Amatoxins are water soluble, heat stable polypeptides found in Amanita (most often Amanita phalloides ), Galerina and some Lepiota species. The main toxin from the species A. phalloides is alpha-amanitin, a cyclic octapeptide. It is a potent inhibitor of RNA polymerases that blocks the production of mRNA and protein synthesis in liver and kidney cells.[1] In one case, an infant developed elevated liver enzymes after nursing once 11.5 hours after maternal ingestion of Amanita phalloides. However, two recent, well-documented cases found no adverse effects in breastfed infants and no amatoxin in the milk. Nevertheless, mothers suspected of having Amanita mushroom poisoning probably should not breastfeed until they have recovered or toxicologic screening of the breastmilk has ruled out.

The genus Amanita contains approximately 600 species of mushrooms, including some that produce amatoxins, which can lead to liver failure and death when ingested. Poisonous mushrooms often resemble and are difficult to distinguish visually from nonpoisonous, edible mushrooms. After above-average late November 2025 rainfall in California, regional mycologists observed numerous Amanita mushroom blooms in regional parks and area wildlands. On November 18, 2025, specialists at the San Francisco division of the California Poison Control System (CPCS) suspected amatoxin-containing mushroom poisoning in two patients who gastrointestinal symptoms and hepatotoxicity after eating foraged wild mushrooms. Over the next 17 weeks (November 18, 2025-March 17, 2026), 39 cases of suspected amatoxin mushroom poisoning in patients who had eaten foraged wild mushrooms were reported to CPCS. These 39 cases were characterized by a pattern of delayed onset of gastrointestinal symptoms and hepatotoxicity; 32 (82%) patients recovered, three (8%) required liver transplants, and four (10%) died. CPCS and the California Department of Public Health Toxicological Outbreak Program coordinated a response that included a statewide health advisory and educational materials translated into multiple languages for the public; collectively, the affected patients spoke at least six languages other than English. This is the largest reported outbreak of mushroom-associated hepatotoxic poisoning in California history and the largest in the United States in several decades. This was also the first outbreak of this size in which some persons ate Amanita ocreata, another poisonous Amanita species. The morbidity and potential lethality associated with amatoxin-containing mushroom ingestion is a serious public health concern. Educational materials, including for non-English-speaking communities, during the late fall to mid-spring when fruiting of amatoxin-containing mushrooms occurs, might reduce the number of poisonings.

Wild mushroom consumption is widespread worldwide and remains an important cause of foodborne intoxication. This concise review analyzes recent literature on the geographic distribution of poisonous wild mushrooms and the epidemiological patterns of intoxication reported in Asia, Europe, and the Americas. Most poisoning incidents occur as a result of the misidentification of toxic species as edible during mushroom foraging. Alongside well-known poisonous mushrooms, several newly identified toxic species have been reported in recent years. The available epidemiological evidence demonstrates clear regional clustering of poisoning incidents, pronounced seasonal peaks associated with mushroom growth, and a predominance of cases in populations where wild mushroom foraging is a traditional practice. Amatoxin-containing species of the genus Amanita remain the leading cause of severe and fatal intoxications worldwide. Overall, the analyzed studies indicate that wild mushroom poisoning continues to represent a significant food safety and public health concern, particularly in Asia and parts of Europe. Improved toxicological surveillance, public awareness, and timely clinical management are essential for reducing morbidity and mortality associated with these intoxications.

Mushroom poisoning remains the leading cause of foodborne morbidity and mortality in China. The mushrooms that cause acute kidney injury (AKI) belong to the species of Amanita genus section Roanokenses. These species exhibit highly similar morphological characteristics, which is a challenge for their identification for non-specialists. Although conventional DNA barcoding identification is reliable, it is time-consuming for rapid diagnosis. In this study, we developed a loop-mediated isothermal amplification (LAMP) method based on the internal transcribed spacer (ITS) region to enable rapid identification of five species within A. sect. Roanokenses which can cause AKI. The optimized LAMP system was rigorously evaluated for specificity and sensitivity, with comparative analysis performed against conventional PCR. The results demonstrated that the established LAMP method achieved visual detection without specialized equipment, exhibiting high specificity and a detection limit of 10 pg per reaction. Critically, this approach can reduce identification time to approximately 1 h and provides sensitivity 100 times greater than that of the conventional PCR protocol.

Deaths from the accidental ingestion of poisonous Amanita mushrooms occur every year due to the lack of a specific antidote against α-amanitin poisoning. Intervention and treatment can be promptly carried out to avoid serious consequences when the toxin can be effectively detected in whole blood before liver toxicity develops. Aptamers are molecular recognition units similar to antibodies, capable of specifically recognizing and detecting small molecules such as α-amanitin for which monoclonal antibodies are difficult to prepare. However, α-amanitin has a small molecular size and limited binding sites, which bring difficulties to aptamer selection. Moreover, achieving highly specific detection of α-amanitin in whole blood remains challenging due to the presence of potentially interfering components, such as human serum albumin (HSA). For these problems, we propose an aptamer selection method for small-molecule target α-amanitin, combining target-immobilized and library-immobilized SELEX to select high-affinity aptamers. To exclude HSA interference, counter-selection was introduced to remove HSA-bound sequences. Through these strategies, we successfully selected a highly specific α-amanitin aptamer with nanomolar affinity.

The death cap mushroom (Amanita phalloides) is one of the most toxic fungi worldwide, with α-amanitin (α-AMA) identified as its primary lethal toxin. Mitophagy selectively eliminates damaged mitochondria via the autophagy pathway and plays a critical role in maintaining mitochondrial quality and cellular homeostasis. However, its function in α-AMA-induced liver injury remains unclear. To elucidate the role and underlying mechanism of mitophagy in α-AMA hepatotoxicity, this study investigated its effects on α-AMA-exposed hepatocytes using both in vitro and in vivo models. The results showed that α-AMA treatment significantly reduced hepatocyte viability and increased reactive oxygen species (ROS) levels, confirming its hepatotoxic effects. Subsequently, mitophagy was activated to assess its functional role. Activation of mitophagy markedly alleviated α-AMA-induced hepatocyte damage. Further mechanistic analysis revealed that mitophagy activation also significantly attenuated oxidative stress and apoptosis-two key pathological processes associated with mitochondrial dysfunction under α-AMA toxicity. In summary, this study provides new evidence that enhancing mitophagy protects hepatocytes against α-AMA-induced injury. These findings highlight mitophagy as a promising therapeutic target for developing treatment strategies against life-threatening α-AMA poisoning.

BACKGROUND: Amanita muscaria (fly agaric) is a poisonous mushroom containing ibotenic acid (IBA) and muscimol (MUS), two neuroactive alkaloids capable of causing severe or fatal intoxication. While human poisoning is well documented, information on fatal intoxication in birds is limited. This report presents the first documented case of fatal poisoning of Old Polish ducks following ingestion of A. muscaria, confirmed by anatomopathological and toxicological analyses. METHODS: Post-mortem specimens, including blood, heart, brain, kidney, liver, lung, pectoral and femoral muscles, and gastrointestinal contents, were subjected to LC–MS/MS analysis for the determination of IBA and MUS. Tissue samples were homogenized, extracted, derivatized, and quantified using multiple reaction monitoring. Mushroom caps and stems collected from the environment were analyzed using the same analytical approach. To exclude alternative toxicological etiologies, liver, muscle, kidney, and gastric contents were screened for rodenticides, pesticides, mycotoxins, and other chemical toxicants by LC–MS/MS. Viral infections were excluded by PCR and RT-PCR assays targeting DNA and RNA viruses commonly affecting waterfowl. In addition, comprehensive bacteriological, mycological, and parasitological examinations were conducted. RESULTS: Post-mortem examination revealed lamellar mushroom fragments in the glandular stomach and congestion in the caeca and brain. Ibotenic acid (IBA) concentrations across tissues ranged from 4 to 1987 µg/kg, while muscimol (MUS) ranged from 2 to 66 µg/kg. In gastrointestinal contents, IBA and MUS concentrations ranged from 16.2 to 1110.5 µg/g and from 2 to 41.3 µg/g, respectively. Analysis of environmental mushroom material showed higher toxin levels in caps (871.7 µg/g IBA; 197.5 µg/g MUS) than in stems (206.6 µg/g IBA; 15.3 µg/g MUS). Screening of liver, muscle, kidney, and gastric contents excluded the presence of rodenticides, pesticides, mycotoxins, and other chemical toxicants, while PCR/RT-PCR and comprehensive bacteriological, mycological, and parasitological examinations ruled out viral, bacterial, fungal, and parasitic infections. CONCLUSION: The presence of IBA and MUS in all organs confirms A. muscaria poisoning as the cause of death. This case highlights the toxicological risk of fly agaric ingestion in waterfowl and indicates that meat and tissues from affected birds are unsafe for consumption.

Amanita pseudoporphyria (local name:) typically causes nephrotoxic injury, while severe hepatotoxic damage is rarely reported. This study reports a familial poisoning cluster involving six individuals in Zhejiang, China, including one pregnant woman. Epidemiological investigation, morphological and molecular identification, and toxin detection were conducted. Two adults developed severe hepatotoxicity with coagulopathy. The pregnant patient exhibited mild liver injury and coagulopathy. Amanitin was detected in patient samples and the implicated mushroom soup. Phylogenetic analysis confirmed the species as Amanita pseudoporphyria. This is a detailed report of severe hepatotoxicity with coagulopathy induced by Amanita pseudoporphyria, and the first documented case in a pregnant woman. The findings underscore the expanded toxic profile of this species and highlight the importance of rapid diagnosis and blood purification in management.

Amanitin (AMA), a highly toxic octapeptide from Amanita mushrooms, poses severe poisoning risks due to misidentification. Herein, we developed a flexible SERS substrate integrating MIL-101(Cr), gold nanobipyramids (AuBPs) and cellulose nanofibers (CNF) with a "dual-sieve" impurity-exclusion mechanism. This platform achieves ultra-sensitive (LOD: 10-8 mg/mL) and rapid discrimination of α-, β-, and γ-AMA subtypes, with robust anti-matrix interference performance. It enables efficient AMA subtyping, providing a portable, reliable strategy for emergency mushroom poisoning screening and food safety diagnostics.

Mushrooms are widely consumed for their culinary and nutritional value; however, some species pose serious toxicological risks. While edible varieties such as Agaricus bisporus dominate global and US markets, others, including Amanita phalloides, contain potent amatoxins associated with high morbidity and mortality. Mushroom poisoning, or mycetism, occurs across diverse populations and commonly results from accidental ingestion or species misidentification. Diagnosis is often delayed due to difficulties in accurate identification, complicating timely management. This report aims to describe two cases of severe Amanita poisoning to illustrate the clinical presentation, diagnostic challenges, and management strategies, including supportive care, antidotal therapy, and consideration for liver transplantation. It also aims to highlight the public health impact of amatoxin-containing mushrooms and underscore the need for early recognition, culturally sensitive education, and effective preventive measures to reduce mushroom-related health risks.

α-amanitin (α-AMA), the primary lethal toxin of amanita, primarily targets the liver with a high toxicity and a low lethal dose. As the precise mechanism of intoxication is unclear, and specific antidotes are lacking, α-AMA-induced liver injury has a high mortality rate. As a selective PPAR-γ agonist, Rosiglitazone (RSG) alleviates liver injury by upregulating the PPAR-γ/Nrf2 signaling pathway, thereby enhancing antioxidant effects, mitigating inflammation, and reducing apoptosis. This study investigated the protective role and mechanism of action of RSG in α-AMA-induced acute liver injury in ICR mice. We established an experimental model and examined hepatic injury markers, focusing on PPAR-γ/Nrf2 pathway activation. Overall, α-AMA intoxication led to dose-dependent increases in serum ALT/AST levels, accompanied by hepatocellular necrosis. This was associated with the onset of oxidative stress, characterized by the accumulation of malondialdehyde (MDA), excessive ROS production, and reduced activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). Furthermore, we observed the upregulation of pro-inflammatory mediators (TNF-α, IL-6, and IL-8), suppression of the PPAR-γ/Nrf2 cytoprotective axis, and hepatocyte apoptosis induced via activation of the P53/caspase-3 pathway, ultimately resulting in murine mortality. RSG treatment alleviated oxidative stress and the inflammatory response, reduced hepatocellular necrosis and apoptosis, and improved survival rates in α-AMA-intoxicated mice by upregulating the PPAR-γ/Nrf2 signaling pathway in hepatocytes. Early RSG intervention can thereby effectively mitigate α-AMA-induced acute liver injury by upregulating the PPAR-γ/Nrf2 signaling pathway. Future studies should focus on exploring the clinical potential of RSG as a therapeutic agent for amanita mushroom poisoning.

Numerous severe cases of neurotoxic mushroom poisoning worldwide are caused by ibotenic acid and muscimol produced by specific species belonging to section Amanita of the genus Amanita. Recent studies have demonstrated that both toxins are produced through the ibotenic acid biosynthetic gene cluster (iboBGC) in these species. In addition to these two toxins, section Amanita is also thought to include several species producing another neurotoxic compound, muscarine. However, the taxonomic distribution and evolutionary history of these toxins within the section remain poorly understood. In this study, phylogenetic analyses based on nucleotide sequences of two loci (ITS and LSU) and five loci (ITS, LSU, RPB2, TEF1, and TUB2), together with a phylogenomic analysis using 467 single-copy genes, were conducted to reconstruct the phylogenetic framework of section Amanita. BEAST analysis was used to estimate divergence times within the section. Gene identification of the iboBGC was conducted using 25 Amanita genomes, followed by phylogenetic analyses of each ibo gene. Biochemical analysis of muscarine was performed on 31 representative species. Based on these analyses, ibo genes were detected in 21 species forming a major monophyletic clade within the section Amanita, whereas muscarine was detected in eight species that constituted a small subclade nested within this clade. Finally, our phylogenetic, phylogenomic, chemotaxonomic, and molecular dating results indicate a monophyletic distribution of the iboBGC and muscarine within the section Amanita, with independent origins approximately 28 million years ago (Mya) and 15 Mya, respectively, and no evidence of subsequent losses.