Ingestion of mushrooms from the genus Amanita can present detrimental consequences to the human body. The mushroom is frequently found in the coastal Pacific Northwest, Pennsylvania, New Jersey, and Ohio. Amanitin, one of the two distinct toxins isolated from the Amanita mushroom, is responsible for the majority of symptoms and signs seen with mushroom poisoning. Clinically, ingestion of these mushrooms can result in a wide range of clinical symptoms including nausea, vomiting, crampy abdominal pain, and diarrhea. There have been several case reports of patients who developed severe hepatic failure that required liver transplantation. Thus, it is important to recognize the symptoms early and treat the patients with the available agents including multidose activated charcoal, N-acetylcysteine, penicillin G, and Silybum. Through an extensive literature search, we found no published literature on amatoxin poisoning in the state of Texas. With new cases of amatoxin poisoning emerging in the state, it is important for healthcare providers and workers to have a better awareness and early recognition of the detrimental effects of Amanita species poisoning and to be educated to provide the proper care for this group of patients.
We present a woman with acute onset of bilateral ophthalmoparesis and ataxia occurring 4 weeks after gastroenteritis. Serum antibody titers against asialo-GM1 and GD1a, typically associated with inflammatory axonal neuropathies, were elevated but titers against anti-GQ1b, the most commonly found antibody found in the Miller Fisher variant of Guillain-Barre syndrome were not. No other etiology for ophthalmoparesis was found despite extensive patient evaluation. Intravenous immunoglobulin was administered, and the patient gradually improved over subsequent months. This case is unique for its antiganglioside antibody profile associated with Miller Fisher syndrome.
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