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Diagnosis and Treatment of Amanita Phalloides-Type Mushroom Poison- Ing-Use of Thioctic Acid

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Diagnosis and Treatment of Amanita Phalloides-Type Mushroom Poison- Ing-Use of Thioctic Acid Refer to: Becker CE, Tong TG, Boerner U, et al: Diagnosis and treatment of Amanita phalloides-type mushroom poison- ing-Use of thioctic acid. West J Med 125:100-109, Aug 1976 Diagnosis and Treatment of Amanita Phalloides-Type Mushroom Poisoning Use of Thioctic Acid CHARLES E. BECKER, MD; THEODORE G. TONG, PharmD; UDO BOERNER, DSc; ROBERT L. ROE, MD; ROBERT A. T. SCOTT, MD, and MICHAEL B. MacQUARRIE, MD, San Francisco; and FREDERIC BARTTER, MD, Bethesda The number of cases of mushroom poisoning is increasing as a result of the increasing popularity of "wild" mushroom consumption. Amanitin and phal- loidin cytotoxins found in some Amanita and Galerina species produce the most severe and frequent life-threatening symptoms of Amanita phalloides- type poisoning. Delay in onset of symptoms, individual susceptibility variation and lack of rapid and reliable identification have contributed to the significant morbidity and mortality of this type of poisoning. A rapid chromatographic assay for identifying the potent cytotoxins and apparently successful management using thioctic acid of two cases of A. phal- loides-type mushroom poisoning are reported. All known cases of A. phal- loides-type mushroom poisoning treated with thioctic acid in the United States are summarized. THE GATHERING AND EATING of wild mushrooms lieve that poisonous varieties can be identified is a popular pastime in the United States, partly easily2'3 and many have the erroneous notion that owing to increased interest in "organic" foods and some toxic species can be rendered harmless by in the hallucinogenic substances found in certain cooking in a particular manner. As a result, even species. Severe and life-threatening poisonings experienced mushroom seekers have been stricken from the ingestion of wild mushrooms have in- when they harvested and ate poisonous varieties. creased in frequency. Of the 2,000 or so species From 1957 to 1964, 30 deaths from ingestion of mushrooms known to exist, fewer than 50 are of wild mushrooms were reported in the United poisonous to man.' Many mushroom hunters be- States; 11 of these occurred in California.2 From From the Medical Service (Drs. Becker, Tong, Roe, Scott and 1964 to 1974, 57 cases of mushroom poisoning, MacQuarrie), and the Toxicology Laboratory (Dr. Boerner), San Francisco General Hospital, and the 'Department of Medicine, including eight deaths, occurred in California SChool of Medicine (Drs. Becker and Roe), and the Division of alone (Table 1); 18 of the poisonings and four Clinical Pharmacy, School of Pharmacy (Dr. Tong), University of California, San Francisco, and the National Heart and Lung In- of the deaths occurred in 1972. stitute, Bethesda, Maryland (Dr. Bartter). Submitted December 4, 1975. The principal toxins of the most poisonous Reprint requests to: Editorial Office, Room 4101, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, CA 94110. mushrooms are complex proteins containing 100 AUGUST 1976 * 125 * 2 0 "I 19 04 CA0~~~~~~~ > > >> o > >>> >> >;> (L) 4) 4.) ° C) 0 04L C) 4) C)4)4) 0 oj *0 0 to C) 0 cts CO) CO CIO 0 0 0 o aaav 4) - 0-) 0 00 0 .° n Ol O- cl Oco oc- i,9 0) )- -- < u 4), . C', S.c 0 E s 0 C) co. E E 'E E 0 o00 co 0 o o _ o0 o_ 0) a - 4 0_ 0 co 4- 0E 4) 4 Ct.. N t e ' N o ' ' S > 4) - u 0? c Ai ~~~~~~~ > > I > vaG Q (A, C~-. -4 %DC. - V- , ,- "..4 T4 r " o _ w co0 00 0 N Cl4 r4N N N- N N N o 00o 000%oo Nl- C> Ntb 0- t ,en It .o0o C r . 0 '_% C? N- N- C4 t, ;* N e.. e-. e!. e-' *- _.4 e t7 *--i -4 -4 '4 cn en in 00 0 *r r E0 ~~ -- 0 .,4.C)LI 0 E = a0 m~0 4m<<<,<<<<<<C 0 Go go(a o0 Go.45. Go co co E) Ca a °a C's I" c4 -J O4) 0 2;0 ) 0 0 4 F- |O 0 0 0'0 0 0 0 00 0 0 O ^^ fi cow .0 0%00 4s40 'e cd CO O0Z 0 O40 f 00 h OO _4 ~~ ~~~dC C dc 'r0 * 0 0.n% ,4 MUSHROOM POISONING TABLE 2.-Diagnosis of Mushroom Poisoning Toxic Cause Constituents1'"0 Genus and Species Comments Cellular Toxins Amanitins Amanita (Sp. phalloides, Found mostly in wooded areas, frequently during Phalloidins verna, virosa) late summer and fall seasons. No obnoxious taste or smell. Gastrointestinal symptoms occur 6 to 24 hours after ingestion. A transient period of im- provement is followed by metabolic disturbances and renal and hepatic impairment. Most fatalities occur within several days. As little as one third of a single cap can be fatal in a child. Mortality is 40 to 90 percent. These species of Amanita ac- count for nearly 90 percent of all cases of severe mushroom poisoning. Amanitins Galerina (Sp. autumnalis, These species are found in the western and mid- marginata, venenata) western United States on lawns, meadows, and de- caying wood. Symptoms are similar to those of A. phalloides-type poisoning. Despite absence of the phalloidin toxin, the mortality risk from ingestion of these species should be considered as significant as for A. phalloides due to presence of amanitin. Enzyme Toxins Monomethyl- Gyromita (Sp. esculenta) These species (except underwoodii) are not con- hydrazine Helvella (Sp. esculenta, fined to any particular habitat or geographic (Gyromitrin) underwoodii) region. These mushrooms produce symptoms simi- lar to intoxication by amanitin but less severe, appearing 6 to 12 hours or more after ingestion. Symptoms are primarily gastrointestinal. Hemol- ysis and central nervous system effects are asso- ciated with these mushrooms. Certain people are resistant to their effects. Cooking may attenuate toxicity. Estimated mortality is 2 to 4 percent. Neurologic Muscarine Inocybe (Sp. napipes) Toxins produce "muscarinic" effects, e.g. saliva- Toxins Clitocybe (Sp. rivulosa, tion, lacrimation, nausea, bronchospasm, abdomi- trunicola, cerussata, nal pain, vomiting, diarrhea, headache and miosis olearia, dealbata) within 15 to 30 minutes after ingestion. Brady- cardia, hypotension and shock may also occur. Death is infrequent. Treatment is primarily sup- portive and symptomatic. Atropine is a specific antidote for muscarine intoxication. There appear to be species differences because only some have caused death. Isoxazole Amanita (Sp. muscaria, Commonly fouind in wooded areas, especially Derivatives: pantherina, cokeri, crenulata, conifer forests of western United States in spring Muscimol solitaria) and fall. These mushrooms are also known as "fly Muscazone mushroom" or "fly agaric." These species have Ibotenic Acid been associated with the toxin muscarine, but in Pantherin fact contain toxicologically insignificant quantities Tricholomic of it. They produce symptoms resembling the cen- Acid tral nervous system effects of excessive atropine and display anticholinergic and mild hallucinogenic properties. Symptoms occur within 1/4-2 hours after ingestion and frequently resemble alcohol intoxication. Severity and duration of symptoms vary with individual. Muscle spasms can occur after ingestion of large quantities. Prognosis for recovery is good. Avoid use of sedatives; atropine is contraindicated in treatment. Death is rare. Psilocybin Psilocybe (Sp. cubensis, Psychotropic "LSD-like" manifestations begin about Psilocin eaerulescens, silvatica) 30 to 60 minutes after ingestion and may continue Panaeolus (Sp. foenisecii for several hours. Recovery is spontaneous and usually within a day. Treatment is symptomatic. 102 AUGUST 1 976 125 * 2 MUSHROOM POISONING TABLE 2.-Diagnosis of Mushroom Poisoning (Continued) Toxic Cause Constituents'"" Genus and Species Comments Gastrointestinal Not Yet *Boletus (Sp. satanas, eastwoodii) Irritating constituents have not been identified. Irritants Identified Clitocybe (Sp. nuda, illudens) Probably many toxins are involved. Mild to severe Chlorophyllum (Sp. molybdites) nausea, vomiting, diarrhea, abdominal cramps, and Russula (Sp. emetica) other gastrointestinal symptoms occur 1/2 to 2 Tricholoma (Sp. venenatum, hours after ingestion and may persist for several pardinum) hours. The incidence and severity of gastrointesti- Catharellus (Sp. floccosus) nal symptoms are greater with raw mushrooms. Hebeloma (Sp. crystuliniforme) Treatment is supportive, and symptoms usually Lactarius (Sp. torminosus, terminate spontaneously within a short time. Rare glaucescens) fatalities have been reported. Naematoloma (Sp. fasciculare) Rhodophyllus (Sp. sinuatus) Disulfiram-like Monomethyl- Coprinus (Sp. atramentarius) Disulfiram reaction-like symptoms of flushing, Constituents hydrazine palpitation, hyperventilation and tachycardia occur only if alcohol is consumed in combination with these mushrooms. These effects may take place up to 48 hours between ingestion of mushroom and alcohol and last for a short time. Gastrointestinal symptoms of nausea, vomiting, and diarrhea have also occurred. The severity of symptoms is greatest after ingestion of raw mushrooms. Treatment is supportive and alcoholic beverages should be avoided. *These species have been the most frequently associated with gastrointestinal irritants. cyclic heptapeptides (phalloidins) and cyclic though not all species of these genera contain octapeptides (amanitins).4 Phalloidin appears to these toxins (Table 2). In Europe, A. phallqides disrupt hepatic cell membranes and to change the is the most frequent cause of mushroom poison- structure of the hepatic endoplasmic reticulum ing; nearly 90 percent of all such deaths are at- adversely. The role of phalloidin in the produc- tributed to A. phalloides, the "death cap." tion of symptoms and pathologic changes in the In the United States, Amanita verna (the "de- liver of a poisoned patient is unclear because stroying angel"), Amanita virosa and A. phal- some species now known to contain this cyclo- loides are the common causes of mushroom poi- peptide and no amanitin have been consumed soning and death (90 percent). Recent deaths in without causing the undue effects. The toxicity of California have been attributed to A. phalloides. amanitin has been compared in vitro with that of Cases of severe mushroom poisoning by Galerina phalloidin and found to be 10 to 20 times greater.
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