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 CHAPTER 114 539 following is another clinical syndrome Other rare manifestations The second phase begins 24-36 hours where there is there is where hours 24-36 begins phase second The laboratory hepatoxicity of evidence though clinical patients. in observed is improvement is the onset after 48 hours phase, seen In the third coma, to hepatic hepatitis progressing of fulminant more which becomes and renal failure, hemorrhage in death. 4-7 days, resulting evident within toxicity: Intake gastroenteritis and liver Seizures, delayed are known to cause gastroenteritis of gyromitra species causing neurological and hepatic poisoning with severe gyromitirn manifestations. The is present in most of the gyromitra mushrooms. The toxicity can be differentiated amanita species based on seasonal from that of the and early as they grow more in spring considerations that are species Amanita to the compared summer Apart from the seasonal the season. seen in the fall of like appearance’ of the gyromitra the ‘brain consideration, mushroom help in differentiating it fromgyromitrin toxicity of clinical manifestations The species. the Amanita headache, seizures, gastroenteritis, includes: delayed hepatitis, hemolysis and methemoglobinemia. renal failure: This is seen with the toxins orellanine, Delayed A, cortinarin B causes interstitial nephritis and cortinarin tubulointerstitial fibrosis found and Omphalatus Cortinarius orellanus, Mycena pura mushroomin species ingestion requires orarius. Treatment for Cortinarius care for acute kidney injury and hemodialysis supportive should be considered for few individuals. rhabdomyolysis Delayed seen with Tricholoma equestre species. Onset of after consumption, symptoms occurs within 24-72 hours On weakness. and progressive which results in myalgia, with raised there is hyperkalemia laboratory evaluation creatinine phosphokinase. Rare manifestations: are less lethal are of mushroom poisoning which encephalopathy, allergic erythromelalgia, delayed hemolytic mediated and immune bronchioalveolitis, anemia. Diagnosis onset Any patient presenting to the ED with the delayed or more hours six diarrhoea of vomiting and be presumed must of foraged mushrooms consumption otherwise. The key an amatoxin poisoning until proven poisoning a patient with mushroom element in evaluating includes proper history, identification ofthe mushroom species, symptoms and signs that leads to a particular resulting wild mushrooms syndrome. The commonest in morbidity and mortality the are amanita species that grows in woodlands, on dead stumps and near pine trees in deciduous forests. Toxicity of most lethal mushrooms gastrointestinal the affecting ingestion post hours 6 occurs and the kidneys. tract, liver that can be a guide to The baseline investigations the different function tests, PT/INR, hemogram, renal and liver clinical syndromes includes complete Full recovery Full recovery Full recovery Full recovery Full recovery Full recovery Full recovery Full recovery Full recovery End stage renal failure 11% Renal transplant 13 % 0-10% 2-30 percernt Mortality Lycoperdon species Paxillus involutus Paxillus Clitocybe acromelalga Chlorophyllum Chlorophyllum molybdites Clitocybe nebularis Omphalates illudens Psilocybe cubensis P.mexicana Conocybe cyanopus Gymnopilus aeruginosa Amanita muscaria A.pantherina A.gemmata Citocybe dealbata C.illudens Inocybe fastigiata Boletus calopus Coprinus atramentarius Clitocybe clavipes Amanita smithiana Cortinarius orellanus C.speciosissinus Mycena pura Omphalatus olearius Gyromitra esculenta G.infula Sarcosphaera coronaria macropus Cyathipodia Amanita phalloides Amanita A.virosa A.verna A.bisporigera marginata Galerina G.venenata Lepiota helveola Mushroom species Mushroom Allergic to spores of Lycoperdon species Antibodies to Paxillus involutus Acromelic acid GI irritants Psilocybin , psilocin Ibotenic acid, muscimol Muscarine Coprine Allenic norleucine Orellanine, orelline, cortinarin Gyromitrin Cyclopeptides : Cyclopeptides Amatoxins, Phallotoxins Table 1: Different types of mycotoxins of types 1: Different Table Mycotoxins species are known to be the most fatal. This particular syndrome presents in three distinct clinical phases. The first phase startswith cholera –like diarrhoea, vomiting, mushroom 6 hours abdominal pain, and subsequent dehydration. after ingestion of the 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 6 to 8 hours. exposure. Octreotide effectively inhibits bile outflow
POISONING from the common bile duct and gallbladder by raising A medical toxicologist and professional mycologist pressure at the Sphincter of Oddi and enhances GB filling are known to contribute in identification of the toxic by reducing GB intraluminal pressure. mushrooms and their toxins. A rapid and specific diagnostic ELISA test for detection of amatoxin in serum SPECIFIC ANTIDOTES IN DIFFERENT TOXINS INDUCED and urine is there but is not available for clinical use. MUSHROOM POISONING Management Amanita poisoning Supportive care is the mainstay of therapy of most patients Amatoxin uptake inhibitors like silibinin or intravenous with mushroom poisoning. Specific therapy is guided by penicillin G have been shown to be associated with higher the clinical presentation (clinical syndrome). levels of patients survival. This blockade or inhibition results in the diversion of amatoxin back into the general Gastrointestinal decontamination with activated charcoal circulation for renal clearance, therefore maintaining benefits maximum when patients presents within one renal function and a brisk urine output is crucial to the hour of the toxin mushroom ingestion. Gastric emptying success of the drug. The recommended doses for silibinin by gastric lavage or ipecac syrup has shown minimal is 5 mg/kg bolus then followed by 20 mg/kg/day for 6 benefits, with increased risk of aspiration. Elimination days or till patient recovers. Intravenous Penicillin G is enhancement with multiple activated charcoal has been considered when silibinin is not available given at the shown to decrease circulation of the amatoxins after dose of 300,000 -1,000,000 units /kg/day as continuous ingestion of the toxins. The recommended doses is 50 gm infusion for the same duration. Penicillin G probably acts (0.5gm/kg) every four hourly for four days. by competitive inhibition of plasma protein binding of Hemodialysis or hemoperfusion do not remove amatoxin and thus causing excess urinary excretion and significant amounts of mushroom toxins hence is not also as uptake inhibitor. Other amatoxin uptake inhibitors recommended for toxin removal unless patient s have which have been found to be effective include silymarin signs of acute renal failure requiring hemodialysis in the and ceftazidime. A dose of silymarin is given in high form of hyperkalemia, metabolic acidosis, uremic signs doses 150 -360 mg every 8 hourly upto 2 gm /day for 6 and encephalopathy. days or till recovers. Injection ceftazidime is also given in Biliary drainage by interventional radiology (Simple/ high dose of 4 gm every 2 hourly. Serial gallbladder aspiration, percutaneous Antioxidants are also indicated in amatoxin poisoning cholecystostomy), general surgery (open cholecystostomy), as the toxins are known to enhance lipid peroxidation or GI (Nasobiliary drainage with suction placed by ERCP) that contributes to membrane instability and cell death. has been demonstrated to be effective in a growing Antioxidant prevents lipid peroxidation. Among the number of case reports. Removing amatoxin laden bile antioxidants injectable N acetylcysteine (NAC) is preferred from the gallbladder provides definitive protection in the dose 150 mg/kg bolus over 1 hour, followed by 12.5 to uninvolved hepatocytes by eliminating further mg/kg over 4 hours, 6.25 mg /kg over 16 hours. enterohepatic exposure to the poison. Simple ultrasound Gyromitrin toxicity with seizures should receive guided gallbladder aspiration appears to be the fastest, pyridoxine (70 mg/kg to 5 gm) per day along safest, easiest, and most efficient means of permanently with anticonvulsant therapy. Pyridoxine acts by removing accumulated amatoxin from the biliary tract. It reversing pyridoxal 5 phosphate deficiency in the can be accomplished using a transhepatic approach early central nervous system mediated by toxic metabolite in the clinical course or via a transperitoneal approach if monomethylhydrazine. Methemoglobinemia also seen the INR is above 2. The collected bile sample should be in gyromitrin poisoning when detected should receive labeled and frozen carefully for subsequent analysis of intravenous methylene blue. amatoxin content. Cholinergic excess from muscarine toxins should receive Intravenous Octreotide (200 mcg bolus followed by CHAPTER 114 541 9th ed. Toxicology 2014; 4:361-5. Toxicon 1993; 31:1513-40. 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CONCLUSION More studies are required in mushroom poisoning in our More studies are required in mushroom types of mushroom country for proper judgment of the programs in Awareness causing morbility and mortality. supportive early and out carried be should area affected the population. therapy should be the goal in affected Supportive care the toxin of by most cause are diarrhoea and Vomiting containing which can be mushrooms treated with antiemetic. fluids and intravenous treated with are delirium and hallucination Agitation, by mushrooms Seizures caused benzodiazepines. are gyromitrin and ibotenic acid containing muscimol, midazolam acting benzodiazepines treated with short if no responds phenytoin or lorazepam and sodium is the epilepsy protocol management. considered as per species by tricholoma equestra caused Rhabdomyolysis with raised creatinine phosphokinase characterized by granular urine showing pigmented or brown casts, a red to is primary treatment The urine supernatant. of color give aggressive intravenous fluids saline 20-40 ml/kg/hour upto 1 litre/hour. preferable normal should be Renal failure when present hemodialysis considered in candidates with fluid overload, refractory to diuretics, hyperkalemia, metabolic acidosis and signs decline in mental of uremia (pericarditis, unexplained status). should prompt the Fulminant hepatitis when present transplant liver patient to a early transfer of for physician not hepatotoxicity does when patient with center and therapy. after 4 days of supportive even improved atropine or glycopyrrolate. or glycopyrrolate. atropine agent anticholinergic Repeat dried. have secretions bronchial until as needed