5. Hasegawa K, Gonmori K, Fujita H, et al.: Determination of ibotenic acid and muscimol, the amanita mushroom toxins, in human serum by liquid chromatography–tandem mass spectrometry. Forensic Toxicol 2013; 31: 322–7

e6. Zhuk O, Jasicka-Misiak I, Poliwoda A, et al.: Research on acute toxicity and the behavioral effects of methanolic extract from psilocybin mushrooms and psilocin in mice. Toxins (Basel) 2015; 7: 1018–29

e7. Sticht G, Käferstein H: Detection of psilocin in body fluids. Forensic Sci Int 2000; 113: 403–7

e8. Chen J, Li M, Yan X, et al.: Determining the pharmacokinetics of psilocin in rat plasma using ultra-performance liquid chromatography coupled with a photodiode array detector after orally administering an extract of Gymnopilus spectabilis. J Chromatogr B Analyt Technol Biomed Life Sci 2011; 879: 2669–72

e9. Martin R, Schürenkamp J, Pfeiffer H, Köhler H: A validated method for quantitation of psilocin in plasma by LC-MS/MS and study of stability. Int J Legal Med 2012; 126: 845–9

e10. Flammer R, Gallen S: Hämolyse bei Pilzvergiftungen: Fakten und Hypothesen. Schweiz Med Wochenschr 1983; 113: 1555–61.

e11. Moss MJ, Hendrickson RG. Toxicity of muscimol and ibotenic acid containing mushrooms reported to a regional poison control center from 2002–2016. Clin Toxicol (Phila) 2019; 57: 99–103

e12. Horowitz KM, Kong EL, Horowitz BZ: Gyromitra mushroom toxicity. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2020. (last update: 29 May 2020).

e13. Arshadi M, Nilsson C, Magnusson B: Gas chromatography-mass spectrometry determination of the pentafluorobenzoyl derivative of methylhydrazine in false morel (Gyromitra esculenta) as a monitor for the content of the toxin gyromitrin. J Chromatogr A 2006; 1125: 229–33

e14. Saviuc P, Harry P, Pulce C, Garnier R, Cochet A: Can morels (Morchella sp.) induce a toxic neurological syndrome? Clin Toxicol (Phila) 2010; 48: 365–72

e15. Frank H, Zilker T, Kirchmair M, et al.: Acute renal failure by ingestion of cortinarius species confounded with psychoactive mushrooms: a case series and literature survey. Clin Nephrol 2009; 71: 557–62

e16. Anantharam P, Shao D, Imerman PM, et al.; Improved tissue-based analytical test methods for orellanine, a biomarker of cortinarius mushroom intoxication. Toxins (Basel) 2016; 8: 158

e17. Rohrmoser M, Kirchmair M, Feifel E, et al.: Orellanine poisoning: rapid detection of the fungal toxin in renal biopsy material. J Toxicol Clin Toxicol 1997; 35: 63–6

e18. Rapior S, Delpech N, Andary C, Huchard G: Intoxication by Cortinarius orellanus: detection and assay of orellanine in biological fluids and renal biopsies. Mycopathologia 1989; 108: 155–61

e19. Bedry R, Baudrimont I, Deffieux G et al.: Wild-mushroom intoxication as a cause of rhabdomyolysis. N Engl J Med 2001; 345: 798–802

e20. Laubner G, Mikulevičienė G: A series of cases of rhabdomyolysis after ingestion of Tricholoma equestre. Acta Med Litu 2016; 23: 193–7

e21. Klimaszyk P, Rzymski P: The yellow knight fights back: toxicological, epidemiological, and survey studies defend edibility of Tricholoma equestre. Toxins (Basel) 2018; 10: 468

e22. Cho JT, Han JH: A case of mushroom poisoning with Russula subnigricans: development of rhabdomyolysis, acute kidney injury, cardiogenic shock, and death. J Korean Med Sci 2016; 31: 1164–7

e23. Lin S, Mu M, Yang F, Yang C: Russula subnigricans poisoning: from gastrointestinal symptoms to rhabdomyolysis. Wilderness Environ Med 2015; 26: 380–3

e24. Matsuura M, Saikawa Y, Inui K, et al.: Identification of the toxic trigger in mushroom poisoning. Nat Chem Biol 2009; 5: 465–7

e25. Matsuura M, Kato S, Saikawa Y, Nakata M, Hashimoto K: Identification of cyclopropylacetyl-(R)-carnitine, a unique chemical marker of the fatally toxic mushroom Russula subnigricans. Chem Pharm Bull (Tokyo) 2016; 64: 602–8

e26. Persson HE, Sjöberg GK, Haines JA, Pronczuk de Garbino J: Poisoning severity score. Grading of acute poisoning. J Toxicol Clin Toxicol 1998; 36: 205–13