Background
The kingdom Fungi constitutes a huge and overlooked source of agents with extensive health benefits. There is a vast body of evidence indicating that mushrooms demonstrate immunomodulatory, antiviral, antibacterial, antidiabetic, antitumor, antioxidant, and hypocholesterolemic effects [1,2,3,4,5]. But aside from the positive effects, they can also be toxic.
Geopolitical and climate changes that form the background of the current migration crisis [6] unexpectedly also caused the problem of mushroom poisoning in countries where it was not a major problem so far. Due to low socioeconomic level and hunger refugees collect and eat mushrooms, and thus the mushroom poisoning phenomenon is observed more and more frequently [7]. In 2016 Azerbaijan Medical Association Journal published a paper on the death of 6 Syrian asylum seekers after eating poisonous mushrooms specified as Amanita phalloides [8]. Also, a Danish media report from 2017 pertained to the death of two children and hospitalization of nine other family members of the same family, possibly from Congo, after mushroom poisoning caused by an unknown species [9]. At the same time, press reports indicate that the cases of mushroom poisoning in Germany are on the rise since the beginning of the refugee crisis, e.g., five asylum seekers from Eastern Europe received medical treatment after eating Amanita phalloides. The same article mentions that in 2016 30 asylum seekers were hospitalized in one of Hanover’s hospitals after eating death cap mushrooms [10].
Amanita phalloides
The most serious food poisonings are caused by lamellar mushrooms, and the most dangerous of that kind is Amanita phalloides, also known as the death cap; this species has been responsible for up to 90–95% of deaths caused by poisonous mushroom ingestion in Poland [11, 12]. In Europe, this kind of mushroom is often mistaken for edible mushrooms, such as Russula virescens, Tricholoma equestre, or Macrolepiota procera [13], but the problem is worldwide [14,15,16]. While A. phalloides mushrooms can emit an unpleasant odor of cat urine after drying, they are tasty and have a sweet scent when fresh and therefore may not raise any suspicion that they may be dangerous when consumed. Most importantly, thermal processing does not neutralize the toxins present [17].
Children are more likely to demonstrate a severe and often fatal course of poisoning [11, 18,19,20]. A typical example is the event that took place at the end of August 2021, when several Afghan citizens evacuated from Kabul and located in a refugee camp in Poland became poisoned with A. phalloides. Two boys, aged 5 and 6 years, died despite treatment.
Our article presents a case of poisoning with Amanita phalloides in a 28-year-old man and the incorrect medical procedures of the medical emergency unit. It is important for healthcare professionals to be aware of the possibility of mushroom poisoning and its potentially fatal consequences.
Symptoms and mechanism of toxicity
It is believed that a single fruiting body of A. phalloides weighing approximately 50 g may contain a lethal dose for an adult human (about 0.1 mg per kg body weight) [19]. The key toxic agent is α-amanitin, an RNA polymerase II inhibitor [15, 17]. Unfortunately, A. phalloides poisoning is characterized by a delayed onset of symptoms and, hence, an increased risk of complications.
The initial symptoms usually appear within the first 8–24 h of ingestion. The toxin has a great affinity for fast-dividing cells, such as hepatocytes, intestinal villi cells, renal tubular cells, and lymphocytes. The most common symptoms include nausea, vomiting, general weakness, severe abdominal pain, headaches, and watery cholera-like stools [17]. However, it should be noted that these symptoms are not pathognomonic and may also be associated with other disorders. Physical examination of the patient will reveal tenderness in response to palpation of the epigastrium, as well as hepatomegaly. This symptomatic stage may be followed by an apparent improvement, which may last even up to 2 days; however, the symptoms invariably recur and at this point the patient typically seeks medical help. The concentration of liver indicators (transaminases and bilirubin) typically increases 24 h after mushroom ingestion and liver failure is observed after 4 to 5 days [19].
Diagnosis
The diagnosis is based on an in-depth interview of the patient, with particular consideration paid to the time of consumption and the amount of mushrooms ingested, and a urine test to determine the presence of amanitin. Amatoxins are rapidly absorbed in the digestive system. They may be present in the blood for up to 36 h and in the urine for a couple of days. If possible, the leftovers of the mushroom meal consumed, or the vomitus of a sick person should be preserved for mycological examination. However, such analyses may be difficult to perform, especially when only vomitus is available, because mushrooms will be in a changed form. Therefore, genetic testing-based methods are becoming increasingly popular to identify the species [17]. In fatal cases, autopsies usually reveal signs of jaundice, cerebral oedema, subserosal petechiae, pulmonary congestion, liver steatosis, renal congestion with ecchymosis, and hemorrhages in the cortical part.