Mushrooms that contain amatoxin may also contain phallotoxins, virotoxin, and toxophallin (l-amino acid oxidase). While the amount of amatoxin varies among species, a single mushroom may contain 5–7 mg of amatoxin and could be fatal if ingested [36, 37, 84–88]. Children are particularly sensitive to amatoxin [14, 37,89–92]. Toxophallin is an enzyme that induces chromatin condensation, DNA and nucleus fragmentation, and apoptosis. It is hypothesized that toxophallin induces cell damage via generation of free radicals and oxidants, resulting in apoptosis [2, 93]. Phallotoxins are not absorbed from the intestine and are not thought to contribute significantly to clinical toxicity [84, 85]. Virotoxin appears to be restricted to A. virosa [85].
Amatoxins are generally accepted as the principal toxins producing hepatotoxicity. There are ten known amatoxins, including alpha-, beta- and gamma-amanitins. Alpha-amanitin, the primary toxin, is a heat-stable, bicyclic octapeptide which damages the liver and kidneys by irreversibly binding to RNA polymerase II. This diminishes mRNA production, which diminishes protein production, and eventually produces cell death [34–36,89, 94]. Alpha-amanitin may also be transformed into free radical intermediates that increase production of reactive oxygen species such as hydrogen peroxide, superoxide, and hydroxyl radicals. This contributes to cell membrane damage [34]. Alpha-amanitin may also act synergistically with endogenous cytokines, such as tumor necrosis factors, to produce cell damage and induce apoptosis [84, 85].
Alpha-amanitin is easily absorbed in the intestines. Gastrointestinal epithelial cells, hepatocytes, and proximal tubular cells are very susceptible to amatoxins, in part, due to increased amatoxin uptake via organic anion-transporting polypeptides within cell membranes [19, 35, 89]. Alpha-amanitin may also be transported into the cell via Na + −taurocholate cotransporter polypeptides [19]. Ultimately, hepatic necrosis and acute tubular necrosis of the kidneys ensue [35, 89, 95].
Clinical Presentation
Clinical progression may be divided into four stages: (1) latency or quiescent phase, (2) gastrointestinal phase, (3) clinical remission (progressive organ damage despite apparent clinical improvement), and (4) acute liver failure or multiorgan failure [84, 85]. Typically, an asymptomatic latency of 6–24 h proceeds severe gastroenteritis; however, shorter latencies have been reported [6, 27, 89]. Others have reported latencies as long as 40 h [84]. Gastroenteritis, including vomiting, watery diarrhea, and abdominal pain follows and typically lasts 1–2 days. This may be associated with tachycardia, hypotension, and electrolyte abnormalities. Gastroenteritis may be followed by a brief clinical remission. Liver enzymes begin to rise within 16–48 h of ingestion and can increase despite apparent clinical improvement [38, 84]. The final stage is hepatorenal or multiorgan failure within 2–7 days of mushroom ingestion. Fulminant hepatic failure is characteristic of severe toxicity. Liver pathology is characterized by fatty degeneration and centrilobular necrosis [84, 90, 94, 96]. Acute tubular necrosis, with damage to the proximal tubules, can also be seen [84, 85]. Death, when it occurs, is generally at 4–16 days but may occur later [6, 83, 84, 89, 94, 96–101]. Less severely poisoned patients may recover, rather than progress to fulminant hepatic failure [84]. Approximately 20 % of survivors develop immune complex-mediated chronic hepatitis with anti-smooth muscle autoantibodies [29, 102, 103]. Pancreatitis, prior to the development of fulminant hepatic failure, has been reported after Lepiota subincarnata ingestion [14]. Thrombocytopenia may occur and is generally noted 3 days after ingestion [38].
Toxin Detection
The Meixner test can be performed by adding hydrochloric acid to a sample of mushroom placed on newspaper. A blue color change suggests amatoxin is present; however, the test may produce false positives [36, 86]. Alpha-amanitin can be detected in serum by HPLC [38, 89, 103]. Amatoxins can also be detected in the urine [85, 101]. Some have used RIA, ELISA, or EPLC to detect amatoxin [84]. Others have developed LC/MS/MS and mass LC/MS methods to detect these toxins [104]. Recently, a DNA-based macroarray was developed to detect Amanita species from left-over mushroom meals [103].
Prognosis
Mortality rates have historically been reported as high as 20–30 % in adults and >50 % in children; however, more recent data indicates that the mortality rates are declining and are currently often reported at <10 %; however, in some current reports, mortality rates continue to be higher than 10 % [26, 31, 36, 38]. Trabulus found that patients who died were more likely to have low mean arterial pressures (MAP < 70 mmHg), encephalopathy (confusion, stupor, and coma), mucosal hemorrhage, and oliguria–anuria. The laboratory studies of patients who died revealed greater elevation of urea, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), total bilirubin, prothrombin time (PT), INR and partial thromboplastin time (PTT) levels, but lower sodium concentrations, platelet counts (platelet count < 100,000/μl) and plasma glucose levels (<60 mg/dl) [38]. All patients who died developed acute hepatic failure with encephalopathy and died within 1–7 days of hospitalization. Encephalopathy was the strongest predictor of death from amatoxin-containing mushroom poisoning [odds ratio (OR) of 232], followed by oliguria–anuria (OR of 52) and thrombocytopenia (OR of 15.5) [38]. Similarly, Fantozzi et al. [105] reports that elevation of ALT or AST > 2000 IU, hepatic encephalopathy, or PT > 50 s are prognostic of impending death. Jan et al. [106] reports that, in children (as in adults), signs of hepatic encephalopathy, prolonged PT, and elevation of hepatic transaminases are associated with increased mortality. It is rare for a patient without encephalopathy to succumb to multi-organ failure after Amanita sp. poisoning [25]. Death from hepatic failure may be secondary to sepsis, brain herniation, or bleeding complications.
Treatment
There are not universally accepted antidotes or standardized treatments for amatoxin poisoning. Treatment generally comprises intensive supportive care, with attention paid to fluid and electrolyte imbalances, coagulation disorders, and hypoglycemia [38]. Standard treatments for acute liver failure (ALF) should be utilized [107–109]. Some recommend multiple-dose activated charcoal (20–40 g every 3–4 h for 24 h or 50 g every 6 h) and nasoduodenal suctioning to limit enterohepatic recirculation of amatoxin, because approximately 60 % of absorbed alpha-amanitin is excreted into the bile and is then returned to the liver via recirculation [29, 38, 73, 84,85]. The antidotes benzylpenicillin, ceftazidime, N-acetyl-cysteine (NAC), rifamycin, and silibinin have been advocated by some [26, 34, 36, 88, 110–112], and questioned by others [113, 114]. Of these, silibinin and NAC show the most promise [32, 34, 111, 115]. Magdalan [34] performed cell culture studies and found that hepatocytes poisoned with alpha-amanitin and simultaneously treated with NAC or silibinin showed less evidence of lipid peroxidation than poisoned hepatocytes simultaneously treated with benzylpenicillin or without an antidote treatment. Studies performed in beagle dogs poisoned with lyophilized A. phalloides reveal silibinin treatment lessened lab abnormalities associated ALF, hemorrhagic necrosis of the liver and mortality [85]. Silibinin is the most active component of silymarin, found in Silybum marianum (milk thistle). It is a scavenger of free radicals, has anti-inflammatory effects, stimulates protein synthesis, and inhibits amatoxin uptake by hepatocytes [26, 34]. If silibinin is available, its administration seems reasonable [19, 31, 85, 97, 111, 115, 116]. Silibinin could potentially be obtained by contacting the researchers using this antidote through clinicaltrials.gov, using identifierNCT00915681. In Europe, Legalon® SIL is available. Its active ingredient is silibinin-C-2′3-dihydrogen sussinate, disodium salt [85]. Amanita virosa decreases intracellular glutathione content; NAC may be useful as a glutathione precursor [34]. Since NAC is readily available and relatively safe, its administration seems reasonable [19, 85, 111] (Table 3).
There are not randomized, controlled trials evaluating extracorporeal treatments for amatoxin-poisoned patients; thus, these treatments remain controversial. Patients studied by Trabulus received hemoperfusion (HP) upstream of concurrent hemodialysis (HD) and had a relatively low mortality rate; however, HP–HD was not compared to optimal medical care without extracorporeal decontamination [38]. Mullins reported on the apparent futility of HP and HD in the treatment of A. phalloides poisoning after noting that amatoxin was not detected before, during or after HP and HD treatments in blood or in HP or HD circuits of two patients treated with HP and HD after A. phalloides poisoning [117]. This is not surprising, since amatoxin is rapidly absorbed and distributed into body compartments. Amatoxins are rarely detected in plasma 36–48 h after mushroom ingestion; despite being detectable in the liver and kidneys after 5 days [31, 84, 89]. Amatoxins may be detectable in the urine for 4 days [31]. Similarly, some report that plasmapheresis reduces mortality [26, 99, 118]; others doubt its efficacy [8, 32,33]. Liver albumin dialysis [molecular absorbent recirculating system (MARS) or fractionated plasma separation and adsorption with high-flux dialysis (Prometheus)] has been successfully utilized, while awaiting liver transplantation; however, patients may die awaiting organ donation [3, 25, 31, 37, 38, 83, 90, 94, 119–121].
MARS is an extracorporeal decontamination technique that removes albumin-bound substances that may play a role in ALF. Blood is dialyzed against an albumin-containing solution across a high flux permeable membrane [89]. While MARS would not likely remove amatoxins, it could remove protein-bound endogenous toxins, allowing the liver to spontaneously recover. Treatment with MARS could improve medical conditions enough that a critically ill patient would better tolerate, or survive until, liver transplantation [89]. Sorodoc et al. [37] evaluated six patients with amanitin-induced fulminant hepatic failure treated with either MARS or optimal intensive care alone and found that MARS treatments decreased ammonia, ALT, PT, and mortality rate (from 100 % to 66.7 %). However, it is difficult to draw prognostic conclusions about MARS treatment from Sorodoc’s data because only 1/6 patients survived. The surviving patient received MARS, but was also the only patient with normal vital signs on admission (non-survivors had hypotension and/or tachycardia on admission). The surviving patient also had the lowest initial model for end-stage liver disease (MELD) score [37]. Sorodoc et al. [37] also notes that the survivor consumed the smallest meal of mushrooms. Based on history and initial presentation, one might have predicted this patient would be the most likely to survive, with or without MARS. Covic utilized MARS treatment in six children with hepatic encephalopathy after mushroom poisoning. Covic et al. [119] found that 4/6 patients survived with intact liver function, compared to matched controls in which MARS was not utilized and 6/6 died (mortality rate of 33 % compared to 100 %). Faybik reports on six patients treated with extracorporeal albumin dialysis after A. phalloides poisoning and notes that: two patients had spontaneous regeneration of liver function; two patients were bridged to liver transplantation; one patient avoided re-transplantation after graft dysfunction following liver transplantation; and one patient died secondary to cerebral herniation [122]. MARS has been utilized in a pregnant patient with hepatic encephalopathy due to A. phalloides poisoning. Her hepatic encephalopathy resolved after MARS treatment, after initial HP–HD, plasma exchange, and aggressive supportive care had been ineffective [27]. Wittebole reviewed the cumulative, international, experience of MARS use in 48 cases of A. phalloides-related liver failure [89]. Wittebole and Hantson [89] note improvement of encephalopathy, often with resolution of encephalopathy, and improvement of hemodynamic parameters.
Vardar evaluated a fractionated plasma separation and adsorption system (FPSA, Prometheus) in eight patients with hepatic failure after wild mushroom ingestion in Turkey. All patients received FPSA, Penicillin G, and NAC. Vardar noted improvement of AST and ALT, a complete response rate of 75 %, and a survival rate of 87.5 % [121]. More recently, Bergis et al. [31] studied 20 patients with proven A. phalloides intoxication (positive urinary amanitin toxin by ELISA). In this study, 9/20 received Prometheus treatment, 11/20 did not. All 20 patients received activated charcoal, fluids, NAC, and silibinin. The study was not randomized and used matched controls; however, some of the matched controls were treated years earlier than some of the patients in the treatment group (some are historical controls). Bergis et al. found that mean urinary amanitin levels and mortality were reduced by Prometheus, with a mortality rate of 0 %, without liver transplantation. The mortality rate for the control group was 9 %; however, this difference was not statistically significant [31].
In the absence of randomized controlled trials, limited numbers of patients treated with liver albumin dialysis, and differences in supportive care measures, it is difficult to make definitive recommendations regarding liver albumin dialysis treatment. However, it appears that liver albumin dialysis treatments often improve encephalopathy and hemodynamic parameters, lower AST, ALT, and ammonia levels, and allow some patients to undergo liver transplantation in better condition [31, 37, 89, 98, 121]. Conversely, there are also case reports of patients with fulminant hepatic failure and encephalopathy who recover without MARS, FPSA, or liver transplantation [123].
Liver transplantation dramatically increases the survival rate of amatoxin-induced ALF [116]. While orthotopic liver transplantation (OLT) has been generally considered the gold-standard treatment of amatoxin-induced ALF, there are also reports of auxiliary partial liver transplantation resulting in eventual regeneration of the native liver, allowing for eventual successful cessation of immunosupressive therapy. Therefore, auxiliary, rather than orthotopic, liver transplantation may be considered in some cases [25, 124]. The specific criteria for emergent transplantation have been debated and many sets of criteria exist [100, 116, 125, 126] (see Table 4). Various reports discuss the successful and unsuccessful application of these criteria. Ferreira et al. [100] reported on ten patients poisoned with A. phalloides, including four deaths, and found that the Escudie’s criteria provided better prognostic indicators than Clichy or King’s College criteria. However, some have criticized Escudie’s criteria because the study analyzed data assuming that transplanted patients would have otherwise died; half of the patients in the ‘fatal intoxication group’ actually received OLT [127]. Escudie has criticized Ganzert’s criteria after finding that 2/19 patients that meet Ganzert’s criteria for transplant recovered without transplantation, while one patient died despite not meeting Ganzert’s criteria [128]. Escudie found that both the Clichy’s and Ganzert’s criteria failed to predict some fatal outcomes. Escudie et al. [25] reports that later in a patient’s clinical course, King’s College criteria were superior to Clichy’s and Ganzert’s criteria. However, Ganzert et al. [127] rebuts, stating that Escudie did not implement the Ganzert’s criteria correctly to draw these conclusions. Garcia de la Fuente reports on an infant that survived amatoxin-induced ALF without transplantation, noting that the King’s College criteria and Clichy’s criteria predicted a poor outcome, while Ganzert’s and Escudie’s criteria correctly predicted a good outcome [116]. In an Australian case series, the prognostic value of (1) onset of diarrhea < 8 h after mushroom ingestion and INR ≥ 6 on day 4 was compared to (2) INR ≥ 2.5 and serum Cr > 106 μmol/l on Day 3, based on previous reports by Ferreira and Ganzert [36, 100, 127]. These prognostic factors for mortality did not prove useful in this series. In this Australian report, patients who died had higher blood lactate levels (>5 mmol/l), compared with survivors [36]. These conflicting reports and debates among experts in the field make utilizing appropriate predictors of outcome and need for OLT difficult. Further, the studies generally have limitations of: limited patient enrollment, retrospective analyses, and utilization of historical controls.
Table 4
Table 4
Various liver transplant criteria (e.g. poor prognosis without transplantation)
Nephrotoxins
Most severe, mycetism-induced renal failure is due to Cortinarius species [5].
Toxins and Pathophysiology
Orellanine (which occurs as orellanine-4,4′-diglucopyranoside in some species) is a nephrotoxic bipyridine N-dioxide found in some Cortinarius species, including C. orellanus (Fool’s Webcap),C. speciosissimus, or C. rubellus (Deadly Webcap), and Cortinarius orellanosus [2, 8, 10, 18, 29, 30, 129,130]. C. orellanosus has been found in Michigan, while C. orellanus is found in Europe [129]. These mushrooms have been mistaken for edible Cantharellus cibarius, Cantharellus tabaeformis, Boletus edulis (Ceps or Porcinis) and for hallucinogenic Psilocybe mushrooms [2, 18, 130]. Orellanine is concentrated in the kidney [10]. Further, oxidation of orellanine in renal tissue may accumulate quinone compounds, producing cell damage [2]. Orellanine interferes with RNA polymerase B and inhibits alkaline phosphatase in the proximal tubule cells, leading to disruption of ATP production [10, 15]. Extracts of Cortinarius orellanus diminish the number of sulfhydrilic groups and deplete glutathione in renal and hepatic tissue [10]. Oxygen-free radical formation may contribute to the cytotoxic damage as well [10, 130]. The tubular epithelium is the toxin’s primary target [131].
Clinical Presentation
This presentation is sometimes referred to as the “Orellanus syndrome” [4]. Patients present with delayed vomiting and diarrhea followed by oliguria or anuria [129–132]. A clinical latency of 36 h to 21 days has been reported. A shorter latency period is associated with a poorer prognosis [10]. Typically, vomiting and diarrhea occur 3 days after ingestion, which is followed by intense thirst, chills and evidence of acute renal failure which develops 8–9 days after ingestion [2, 129, 132]. Patients may present with fatigue, nausea, vomiting, headache, weakness, myalgias, and flank pain [10]. Polyuria is followed by oligo-anuria [10]. Creatinine and BUN rise. Associated electrolyte abnormalities, such as hyponatremia, hyperkalemia, and acidosis, may be noted [10, 129, 131]. Ultrasound may reveal enlarged kidneys with reduced echogenicity of the medulla and papillae [10]. Renal biopsy reveals evidence of acute tubular necrosis with interstitial nephritis and edema. The glomeruli and renal vessels are typically intact [10, 33, 129, 131]. Progressive fibrosis may ensue [123].
Toxin Detection
Diagnosis may be made by microscopic evaluation of mushroom spores [10, 131]. Alternatively, orellanine can be tested for by adding a drop of 2 % iron (III) chloride in 0.5 N HCl to the liquid pressed from fresh or rehydrated mushroom fragments. If orellanine is present, the initially yellow liquid immediately stains purple red to violet [5, 10]. Orellanine can be detected by thin-layer chromatography (TLC), electrophoresis, UV detection, and HPLC-ESI-MS/MS [130]. If orellanine is going to be assessed in renal biopsy tissue, care must be taken to protect the specimen from light, as orellanine is light-sensitive [5]. In renal biopsy tissue, orellanine is detectable TLC up to 6 months after poisoning [10].
Prognosis
Acute renal failure occurs in 30 % to 75 % of patients [10, 29, 30]. As many as 50 % of those requiring early dialysis will develop chronic renal failure [10, 123, 129, 131, 133]. Some patients, who do not require hemodialysis, will still show evidence of chronic renal insufficiency. Only 30 % of those poisoned have complete recovery of renal function [10, 131]. Case series suggest that children may suffer a worse prognosis than adults [131].
Treatment
Treatment is supportive and includes renal replacement therapy. Some have recommended anti-oxidant treatment with steroids and NAC; however, these treatments are based on anecdotal reports [10, 131,134]. Furosemide may worsen injury, possibly due to concentrating orellanine in the kidney [131]. Renal transplantation has been utilized [10, 32, 129, 131].
Other Nephrotoxic Mushrooms
Relatively accelerated nephrotoxic mushroom syndromes are described afterAmanita proxima (Mediterranean Amidella) and Amanita smithiana (toxic Lepidella Amanita or North American Lepidella) ingestions [4]. This is sometimes referred to as the “Amanita nephrotoxic syndrome” [4]. A. smithiana has been found along the Pacific coast of North America and less commonly in Idaho, Nevada and New Mexico [135]. A. smithiana contains A. smithiana toxin. Amanita boudieri, A. echinocephala, and A. gracilior also contain A. smithiana toxin and present similarly [4, 5, 129, 135–139]. A. smithiana toxin is not present in A. proxima, but the presentation, is nonetheless, similar [5, 46]. A. smithiana toxin may be detected by TLC [135].
A 20 min–24 h latency period is followed by GI symptoms. The GI symptoms occur more rapidly when the mushrooms are ingested raw. This is followed by nephrotoxicity within 1–6 days. Tubulointerstitial nephritis is characteristic. Mild cytolytic hepatitis can also be seen and the liver enzymes may rise before the creatinine rises [4, 15, 32, 129, 135–138]. De Haro et al. [140] reported on 53 patients poisoned by A. proxima and found 38 % had an increased creatinine, 32 % were oliguric or anuric, and 24.5 % required hemodialysis. The renal failure is secondary to interstitial nephritis and is generally reversible [5]. Some patients require hemodialysis, but this requirement generally resolves within several weeks [5].
Amanita psuedoporphyria Hongo ingestion has also been associated with delayed onset acute renal failure. This mushroom does not contain A. smithiana toxin, but it does contain 2-amino-4,5-hexadienoic acid (allenic norleucine), which is also found in A. smithiana [4, 5, 135, 137]. However, allenic norleucine is no longer thought to be responsible for A. proxima or A. smithiana toxicity [4, 5, 135]. Regardless, acute tubular necrosis is seen and hemodialysis may be required for several weeks [137].
A. phalloides can produce acute renal failure characterized by tubular necrosis particularly of the proximal renal tubules. Biopsy has revealed epithelial damage with tubular epithelial cell-shedding, apoptosis, and tubular epithelium atrophy. The renal failure associated with A. phalloides ingestion may ensue after the liver has recovered or after OLT. Renal replacement therapy has been utilized and long-term hemodialysis is occasionally required [14, 95, 123].
Mushroom ingestions that cause rhabdomyolysis (discussed next) may also produce renal injury.
Myotoxins
Rhabdomyolysis has been associated with repetitive ingestions of T. equestre (also known as T. flavovirens, T. auratum, and Yellow Trich or Yellow Knight or Man on Horseback). Several, generally three to nine consecutive, meals of T. equestre mushrooms (100–400 g) must be consumed to develop toxicity [2]. Rhabdomyolysis also follows ingestions of R. subnigricans (Blackening Russula), and some Cortinarius species [10, 15, 33, 49, 141].
Clinical presentation
Four patients presented after consuming T. equestre for several days. Adults presented with fatigue, muscle weakness, myalgias, nausea, and profuse diaphoresis, 1–2 days after their last mushroom meals. A young child presented with coma, cyanosis, hypertonia, and convulsions within 4 h of his last mushroom meal. Two of four patients required ventilatory support for respiratory failure, and one died from cardiac arrest. The maximal CK was nearly 50,000 U/l [141]. In other case reports, the CK has risen to 600,000 U/l. Moderate elevation of liver transaminases is also reported (AST 800 to 2,000 U/l; ALT 400 U/l) in some patients; this may be secondary to rhabdomyolysis. Occasionally, marked elevation of liver transaminases is noted (AST > 8,000 U/l); this may represent hepatic injury [142]. The mortality rate is 20 % [141].
R. subnigricans contains cycloprop-2-ene carboxylic acid, which triggers rhabdomyolysis [143]. In Asia, ingestion of R. subnigricans typically results in nausea, vomiting, and diarrhea within 30 min to 2 h of ingestion. Patients may recover or may present with delayed complaints of muscle pain and weakness, with associated rhabdomyolysis, myoglobinuria, renal failure, and hyperkalemia. Speech impairment, convulsions, and loss of consciousness have also been reported [143, 144].
Myotoxic mushrooms may cause profound muscle weakness and patients may be unable to sit or stand, require mechanical ventilation, and require prolonged bladder catheterization [141]. When patients recover, they may experience muscle weakness for several weeks to months [71, 72, 143, 144].
Myotoxic mushrooms may injure cardiac muscle, resulting in cardiopulmonary complications including respiratory failure, pulmonary edema, myocarditis, dysrhythmias (e.g., ventricular tachycardia), and cardiovascular collapse. Death may occur. This is reported after ingestions of R. subnigricans and T. equestre [141].
Muscle biopsies after T. equestre poisoning have revealed myofibrils that appear nibbled and separated by edema. Autopsies have revealed acute myopathy of skeletal muscle, diaphragm muscle, and myocardium [32, 71,72, 141].
Immunologic/Hematologic Toxins
Repeated ingestion of Paxillus involutus (Poison Pax; Brown Roll-Rim) may produce immunohemolytic anemia. Antibodies against the mushroom produce immune-complex-mediated hemolysis. Symptoms may begin < 6 h from ingestion and include gastroenteritis and shock. Interstitial nephritis and hepatorenal failure may ensue. Hemodialysis may be required. Some have recommended corticosteroid and plasma exchange treatment [32, 49,145, 146].
Yoon reports [17] that, in northeast Asia, a reversible pancytopenia, with a normocytic, normochromic anemia, and associated fever has been reported after consuming a decoction of Ganoderma neojaponicum Imazeki, as an herbal medicine.
In Japan, China, Korea, and Java, Podostroma cornu–damae may produce toxicity. In one case series, misidentification for Ganoderma lucidum, which is nontoxic, lead to poisoning. Podostroma cornu–damaecontains trichothecene mycotoxins including satratoxins, tratoxin, roridin, and verucarin. Ingestion produces GI distress, followed by dehydration and hypotension, oliguria, altered mental status, leukopenia, thrombocytopenia, lamellar desquamation of the palms and face, and alopecia. Multiple organ failure and death may occur. Patients may succumb to sepsis secondary to pancytopenia. Treatment includes supportive care, antibiotics to cover neutropenic fever, and granulocyte colony-stimulating factor for pancytopenia [147].
Allergic reactions to mushrooms have been described with B. edulis (Porcini; King Bolete), Agaricus bisporus(Button Mushroom) and Lentinula edodes (Shiitake). A diffuse, pruritic dermatitis has been reported after touching or eating Shiitake mushrooms [49].
Mitochondrial Toxins
P. porrigens (Angel’s Wing), G. frondosa, and P. eringii are cyanogenic. Poisoning may present like an encephalopathic syndrome. The convulsive encephalopathy seen after P. porrigens ingestion is discussed above, under epileptogenic syndromes [49, 50, 148, 149].
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Summary
New toxic mushroom species continue to be identified. Some species initially classified as edible are later reclassified as toxic. This results in a continually expanding list of toxic mushrooms. As new toxic species are identified, some classic teachings about mycetism no longer hold true. One example is the utilization of a time line for development of GI systems as a prognosticator. We now recognize that this time line is flawed, since patients who have early GI symptoms may develop significant systemic toxicity after mushroom ingestion. As more toxic mushrooms are identified and more toxic syndromes are reported, older classification systems fail to effectively accommodate mycetism. This review classified mushroom poisonings by the primary organ system affected and subclassified mushroom poisonings by the type of syndrome produced within each organ system affected. This classification permits expansion, as new, toxic mushroom species are discovered, and it allows clinicians to determine the species most likely responsible for illness in their patients. This approach may facilitate ordering specific diagnostic tests and providing specific treatments in conjunction with intensive, supportive care.
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