To the Editor:
Wild mushroom poisonings are frequently reported all around the world. Although the majority of mushroom intoxications are benign, some result in significant toxicity, such as the phalloides syndrome, which can induce life-threatening situations. The most frequent species implicated in the origin of phalloides syndrome belong to the Amanita genus: Amanita phalloides, Amanita verna, and Amanita virosa. However, it is possible to observe such a poisoning with other species like taxa from the Galerina or Lepiota genus. 1 We report a collective case of poisoning after consumption of Lepiota brunneoincarnata (Figure 1), identified by mycologists of the Marseille Poison Control Center, in southeastern France.

Lepiota brunneoincarnata, a hepatotoxic mushroom, picked and eaten by the patients in this report. They are small cream-colored mushrooms with free white lamellae and a cap covered with brown scales.
After a heavy rainfall in November 2011, a patch of brown mushrooms sprouted in the countryside near the city of Salon-de-Provence. Mistaking these mushrooms for a well-known edible local species (Tricholoma terreum, Figure 2), a mother and 2 children picked a basketful of only one type of mushrooms that they cooked and ate for dinner in the evening. After specific questioning, the mother reported that the mushrooms were delicious and stated that she consumed most of them while her 8-year-old son ate a smaller portion and her 11-year-old daughter only tasted a bite. The next morning, approximately 9 hours after the meal, all 3 family members presented to the local emergency department with stomach cramps and vomiting. Laboratory findings were normal, and the diagnosis of the physicians on duty was common gastroenteritis despite the foraged mushroom meal described to the medical team. They were discharged from the hospital with a prescription for antiemetic and spasmolytic agents and instructions to return if symptoms persisted more than 48 hours. On the second day after ingestion, the mother and the daughter felt better, but the son's conditions worsened with asthenia, fever, abdominal pain, persistent vomiting, and watery diarrhea. On the fourth day, the persistence of symptoms and the occurrence of rectal bleeding led them to consult the pediatric emergency department for the boy. On admission, he was somnolent and confused owing to the intense dehydration that was demonstrated clinically by a dry skin. Blood chemistry values demonstrated major liver failure with elevated transaminase levels (aspartate transaminase, 1018 UI/L; alanine transaminase, 3205 UI/L) and a clotting disturbance (prothrombin time, 18 seconds [normal values, 10–14 seconds]). The findings of the 2 other family members also demonstrated a transient minor liver impairment. In the intensive care unit, all patients received the same treatment using activated charcoal (0.5 g/kg every 4 hours for 12 hours), penicillin G (0.1 MUI/kg × 6/day for 12 hours), silibinin (5 mg/kg × 4/day for 24 hours), and N-acetylcysteine (intravenous loading dose of 150 mg/kg, followed by 50 mg/kg every 4 hours for 12 hours). All family members were discharged home on the eleventh day after ingestion, without complications.

Tricholoma terreum, an edible mushroom. They are small gray mushrooms with a cap covered in fine gray scales and close white lamellae.
This collective poisoning shows that wild mushroom picking could cause severe poisoning. The clinical features of this poisoning vary according to several factors, related to the species and the quantity ingested. Potentially fatal hepatotoxicity in a male adult could be induced by 30 to 50 g of A phalloides and at least of 100 g of L brunneoincarnata [2]. The lower quantity of α-amanitins in the brown Lepiota species could explain the favorable outcome of our patients. However, some deaths, including in pediatric cases, after consumption of Lepiota species have been reported in the medical literature.3,4 Moreover, in a mushroom-poisoned patient, other factors are important such as personal tolerance, body weight, and general health. However, the intensive reaction of the young boy could be explained by the relatively large amount of mushroom eaten and a small body weight (30 kg).
It is important to recognize that onset of digestive symptoms at more than 6 hours after ingestion is a characteristic feature of a potentially toxic mushroom such as phalloides. In this collective poisoning, the real diagnosis was delayed, and this could produce a life-threatening situation implicated by a late treatment of cytolytic hepatitis. Normally, management of phalloides poisoning consists mainly of symptomatic treatment to correct electrolyte imbalances, hemodynamic disturbances, and coagulation changes. In early-stage poisoning, gastric lavage and activated charcoal could be used to clear the toxins from the stomach. No antidote with proven efficacy for treatment of phalloides poisoning is available, but 3 major products have been described as useful at the choleriform stage. 2 ,3,5 Penicillin G may have a preventive effect by inhibiting α-amanitin uptake by hepatocytes. Silibinin has been recommended as a hepatoprotector and a glutathione precursor. N-acetylcysteine can restore redox capacity and may protect the liver. Liver transplantation or albumin liver dialysis, eg, molecular adsorbents recirculation system (MARS) therapy, may be proposed as a last resort. 3
