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Mushroom Poisoning

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Mushroom Poisoning CHAPTER Mushroom Poisoning 114 Bhupen Barman, KG Lynrah, Iadarilang Tiewsoh INTRODUCTION Acute gastroenteritis – A wide variety of non eatable Mushroom poisoning among other forms of poisoning mushrooms when consumed causes nausea, vomiting, contributes to high morbidity and mortality in the diarrhea and abdominal cramps within one to three country. In certain ethnic populations of India, mushroom hours of consumption. These symptoms are caused most is an important constituent of their diet. The incidence of commonly by the chlorophyllum molybdites species are mushroom poisoning in India in the recent years has been also called “backyard mushrooms”. recognized due to increasing awareness and the affected NEUROTOXIC SYNDROMES individuals seeking health care at the earliest. The tropical a. The hallucinogenic effects are produced by the belt of the country with its biodiversity is a mother load ingestion of mushroom containing psilocybin of different fungal mushroom species. As per studies and psilocin. They are known to be abused for conducted in India, there are 1200 species with only 50 recreational purposes. to 100 species known to be poisonous. Twelve groups of the identified mushroom toxins have been identified b. CNS excitation and depression: This syndrome responsible for 14 described clinical syndromes. is caused by Amanita species containing toxins muscimol and ibotenic acid. Muscimol is a CNS EPIDEMIOLOGY depressant whereas ibotenic acid has excitatory From the studies conducted the 50-100 toxic mushrooms effects at glutamic acid receptors in the CNS. produces the mycotoxins responsible for different clinical Symptoms include somnolence, dizziness, syndromes which are described below. In the United hallucination, dysphoria, bizarre behavior and States the North American mycological association seizures. maintains a case registry where instances of mushroom poisoning are being reported. In India mushroom forms c. Cholinergic poisoning ocuurs when there is intake part of the diet especially in the ethnic populations. In of inocybe and clitocybe species which contain most of the cases mushroom poisoning occurs from muscarine toxin. Muscarine is structurally similar consumption of the wild mushrooms. However most of to acetylcholine and causes toxicity by binding the cases are undiagnosed, unreported and epidemics to postganglionic cholinergic neurons in the of mushroom poisoning are reported in press which has autonomic nervous system. Symptoms usually been observed mostly in the monsoon season. Table 1 appear 30 minutes post ingestion in the form of shows the different mushroom species with their toxins bradycardia, diaphoresis, salivation, lacrimation, and mortality percentage. bronchospasm, bronchorrhoea and incontinence. From the case reports in India the reported cases are from Disulfiram like reaction: The toxin coprine found in the the tribal areas of South India, the Eastern Ghats, Northern coprinus atramentarius, the inky cap mushroom and its India and north eastern parts of the country. Most of the species are known to cause this syndrome. The symptoms cases are being reported and documented in newspapers occurs after 2 hours of ingestion in the form of headache, where mortality of such cases are being noticed. As per flushing of face, neck and trunk, nausea and vomiting, the clinical syndromes of most of the fatalities, they are tachycardia, palpitations, chest pain, dyspnoea. very suggestive of Amanita phalloides poisoning (Table Delayed onset syndrome (>6 hours) occurs mostly after 2). ingestion of lethal mushrooms. CLINICAL SYNDROMES Gastroenteritis and delayed renal failure are encountered The 14 types of clinical syndromes caused by the 12 with the Amanita species particularly Amanita smithiana. groups are described below. The syndromes are divided Onset of renal failure is observed 12-24 hours after on the basis of their presentation as early onset (< 6 hours ingestion. General supportive care is the management of of ingestion) and late onset (> 6 hours of ingestion). The choice with few patients requiring hemodialysis. syndromic presentation and their identification help in Delayed gastroenteritis and liver toxicity : Delayed onset making early diagnosis and empirical therapy. of vomiting, diarrhoea, and hepatitis observed more than Early onset syndromes are less toxic and life threatening, 6 hours post ingestion are known to be life threatening however does not exclude the possibility of consumption complications mostly observed with toxic mushrooms, of lethal mushrooms. Aminata, Galerina and Lepiota of which the Amanita Table 1: Different types of mycotoxins The second phase begins 24-36 hours where there is 539 laboratory evidence of hepatoxicity though clinical Mycotoxins Mushroom species Mortality improvement is observed in patients. Cyclopeptides : Amanita phalloides 2-30 In the third phase, seen after 48 hours is the onset Amatoxins, A.virosa percernt of fulminant hepatitis progressing to hepatic coma, Phallotoxins A.verna hemorrhage and renal failure, which becomes more A.bisporigera Galerina marginata evident within 4-7 days, resulting in death. G.venenata Seizures, delayed gastroenteritis and liver toxicity: Intake Lepiota helveola of gyromitra species are known to cause gastroenteritis with severe poisoning causing neurological and hepatic Gyromitrin Gyromitra esculenta 0-10% manifestations. The gyromitirn is present in most of the CHAPTER 114 G.infula gyromitra mushrooms. The toxicity can be differentiated Sarcosphaera coronaria from that of the amanita species based on seasonal Cyathipodia macropus considerations as they grow more in spring and early Orellanine, Cortinarius orellanus End stage summer compared to the Amanita species that are orelline, C.speciosissinus renal failure seen in the fall of the season. Apart from the seasonal cortinarin Mycena pura 11% consideration, the ‘brain like appearance’ of the gyromitra Omphalatus olearius Renal mushroom help in differentiating it from the Amanita transplant species. The clinical manifestations of gyromitrin toxicity 13 % includes: delayed gastroenteritis, headache, seizures, Allenic Amanita smithiana Full hepatitis, hemolysis and methemoglobinemia. norleucine recovery Delayed renal failure: This is seen with the toxins orellanine, Coprine Coprinus Full cortinarin A, cortinarin B causes interstitial nephritis and atramentarius recovery tubulointerstitial fibrosis found in mushroom species Clitocybe clavipes Cortinarius orellanus, Mycena pura and Omphalatus Muscarine Citocybe dealbata Full orarius. Treatment for Cortinarius ingestion requires C.illudens recovery supportive care for acute kidney injury and hemodialysis Inocybe fastigiata should be considered for few individuals. Boletus calopus Delayed rhabdomyolysis is another clinical syndrome Ibotenic acid, Amanita muscaria Full seen with Tricholoma equestre species. Onset of muscimol A.pantherina recovery symptoms occurs within 24-72 hours after consumption, A.gemmata which results in myalgia, and progressive weakness. On Psilocybin , Psilocybe cubensis Full laboratory evaluation there is hyperkalemia with raised psilocin P.mexicana recovery creatinine phosphokinase. Conocybe cyanopus Rare manifestations: Other rare manifestations Gymnopilus of mushroom poisoning which are less lethal are aeruginosa erythromelalgia, delayed encephalopathy, allergic GI irritants Chlorophyllum Full bronchioalveolitis, and immune mediated hemolytic molybdites recovery anemia. Clitocybe nebularis Omphalates illudens Diagnosis Acromelic acid Clitocybe acromelalga Full Any patient presenting to the ED with the delayed onset recovery of vomiting and diarrhoea six hours or more following consumption of foraged mushrooms must be presumed Antibodies Paxillus involutus Full an amatoxin poisoning until proven otherwise. The key to Paxillus recovery element in evaluating a patient with mushroom poisoning involutus includes proper history, identification of the mushroom Allergic to Lycoperdon species Full species, symptoms and signs that leads to a particular spores of recovery syndrome. The commonest wild mushrooms resulting Lycoperdon in morbidity and mortality are the amanita species that species grows in woodlands, on dead stumps and near pine trees in deciduous forests. Toxicity of most lethal mushrooms species are known to be the most fatal. This particular occurs 6 hours post ingestion affecting the gastrointestinal syndrome presents in three distinct clinical phases. tract, liver and the kidneys. The first phase starts 6 hours after ingestion of the The baseline investigations that can be a guide to mushroom with cholera –like diarrhoea, vomiting, the different clinical syndromes includes complete abdominal pain, and subsequent dehydration. hemogram, renal and liver function tests, PT/INR, 540 Table 2: Geographic distribution of mushroom poisoning in India Location Clinical Syndrome Possible mushrooms South India (Eastern Ghats) Acute gastroenteritis Omphalotus olivascens, Mycena pura Chlorophyllum molybdites Karnataka (Mangalore Cholinergic excess Clitocybe species North India (Himachal Pradesh) Acute gastroenteritis, liver failure Amanita species North east India (Assam, Meghalaya, Acute gastroenteritis ,liver failure Amanita species Mizoram, Manipur) *As per case reports and media reports creatinine kinase, serum lactate at presentation, followed 50 mcg per hour) helps to keep amatoxin contained in by serial measurement of CMP, lactate, and PT/INR every the gallbladder and thus limiting further hepatocyte
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