Poisoning by Amanita phalloides ("deathcap") mushrooms in the Australian Capital Territory
Amanita phalloides ("deathcap") mushrooms are widespread in south-eastern Australia. Seven patients presented to hospital in the Australian Capital Territory with poisoning by this mushroom between 1988 and 1998. Three developed hepatoxicity and one died. Because A. phalloides is becoming more widespread, increased community and medical awareness is needed to reduce the frequency and morbidity of poisoning.
Amanita phalloides mushrooms growing under an oak tree on the western shores of Lake Burley Griffin, Canberra.
MJA 1999; 171: 247-249
Geoffrey M Trim, Heino Lepp, Matthew J Hall, Robin V McKeown, Geoffrey
Geoffrey G Duggin and David G Le Couteur
|Introduction||The "deathcap" mushroom, Amanita phalloides, accounts for most deaths after mushroom ingestion.1,2 There are four clinical phases of poisoning: an initial asymptomatic latent phase, a gastrointestinal phase characterised by watery diarrhoea, a honeymoon period when symptoms temporarily resolve, and a final hepatic phase characterised by hepatic and renal failure. In an adult, death may ensue within 7-10 days of ingestion of a single cap.1,2 We report seven cases of poisoning by A. phalloides mushrooms that occurred in the Australian Capital Territory (ACT) between 1988 and 1998. The only other Australian reports have been from Victoria,3,4 and there is now concern that the mushroom may be becoming more widespread in Australia.|
The seven cases are summarised in the Box. Patients comprised six
adults aged 20-46 years and a seven-year-old child. All patients had
eaten cooked mushrooms that they had picked in gardens or streets of
Canberra, except the child, who had eaten part of a raw mushroom she had
picked in her schoolyard. Three Laotians were poisoned at the
same time when they mistook A. phalloides for the
superficially similar-appearing paddy straw mushroom
(Volvariella volvacea), common in South-East Asia.
The dose ranged from a quarter to eight mushrooms. All patients presented after one to two days with diarrhoea and, in most cases, vomiting, except the child, who vomited within two hours and was brought for medical attention immediately. The diagnosis was made on initial presentation in only this child and the other 1998 patient (Patient 2).
In 1995, a 46-year-old man ate eight mushrooms which he had picked in a
north Canberra suburb. He presented with vomiting and diarrhoea the
next day, but, as he was confident that the mushrooms were not A.
phalloides, he was discharged home after receiving intravenous
rehydration. He presented again two days later with hepatic and renal
Initial investigations revealed the following serum levels: alanine aminotransferase (ALT) > 10 000 U/L (reference range [RR], 5-55 U/L); bilirubin, 114 µmol/L (RR, 3-20 µmol/L); creatinine, 535 µmol/L (RR, 40-90 µmol/L); and prothrombin time - international normalised ratio (PT-INR) > 10. A mycologist identified A. phalloides growing in the street where the patient had picked the mushrooms and also identified the mushroom stalks that he had discarded in a rubbish bin.
The patient was transferred to a liver transplant unit but died from hepatic failure six days after mushroom ingestion. Postmortem examination of his liver revealed complete necrosis of parenchyma, with one residual island of intensely vacuolated hepatocytes with severe intracanalicular biliary stasis. No viable hepatocytes were seen.
In 1998, a 39-year-old man ate three mushrooms picked from his back
garden in an inner Canberra suburb. The mushrooms were cooked
as a pasta sauce. He had been previously well but had been taking
griseofulvin for six months to treat a fungal toenail infection.
Eighteen hours after ingestion, he developed watery diarrhoea. He
presented to hospital with dehydration and epigastric discomfort 36
hours after ingestion.
Initial investigations revealed the following serum levels: ALT, 914 U/L; bilirubin, 24 µmol/L; and creatinine, 102 µmol/L. He had evidence of metabolic acidosis, with pH of 7.30 (RR, 7.34-7.44) and bicarbonate level of 18.6 mmol/L (RR, 22-26 mmol/L). The mushrooms were identified as A. phalloides by a mycologist.
The patient was transferred to a liver transplant unit and treated with intravenous fluids, high dose penicillin and N-acetylcysteine. Three days after mushroom ingestion, his serum ALT level peaked at 8199 U/L, and PT-INR at 4.7, but he did not develop encephalopathy. He subsequently made an uneventful recovery.
Our seven patients poisoned by A. phalloides mushrooms in the
ACT is the only series reported in Australia. In five of our seven
patients, the diagnosis was not made on initial presentation, and in
one it was not suspected at all, despite a history of mushroom
ingestion and characteristic clinical picture. Three patients
developed significant hepatic dysfunction, two were transferred to
a liver transplant unit and one died. There have been only two other
reports of poisoning by A. phalloides mushrooms in
Australia,3,4 both in Victoria. Neither
case was diagnosed on initial presentation, and one was
A. phalloides is a mycorrhizal fungus (ie, it grows in a symbiotic association with the roots of trees, primarily oak trees). It produces a range of toxins (amatoxins). The major toxin, a cyclic peptide, amanitin, inhibits RNA polymerase II and is not inactivated by cooking, freezing or drying. The lethal dose is about 0.1 mg/kg, which may be contained in as little as one mushroom.5 Amanitin is usually cleared rapidly, mainly by renal excretion.6
Recommended treatment of A. phalloides poisoning includes vigorous gastrointestinal decontamination.7 Early and aggressive decontamination may have prevented toxicity in the seven-year-old child. Supportive care, including intravenous rehydration, is thought responsible for most of the improvement in mortality, from well over 50% early this century to 20%-30% in recent decades.1 Many specific antidotes have been used, although no prospective-trial evidence is available. Retrospective clinical studies and animal studies support the use of high dose penicillin (0.5-1 million units/kg per day) and parenteral silibinin, an extract of milk thistle available only in Europe. Both are thought to act by inhibiting amatoxin uptake into hepatocytes and by interfering with its enterohepatic circulation.1,7 Cimetidine, a hepatic enzyme inhibitor, may be harmful.8 We speculate that, in Patient 1, long-term use of griseofulvin (a hepatic enzyme inducer) before poisoning may have increased the rate of detoxification of amatoxin and thereby contributed to survival. Liver transplantation may be used in cases that fail to respond to more conservative measures. It has been performed successfully for this indication in the United States since 1985,9 but has not been attempted for this indication in Australia.
A. phalloides mushrooms have been described in many regions of south-eastern Australia. Collections have been made in several Melbourne suburbs,4,10,11 and the Victorian country centres of Riddells Creek, Morwell and Walhalla.11 The National Herbarium of Victoria and the State Herbarium in Adelaide hold collections of A. phalloides or very similar species from New South Wales, Tasmania and Victoria. A. phalloides mushrooms were first reported in Canberra in 19614 and are now widespread in the ACT.
Although A. phalloides is found primarily in association with oak trees, there is concern among mycologists and toxicologists that it may develop the ability to grow in association with other trees, particularly Australian natives, and thereby spread dramatically. Associations between Eucalyptus spp. and Amanita spp. other than A. phalloides have been reported in other countries,12 and between Eucalyptus spp. and A. phalloides itself in Africa.13,14 There is anecdotal evidence of A. phalloides forming mycorrhizae with Eucalyptus spp. in Canberra (Richard Windsor, consultant botanist, Canberra, ACT, personal communication).
A. phalloides is not the only mushroom to contain amatoxins. In the northern hemisphere, these toxins are found in other Amanita species and in species within the genera Conocybe, Galerina and Lepiota,1 which also occur in Australia. Four cases of Lepiota helviola poisoning have been reported from Adelaide. In each, hepatotoxicity occurred and amatoxins were identified.4,15
A. phalloides is now widely distributed in south-eastern Australia, and may become more widespread if it develops the ability to grow in association with eucalyptus trees. Increased community and clinician awareness is needed to reduce the incidence of poisoning and to improve outcomes. Wild mushrooms should not be eaten unless definitely identified as non-poisonous. Clinicians should consider A. phalloides poisoning in patients with vomiting, diarrhoea or abnormal liver function.
|We thank Graham Bell (State Herbarium, Adelaide) and Tom May (National Herbarium of Victoria) for information about Amanita phalloides collections in their herbaria, and Richard Windsor (Canberra, ACT) for his comments about A. phalloides and Eucalyptus spp. in Canberra.|
(Received 11 Feb, accepted 24 Jun, 1999)
Canberra Hospital, Canberra, ACT.
Geoffrey M Trim, MB BS, Clinical Pharmacology Registrar;
Robin V McKeown, PhC, Poisons Information Service;
David G Le Couteur, FRACP, PhD, Associate Professor, The Canberra Clinical School of the University of Sydney.
Australian National Herbarium, Centre for Plant Biodiversity
Research, Canberra, ACT.
Royal Prince Alfred Hospital, Sydney, NSW.
Reprints will not be available from the authors.
|Amanita phalloides mushrooms at different stages of the lifecycle. A mature "deathcap" typically has a greenish-brown to white cap, white gills on the underside of the cap, a white frill-like ring on a white to pale yellow-green stem, and a white underground cup. The deathcap may be mistaken by those unfamiliar with fungi for mushrooms of the genus Agaricus, the type most commonly grown for consumption. The deathcap also superficially resembles the edible paddy straw mushroom (Volvariella volvacea).|
|Seven cases of poisoning by Amanita phalloides in the Australian Capital Territory, 1988-1998|
|Year||Age (years) sex||Mushrooms ingested (identified*)||Symptoms||Results of liver function tests||Treatment||Outcome|
|1988||20, M†||Several (yes)||Diarrhoea after 1-2 days||Normal||Nil||Recovered|
|20, M†||Several (yes)||Diarrhoea after 1-2 days||Normal||Nil||Recovered|
|20, F†||Several (yes)||Diarrhoea, vomiting after 1-2 days||Normal||Intravenous fluids||Recovered|
|1995||46, M‡||8 (yes)||Diarrhoea, vomiting after 1-2 days||ALT > 10 000 U/L; PT-INR > 10; creatinine 535 µmol/L||Transferred to transplant unit, intravenous fluids, high dose penicillin, N-acetylcysteine||Died|
|1997||45, M||Several (no)||Diarrhoea, vomiting after 2 days||ALT, 2938 U/L; PT, 19 s; creatinine, 216 µmol/L||Intravenous fluids||Recovered|
|1998||39, M§||3 (yes)||Vomiting, diarrhoea after 1-2 days||ALT, 8199 U/L; PT-INR, 4.7||Transferred to transplant unit, intravenous fluids, high dose penicillin, N-acetylcysteine||Recovered|
|7, F||1/4 (yes)||Vomiting within 2 hours||Normal||Intravenous fluids, whole bowel irrigation, multiple dose activated charcoal, high dose penicillin||Recovered|
|ALT = serum alanine aminotransferase level (reference range [RR], 5-55 U/L). PT-INR = prothrombin time, international normalised ratio. PT = prothrombin time (RR, 8-14 s). Creatinine = serum creatinine level (RR, 40-90 µmol/L). * Identity confirmed by a mycologist. † These three people from Laos were poisoned at the same time when they ate mushrooms picked from a Canberra street. ‡ Patient 1. § Patient 2.|
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