Toxicon 47 (2006) 605–607 www.elsevier.com/locate/toxicon
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Panther cap Amanita pantherina poisoning case report and review Leszek Satora *, Dorota Pach, Krzysztof Ciszowski, Lidia Winnik Department of Clinical Toxicology, Poison Information Center, Collegium Medicum, Jagiellonian University, Os. Złotej Jesieni 1, 31-826 Krako´w, Poland Received 28 October 2005; accepted 6 January 2006 Available online 24 March 2006
Abstract An analysis of patients with mushroom poisoning hospitalized in the Clinic of Toxicology in Cracow revealed that only a small percentage of cases had been caused by the death cap Amanita phalloides (Vaill. ex Fr.) Secr. The most important factors contributing to intoxication are confusion of toxic mushrooms with edible species, and non-specific mushroom poisoning. The genus Amanita has a global distribution and is one of the most well-known genera of macrofungi. Active toxins present in the panther cap (A. pantherina) (DC ex Fr.) Secr are ibotenic acid and muscimol, which are rapidly absorbed from the gastrointestinal tract. It is likely that other substances also participate in the psychotropic effects. Five frayed panther cap fruiting bodies were eaten by mistake by two persons (27 and 47 years of age). Symptoms onset occurred after 120 min with central nervous system (CNS) depression, ataxia, waxing and waning obtundation, religious hallucinations and hyperkinetic behaviour. In the present case, successful general symptomatic treatment was administered, which consisted of controlling the nervous symptoms and stabilizing the electrolyte balance. The poisoning regressed with no organ complications. q 2006 Elsevier Ltd. All rights reserved. Keywords: Amanita pantherina; Panther cap; Mushroom poisoning
1. Introduction Mushroom poisoning in Poland is common, especially in summer and autumn and is associated with traditional wildmushroom picking and cookery. An analysis of patients with mushroom poisoning hospitalized at the Clinic of Toxicology in Cracow revealed that only a small percentage of cases had been caused by the death cap (Satora, 2004). The most important factors contributing to intoxication are confusion of toxic mushrooms with edible species, as considerable experience is required to differentiate these, and the recently emerging but widespread practice of deliberate use of hallucinogenic mushrooms for ‘recreational purposes’. The psychotropic properties of Amanita pantherina (panther cap) and A. muscaria (L. ex Fr.) Hooker (fly agaric) have been known since ancient times. The use of * Corresponding author. Tel./fax: C48 12 6468905. E-mail address:
[email protected] (L. Satora).
0041-0101/$ - see front matter q 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.toxicon.2006.01.008
the panther cap and the fly agaric is connected with mysticism (Michelot and Melendez-Howell, 2003). A. pantherina is commonly found in coniferous forests throughout Poland from July to October. The panther cap grows in deciduous woods, especially beech and birch woods, as well as coniferous woods. The cap of A. pantherina has a diameter of 5–10 cm and is grey or grey brown, grey yellow, paling when old, with small pure white flakes. In Poland, in some accidental poisoning cases, this species has been mistaken for the edible A. rubescens (Pers. ex Fr.) Gray, A. spissa (Fr.) P. Kumm. and Macrolepiota procera (Scop. ex Fr.) Sng. Colour is not a reliable characteristic for identification because it varies with weather, soil condition, age and other factors.
2. Case study 47-year-old mother and 27-year old daughter ate five fried mushroom caps thinking that they were eating parasol
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mushrooms M. procera. Approximately 2 h after ingestion, the patients had nausea, stomach ache and diarrhoea and vomited several times. Initially, the mother was conscious, intermittently anxious and maintained verbal contact, and had efficient respiration, blood pressure (BP) of 150/90 mmHg and heart rate (HR) of 100 beats per minute (bpm). Within around 30 min restlessness, moria and increased psychomotor drive were observed. The patient was agitated, maintained logical verbal contact with maintained criticism, talked incessantly, and reported mystical experiences. In the physical examination on admission to the hospital showed respiration, a transient increase of BP to 170/100 mmHg, regular HR of 80 bpm, mildly dilated and properly light-responsive pupils. The patient complained of cramping pains in the epigastric region of the abdomen, vertigo and paraesthesias of the left arm. The patients condition worsened 2–3 h after admission to the hospital, and she became more anxious, intermittently without logical verbal contact, but with maintained visual contact. Her speech was intermittent, with stammering and perseverations, her breathing was shallow and she gasped for breath, and complained of a heavy feeling in her chest. The patient remained hospitalized for several days and was conscious, maintained full logical contact, was fully aware, and had sharpened perceptions and reactions to external stimuli. Her mood was changeable, switching from extreme merriment to crying. She complained of difficulties with her perception of her own body and inability to speak properly. She had paroxysmal stuttering and her speech was quite clear, but intermittent and fast. The patient was mildly hyperreactive, but did not have significant problems with motor coordination. The 27-year-old daughter of the abovedescribed patient was conscious on the spot, maintained logical verbal contact and had efficient respiration, BP of 140/80 mmHg and HR of 96 bpm. She complained of dizziness, anxiety, nausea, and humming and throbbing in her head. On admission to the Toxicological Department she was conscious, unwell, and her perceptions were not impaired, but she continued to complain of nausea and a feeling of ‘waving’ inside her body. The patient was treated with activated charcoal with laxatives. Symptomatic treatment was also administered, i.e. i.v. infusions, electrolytes supplementation and a light diet. The treatment resulted in improvements in her state of consciousness and the general physical and mental state of both patients improved. All symptoms disappeared after about 6 h. Mushrooms were identified from complete specimens and mycological analysis (vomited matter). Urine samples were collected 3 h after mushroom ingestion and were analysed for THC, amphetamine, opiates and amanitin. The results were negative. Additional laboratory tests revealed only hyperbilirubinaemia (50.8 mmol/l) and mildly elevated levels of aminotransferases (54 U/l and ALT 66 U/l) in the younger patient, which were present before the mushroom poisoning. After the several days’ hospitalization, both patients were discharged from the hospital in a normal
clinical state. Throughout the hospitalization period, any disturbances of the consciousness were observed.
3. Discussion From a clinical and diagnostic perspective in humans, toxic mushrooms are grouped by Lampe (1978) according to the six main syndromes encountered: 1. A diverse group usually responsible for transient gastrointestinal irritation, associated with a variety of toxins. 2. The Amanita phalloides group, containing cyclic polypeptides, responsible for the most serious and often fatal intoxication: delayed, irreversible cytotoxicity predominantly affecting the liver and kidney. 3. The Gyromitra group, containing methylhydrazine derivatives and causing similar but less severe cytotoxicity. 4. A group muscarine-related symptoms such as salivation and increased gastrointestinal motility. 5. A group that causes sensitivity to alcohol by inhibition of acetaldehyde dehydrogenase. 6. The hallucinogenic mushrooms. This category can be subdivided into the Psilocybe group, causing a hallucinogenic syndrome, and a group causing delirium associated with sleep or coma. Both A. pantherina and A. muscaria fall into the latter group. An important diagnostic factor is the interval between the ingestion of the food and the occurrence of symptoms in the gastrointestinal tract. If these begin after between 30 min and approximately 4 h, it usually indicates poisoning by mushrooms that do not cause damage to the organs. It should be remembered, however, that there may also have been very dangerous or even mushrooms in the food, which have a delayed effect (Satora, 2004). Hallucinogenic substances are found in mushrooms commonly gathered in the Central and North Europe. Common Amanitas include A. phalloides (Death Cap or the Green Death Cap), A. citrina (Schaeff.) Pers. (False Death Cap), A. regalis (Fr.) Sacc., A. verna (Bull. ex Fr.) Pers. (Destroying Angel) and three species that can be considered as edible: A. caesarea (Scop. ex Fr.) Sacc. (Cesar’s Mushroom), A. rubescens and A. spissa (Bonnet and Basson, 2002). The name Amanita is derived from the Greek meaning ‘a king of fungus’. The panther cap and the fly agaric contain the toxins ibotenic acid and muscimol (isoxazoles). Muscimol and ibotenic acid seem to cross the blood–brain barrier via an active transport system and exert their effects primarily on the CNS, where they act as neurotransmitter agonists (Satora et al., 2005; Michelot and Melendez-Howell, 2003). Ibotenic acid (pantherin, agarin) is readily soluble in cold water, mimics the excitatory amino acid glutamic acid and acts most strongly at N-methyl-D-aspartic acid (NMDA)
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receptors. Muscimol is a potent agonist of GABA-A receptors and exerts pronounced CNS effects similar to those produced by therapeutic doses of diazepam. In small doses muscimol decreases motor activity and in large doses, caused ataxia (Michelot and Melendez-Howell, 2003). The lethal dose of muscimol is estimated to be about 12 mg. Ibotenic acid and muscimol, together with their metabolites, appear to be responsible for the symptoms of this poisoning: nausea, hallucinations, delirium, muscular spasm and sleep. The levels of muscimol detected in the samples were of 0.19% d.w. A. muscaria and 0.3% d.w. A. pantherina (Michelot and Melendez-Howell, 2003). Both ibotenic acid and muscimol are found in human urine 1 h after consumptions. Glutamic acid is a major excitatory neurotransmitter in mammalian CNS and its receptors are implicated in neurological disorders such as Huntington’s disease and epilepsy. Inhibitory glutamate receptors (IgluRs) constitute a class of ion channel proteins equivalent to glycine and GABA receptors. Ibotenic acid acts on IgluRs (Cleland, 1996). Another compounds reported in A. pantherina and A. muscaria is muscazone which exhibits minor pharmacological activities compared with the substances mentioned above. Muscazone induces effects on the CNS, but with a longer latency period: these include confusion, somnolence, and nervousness (Michelot and Melendez-Howell, 2003). Other active components reported in the panther cap are (2R), (1R)-2-amino-3-(1,2-dicarboxyethylthio) propanoic acid and (2R), (1S)-2-amino-3-(1,2dicarboxyethylthio) propanoic acid. These are antagonists of NMDA receptors KI-II-A and KI-II-B, respectively (Michelot and Melendez-Howell, 2003). The panther cap contains additional compounds, such as stizolobic and stizolobinic acid, which exhibit an excitatory action an isolated rat spinal cord (Michelot and Melendez-Howell, 2003). There are regional differences in the toxin concentration of mushrooms of the same species and local ecological factors may play an important role. In spring and summer mushrooms may contain up to 10 times as much ibotenic acid/muscimol compared to autumn fruitings (Benjamin, 1992). The effects of the panther cap have a short latency period. Cooking does not notably lower toxicity. Clinical symptoms have been reported in humans
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30 min to 2 h after ingestion of A. pantherina. In most cases, one cap is sufficient to cause psychotropic effects. The poisoning syndrome due to the panther cap and fly agaric has been called ‘mycoatropinic’, but tropanic alkaloids are not present (Michelot and Melendez-Howell, 2003). The first manifestation is usually CNS depression with lethargy, progressive obtundation and ataxia. A deep sleep ends the poisoning, which generally lasts 8 h (Benjamin, 1992; Davis and Williams, 1999). First aid consists of eliminating the toxic substances from the gastrointestinal tract, or administering activated charcoal and purging. Physostigmine has been recommended as it counteracts the effects of poisoning by atropine and related antimuscarinic drugs (Michelot and Melendez-Howell, 2003). In the present case, successful general symptomatic treatment was administered, which consisted of controlling the nervous symptoms and stabilizing the electrolyte balance.
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