Les atroces souffrances infligées par "le flamboyant " (カエンタケ 症状)

Podostroma cornu-damae (Pat.) Hongo & Izawa 1994

Kaen-také, Cornes de daim rutilantes, Champignon flamboyant (カエンタケ)

Hommage à Masana IZAWA 伊沢正名 先生
et Shinnosuké MIYAUCHI

Champignon très dangereux, même à la manipulation (brûlures et desquamation!), mortel si ingéré, le Kaen-také ("champignon flamboyant") emblème des Samouraïs par sa forme de Kabuto et sa couleur de feu, continue de nos de jours de défier les matchos qui le consomment par bravade, comme ce fut le cas en 1999 à Niigata : cinq adultes se sont partagés un morceau de 3 cm macéré dans l'eau de vie : l'un deux décède dans d'horribles souffrances deux jours après avoir consommé environ un gramme du champignon. L'année suivante un ramasseur de champignon décède également dans le département de Gunma, après avoir consommé un carpophore du champignon frit.

Au Japon, l'Atlas de Materia Medica datant de l'ère Bunsei (1818 -1829) mentionne déjà le "poison foudroyant" du Kaen-také, en donnant la description d'une intoxication mortelle. La dose létale est extrêmement faible, seulement 3 g (poids frais des fructifications). Ont été rapportés 6 cas d'empoisonnement au Japon dont 3 décès.

Kabuto, casque de guerrier japonais

Le kabuto correspond au "casque". Il fait parti intégrante de l'équipement des ("Sujikabuto", " Mononari", " Boshi Kabuto ", " Kawari Kabuto "... guerriers japonais. Les premiers casques ont été largement influencés par les modes et techniques de l'empire chinois tout proche. La kabuto est un bon indicateur de la société japonaise au travers les âges.

――058――

妖怪名：【振袖火焔】フリソデカエン
モデルになったきのこ：【カエンタケ】 ニクザキン目ニクザキン科

きのこ妖怪の森
http://blog.livedoor.jp

 

Ne pas toucher ! Non, ce n'est pas un Dildoo...

Les symptômes apparaissent en peu de temps, environ 10 minutes après l'ingestion.

• Les premiers symptômes sont digestifs, avec des douleurs abdominales, vomissements et diarrhée.
• Puis des paresthésies, engourdissement des membres, étourdissements, difficultés respiratoires et déficience des globules blancs et plaquettes avec échec de la fonction hématopoïétique, ulcérations dermiques dans tout l'organisme, insuffisance hépatique, insuffisance rénale et insuffisance respiratoire, taux de létalité élevé.
• Les séquelles des survivants consistent en l'atrophie du cervelet et de la langue, troubles du mouvement ou perte de cheveux et desquamation de la peau.

文 政年間（1818 - 1829年）の植物図鑑『本草図譜』に「大毒ありといへり」との記述があることから、古くから中毒・死亡事故が発生していたという。致死量はわずか 3g（子実体の生重量）程度ときわめて強力である。日本では6例ほどの中毒事例が報告され、計10名の中毒患者が出ており、そのうち2名は死亡している。

摂取後10分前後の短時間で症状が現れる。初期には消化器系の症状が強く、腹痛・嘔吐・水様性下痢を呈する。その後、めまい・手足のしびれ・呼吸困難・言語障害・白血球と血小板の減少および造血機能障害・全身の皮膚のびらん・肝不全・腎不全・呼吸器不全といった多彩な症状が現れ、致死率も高い。また回復しても、小脳の萎縮・言語障害・運動障害、あるいは脱毛や皮膚の剥落などの後遺症が残ることがある。
毒成分 [編集]

マイコトキシンとして知られているトリコテセン類（ロリジンE、ベルカリンJ（ムコノマイシンB）、サトラトキシンHおよびそのエステル類の計6種類）が検出されている。これらの成分には皮膚刺激性もあるため、手にとって観察するだけでも皮膚炎を起こす可能性がある。

Podostroma cornu-damae (Japanese : Kaen-také カエンタケ "fire fungus") is a species of fungus in the Hypocreaceae family.

The fruit bodies of the fungus are highly toxic, and have been responsible for several fatalities in Japan. The fungus contains several trichothecene mycotoxins.

Taxonomy: The species was originally described as Hypocrea cornu-damae by the French mycologist Narcisse Théophile Patouillard in 1895, and later transferred to the genus Podocrea in 1905 by the Italian botanist and mycologist Pier Andrea Saccardo.

In 1994, the Japanese mycologist Tsuguo Hongo placed the species in the genus Podostroma.

Description: The conidiophores (specialised fungal hyphae that produce conidia) are up to 400 μm high and about 2–4 μm wide in the main axial hyphae.
The phialides are arranged in tufts with narrow angles at the top, similar to the branching hyphae found in Trichoderma species.
The conidia are roughly spherical with a truncate base in each spore, pale green in color, and measure 2.5–3.5 μm in diameter.
Their surfaces are almost smooth, but sometimes appearing very faintly roughened with light microscopy.

Toxicity : Several poisonings have been reported in Japan resulting from consumption of the fungus.
In 1999, one of a group of five people from Niigata prefecture died two days after consuming about 1 g of fruit body that had been soaked in saké.
In 2000, an individual from Gunma prefecture died after eating the fried mushroom.
Symptoms associated with consumption in these cases included stomach pains, changes in perception, decrease in the number of leukocytes and thrombocytes, peeling skin on the face, hair loss, and shrinking of the cerebellum, resulting in speech impediment and problems with voluntary movement.

In another instance, an autopsy revealed multiple organ failure, including acute kidney failure, liver necrosis and disseminated intravascular coagulation.
In one case of poisoning, the patient suffered from hemophagocytosis, in addition to severe leukocytopenia and thrombocytopenia seven days after ingesting the fungus. Plasmapheresis and administration of granulocyte colony-stimulating factor were used to treat the blood disorders.

The authors suggested that these treatments, in addition to the large volume of administered intravenous fluid (9 litres over a 12-hour period) were responsible for his successful recovery.

The poisoning symptoms are similar to these observed previously with animals that have consumed trichothecene mycotoxins. Japanese researchers detected the presence of the macrocyclic trichothecenes satratoxin H, satratoxin H 12′,13′-diacetate, satratoxin H 12′-acetate, and satratoxin H 13′-acetate.
When grown in liquid culture the fungus additionally produces roridin E, verrucarin J, and satratoxin H.
With the exception of verrucarin J, a 0.5 g dose of all of these compounds, when injected into the abdomen of mice, will result in their death the following day.

---

• Ascomycota / Sordariomycetes / Hypocreales / Hypocreaceae

• Synonymes :
  Hypocrea cornu-damae Pat., Bulletin de la Société Mycologique de France 11: 198 (1895) ;
  Podocrea cornu-damae (Pat.) Sacc. & D. Sacc., Sylloge Fungorum 17: 799 (1905)

• Fructification : Stroma simple et cylindrique à étroitement clavé à flabelliforme, souvent bifide à branchu, ramifié en forme de bois de daim (inde nomen), 7-9 cm de haut, aplani, 0,5-1 cm d'épaisseur, plusieurs stromatas cylindriques issus d'une base commune, rouge orangé à rouge corail brillant; surface glabre, lisse, périthèces non visibles, ostioles sous forme de minuscules points orange.

• Stipe stérile

• Conidiophores jusqu'à 400 μm de haut x 2–4 μm de large ; Phialides en bouquets, aigus au sommet, rappelant les hyphes ramifiées des Trichoderma; conidies grossièrement sphériques; spore à base tronquée, vert pale, 2,5–3,5 μm; presque lisse à l'optique. Asques cylindriques, 135-158 × 6,5-8,2 µm, épaissies au sommet, annelées.

• Ecologie : sur le bois mort, peu commun. Tibet, Japon, Chine, Corée.

• Mortel

• Références bibliographiques : IH2 p. 279 ; IOH p. 587 ; Kinoko Field Book p. 331 ; Saikawa Y. et al., Tetrahedron, Volume 57, No. 39, 24 Sept. 2001 , pp. 8277-8281

Trois mycotoxines ont été identifiées en 2001 par Mademoiselle SAIKAWA Y., MM. OKAMOTO H. & INUI Y., de type trichotecene: roridine E, verrucarine J, et satratoxine H.

---

Toxic principles of a poisonous mushroom Podostroma cornu-damae, Saikawa Y.; Okamoto H.; Inui T.; Makabe M.; Okuno T.; Suda T.; Hashimoto K.1; Nakata M.,
Tetrahedron, Volume 57, Number 39, 24 September 2001 , pp. 8277-8281

From the culture broth of a poisonous mushroom Podostroma cornu-damae, roridin E, verrucarin J, and satratoxin H were isolated. From the fruit bodies of the same fungus, satratoxin H, satratoxin H 12′,13′-diacetate, satratoxin H 12′-acetate, and satratoxin H 13′-acetate were isolated. All these macrocyclic trichothecenes except for verrucarin J had a lethal effect on mice by at least 0.5 mg per capita.

Toxic principles of a poisonous mushroom Podostroma cornu-damae.

Yoko Saikawa, Hiroki Okamoto, Taichi Inuia, Midori Makabe, Toshikatsu Okuno, Takashi Suda, Kimiko Hashimoto, Masaya Nakata

Chudoku Kenkyu. 2002 Apr;15(2):177-82.

Successful treatment in a case of podostroma cornu-damae poisoning, a deadly poisonous mushroom

[Article in Japanese]

Suzuki M¹, Katoh Y, Kumagai H, Saitoh M, Ishikawa H, Itoh H, Shimazu K.

Abstract

In this case study, a 62-year-old man ate a piece of Podostroma cornu-damae, poisonous mushroom, by mistake and suffered from severe diarrhea, vomiting and dehydration. The next day he received about 9 liters of solution intravenously over a 12 hour period at his neighboring hospital. The mushroom was identified as Podostroma cornu-damae and he was transported to our hospital on the same day. When he arrived, hypotension due to high capillary permeability accompanied by protein leakage, Leukocytosis, and faint erythema on the body were observed. He was immediately treated by continuous hemodiafiltration (CHDF) and large quantities of solution were given while monitoring the patient's pulmonary capillary wedge pressure and cardiac output. On the seventh day, Leukocytopenia and thrombocytopenia became severe and hemophagocytosis was observed. Plasma exchange (PE) and granulocyte colony stimulating factor (GCSF) were effectively used to treat these hematological disorders. In addition, hypouricemia was also observed, severe depilation occurred, and the skin lesions gradually changed to lameller desquamation. The patient needed over 30 days to recover from leukocytopenia.

CONCLUSION:

It is important to infuse large quantities of solution in the initial treatment of Podostroma cornu-damae poisoning, and blood purification therapy (CHDF and PE) may be highly recommended.
----------------------------------------------------------------------------------------------------

Korean cases :

Yonsei Med J. 2013 Jan 1; 54(1): 265–268. Published online 2012 Nov 28. 

Two Cases of Mushroom Poisoning by Podostroma Cornu-Damae

Jin Young Ahn,^1,* Soon Ja Seok,^2,* Je Eun Song,¹ Jung Ho Choi,¹ Sang Hoon Han,¹ Jun Yong Choi,¹ Chang Oh Kim,¹ Young Goo Song,¹ and June Myung Kim¹

 A 64-year old man visited the emergency department with a 10-day history of fever, desquamation on his palms, soles and scalp (Fig. 1). He had a medical history of hypertension and was currently taking medication. Upon admission, his vital signs included a blood pressure of 77/55 mm Hg, heart rate of 114 beats/min, respiratory rate of 18 times/min and a body temperature of 38.2℃. He complained of a fever, chilling sensation, generalized weakness, mild headache, and a sore throat. He did not complaint of chest pain, dyspnea, abdominal pain or diarrhea. Also there were no symptoms of paresthesia or visual disturbance. Physical examination revealed an alert mentality, poor skin turgor, a dried tongue and lips, mild throat injection, desquamation on his palms and soles, and hair loss. Initial laboratory tests showed pancytopenia with a white blood cell (WBC) count of 120/µL [absolute neutrophil count (ANC) 20/µL], hemoglobin (Hb) of 11.2 g/dL, and a platelet count of 5000/µL; elevated erythrocyte sedimentation rate (135 mm/hr) as well as C-reactive protein (159 mg/L) and ferritin (898 µg/L); and normal blood urea nitrogen (BUN), serum creatinine (Cr) (20.4/0.82 mg/dL), aspartate aminotransferase (AST)/alanine aminotransferase (ALT) (15/20 IU/L) and total bilirubin (0.8 mg/dL). A simple chest X-ray did not reveal any abnormal findings, and an abdominal-pelvic CT scan, which was performed to evaluate the causes of the pancytopenia and intraabdominal infection focus, did not show any hepatosplenomegaly or infiltrating mass lesion in the liver or spleen, abnormal enlargement of intraabdominal lymph nodes, or any abnormal finding as to the cause of the severe sepsis. Treatment comprising fluid resuscitation with crystalloid and the use of norepinephrine was also performed. Also, intravenous penicillin G (400 million IU, q 4 hrs), clindamycin (600 mg, q 8 hrs), and intravenous immunoglobulin (2 g/kg) were administered considering the possibility of streptococcal toxic shock syndrome.

Case Report

Clin Exp Emerg Med 2016; 3(3): 186-189.

Published online: September 30, 2016

DOI: https://doi.org/10.15441/ceem.15.028

Hee Nyung Kim, Han Ho Do, Jun Seok Seo, Hee Young Kim

Department of Emergency Medicine, Dongguk University Ilsan Hospital, Goyang, Korea

Case 1

A 62-year-old woman, previously diagnosed with hypertension, was admitted to the emergency department due to desquamation of the hands and feet (Fig. 3) and alopecia (Fig. 4). The symptoms had started 7 days previously, and she tried taking oral medication and applying lotions prescribed by her dermatologist without improvement. The symptoms worsened, and she developed general weakness and mild nausea. Upon further questioning, she admitted that she had gathered wild mushrooms from a nearby mountain and had made tea from the mushrooms. She had been drinking 2 or 3 cups of mushroom tea for the previous 12 days.

On admission, her blood pressure was 115/64 mm Hg, heart rate was 97 beats/min, and temperature was 37.7°C. She complained of general weakness, fever, and light abdominal discomfort, and she had desquamation of the hands and feet and alopecia. There were no respiratory or gastrointestinal symptoms. Her physical examination showed no neurological deficits.

Blood tests showed severe bicytopenia with a white blood cell (WBC) count of 6,200/µL and an absolute neutrophil count <10, as well as a hemoglobin (Hb) level of 11.5 g/dL and platelet count of 29,000/µL. Electrolyte panels and biochemical laboratory measurements were carried out. The patient’s C-reactive protein (CRP) level was 21.18 mg/dL, which was elevated above the normal range. Other test results were within normal limits (blood urea nitrogen 33.8 mg/dL, creatinine 0.94 mg/dL, aspartate aminotransferase 7 IU/L, alanine aminotransferase 10 IU/L, creatine kinase-MB 0.51 ng/dL, and troponin T 0.019 ng/dL). A peripheral blood smear showed severe neutropenia, while a chest radiograph and electrocardiograms showed normal findings.

Although her history suggested mushroom intake to be the cause of her abnormal laboratory measurements, she was admitted and treated with prophylactic antibiotics and granulocyte colony-stimulating factor (G-CSF). We tested for Hantaan virus, tsutsugamushi, leptospirosis, and malaria antibody to rule out other infections, and two sets of blood cultures were performed immediately. All of the results were negative. A bone marrow biopsy showed hypocellular bone marrow.

Neutropenia persisted during her hospitalization, and on the third hospital day, her platelet count decreased to 10,000/µL. After 4 pints of platelet infusion and continuous G-CSF infusion, her blood cell count improved without any other infective, renal, or cardiovascular complications. On the thirteenth day of her hospitalization, the laboratory measurements showed a WBC count of 2,000/µL, absolute neutrophil count (ANC) of 710, segmented neutrophil count of 42%, Hb level of 7.9 g/dL, and platelet count of 144,000/µL. She was then discharged. One week later, at an outpatient follow-up visit, her blood cell count had recovered fully.

Case 2

The patient was a 62-year-old man and the husband of case 1. He did not have gastrointestinal or cardiovascular symptoms, alopecia, or desquamation. However, he admitted to having drunk mushroom tea with case 1. On admission, his blood pressure was 133/66 mmHg, heart rate was 66 beats/min, and body temperature was 37.5°C. He was alert with no abnormalities upon physical examination. Initial laboratory results showed a WBC count of 1.75×10³/μL, ANC of 820, Hb level of 14.3 g/dL, platelet count of 12×10³/μL, CRP level of 2.05 mg/dL, blood urea nitrogen level of 15.0 mg/dL, creatinine level of 0.99 mg/dL, aspartate aminotransferase level of 18 U/L, alanine aminotransferase level of 19 IU/L, and procalcitonin level of 0.07 ng/dL. He was admitted and treated with prophylactic antibiotics and G-CSF.

On the fourth day of his admission, his neutropenia was aggravated, without fever. His ANC fell to <10, and his CRP level was 13.33 mg/dL. Under suspicion of concealed infection, prophylactic vancomycin was administered. This treatment was discontinued after cultures showed no growth. His antibody tests and cultures all yielded negative results (similar to case 1). On the twelfth day of his admission, his bicytopenia started to improve. On the eighteenth day of his admission, his complete blood cell count normalized, with a WBC count of 7,380/µL, Hb level of 11.0 g/dL, and platelet count of 30,000. He was subsequently discharged.

DISCUSSION

Podostroma cornu-damae is an ascomycete fungus and was originally described by Narcisse Patouillard as Hypocrea cornu-damae (1895) and said to originate in Tibet. Podostroma cornu-damae was next described by Boedijn et al. (1934) and Doi et al. (1973). It was then published in Saccardo’s famous Sylloge Fungorum (1905) and was named since [4]. Many accidental poisonings by Podostroma cornu-damae can be attributed to its similarity to antler Ganoderma lucidum and Cordyceps (Figs. 1, 2). Podostroma cornu-damae is known to inhabit the Java Islands, Korea, Japan, and China [5,6].

In 1999, five people in Japan drank home saké made from about 1 g of this toxic mushroom, resulting in a death 2 days later despite intensive treatment [5]. Another Japanese report documented 13 cases of ingestion, including 2 people who died [3]. In Korea, 4 people have reportedly been intoxicated by this mushroom, of whom 3 drank tea made from its fruit body. One died of multi-organ failure [7], and the 2 others were discharged from the hospital without complications [7,8]. One man was reported to have boiled the mushroom and eaten it. He developed nausea, vomiting, and fever within 3 hours of consumption. His lungs showed hemorrhagic and necrotic changes, and he died within 12 days due to multi-organ failure [9].

The case reported by Ahn et al. [7], is similar to ours in many ways. The patient consumed the mushroom in tea form and showed similar symptoms such as fever, generalized weakness, alopecia, and desquamation of the palms and soles (as in case 1). Both were treated with prophylactic antibiotics, G-CSF, and platelet transfusion. Our patient recovered gradually, while the patient described by Ahn et al. [7], despite being intubated and treated with continuous renal replacement, experienced worsening bilateral lower lung field consolidation and died due to multi-organ failure.

The most common complaints were abdominal pain, desquamation of the hands and feet, alopecia, perception changes, and speech impediment. Further evaluation showed blood cell count anomalies, such as pancytopenia or bicytopenia, and cerebellal atrophy. Autopsies showed that the patients died of multi-organ failure, including disseminated intravascular coagulation, kidney failure, and hepatic failure [10]. These symptoms were similar to animals dosed with trichothecene mycotoxin. In Japan, researchers have identified macrocyclic trichothecene toxins, such as satratoxin H, satratoxin H 12’, 13’-diacetate, satratoxin H 12’-acetate, and satratoxin H 13’-acetate. The mice died the next day after they were injected with 0.5 g of the toxin [5].

No specific treatment has been found for poisoning with this lethal mushroom, but one patient who showed severe hemophagocytosis and bicytopenia was treated with abundant intravenous fluids (12 liters over 9 hours), plasmapheresis, and G-CSF. He recovered fully after over 1 month of intensive treatment [6]. Other patients, like ours, were treated using G-CSF and prophylactic antibiotics and recovered without complications.

The onset of symptoms depends on the amount and manner of oral intake. Cases in which a person drank or ate the fruit body itself resulted in intake of large amounts of the toxin, thereby leading to symptoms within only a few hours or few days. When patients make tea and drink small amounts of the mushroom over a long period, it takes 2 to 4 weeks for symptoms to appear.

In the current case, the patients complained of alopecia and desquamation of the hands, with no other symptoms. It took 2 weeks for these symptoms to develop. Both were treated with G-CSF, and their symptoms and abnormal laboratory measurements remitted without any complications. The mechanism by which alopecia and desquamation appears has not yet been discovered.

We hope these cases will help treat future patients who present with an unknown cause of neutropenic fever and pancytopenia as well as desquamation on their palms and soles. Furthermore, as the number of cases of Podostroma cornu-damae poisoning is increasing, physicians should be sure to ask patients about any history of ingesting wild mushrooms when such symptoms appear.

We report four cases of Podostroma cornudamae intoxication. All patients experienced pancytopenia with anaemia, leukopenia,and thrombocytopenia.One patient developed life-threatening sepsis. The other three had only feve and were successfully treated with a treatment regimen similar to that used for chemotherapy patients with severe bone marrow suppression including GCSF, antibiotics, blood transfusions, and isolation in aseptic rooms.

Table1. Characteristic early and delayed symptoms of Podostroma cornu-damae intoxication

            Early symptoms                                     Delayed symptoms

Diarrhea, vomiting, dehydration                  Palmar lamellar desquamation

Anuria, hypotension, polypnoea                  Depilation

Consciousness disturbance                         Leukocytopenia

Multiple organ failures                                 Thrombocytopenia