PHALLOID SYNDROME
It is caused by the spontaneous flora fungi ingestion. For 80% of the poisonings leading to death the responsible fungus was : AMANITA PHALLOIDES and for the remaining cases the fungi responsible were: AMANITA VERNA (for approximately 15%) , AMANITA VIROSA(5% of the cases) .(Victor a Voicu 1999) . The evolution of the poisonings depends on the immune system reaction. If a person whose immune system is sensitive to Ammanita Virosa poisoning, is affected by the Amanita Phalloides intoxication, it will be a less severe form of poisoning.
There also exists the para-phalloid syndrome with similar manifestations, which is caused by a series of Lepiota fungi ( L. Helveolla , L. Bruneoincarnata , L. Subincarnata ) and Galerina species ( G. Tumnalis , G. Venenata , G. Marginata )
The clinical manifestations of the phalloid can be broken down into three stages just like the clinical symptoms of the HIV-AIDS virus infection Latent phase: with no important clinical signs and duration of 6-40 hours, the main symptoms being psychological and not physical.
The aggressive phase: starts after 2 -5 days, and the patients have the signs and symptoms of a severe gastroenteritis with sudden beginning; they vomit frequently and abundantly, have nausea and total gastric intolerance. Diarrhea begins to manifest itself after a few hours from the digestive signs debut; the feces are aqueous, fetid, abundant, with mucus, and sometimes hemorrhagic. Approximately 70 % of the poisoned patients have abdominal pains, which can be of two kinds: either as cramps or as severe epigastric burns, excessive vomiting, or colic type pains. The digestive disorders take place during the first 12-24 hours, including a total dehydration (asthenia, adynamia, intense thirst, arterial hypotension, tachycardia and finally a state of shock with anuria). Muscular cramps, mainly in the shanks can be observed. Successively hyperthermia accompanied by extra and intra-cellular dehydration signs appears.
Parenchymatous phase: in which intensify or reappear some digestive signs less specific like anorexia, nausea, vomiting, intense asthenia. The clinical examination shows a discrete hepatomegaly, generally painful, sub-jaundice or a general jaundice. The acute toxic hepatitis appears in the severe types of poisoning and in nearly 50% of the cases. The biologic hepatic cytolysis syndrome is caused (Sicot and collaborators 1970); the increase of the seric transaminases and of bilirubin, hepatic and coagulation functions alterations. The hepatocellular deficiency syndrome is of major importance because it is the one which conditions the poisoning evolution. The hepatic lesions that cause it consist in the central lobe steatosis, which in the lethal cases affect the entire hepatic lobe. Their evolution is either complete cure or massive hepatic cytolysis followed by death. There were not any cases of fibrose transformation or hepatic cirrhosis. In some cases the frequent symptoms are acute tubular nephritis with benign evolution which can be cured rapidly in a few days, (the blood urea concentration decreases and the urinary urea concentration increases rapidly). The kidney lesions come in second after the hypovolaemia and arterial hypotension.
