amatoxin and Mushroom-Poisoning

Amatoxins are toxic bicyclic octapeptides found in certain wild mushroom species, particularly Amanita phalloides. These mushrooms contain predominantly α- and β-amanitin, which can lead to severe health risks for humans and animals if ingested. Rapid and accurate identification of these toxins in mushroom and biological samples is crucial for diagnosing and treating mushroom poisoning. Analytical methods for the determination of amatoxins are critical to ensure food safety and prompt medical treatment. This review provides a comprehensive overview of the research literature on the determination of amatoxins in clinical specimens, biological and mushroom samples. We discuss the physicochemical properties of toxins, highlighting their influence on the choice of the analytical method and the importance of sample preparation, particularly solid-phase extraction with cartridges. Chromatographic methods are emphasised with a focus on liquid chromatography coupled to mass spectrometry as one of the most relevant analytical method for the determination of amatoxins in complex matrices. Furthermore, current trends and future perspectives in amatoxin detection are also suggested.

Topics: Animals; Chromatography, High Pressure Liquid; Chromatography, Liquid; Humans; Mass Spectrometry; Mushroom Poisoning; Toxins, Biological

Amanita neoovoidea (genus Amanita Pers.) poisoning leads to acute renal failure. Here, we present seven case reports of acute renal failure with acute hepatic failure due to ingestion of A. neoovoidea. Clinical manifestations included gastrointestinal symptoms 1-72 h after ingestion; elevation of renal parameters and blood uric acid, blood urea nitrogen, and creatinine levels; a few abnormal hepatic parameters, primarily albumin decrease and alanine aminotransferase increase; and elevation of zymogram parameters such as cholinesterase and lactate dehydrogenase. To determine whether the hepatic/renal lesions were caused by amanitins, we analyzed the blood and urine samples of patients and specimens of poisonous mushrooms. Morphological and molecular biological analyses indicated that the mushroom was A. neoovoidea. However, no amatoxins and phallotoxins were detected in its basidiomata.

Topics: Acute Kidney Injury; Adult; Aged; Aged, 80 and over; Amanita; Amanitins; Blood Urea Nitrogen; China; Chromatography, High Pressure Liquid; Creatinine; Female; Humans; Male; Middle Aged; Mushroom Poisoning; Uric Acid

Amatoxins are produced primarily by 3 species of mushrooms: Amanita, Lepiota, and Galerina. Because amatoxin poisonings are increasing, the objective of this review was to identify all amatoxin-containing mushroom species, present a toxidromic approach to earlier diagnoses, and compare the efficacies and outcomes of therapies. To meet these objectives, Internet search engines were queried with keywords to select peer-reviewed scientific articles on amatoxin-containing mushroom poisoning and management. Descriptive epidemiological analyses have documented that most mushroom poisonings are caused by unknown mushrooms, and most fatal mushroom poisonings are caused by amatoxin-containing mushrooms. Amanita species cause more fatal mushroom poisonings than other amatoxin-containing species, such as Galerina and Lepiota. Amanita phalloides is responsible for most fatalities, followed by Amanita virosa and Amanita verna. The most frequently reported fatal Lepiota ingestions are due to Lepiota brunneoincarnata, and the most frequently reported fatal Galerina species ingestions are due to Galerina marginata. With the exception of liver transplantation, the current treatment strategies for amatoxin poisoning are all supportive and have not been subjected to rigorous efficacy testing in randomized controlled trials. All patients with symptoms of late-appearing gastrointestinal toxicity with or without false recovery or quiescent periods preceding acute liver insufficiency should be referred to centers providing liver transplantation. Patients with amatoxin-induced acute liver insufficiency that does not progress to liver failure will have a more favorable survival profile with supportive care than patients with amatoxin-induced acute liver failure, about half of whom will require liver transplantation.

Topics: Agaricales; Amanita; Amanitins; Hepatic Insufficiency; Humans; Liver Failure, Acute; Liver Transplantation; Mushroom Poisoning

Amanita phalloides poisoning with a high mortality is a serious health problem in the world. The typical clinical manifestations are usually characterized by the absence of any symptoms followed by severe gastrointestinal disorders and acute liver failure. Inhibition of RNA polymeraseII (RNAP II) activity, apoptosis, and oxidative stress are considered as the major mechanism of amatoxins intoxication. The current treatment measures mainly include prevention of amatoxins absorption, elimination of absorbed amatoxins, potential antidotes therapy, and liver transplantation. Nevertheless, there are no widely accepted treatment criteria for Amanita phalloides poisoning. This paper will focus on the treatment measures based on the previous studies and provide the currently available information for clinicians.

Topics: Acetylcysteine; Amanita; Amanitins; Antidotes; Bile Ducts; Charcoal; Diuresis; Gastric Lavage; Humans; Liver; Liver Failure, Acute; Liver Transplantation; Mushroom Poisoning; Penicillin G; Silymarin

Topics: Acute Disease; Adult; Aged; Amanitins; Female; Glasgow Coma Scale; Hepatic Encephalopathy; Hong Kong; Humans; Liver Transplantation; Male; Middle Aged; Mushroom Poisoning

A shortcut review was carried out to establish whether silibinin is better than conservative management at reducing liver transplantation and death after poisoning with amatoxin-containing mushrooms. Thirty-eight papers were found in Medline and 86 in EMBASE using the reported searches. Of these, five presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these best papers are tabulated. It is concluded that the evidence is limited, but given the lack of alternative treatments in patients with suspected amatoxin-containing mushroom poisoning and the relatively few adverse effects, silibinin should be considered in some patients.

Topics: Amanitins; Antioxidants; Evidence-Based Emergency Medicine; Humans; Mushroom Poisoning; Silybin; Silymarin

Topics: Acetylcysteine; Amanita; Amanitins; Bile; Blood Component Removal; Charcoal; Chromatography, High Pressure Liquid; Drainage; Gastric Lavage; Humans; Japan; Laxatives; Liver Transplantation; Mushroom Poisoning; Penicillin G; Silybin; Silymarin

Topics: Acetylcysteine; Adult; Amanita; Amanitins; Cause of Death; Combined Modality Therapy; Critical Care; Diagnosis, Differential; Hepatic Encephalopathy; Humans; Liver Function Tests; Liver Transplantation; Male; Mushroom Poisoning; Prognosis; Silybin; Silymarin

Diagnosis and management of Amanita mushroom poisoning is a challenging problem for physicians across the United States. With 5902 mushroom exposures and two resultant deaths directly linked to Amanita ingestion in 2009, it is difficult for physicians to determine which patients are at risk for lethal toxicity. Identification of amatoxin poisoning can prove to be difficult due to delay in onset of symptoms and difficulty with identification of mushrooms. Consequently, it is difficult for the Emergency Physician to determine proper disposition. Further, treatment options are controversial.. To review current data to help health care providers effectively identify and treat potentially deadly Amanita mushroom ingestions.. We present two cases of Amanita mushroom ingestion in the northeastern United States treated with N-acetylcysteine, high-dose penicillin, cimetidine, and silibinin, a semi-purified fraction of milk thistle-derived silymarin, as part of their treatment regimen. The mushroom species was identified by a consultant as Amanita Ocreata.. We present the successful treatment of 2 patients who ingested what we believe to be an Amanita species never before identified in the northeastern United States.

Topics: Aged; Amanita; Amanitins; Antioxidants; Female; Humans; Male; Middle Aged; Mushroom Poisoning; Treatment Outcome

More than 90% of all fatal mushroom poisonings worldwide are due to amatoxin containing species that grow abundantly in Europe, South Asia, and the Indian subcontinent. Many cases have also been reported in North America. Initial symptoms of abdominal cramps, vomiting, and a severe cholera-like diarrhea generally do not manifest until at least six to eight hours following ingestion and can be followed by renal and hepatic failure. Outcomes range from complete recovery to fulminant organ failure and death which can sometimes be averted by liver transplant. There are no controlled clinical studies available due to ethical reasons, but uncontrolled trials and case reports describe successful treatment with intravenous silibinin (Legalon® SIL). In nearly 1,500 documented cases, the overall mortality in patients treated with Legalon® SIL is less than 10% in comparison to more than 20% when using penicillin or a combination of silibinin and penicillin. Silibinin, a proven antioxidative and anti-inflammatory acting flavonolignan isolated from milk thistle extracts, has been shown to interact with specific hepatic transport proteins blocking cellular amatoxin re-uptake and thus interrupting enterohepatic circulation of the toxin. The addition of intravenous silibinin to aggressive intravenous fluid management serves to arrest and allow reversal of the manifestation of fulminant hepatic failure, even in severely poisoned patients. These findings together with the available clinical experience justify the use of silibinin as Legalon® SIL in Amanita poisoning cases.

Topics: Amanitins; Animals; Antidotes; Chemical and Drug Induced Liver Injury; Humans; Molecular Structure; Mushroom Poisoning; Silymarin; Tissue Distribution; Treatment Outcome

Topics: Agaricales; Amanitins; Cyanides; Humans; Japan; Mushroom Poisoning; Peptides, Cyclic

Mushrooms are ubiquitous in nature. They are an important source of nutrition; however, certain varieties contain chemicals that can be highly toxic to humans. Industrially cultivated mushrooms are historically very safe, but foraging for mushrooms or accidental ingestion of mushrooms in the environment can result in serious illness and death. The emergency department is the most common site of presentation for patients suffering from acute mushroom poisoning. Although recognition can be facilitated by identification of a characteristic toxidrome, the presenting manifestations can be variable and have considerable overlap with more common and generally benign clinical syndromes. The goal of this two-part article is to review the knowledge base on this subject and provide information that will assist the clinician in the early consideration, diagnosis and treatment of mushroom poisoning. Part I, presented in this issue of the Journal, reviews the epidemiology and demographics of mushroom poisoning, the physical characteristics of the most toxic varieties, the classification of the toxic species, and an overview of the cyclopeptide-containing mushroom class. Part II, to be published in the next issue of the Journal, will be focused on the presentation of the other classes of toxic mushrooms along with an up-to-date review of the most recently identified poisonous varieties.

Topics: Agaricales; Amanita; Amanitins; Child, Preschool; Humans; Mushroom Poisoning; Mycotoxins

Among fungal toxins causing organ damage in the human body, amatoxins and orellanine remain exceptional. Amatoxins, a group of bicyclic octapeptides occurring in some Amanita, Galerina and Lepiota species, induce deficient protein synthesis resulting in cell death, but might also exert toxicity through inducing apoptosis. Target organs are intestinal mucosa, liver and kidneys. Poisoning will result in dehydration and electrolyte derangement, liver necrosis and possibly kidney damage. In established poisoning the mainstay of treatment is optimum symptomatic and supportive care. No specific treatment is available, but some pharmaceuticals, like silibinin, benzylpenicillin and acetylcysteine, might have a role in limiting the extent of hepatic damage. Orellanine is a nephrotoxic bipyridine N-oxide found in some Cortinarius species. Its mechanism of action is not fully understood, but it has been shown to inhibit protein synthesis and to generate free oxygen radicals. As early symptoms often are lacking or vague, poisoning may initially be overlooked or misinterpreted and the patients usually present with established renal damage. Supportive care is the only therapeutic option. Tricholoma equestre might contain a myotoxin and repeated ingestion may cause significant rhabdomyolysis. Ingestion of Amanita smithiana and A. proxima has been reported to result in kidney damage. Gyromitrin, a toxic compound that is converted to hydrazines in the stomach, occurs in some Gyromitra species. It is mainly neurotoxic, but may also induce moderate hepatic damage and haemolysis.

Topics: 2,2'-Dipyridyl; Acetaldehyde; Amanitins; Basidiomycota; Humans; Kidney Diseases; Mushroom Poisoning; Mycotoxins; Rhabdomyolysis

Amatoxin poisoning is a medical emergency characterized by a long incubation time lag, gastrointestinal and hepatotoxic phases, coma, and death. This mushroom intoxication is ascribed to 35 amatoxin-containing species belonging to three genera: Amanita, Galerina, and Lepiota. The major amatoxins, the alpha-, beta-, and gamma-amanitins, are bicyclic octapeptide derivatives that damage the liver and kidney via irreversible binding to RNA polymerase II.. The mycology and clinical syndrome of amatoxin poisoning are reviewed. Clinical data from 2108 hospitalized amatoxin poisoning exposures as reported in the medical literature from North America and Europe over the last 20 years were compiled. Preliminary medical care, supportive measures, specific treatments used singly or in combination, and liver transplantation were characterized. Specific treatments consisted of detoxication procedures (e.g., toxin removal from bile and urine, and extracorporeal purification) and administration of drugs. Chemotherapy included benzylpenicillin or other beta-lactam antibiotics, silymarin complex, thioctic acid, antioxidant drugs, hormones and steroids administered singly, or more usually, in combination. Supportive measures alone and 10 specific treatment regimens were analyzed relative to mortality.. Benzylpenicillin (Penicillin G) alone and in association was the mostfrequently utilized chemotherapy but showed little efficacy. No benefit was found for the use of thioctic acid or steroids. Chi-square statistical comparison of survivors and dead vs. treated individuals supported silybin, administered either as mono-chemotherapy or in drug combination and N-acetylcysteine as mono-chemotherapy as the most effective therapeutic modes. Future clinical research should focus on confirming the efficacy of silybin, N-acetylcysteine, and detoxication procedures.

Topics: Agaricales; Amanitins; Animals; Chemical and Drug Induced Liver Injury; Emergency Medical Services; Humans; Liver Transplantation; Mushroom Poisoning; Retrospective Studies

The most poisonous mushroom toxins are produced by Amanita phalloides (death cap). The occurrence and chemistry of three groups of toxins (amatoxins, phallotoxins and virotoxins) are summarized. The concentration and distribution of toxins in certain species are variable, with the young fruit body containing lower, and the well-developed fungus higher concentrations, but there is a high variability among specimens collected in the same region. Regarding phallotoxins, the volva (the ring) is the most poisonous. The most important biochemical effect of amatoxins is the inhibition of RNA polymerases (especially polymerase II). This interaction leads to a tight complex and the inhibition is of a non-competitive type. Non-mammalian polymerases show little sensitivity to amanitins. The amatoxins cause necrosis of the liver, also partly in the kidney, with the cellular changes causing the fragmentation and segregation of all nuclear components. Various groups of somatic cells of emanation resistance have been isolated, including from a mutant of Drosophila melanogaster. The phallotoxins stimulate the polymerization of G-actin and stabilize the F-actin filaments. The interaction of phallotoxins occurs via the small, 15-membered ring, on the left side of the spatial formula. The symptoms of human poisoning and the changes in toxin concentrations in different organs are summarized. Conventional therapy includes: (1) stabilization of patient's condition with the correction of hypoglycaemia and electrolytes; (2) decontamination; and (3) chemotherapy with different compounds. Finally, certain antagonists and protective compounds are reviewed, bearing in mind that today these have more of a theoretical than a practical role.

Topics: Amanita; Amanitins; Animals; Humans; Models, Molecular; Molecular Structure; Mushroom Poisoning; Peptides, Cyclic

Hepatotoxic mushroom poisoning (due to Amanita, Lepiota and Galerina species) may be considered as a real medical emergency, since an early diagnosis and immediate treatment are required for a successful outcome. In this review the physio-pathological features and the clinical picture of amatoxin poisonings are described as the basis for diagnosis and therapeutic decisions. The treatment schedule proposed is analyzed in some points: Symptomatic and supportive measures, toxin removal and extraction procedures, and the possibility of using antidotes. Some parameters with prognostic significance are commented on. Finally, the mortality rate and its evolution throughout the present century is also considered.

Topics: Amanitins; Combined Modality Therapy; Humans; Mushroom Poisoning; Prognosis

A 60-year-old man presented with acute gastroenteritis, hypovolemic shock, acute renal failure (BUN/Cr, 56.7/4.24 mg/dl), and aspiration pneumonia. The previous day, he ingested 30 caps of mushrooms of an unknown species. The patient was treated with a massive intravenous infusion, renal replacement therapy, and antimicrobial agents. Late-onset mild liver injury peaked on day 11 (AST/ALT, 62/67 IU/l). Acute renal failure improved once before worsening, with the worst symptoms on day 19 (BUN/Cr, 99/6.61 mg/dl). Thereafter, the patient showed gradual improvement, and renal replacement therapy was discontinued on day 23. His general condition improved fully and he was transferred to another hospital for rehabilitation on day 47. The mushrooms were later identified as Galerina sulciceps by the Basic Local Alignment Search Tool, and toxicologic analysis using liquid chromatography-tandem mass spectrometry revealed an average of 85 ppm α-amanitin and 330 ppm β-amanitin in the tissue of the mushrooms brought in by the patient's family. Galerina sulciceps is distributed mainly in tropical and subtropical regions of Southeast Asia and had never been identified before in Japan. The heat of fermentation generated by the thick layer of wood chips on the ground or global warming may have contributed to its growth in Japan. Interestingly, our patient did not have liver dysfunction, which is one main and typical amatoxin poisoning symptom. Variation in clinical presentation may be attributed to the different ratios of α-amanitin to β-amanitin in different mushroom species.

Topics: Acute Kidney Injury; Agaricales; Alpha-Amanitin; Amanitins; Humans; Japan; Male; Middle Aged; Mushroom Poisoning

About 95% of fatal mushroom poisonings worldwide are caused by amatoxins and phallotoxins mostly produced by species of Amanita, Galerina, and Lepiota. The genus Lepiota is supposed to include a high number of species producing amatoxins. In this study, we investigated 16 species of Lepiota based on 48 recently collected specimens for the presence of amatoxins by liquid chromatography coupled to a diode-array detector and mass spectrometry (UHPLC-QTOF-MS/MS). By comparing the retention times, UV absorptions, and diagnostic MS fragment ions with data obtained from the benchmark species Amanita phalloides, we detected α-amanitin and γ-amanitin in Lepiota subincarnata, α-amanitin and amaninamide in Lepiota brunneoincarnata, and β-amanitin and α-amanitin in Lepiota elaiophylla. Phallotoxins have not been detected any of these species. Two possibly undescribed amatoxin derivatives were found in Lepiota boudieri and L. elaiophylla, as well as one further non-amatoxin compound in one specimen of L. cf. boudieri. These compounds might be used to differentiate L. elaiophylla from L. xanthophylla and species within the L. boudieri species complex. No amatoxins were detected in L. aspera, L. castanea, L. clypeolaria, L. cristata, L. erminea, L. felina, L. fuscovinacea, L. lilacea, L. magnispora, L. oreadiformis, L. pseudolilacea, L. sp. (SeSa 5), and L. subalba. By combining the occurrence data of amatoxins with a phylogenetic analysis, a monophyletic group of amatoxin containing species of Lepiota is evident. These chemotaxonomic results highlight the relevance of systematic relationships for the occurrence of amatoxins and expand our knowledge about the toxicity of species of Lepiota.

Topics: Agaricales; Amanitins; Mushroom Poisoning; Phylogeny; Tandem Mass Spectrometry

Topics: Acetylcysteine; Amanitins; Humans; Mushroom Poisoning

Topics: Acetylcysteine; Amanitins; Humans; Mushroom Poisoning

Mushroom toxicity is the main branch of foodborne poisoning, and liver damage caused by amatoxin poisoning accounts for more than 90 % of deaths due to mushroom poisoning. Alpha-amatoxin (α-AMA) has been considered the primary toxin from amatoxin-containing mushrooms, which is responsible for hepatotoxicity and death. However, the mechanism underlying liver failure due to α-AMA remains unclear. This study constructed animal and cell models. In the animal experiments, we investigated liver injury in BALB/c mice at different time points after α-AMA treatment, and explored the process of inflammatory infiltration using immunohistochemistry and western blotting. Then, a metabonomics method based on gas chromatography mass spectrometry (GCMS) was established to study the effect of α-AMA on liver metabonomics. The results showed a significant difference in liver metabolism between the exposed and control mice groups that coincided with pathological and biochemical indicators. Moreover, 20 metabolites and 4 metabolic pathways related to its mechanism of action were identified, which suggested that energy disorders related to mitochondrial dysfunction may be one of the causes of death. The significant changes of trehalose and the fluctuation of LC3-II and sqstm1 p62 protein levels indicated that autophagy was also involved in the damage process, suggesting that autophagy may participate in the clearance process of damaged mitochondria after poisoning. Then, we constructed an α-AMA-induced human normal liver cells (L-02 cells) injury model. The above hypothesis was further verified by detecting cell necrosis, mitochondrial reactive oxygen species (mtROS), mitochondrial permeability transition pore (mPTP) opening, mitochondrial membrane potential (Δψ m), and cellular ATP level. Collectively, our results serve as direct evidence of elevated in vivo hepatic mitochondrial metabolism in α-AMA-exposed mice and suggest that mitochondrial dysfunction plays an important role in the early stage of α-AMA induced liver failure.

Topics: Amanitins; Animals; Cell Line; Chemical and Drug Induced Liver Injury; Disease Models, Animal; Energy Metabolism; Humans; Liver; Liver Failure; Metabolomics; Mice, Inbred BALB C; Mitochondria, Liver; Mushroom Poisoning; Time Factors

Topics: Acetylcysteine; Amanitins; Humans; Mushroom Poisoning

Topics: Acetylcysteine; Amanitins; Humans; Mushroom Poisoning

Topics: Amanita; Amanitins; Chromatography, High Pressure Liquid; Cooking; Forensic Toxicology; Hot Temperature; Humans; Mushroom Poisoning

To describe the clinical course, treatment, and outcome of 5 dogs following ingestion of toxic Amanita spp. mushrooms containing amatoxins using an adapted version of the Santa Cruz protocol developed for people.. Five dogs were presented with clinical signs compatible with amanitin toxicity with witnessed ingestion noted in 3 of 5 dogs. Clinical findings included acute onset vomiting and diarrhea, lethargy, and hepatopathy including signs of fulminant hepatic failure (increased liver enzyme activities, hyperbilirubinemia, prolonged clotting times, and hypoglycemia were noted among these cases). Urine toxicological screening confirmed the presence of Amanita toxins in 4 cases with expert mycologist speciation in the fifth. Core interventions included percutaneous biliary drainage, use of octreotide, and early nil per os orders. All dogs survived to discharge with this treatment strategy.. This case series describes the use of a modified version of the Santa Cruz protocol to address amatoxin-induced fulminant hepatic failure in dogs. The protocol was safe, well tolerated, and all patients made a full clinical recovery.

Topics: Amanita; Amanitins; Animals; Dog Diseases; Dogs; Humans; Liver Failure, Acute; Male; Mushroom Poisoning

Amatoxin poisoning is the main cause of death from accidental ingestion of poisonous mushrooms and a mortality rate of 27.3% has been reported in Thailand. Symptoms of mushroom ingestion are often confused with food poisoning; thus, gastroenteritis is not recognised as the first phase of poisoning. Our study assessed the efficacy of N-acetylcysteine (NAC) as a treatment for amatoxin poisoning. We retrospectively analysed 74 medical records over 12 years. The majority (70/74) were treated successfully with NAC; death in the remaining 4 (5.4%) patients was attributed to late presentation in three and advanced alcoholic cirrhosis in one.

Topics: Acetylcysteine; Amanitins; Female; Gastroenteritis; Humans; Male; Mushroom Poisoning; Retrospective Studies; Thailand; Treatment Outcome

Topics: Amanita; Amanitins; Antioxidants; China; Female; Humans; Liver; Liver Failure, Acute; Male; Middle Aged; Mushroom Poisoning; Thrombocytopenia

Globally, mushroom poisonings cause about 100 human deaths each year, with thousands of people requiring medical assistance. Dogs are also susceptible to mushroom poisonings and require medical assistance. Cyclopeptides, and more specifically amanitins (or amatoxins, here), are the mushroom poison that causes the majority of these deaths. Current methods (predominantly chromatographic, as well as antibody-based) of detecting amatoxins are time-consuming and require expensive equipment. In this work, we demonstrate the utility of the lateral flow immunoassay (LFIA) for the rapid detection of amatoxins in urine samples. The LFIA detects as little as 10 ng/mL of α-amanitin (α-AMA) or γ-AMA, and 100 ng/mL of β-AMA in urine matrices. To demonstrate application of this LFIA for urine analysis, this study examined fortified human urine samples and urine collected from exposed dogs. Urine is sampled directly without the need for any pretreatment, detection from urine is completed in 10 min, and the results are read by eye, without the need for specialized equipment. Analysis of both fortified human urine samples and urine samples collected from intoxicated dogs using the LFIA correlated well with liquid chromatography-mass spectrometry (LC-MS) methods.

Topics: Amanitins; Animals; Dog Diseases; Dogs; Humans; Immunoassay; Molecular Structure; Mushroom Poisoning; Point-of-Care Testing; Sensitivity and Specificity

Amatoxins, most of which are hepatotoxic, can cause fatal intoxication. While mushrooms in the amatoxin-containing Galerina genus are rare, they can poison humans and animals worldwide. Few studies have profiled the toxicity of Galerina marginata. In addition, many studies indicate that macrofungi can have different characteristics in different regions. In this study, the quantities of toxins present in G. marginata from different provinces in Turkey were analysed using reversed-phase high-performance liquid chromatography with ultraviolet detection (RP-HPLC-UV) and liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS). G. marginata samples were collected from three different regions of Turkey. The taxonomic categorization of mushrooms was based on their micro- and macroscopic characteristics. The presence of toxins α-amanitin (AA), β-amanitin (BA), γ-amanitin (GA), phalloidin (PHD) and phallacidin (PHC) quantities were measured using RP-HPLC-UV and then were confirmed using LC-ESI-MS/MS. BA levels were higher than AA levels in G. marginata mushrooms collected from all three regions. Moreover, the levels of GA were below the detection limit and no phallotoxins were detected. This is the first study to identify and test the toxicity of G. marginata collected from three different regions of Turkey using RP-HPLC-UV. This is also the first study to confirm the UV absorption of amatoxins in G. marginata using LC-ESI-MS/MS, which is a far more sensitive process. More studies evaluating the toxicity of G. marginata in other geographic regions of the world are needed.

Topics: Alpha-Amanitin; Amanitins; Mushroom Poisoning; Toxins, Biological; Turkey

A 34-year-old woman from Thai origin developed acute liver failure after ingestion of a soup which contained the death cap (Amanita phalloides).. In patients with poisoning due to amatoxin-containing mushrooms, gastro-intestinal complaints usually develop several hours after ingestion, followed by acute hepatic failure which occasionally leads to death. The incidence of reported mushroom poisonings in the Netherlands has increased in 2019, which is possibly associated with migration of asylum seekers who regularly pick and eat mushrooms.. In the Netherlands mushroom intoxication is rare. Therefore, there is a lack of knowledge among health care personnel and foragers. The present case report highlights the importance of awareness of the poisonous death cap to prevent intoxications and optimize treatment decisions.

Topics: Adult; Amanita; Amanitins; Female; Humans; Liver Failure, Acute; Mushroom Poisoning; Netherlands

Topics: Adult; Amanita; Amanitins; Breast Feeding; Female; Humans; Infant, Newborn; Middle Aged; Milk, Human; Mushroom Poisoning; Treatment Outcome

Eating mushrooms known to contain amatoxin is fraught with serious complications. The analysis of the relevant literature publications revealed no article with the description of the histological picture of the internal organs in the subjects intoxicated with amatoxin. It is known, however, that such poisoning is associated with the severe irreversible injuries to all intracellular protein structures the character of which depends on time. Specifically, acute amatoxin intoxication produces the well apparent clinical picture within 6 days after intake of the poison. It is characterized by acute renal and hepatic insufficiency in the combination with the injury to the conducting system of heart and the myocrardium itself. Thereafter, the disseminated intravascular coagulation (DIC) syndrome developed accompanied by the signs of progressive tissue hypoxia that ended in death on day 9. The histological study has demonstrated necrotic foci in the liver and oedematous hepatic stroma. Kidneys underwent multiple hemorrhages, necrosis of convoluted tubules and well apparent hydropic protein dystrophy of their epithelium. The adrenal glands showed up signs of necrosis and hemorrhage. It is concluded that poisoning with mushrooms (amatoxin) should be regarded as the most probable cause of the condition requiring differential diagnostics between acute gastroenteritis and renal insufficiency.. Употребление в пищу грибов, содержащих аматоксин, опасно серьезными осложнениями. Анализ источников литературы не выявил ни одного сообщения, в котором бы приводилась гистологическая картина внутренних органов у лиц, отравившихся аматоксином. Известно, что при таких отравлениях необратимые изменения обусловлены повреждением всех клеточных белковых структур и имеют различную временнýю составляющую. В случае острого отравления аматоксином развернутую клиническую картину в виде острой почечной и печеночной недостаточности, а также поражения проводящей системы сердца и самого миокарда наблюдали на 6-е сутки. Смерть наступила на 9-е сутки на фоне массивного ДВС-синдрома и признаков прогрессирующей тканевой гипоксии. При гистологическом исследовании наблюдали очаги некроза и отек стромы печени, множественные кровоизлияния, некроз извитых канальцев почек, резко выраженную белковую гидропическую дистрофию эпителия извитых канальцев, некроз и кровоизлияния в ткани надпочечников. Отравление грибами (аматоксином) необходимо рассматривать в качестве наиболее вероятной причины при дифференциальной диагностике острого гастроэнтерита и почечной недостаточности.

Topics: Amanita; Amanitins; Humans; Kidney; Liver; Mushroom Poisoning

Mushroom poisoning with Amanita phalloides or similar species can lead to liver failure with 10-30% mortality rates. We aimed at defining the prognostic value of urinary amatoxin quantification in patients with hepatotoxic mushroom poisoning.. Data from 32 patients with hepatotoxic mushroom poisoning (Hospital Clínic Barcelona, 2002-16) in whom urinary amatoxins were determined (ELISA) were retrospectively reviewed. Correlations between urinary amatoxin and collected baseline variables with outcomes including hepatotoxicity (ALT>1000 U/L), severe acute liver injury (ALI, prothrombin <50%), acute liver failure (ALF, ALI and encephalopathy), transplantation/death and hospital length-of-stay, were evaluated.. 12/32 patients developed increased aminotransferase activity. Among the 13/32 amatoxin negative patients, 1 developed ALI and 12/13 no hepatotoxicity. Among the 19/32 amatoxin positive patients, 8/19 (42%) developed hepatotoxicity, including 5 who progressed to severe ALI, of whom 3 developed ALF (2 deaths, 1 transplantation). Urinary amatoxin and prothrombin were independent predictors of hepatotoxicity, ALT peak values (along with age) and hospital length-of-stay. In positive amatoxins patients, urinary concentrations > 55 ng/ml (or a baseline prothrombin ≤ 83%), were associated to hepatotoxicity (presented by 8/9 patients with ALT>1000 U/L). Among 5 patients with urinary amatoxin ≥ 70 ng/ml, 4 developed severe ALI.. In patients with hepatotoxic mushroom poisoning, a negative urinary amatoxin quantification within 72h of intake ruled out the risk of hepatotoxicity in 92% of patients, whereas positive urinary amatoxins were associated with hepatotoxicity and severe ALI. Concentrations >55 ng/ml and ≥ 70 ng/ml were predictive of hepatotoxicity and severe ALI, respectively.

Topics: Adolescent; Adult; Aged; Amanitins; Child; Enzyme-Linked Immunosorbent Assay; Female; Humans; Liver Failure, Acute; Logistic Models; Male; Middle Aged; Mushroom Poisoning; Predictive Value of Tests; Retrospective Studies; Spain; Young Adult

The most frequently reported fatal Lepiota ingestions are due to L. brunneoincarnata. We present a case of L. brunneoincarnata poisoning with endoscopic nasobiliary drainage known to be the first in China. The patient suffered gastrointestinal symptoms 9 h post ingestion of mushrooms. The patient was hospitalized 4 days after eating the mushrooms with jaundice. The peak ALT, AST, APTT, TBIL and DBIL values of the patient were as follow: ALT, 2980 U/L (day 4 post ingestion); AST, 1910 U/L (day 4 post ingestion); APTT, 92.8 seconds (day 8 post ingestion), TBIL, 136 μmol/L (day 10 post ingestion), DBIL 74 μmol/L (day 10 post ingestion). UPLC-ESI-MS/MS was used to detect the peptide toxins in the mushroom and biological samples from the patient. We calculated that the patient may have ingested a total of 29.05 mg amatoxin from 300 g mushrooms, consisting of 19.91 mg α-amanitin, 9.1 mg β-amanitin, and 0.044 mg γ-amanitin. Amatoxins could be detected in bile even on day 6 after ingestion of L. brunneoincarnata. With rehydration, endoscopic nasobiliary drainage and intravenous infusion of Legalon SIL, the patient recovered after serious hepatotoxicity developed.

Topics: Agaricales; Amanitins; China; Drainage; Humans; Male; Middle Aged; Mushroom Poisoning; Silymarin

Topics: Amanitins; Critical Care; Humans; Liver; Mushroom Poisoning

Acute liver failure (ALF) induced by amatoxin-containing mushrooms accounts for more than 90% of deaths in patients suffering from mushroom poisoning. However, due to the fact that most hospitals cannot identify the species of mushrooms involved, or detect amatoxins, the early diagnosis of amatoxin intoxication remains a significant challenge in clinical practice.. Two patients were had ingested wild mushrooms 15 hours before admission. Six hours prior to admission they experienced nausea, vomiting, weakness, abdominal pain and diarrhea. The species of mushrooms they had consumed could not be identified.. According to their delayed gastroenteritis, the two patients were clinically diagnosed with amatoxin poisoning. One week after the patients were discharged, the species of the mushrooms was identified as Amanita fuliginea and the diagnosis was confirmed.. The two patients were treated with silibinin, penicillin G and plasma exchange.. Although the two patients progressed to ALF they fully recovered and were discharged on day 10 after admission.. Our case reports suggested that patients with unidentified wild mushroom intoxication with delayed gastroenteritis could be clinically diagnosed with amatoxin poisoning; in such cases, liver coagulation function should be frequently evaluated. Early diagnosis and treatment are crucial for survival in patients with ALF induced by amatoxin poisoning.

Topics: Adult; Amanita; Amanitins; Anti-Bacterial Agents; Antioxidants; Diagnosis, Differential; Early Diagnosis; Female; Humans; Liver Failure, Acute; Middle Aged; Mushroom Poisoning; Penicillin G; Plasma Exchange; Silybin; Silymarin

Cases of mushroom poisoning in Thailand have increased annually. During 2008 to 2014, the cases reported to the National Institute of Health included 57 deaths; at least 15 died after ingestion of amanitas, the most common lethal wild mushrooms inhabited. Hence, the aims of this study were to identify mushroom samples from nine clinically reported cases during the 7-year study period based on nuclear ITS sequence data and diagnose lethal peptide toxins using a reversed phase LC-MS method. Nucleotide similarity was identified using BLAST search of the NCBI database and the Barcode of Life Database (BOLD). Clade characterization was performed by maximum likelihood and Bayesian phylogenetic approaches. Based on BLAST and BOLD reference databases our results yielded high nucleotide similarities of poisonous mushroom samples to A. exitialis and A. fuliginea. Detailed phylogenetic analyses showed that all mushroom samples fall into their current classification. Detection of the peptide toxins revealed the presence of amatoxins and phallotoxins in A. exitialis and A. fuliginea. In addition, toxic α-amanitin was identified in a new provisional species, Amanita sp.1, with the highest toxin quantity. Molecular identification confirmed that the mushrooms ingested by the patients were members of the lethal amanitas in the sections Amanita and Phalloideae. In Thailand, the presence of A. exitialis was reported here for the first time and all three poisonous mushroom species provided new and informative data for clinical studies.

Topics: Amanita; Amanitins; Chromatography, Liquid; Databases, Genetic; Humans; Mass Spectrometry; Mushroom Poisoning; Retrospective Studies; Sequence Analysis, DNA; Thailand

Published estimates of survival associated with mushroom (amatoxin)-induced acute liver failure (ALF) and injury (ALI) with and without liver transplant (LT) are highly variable. We aimed to determine the 21-day survival associated with amatoxin-induced ALI (A-ALI) and ALF (A-ALF) and review use of targeted therapies.. Cohort study of all A-ALI/A-ALF patients enrolled in the US ALFSG registry between 01/1998 and 12/2014.. Of the 2224 subjects in the registry, 18 (0.8%) had A-ALF (n = 13) or A-ALI (n = 5). At admission, ALF patients had higher lactate levels (5.2 vs. 2.2 mm, P = 0.06) compared to ALI patients, but INR (2.8 vs. 2.2), bilirubin (87 vs. 26 μm) and MELD scores (28 vs. 24) were similar (P > 0.2 for all). Of the 13 patients with ALF, six survived without LT (46%), five survived with LT (39%) and two died without LT (15%). Of the five patients with ALI, four (80%) recovered and one (20%) survived post-LT. Comparing those who died/received LT (non-spontaneous survivors [NSS]) with spontaneous survivors (SS), N-acetylcysteine was used in nearly all patients (NSS 88% vs. SS 80%); whereas, silibinin (25% vs. 50%), penicillin (50% vs. 25%) and nasobiliary drainage (0 vs. 10%) were used less frequently (P > 0.15 for all therapies).. Patients with mushroom poisoning with ALI have favourable survival, while around half of those presenting with ALF may eventually require LT. Further study is needed to define optimal management (including the use of targeted therapies) to improve survival, particularly in the absence of LT.

Topics: Acetylcysteine; Adult; Amanitins; Chemical and Drug Induced Liver Injury; Cohort Studies; Female; Humans; Liver Failure, Acute; Liver Transplantation; Male; Middle Aged; Mushroom Poisoning; North America; Penicillins; Registries; Silybin; Silymarin

Mushroom poisoning is a cause of major mortality and morbidity all over the world. Although Hong Kong people consume a lot of mushrooms, there are only a few clinical studies and reviews of local mushroom poisoning. This study aimed to review the clinical characteristics, source, and outcome of mushroom poisoning incidences in Hong Kong.. This descriptive case series review was conducted by the Hong Kong Poison Information Centre and involved all cases of mushroom poisoning reported to the Centre from 1 July 2005 to 30 June 2015.. Overall, 67 cases of mushroom poisoning were reported. Of these, 60 (90%) cases presented with gastrointestinal symptoms of vomiting, diarrhoea, and abdominal pain. Gastrointestinal symptoms were early onset (<6 hours post-ingestion) and not severe in 53 patients and all recovered after symptomatic treatment and a short duration of hospital care. Gastrointestinal symptoms, however, were of late onset (≥6 hours post-ingestion) in seven patients; these were life-threatening cases of amatoxin poisoning. In all cases, the poisonous mushroom had been picked from the wild. Three cases were imported from other countries, and four collected and consumed the amatoxin-containing mushrooms in Hong Kong. Of the seven cases of amatoxin poisoning, six were critically ill, of whom one died and two required liver transplantation. There was one confirmed case of hallucinogenic mushroom poisoning caused by Tylopilus nigerrimus after consumption of a commercial mushroom product. A number of poisoning incidences involved the consumption of wild-harvested dried porcini purchased in the market.. Most cases of mushroom poisoning in Hong Kong presented with gastrointestinal symptoms and followed a benign course. Life-threatening cases of amatoxin poisoning are occasionally seen. Doctors should consider this diagnosis in patients who present with gastrointestinal symptoms that begin 6 hours or more after mushroom consumption.

Topics: Abdominal Pain; Adolescent; Adult; Aged; Aged, 80 and over; Amanitins; Child; Child, Preschool; Diarrhea; Female; Gastrointestinal Diseases; Hong Kong; Humans; Male; Middle Aged; Mushroom Poisoning; Retrospective Studies; Vomiting; Young Adult

BACKGROUND Fractionated plasma separation and absorption (FPSA) is an extracorporeal liver support method that detoxifies accumulated toxins. There are limited data of its use in the treatment of Amanita phalloides intoxication. The objective of this study was to investigate whether FPSA before liver transplantation improves patients' short-term post liver transplantation survival in Amanita phalloides poisoning. MATERIAL AND METHODS The study population consisted of ten patients who had liver transplantation (LT) due to acute liver failure (ALF) caused by Amanita phalloides poisoning. Six patients were treated with FPSA before liver transplantation. All the patients who were started on FPSA were also placed on the liver transplantation list according to emergent liver transplantation criteria. RESULTS Patients treated with FPSA were in a more severe clinical condition presenting in higher mean MELD, total bilirubin, INR and ammonia along with more frequent hypoglycemia and hepatic encephalopathy grade 3/4. FPSA group had longer mean waiting time on the recipient list (3.5 vs. 1.25 days) but inferior thirty-day survival rate (16.5% vs. 100%). CONCLUSIONS When conservative medical modalities are ineffective, the only treatment for Amanita phalloides poisoning is a liver transplant. Although FPSA treated patients had inferior post-LT survival, FPSA was found to prolong the pre surgical waiting time for critically ill patients, consequently giving a chance of life-saving procedure.

Topics: Adult; Aged; Amanita; Amanitins; Female; Humans; Kaplan-Meier Estimate; Liver Failure, Acute; Liver Transplantation; Male; Middle Aged; Mushroom Poisoning; Retrospective Studies; Sorption Detoxification; Time Factors; Waiting Lists; Young Adult

Lethal amanitas (Amanita sect. Phalloideae) are responsible for 90% of all fatal mushroom poisonings. Since 2000, more than ten new lethal Amanita species have been discovered and some of them had caused severe mushroom poisonings in China. However, the contents and distribution of cyclopeptides in these lethal mushrooms remain poorly known. In this study, the diversity of major cyclopeptide toxins in seven Amanita species from Eastern Asia and three species from Europe and North America were systematically analyzed, and a new approach to inferring phylogenetic relationships using cyclopeptide profile was evaluated for the first time. The results showed that there were diversities of the cyclopeptides among lethal Amanita species, and cyclopeptides from Amanita rimosa and Amanita fuligineoides were reported for the first time. The amounts of amatoxins in East Asian Amanita species were significantly higher than those in European and North American species. The analysis of distribution of amatoxins and phallotoxins in various Amanita species demonstrated that the content of phallotoxins was higher than that of amatoxins in Amanita phalloides and Amanita virosa. In contrast, the content of phallotoxins was significantly lower than that of amatoxins in all East Asian lethal Amanita species tested. However, the distribution of amatoxins and phallotoxins in different tissues showed the same tendency. Eight cyclopeptides and three unknown compounds were identified using cyclopeptide standards and high-resolution MS. Based on the cyclopeptide profiles, phylogenetic relationships of lethal amanitas were inferred through a dendrogram generated by UPGMA method. The results showed high similarity to the phylogeny established previously based on the multi-locus DNA sequences.

Topics: Amanita; Amanitins; Chromatography, High Pressure Liquid; Mass Spectrometry; Mushroom Poisoning; Peptides, Cyclic; Phylogeny; Reference Standards

Most of the fatal cases of mushroom poisoning are caused by Amanita phalloides. The amount of toxin in mushroom varies according to climate and environmental conditions. The aim of this study is to measure α-, β-, and γ-amanitin with phalloidin and phallacidin toxin concentrations. Six pieces of A. phalloides mushrooms were gathered from a wooded area of Düzce, Turkey, on November 23, 2011. The mushrooms were broken into pieces as spores, mycelium, pileus, gills, stipe, and volva. α-, β-, and γ-Amanitin with phalloidin and phallacidin were analyzed using reversed-phase high-performance liquid chromatography. As a mobile phase, 50 mM ammonium acetate + acetonitrile (90 + 10, v/v) was used with a flow rate of 1 mL/min. C18 reverse phase column (150 × 4.6 mm; 5 µm particle) was used. The least amount of γ-amanitin toxins was found at the mycelium. The other toxins found to be in the least amount turned out to be the ones at the spores. The maximum amounts of amatoxins and phallotoxin were found at gills and pileus, respectively. In this study, the amount of toxin in the spores of A. phalloides was published for the first time, and this study is pioneering to deal with the amount of toxin in mushrooms grown in Turkey.

Topics: Alpha-Amanitin; Amanita; Amanitins; Chromatography, High Pressure Liquid; Chromatography, Reverse-Phase; Forests; Fruiting Bodies, Fungal; Humans; Mushroom Poisoning; Mycelium; Peptides, Cyclic; Phalloidine; Species Specificity; Spectrophotometry, Ultraviolet; Spores, Fungal; Turkey

Serious to fatal toxicity may occur with amanitin-containing mushrooms ingestions. A Lepiota brunneoincarnata familial poisoning with hepatic toxicity is reported. In such poisonings, acute gastroenteritis may be firstly misdiagnosed leading to delay in preventing liver dysfunction by silibinin or penicillin G. Mushroom picking finally requires experience and caution.

Topics: Administration, Oral; Adult; Agaricales; Amanitins; Antidotes; Charcoal; Child; Diagnosis, Differential; Emergency Service, Hospital; Female; Fluid Therapy; Follow-Up Studies; Humans; Male; Mushroom Poisoning

Mushroom poisonings occur when ingestion of wild mushrooms containing toxins takes place, placing the consumers at life-threatening risk. In the present case report, an unusual multiple poisoning with isoxazoles- and amatoxins-containing mushrooms in a context of altered mental state and poorly controlled hypertension is presented. A 68-year-old female was presented to São João hospital (Portugal) with complaints of extreme dizziness, hallucinations, vertigo and imbalance, 3 h after consuming a stew of wild mushrooms. The first observations revealed altered mental state and elevated blood pressure. The examination of cooked mushroom fragments allowed a preliminary identification of Amanita pantherina. Gas chromatography-mass spectrometry (GC-MS) showed the presence of muscimol in urine. Moreover, through high-performance liquid chromatography-ultraviolet detection (HPLC-UV) analysis of the gastric juice, the presence of α-amanitin was found, showing that amatoxins-containing mushrooms were also included in the stew. After 4 days of supportive treatment, activated charcoal, silybin and N-acetylcysteine, the patient recovered being discharged 10 days post-ingestion with no organ complications. The prompt and appropriate therapy protocol for life-threatening amatoxins toxicity probably saved the patient's life as oral absorption was decreased and also supportive care was immediately started.

Topics: Acetylcysteine; Agaricales; Aged; Alpha-Amanitin; Amanita; Amanitins; Charcoal; Female; Gas Chromatography-Mass Spectrometry; Humans; Isoxazoles; Mushroom Poisoning; Silybin; Silymarin

There are few data estimating the human lethal dose of amatoxins or of the toxin level present in ingested raw poisonous mushrooms. Here, we present a patient who intentionally ingested several wild collected mushrooms to assess whether they were poisonous. Nearly 1 day after ingestion, during which the patient had nausea and vomiting, he presented at the emergency department. His transaminase levels started to increase starting from hour 48 and peaking at hour 72 (alanine aminotransferase 2496 IU/L; aspartate aminotransferase 1777 IU/L). A toxin analysis was carried out on the mushrooms that the patient said he had ingested. With reversed-phase high-performance liquid chromatography analysis, an uptake of approximately 21.3 mg amatoxin from nearly 50 g mushroom was calculated; it consisted of 11.9 mg alpha amanitin, 8.4 mg beta amanitin, and 1 mg gamma amanitin. In the urine sample taken on day 4, 2.7 ng/mL alpha amanitin and 1.25 ng/mL beta amanitin were found, and there was no gamma amanitin. Our findings suggest that the patient ingested approximately 0.32 mg/kg amatoxin, and fortunately recovered after serious hepatotoxicity developed.

Topics: Amanita; Amanitins; Chromatography, High Pressure Liquid; Humans; Male; Middle Aged; Mushroom Poisoning

Topics: Amanita; Amanitins; Fatal Outcome; Female; Humans; Middle Aged; Mushroom Poisoning

Picking wild mushrooms is a popular pastime in Switzerland. Correct identification of the species is difficult for laypersons. Ingestion of toxic mushrooms may result in serious toxicity, including death. The aim of the study is to analyze and describe the circumstances of exposure to mushrooms, and to define the clinical relevance of mushroom poisoning for humans in Central Europe.. We performed a retrospective case study and analyzed all inquiries concerning human exposures to mushrooms (n = 5638, 1.2% of all inquiries) which were reported to the Swiss Toxicological Information Centre between January 1995 and December 2009.. The most frequent reason for contacting the poison center in cases of adult exposure was toxicity resulting from edible species. Pediatric exposure predominantly occurred from mushrooms found around the home. Severe symptoms have not only been observed after ingestion of non-amatoxin-containing toxic mushrooms, i.e. Boletus sp. and Cortinarius sp., but also after meals of edible species. The mortality of confirmed amatoxin poisonings was high (5/32) compared to other reports.. Inquiries regarding mushroom poisoning were a relatively infrequent reason for contacting the poison center. Nevertheless, accidental ingestion of toxic mushrooms can be responsible for severe or fatal poisonings. Although pediatric exposure to mushrooms found around the home has not led to serious toxicity in this study, prevention of exposure is warranted. Inspection of wild mushrooms by a certified mushroom expert or a mycologist seems to be a safe procedure which should be recommended.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Amanitins; Child; Child, Preschool; Eating; Female; Humans; Infant; Male; Middle Aged; Mushroom Poisoning; Poison Control Centers; Seasons; Switzerland; Young Adult

OBJECTIVE. We aimed to determine clinical and laboratory findings that were different between those patients who died and those who survived and to look for factors associated with the mortality in amatoxin-containing mushroom poisoning. METHODS. The mushroom poisoning patients who were admitted to our clinic between 1996 and 2009 were retrospectively evaluated. The diagnosis was based on a history of mushroom ingestion, clinical picture and the presence of serum alpha-amanitin. Patients were divided into two groups as the survival group and the fatality group. Clinical and laboratory findings were compared between the two groups. Relation between variables and clinical outcome was analyzed. RESULTS. A total of 144 amatoxin poisoning patients were included in this study. Patients who died were more likely to have demonstrated low mean arterial pressure, encephalopathy, mucosal hemorrhage, oliguria-anuria, hypoglycemia, and thrombocytopenia during the hospitalization. Low sodium values and high urea, AST, ALT, total bilirubin, LDH, prothrombin time, international normalized ratio, and activated partial thromboplastin time values were associated with increased likelihood of mortality. Nineteen patients developed acute renal failure. Fourteen patients developed acute hepatic failure. All the 14 patients who died developed acute hepatic failure. The mortality rate was 9.7%. CONCLUSIONS. The factors associated with mortality determined in this retrospective study may be helpful for clinical outcome assessment and monitoring of patients with amatoxin-containing mushroom poisoning.

Topics: Adult; Amanitins; Female; Hemoperfusion; Humans; Liver Failure, Acute; Male; Middle Aged; Mushroom Poisoning; Retrospective Studies

Ninety percent of fatal higher fungus poisoning is due to amatoxin-containing mushroom species. In addition to absence of antidote, no chemotherapeutic consensus was reported. The aim of the present study is to perform a retrospective multidimensional multivariate statistic analysis of 2110 amatoxin poisoning clinical cases, in order to optimize therapeutic decision-making. Our results allowed to classify drugs as a function of their influence on one major parameter: patient survival. Active principles were classified as first intention, second intention, adjuvant or controversial pharmaco-therapeutic clinical intervention. We conclude that (1) retrospective multidimensional multivariate statistic analysis of complex clinical dataset might help future therapeutic decision-making and (2) drugs such as silybin, N-acetylcystein and putatively ceftazidime are clearly associated, in amatoxin poisoning context, with higher level of patient survival.

Topics: Acetylcysteine; Algorithms; Amanitins; Anti-Bacterial Agents; Antioxidants; Ceftazidime; Databases, Factual; Decision Making; Decision Theory; Factor Analysis, Statistical; Humans; Multivariate Analysis; Mushroom Poisoning; Retrospective Studies; Silybin; Silymarin; Survival; Survival Rate

There is a paucity of knowledge about prenatal and perinatal risks through maternal amatoxin poisoning. No symptoms of amatoxin intoxication, except for a slight temporary increase in liver enzymes activity, occurred in a term newborn after delivery despite an Amanita phalloides intoxication of the mother 2 days before. Considering previous reports, severe fetal intoxication may not occur during the entire pregnancy.

Topics: Adult; Amanitins; Female; Humans; Infant, Newborn; Liver Function Tests; Male; Mushroom Poisoning; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Risk Factors

Topics: Alpha-Amanitin; Amanitins; Animals; Antidotes; Chemical and Drug Induced Liver Injury; Cimetidine; Humans; Mice; Mushroom Poisoning

Current treatment of amatoxin poisoning includes the administration of silibinin and penicillin in combination or silibinin alone. The aim of this study was to compare both therapeutic regimes.. Of 604 patients with the suspected diagnosis of amatoxin poisoning 367 were retrospectively analysed: 118 patients had received silibinin alone and 249 patients silibinin in combination with penicillin. Logistic regression analyses were applied to investigate the efficacy of both therapeutic regimens by comparing death and liver transplantation rates. A potentially independent effect on outcome of age, sex, year of treatment, latency period of symptoms and start of silibinin therapy was taken into account.. In the group who had received the combination of silibinin and penicillin 8.8% died or underwent liver transplantation compared to 5.1% in the group of those who had received silibinin alone. The risk of death or organ transplantation was thus reduced by nearly 40% in the latter group (adjusted odds ratio: 0.58; 95% CI: 0.21-1.57; p=0.28). A longer latency period (< or =12h vs. >12h) was associated with a significant reduction of this risk (adjusted OR.: 6.10; 95% CI:1.77-21.3; p=0.004). A later start of silibinin therapy (>24h vs. < or = 24h) was associated with a tendency toward an increased frequency of death or organ transplantation (adjusted OR.: 3.0; 95% CI: 0.96-9.20; p=0.059).. A lower death and transplantation rate was observed in the silibinin treatment group than in group treated with silibinin combined with penicillin. However, this difference was not statistically significant. The high risk ratio relating to the time-dependent effect of silibinin suggests its efficaciousness in the treatment of amatoxin poisoning. The latency period was assessed as an independent prognostic factor.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Amanita; Amanitins; Antidotes; Antioxidants; Child; Child, Preschool; Drug Therapy, Combination; Female; Humans; Liver Transplantation; Logistic Models; Male; Middle Aged; Mushroom Poisoning; Penicillins; Prognosis; Retrospective Studies; Severity of Illness Index; Silybin; Silymarin; Time Factors

Two patients, a 54-year-old man and a 51-year-old woman, presented with abdominal pain, vomiting and diarrhoea; these symptoms developed 9 and 15 hours, respectively, after consumption of soup from mushrooms that they had picked themselves. As a result of these events, a third patient, a 55-year-old woman with diarrhoea who had also eaten the soup, also presented herself. The first patient recognised deathcap or death angel mushrooms (Amanita phalloides) on a photograph. All three patients were treated for amatoxin poisoning with a combination of high-dose penicillin G, silibinin and acetylcysteine intravenously. The poisoning was later confirmed by the results of urinalysis. The patients were discharged in good condition 8 days later.

Topics: Acetylcysteine; Amanita; Amanitins; Antioxidants; Drug Therapy, Combination; Female; Humans; Male; Middle Aged; Mushroom Poisoning; Penicillin G; Silybin; Silymarin; Treatment Outcome; Urinalysis

The foraging of wild mushrooms can be complicated by toxicity from several mushroom types. Amatoxin, a peptide contained in several mushroom species, accounts for the majority of severe mushroom poisonings by binding to RNA polymerase II irreversibly, leading to severe hepatonecrosis. There is no effective antidote for severe amatoxin poisoning. We compare the effectiveness of 5 potential antidotal therapies in limiting the degree of hepatonecrosis in a randomized, controlled, murine model of amatoxin-induced hepatotoxicity.. One hundred eighty male Institute of Cancer Research mice were randomized into 6 equal groups. Within each group, 21 mice were intraperitoneally injected with 0.6 mg/kg of alpha-amanitin (amatoxin); the remaining 9 were injected with 0.9% normal saline solution. Four hours postinjection, each group of 30 mice was randomized to 1 of 5 intraperitoneal treatments (N-acetylcysteine, benzylpenicillin, cimetidine, thioctic acid, or silybin) or normal saline solution. Repeated dosing was administered intraperitoneally every 4 to 6 hours for 48 hours. After 48 hours of treatment, each subject was killed, cardiac blood was aspirated for hepatic aminotransferase measurements (alanine transaminase and aspartate transaminase), and liver specimens were harvested to evaluate the extent of hepatonecrosis. The degree of hepatonecrosis was determined by a pathologist blinded to the treatment group and divided into 5 categories according to percentage of hepatonecrosis.. Amanitin significantly increased aspartate transaminase in treated mice compared with normal saline solution-treated controls (mean [SD] 2,441 [2,818] IU/L versus 310 [252]; P=.03). None of the antidotal therapies were found to significantly decrease the increase in aminotransferases compared with controls. Further, none of the antidotal therapies demonstrated an important decrease in hepatonecrosis compared with controls when a histologic grading scale was used.. In this murine model, N-acetylcysteine, benzylpenicillin, cimetidine, thioctic acid, and silybin were not effective in limiting hepatic injury after alpha-amanitin poisoning. Increases of aminotransferases and degrees of histologic hepatonecrosis were not attenuated by these antidotal therapies.

Topics: Acetylcysteine; Alanine Transaminase; Amanitins; Animals; Antidotes; Aspartate Aminotransferases; Chemical and Drug Induced Liver Injury; Cimetidine; Disease Models, Animal; Male; Mice; Mushroom Poisoning; Penicillin G; Random Allocation; Silybin; Silymarin; Thioctic Acid

Topics: Amanitins; Creatinine; Emergency Medical Services; Humans; Liver Transplantation; Mushroom Poisoning; Predictive Value of Tests; Prothrombin

Topics: Amanitins; Humans; Liver Failure, Acute; Mushroom Poisoning

Indication of liver transplantation in acute liver failure following amatoxin intoxication is still uncertain.. One hundred and ninety-eight patients were studied retrospectively. The laboratory parameters alanine-aminotransferase, serum bilirubin, serum creatinine and prothrombin index were analyzed over time. Predictors of fatal outcome and survival were determined by receiver-operating-characteristic and sensitivity-specificity analysis.. Twenty-three patients died in the median 6.1 days (range, 2.7-13.9 days) after ingestion. Using a single parameter as predictor of fatal outcome the area under the receiver-operating-characteristic curve of prothrombin index (0.96) and serum creatinine (0.93) were both significantly greater (P<0.05) compared with serum bilirubin (0.82) and alanine-aminotransferase (0.69). Prediction of fatal outcome had an optimum, if a prothrombin index less than 25% was combined with a serum creatinine greater than 106 micromol/l from day 3 after ingestion onwards (sensitivity 100%, 95% confidence interval 87-100; specificity 98%, 95% confidence interval 94-100). The median time period between the first occurrence of this predictor in non-survivors and death was 63h (range, 3-230h).. A decision model of liver transplantation following amatoxin intoxication using prothrombin index in combination with serum creatinine from day 3 to 10 after ingestion enables an early and reliable assessment of outcome.

Topics: Adolescent; Adult; Alanine Transaminase; Amanitins; Bilirubin; Child; Humans; Liver Failure; Liver Transplantation; Mushroom Poisoning; Predictive Value of Tests; Prothrombin Time; Retrospective Studies; Survival Analysis

This paper presents species of fungi of high toxicity. Their consumption might have serious consequences for health and in many cases it might lead to death. Toxic compounds present in fungi have also been characterised, mechanisms of their toxic activity have been presented and clinical symptoms of poisoning have been described. Hallucinogenic mushrooms have also been mentioned as they have recently become a serious problem: many people use them to intoxicate themselves. There are also species of mushrooms that can be consumed under certain conditions since they can occasionally trigger off serious disturbances for the functioning of organisms.

Topics: Amanita; Amanitins; Cross-Sectional Studies; Humans; Incidence; Mushroom Poisoning; Peptides, Cyclic; Poland; Structure-Activity Relationship

Experiences of liver transplantation after Amanita phalloides poisoning were analysed in anaesthetic and intensive therapist point of view based on 3 cases. Cardiac problems were found at all patients during the postoperative period. Probably the amatoxin has cardiotoxic effect or a part of phallotoxins are absorbed despite cooking and caused reversible cardiac function impairment. Pancreatitis, DIC, gastrointestinal bleeding, acute renal failure were found at all patients, therefore liver transplantation is only a part of the treatment, complex therapy is necessary in this cases.

Topics: Acute Kidney Injury; Adult; Amanita; Amanitins; Anesthesia, General; Child; Combined Modality Therapy; Critical Care; Disseminated Intravascular Coagulation; Electrocardiography; Gastrointestinal Hemorrhage; Heart Conduction System; Humans; Liver Failure; Liver Transplantation; Male; Mushroom Poisoning; Pancreatitis

We report here three cases of Amanita virosa induced toxic hepatitis. Two of the three cases recovered but the other died 10 days after mushroom ingestion. Since the mortality of Amanita mushroom induced toxic hepatitis is very high, prompt diagnosis and aggressive therapeutic measures should be initiated as soon as possible. Our cases showed that the initial serum aminotransferase levels might not predict the clinical outcome of the patient, but that the prothrombin time (PT) seemed to be a more useful prognostic marker. Close monitoring of aminotransferase levels and PT as well as appropriate therapy are recommended. All three cases showed signs of proteinuria and we were able to characterize mixed tubular and glomerular type proteinuria at 3 or 4 days after ingestion in two cases. Among the previously reported Korean cases of suspected Amanita induced toxic hepatitis, most species could not be identified except for four cases of Amanita virosa. No cases of Amanita phalloides induced toxic hepatitis have been identified in Korea so far.

Topics: Adult; Amanita; Amanitins; Chemical and Drug Induced Liver Injury; Female; Humans; Male; Middle Aged; Mushroom Poisoning; Proteinuria

Topics: Adolescent; Adult; Aged; Amanita; Amanitins; California; Cause of Death; Charcoal; Child; Colic; Diarrhea; Female; Fluid Therapy; Histamine H2 Antagonists; Humans; Male; Middle Aged; Mushroom Poisoning; Nausea; Vomiting

Four cases of severe Lepiota poisoning, including three which developed toxic fulminant hepatitis treated by orthotopic hepatic transplantation, are reported here. The toxicity of the Lepiota is discussed as well as the indications for hepatic transplantation in poisonings due to amatoxin-containing mushrooms.

Topics: Adult; Amanitins; Child; Electroencephalography; Female; Humans; Liver Failure; Liver Transplantation; Male; Mushroom Poisoning

We report four cases of poisoning with amatoxin-producing mushrooms in suburban Long Island. All occurred when amateur mushroom hunters picked mushrooms from neighboring lawns. Two patients presented 30 hours post ingestion with evidence of acute hepatic dysfunction. One survived, after treatment with charcoal and penicillin; the other, a 90-year-old woman with prior cardiac disease soon developed shock and subsequently died. The other two patients were admitted 18 hours after ingestion of Lepiota chlorophyllum and received prompt charcoal hemoperfusion. Both did well, although one had a mild elevation of transaminases. Although most reports of amatoxin poisoning originate in Europe, these cases confirm that amatoxin-producing mushrooms, including Lepiota chlorophyllum, may be found in northeastern American suburbs. Such patients who present prior to 24 hours after ingestion should receive charcoal hemoperfusion if a lethal dose (> 50 g of mushroom) has been eaten.

Topics: Adult; Aged; Aged, 80 and over; Amanita; Amanitins; Basidiomycota; Fatal Outcome; Female; Heart Block; Humans; Hypertension; Male; Middle Aged; Mushroom Poisoning; New York; Thyroiditis, Autoimmune

Mushroom poisonings caused by amatoxins are mostly lethal. Information about mycetisms caused by white species of Amanita is scarce. The present paper describes a case of mushroom poisoning caused by A. virosa. A prolongated latency period (6-10 hours), followed by cholera-like, improvement and visceral complication phases confirmed the amatoxin poisoning. The consumption of about 3 pounds of the toadstool by seven persons caused the death of five. Two patients survive the ingestion.

Topics: Adolescent; Adult; Aged; Amanita; Amanitins; Fatal Outcome; Female; Humans; Male; Mexico; Mushroom Poisoning

Twelve patients with Galerina Autumnalis (GA) poisoning were treated. Amatoxin and phallotoxin are the principal toxins of GA. After absorption from intestine into the liver, the toxins combine with RNA polymerase, resulting in block of messenger (mRNA) synthesis, hepatocellular damage, hepatitis, hepatic necrosis, serious coagulation abnormalities and DIC. The clinical characteristics are long latent period, short period of "pseudo-remission" and serious liver dysfunction. These were pathologically confirmed by autopsy. Our experiences with this poisoning are as follows: treatment should be carried out as early as possible, especially with gastric lavage and catharsis and special attention paid to the "pseudo-remission".

Topics: Adolescent; Adult; Agaricales; Amanitins; Child; Female; Gastric Lavage; Humans; Liver; Male; Mushroom Poisoning; Necrosis

The kinetics of alpha and beta amanitin were studied in 45 patients intoxicated with Amanita Phalloides. The amatoxins were analyzed by high performance liquid chromatography in plasma (43 cases), urine (35 cases), gastroduodenal fluid (12 cases), feces (12 cases) and tissues (4 cases). All patients had gastrointestinal symptoms and 43 developed an acute hepatitis. Two patients underwent successful liver transplantation. Eight patients, of whom three were children, died. The detection of amatoxins in the biological fluids was time dependent. The first sample was obtained at an average of 37.9 h post ingestion in the patients with positive results and at 70.6 h in the samples without detectable amatoxins. Plasma amatoxins were detected in 11 cases at 8 to 190 ng/mL for alpha and between 23.5 to 162 ng/mL for beta. In 23 cases amatoxins were detected in urine with a mean excretion per hour of 32.18 micrograms for alpha and 80.15 micrograms for beta. In 10 patients the total amounts eliminated in the feces (time variable) ranged between 8.4 and 152 micrograms for alpha amanitin and between 4.2 and 6270 micrograms for beta amanitin. In three of four cases amatoxins were still present in the liver and the kidney after day 5. Amatoxins were usually detectable in plasma before 36 h but were present in the urine until day 4. The rapid clearance indicates that enhanced elimination of amatoxins requires early treatment. Clearance of circulating amatoxins by day 4 spares the transplanted liver.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Amanita; Amanitins; Child; Child, Preschool; Chromatography, High Pressure Liquid; Female; Humans; Liver Function Tests; Liver Transplantation; Male; Metabolic Clearance Rate; Middle Aged; Mushroom Poisoning; Prognosis; Time Factors; Tissue Distribution

Ingestion of mushrooms followed after 6-12 hours by gastrointestinal symptoms and after 3-4 days by hepatic symptoms is diagnostic for the life-threatening amatoxin intoxication and should be treated as soon as possible. Four case histories are reported and recommendations for treatment are given.

Topics: Acute Kidney Injury; Adult; Amanita; Amanitins; Combined Modality Therapy; Female; Humans; Liver Function Tests; Male; Middle Aged; Mushroom Poisoning

Twenty-seven consecutive mushroom poisoning cases were followed up over a period of 14 days. Fourteen out of 27 died of liver failure. There were no deaths from renal failure. The mushrooms were identified as the amatoxin-containing Lepiota species. Therapeutic measures included nasogastric lavage, charcoal, vitamin C, vitamin B, penicillin G, corticosteroids, oral streptomycin and, in the case of a few patients, limited amounts of thioctic acid. Of the ten haemodialysed, nine died. Unfortunately charcoal haemoperfusion was not available. It appeared that therapeutic measures were ineffective and it also seemed that the amount of mushroom ingested was the determining factor for the prognosis. An important point to make is that renal failure does not occur and liver failure is always delayed (group II). For this reason all suspected cases of mushroom poisoning, regardless of absence of clinical signs and symptoms, must be hospitalised for a period of at least one week. The poisonous properties of wild mushrooms have been recognized since ancient times. However, despite awareness of their inherent dangers, serious poisoning continues to occur. Fatal intoxications can be attributed almost entirely to the amtoxin-containing species. Amanita phalloides have been blamed for over 90% of poisoning deaths in North America. There are reports of intoxications of other amatoxin-containing species in Europe, but fatalities due to Lepiota species are reported only rarely. It was previously acknowledged that the interval between ingestion of mushrooms and the onset of symptoms is longer than expected in serious poisonings.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Amanitins; Chemical and Drug Induced Liver Injury; Child; Coma; Female; Humans; Male; Middle Aged; Mushroom Poisoning; Prognosis; Renal Dialysis; Thioctic Acid; Time Factors

In 1986-88, 46 poisonings (4 of which were fatal) caused by amatoxin mushroom were reported. The fatalities were males aged between 7 and 65 years. They all had gastrointestinal symptoms and three of the patients died of acute hepatic insufficiency. The fourth died as a result of an intestinal perforation. The clinical and pathological alterations are compared with the findings of other authors.

Topics: Adolescent; Adult; Aged; Amanitins; Child; Humans; Male; Mushroom Poisoning; Spain

A monoclonal antibody, with high affinity against the mushroom toxin alpha-amanitin, was prepared. Administration of the Fab fragment of the monoclonal antibody to mice caused a 50-fold increase in alpha-amanitin toxicity. Electron micrographs showed normal appearance of hepatocytes but typical, amanitin-induced lesions in cells of the proximal convoluted tubules of the kidney. The pronounced nephrotoxicity is mainly explained by glomerular filtration and tubular reabsorption of the Fab-amatoxin complex and, to a lesser extent, of the immunoglobulin-amatoxin complex, which is still c. Twice as toxic as free alpha-amanitin. To our knowledge this is the first reported case where immunoglobulins or their fragments enhance rather than decrease the activity of a toxin. Accordingly, immunotherapy of Amanita mushroom poisoning in humans does not appear promising.

Topics: Amanitins; Animals; Antibodies, Monoclonal; Female; Immunoglobulin Fab Fragments; Kidney Tubules; Mice; Mice, Inbred Strains; Microscopy, Electron; Mushroom Poisoning

Topics: Amanita; Amanitins; Humans; Mushroom Poisoning

Four incidents of mushroom poisoning, representing four of the seven established groups of toxic mushrooms, are presented. These case reports illustrate the range of gastrointestinal and neurological symptoms caused by mushroom poisoning and reflect a nationwide increase in reports of serious poisonings in recent years. Severity of poisonings often parallels the time span between consumption and onset of symptoms, with serious poisonings having longer incubation periods. New therapies for amatoxin poisoning may reduce mortality caused by these poisonings.

Topics: Acute Kidney Injury; Adult; Aged; Amanitins; Child; Diarrhea; Female; Hallucinations; Humans; Male; Middle Aged; Mushroom Poisoning; New York; Respiratory Distress Syndrome; Thioctic Acid; Time Factors

Topics: Amanitins; Humans; Mushroom Poisoning; Pyridoxine

Topics: Adult; Amanita; Amanitins; Female; Humans; Infant, Newborn; Maternal-Fetal Exchange; Mushroom Poisoning; Pregnancy; Pregnancy Complications

Topics: Amanitins; Antidotes; Cyclopropanes; Gastric Lavage; Glutamine; Humans; Monomethylhydrazine; Muscarine; Muscimol; Mushroom Poisoning; Psilocybin

Topics: Amanita; Amanitins; Humans; Mushroom Poisoning