Three people are dead and one is in a critical condition in a Melbourne hospital from suspected mushroom poisoning after eating a beef wellington pie in the Victorian town of Leongatha.
Police have said their symptoms were consistent with having eaten death cap mushrooms, although the official cause of death has not yet been confirmed.
The death cap, Amanita phalloides, is responsible for about 90% of mushroom-related deaths globally. It can be mistaken for edible mushroom varieties such as the field mushroom or the straw mushroom.
“It’s quite upright, it’s very bright white … it’s eye-catching,” says Dr Michael Taylor, a mycology expert at Flinders University.
The cap of a typical Amanita phalloides mushroom may measure about 10cm across, Taylor says. “Half of that would be toxic, probably enough to kill a person. That might be, once it’s cooked down, a mouthful – maybe two or three mouthfuls of actual mushroom … at absolute most.”
The toxicity of individual mushrooms may vary depending on geographical location, Taylor says. Death caps are not native to Australia and are usually only found in Victoria and the Australian Capital Territory.
What are the effects of eating a death cap mushroom?
“Death cap mushrooms contain three broad classes of toxins: the amatoxins, the phallotoxins and the virotoxins,” says Dr Ian Musgrave, a molecular pharmacologist at the University of Adelaide.
The most toxic of these is an amatoxin known as α-Amanitin. Amatoxins inhibit an enzyme called RNA polymerase II, preventing cells from carrying out essential functions such as creating proteins. The toxin cannot be destroyed by cooking or drying.
Once a death cap is eaten, people are often asymptomatic for several hours before its effects become apparent. Nausea, diarrhoea and other symptoms of gastrointestinal upset develop from about six to 12 hours after ingestion, though this may occur sooner if a high dose is ingested, Taylor says.
The primary site of α-Amanitin toxicity is the liver, where it first travels after being absorbed from the lining of gastrointestinal tract. “It’ll stop the liver functioning and then after a period of time, the liver will die,” Taylor says.
The toxin has the same effect on all the cells it interacts with.
“Quite often you have … a period of remission in which you stop being immediately sick, the nausea calms down, you start feeling pretty well again,” Taylor says. “Then you hit that 24-hour-plus mark if you’ve had a relatively low dose. That’s when you start to get the secondary toxic effects … the liver and other organs start to shut down.”
Within one to seven days of ingestion, the death cap can result in liver failure, kidney failure, encephalopathy and death.
How is death cap poisoning treated?
Antidotes to α-Amanitin are “mostly not very good”, Musgrave says. “The binding of the amatoxin to its target is largely irreversible – it’s very hard to get around it.”
A compound called silibinin can be used to treat death cap poisoning. It works by competitively binding to the same receptors in the liver that α-Amanitin binds to.
But it is only effective if administered before the toxin starts to irreversibly bind to cells – which may be before a person begins to show symptoms, depending on the dose.
“The quicker that you are administered it, the far better is the prognosis,” Taylor says. “Some people have … had silibinin and it’s reduced the degree of organ damage.”
People treated with death cap poisoning in hospital may also be given supportive care in the form of intravenous fluids and activated charcoal. In the case of liver failure, and if a patient is well enough, they may receive a liver transplant.
Scientists announced in May that they had identified a potential antidote to the death cap toxin. Researchers identified that indocyanine green, a medical imaging dye, appeared to block the toxic effects of α-Amanitin. The research has not been tested in humans yet.
Indocyanine green appears to work in a similar way to silibinin, Taylor says. He suggests there has been limited research investment into antidotes for death cap toxins because the of the relatively small number of poisonings globally.
“I can’t imagine that a drug company would ever put enormous amounts of time and energy into [developing one], because it may only be used 50 … or 100 times a year.”
