MedQA_jp

ProMED-mail Archive Number 20101121.4211
Published Date 21-NOV-2010
Subject PRO/AH/EDR> Foodborne illness, fatal – Micronesia: (CH) turtle meat

日本語概要 投稿者ブログ
URL http://outbreaks.biz/2010/11/22/chelonitoxism-micronesia/
に続く。
[Mod. TG氏解説(続):
他に オサガメ、アカウミガメも中毒を起こすことがある。
However, other species may be toxic including the leatherback turtle ( Dermochelys coriacea [カメ目オサガメ科オサガメ属オサガメ 長亀/ワシントン条約 絶滅寸前 CR]) and the loggerhead turtle ( Caretta caretta [ウミガメ科アカウミガメ属アカウミガメ /ワシントン条約]).
…
…
The clinical signs of chelonitoxism are clearly distinguishable from other types of seafood poisonings (Brodin, 1992; Isbister and Kiernan, 2005) and are relatively stereotyped.
Onset occurs from few hours to 4 days after consumption. The onset period is characterized by the appearance of gastrointestinal signs (nausea, vomiting, epigastric pain and, occasionally, diarrhea). Other symptoms possibly present at onset include dizziness, malaise, sweating, sore throat, and chest pain. Most patients do not develop any further effects and recover over a week (Bagnis and Bourligueux, 1972).
The typical moderate poisoning is characterized by pathognomonic oral and pharyngeal involvement with a burning mouth and throat sensation and dysphagia with hypersialorrhea followed by glossitis (25-75 percent of patients depending on series). Ulcerative oeso-gastro-duodenal lesions have also been reported. At this stage neurological manifestations, best indicators of severity, may appear with alternating periods of drowsiness and full consciousness (or psychomotor agitation). Most patients with moderate forms (grade 2) recover fully within about 3 weeks.
However some patients may lapse into coma as an initial phase of a more severe grade characterized by multiorgan involvement (tubular nephropathy, liver cytolysis, hypotonic coma, respiratory distress). The most frequent abnormal laboratory test findings are metabolic acidosis, hyperuricemia, hyponatremia, hypocalcemia, hypoglycemia, neutropenia, and thrombopenia (Brodin, 1992). Mortality is high among patients with severe forms especially in children. Upon emerging from coma, survivors often present complex central and/or peripheral neurological sequels (such as, hemiplegia, tetraplegia, dementia, sensorimotor deficit, cerebellar syndrome).
There is no antidote for sea turtle poisoning and treatment is strictly supportive and symptomatic with intensive care if necessary.

The sea turtle species most commonly cited in the literature and apparently responsible of the highest mortality is Eretmochelys imbricata [ウミガメ科タイマイ属タイマイ]. Most authors stress that all organs of this chelonian [カメ目] are potentially toxic regardless of preparation (thermoresistant toxin ?) (Pillai et al, 1962; Ariyananda and Fernando, 1987; Champetier de Ribes et al, 1999).
It has also been noted that toxic effects are dose dependent since symptoms are most severe in victims that eat the most flesh.
Another feature of chelonitoxism described in the literature is passage of toxins into breast milk with several reported cases of poisoning in breast-fed children that did not consume the turtle flesh itself (Dewdney, 1967; Ariyananda and Fernando, 1987; Ranaivoson et al, 1994).
Transplacental contamination may have also occurred in a case in which the fetus died at the beginning of the severe phase when the metabolic status of the mother was still under control.

It should be stressed that the causative toxins for sea turtle poisoning have not been identified. The symptoms and outcomes are known, but toxin remains a mystery.
Portions of this comment have been extracted from
URL http://www.seaturtle.org/PDF/Fussy_2007_Toxicon.pdf – Mod.TG]

[Another article adds: “The toxic compounds identified to date as the causative agents are lyngbyatoxins, which are accumulated through the food chain into the flesh of marine turtles following ingestion of the cyanobacterium Lyngbya majuscula, that grows on seagrass, sand and rocky outcrops.”
(Magnino S, Colin P, Dei-Cas E, Madsen M, McLauchlin J, Nöckler K, Maradona MP, Tsigarida E, Vanopdenbosch E, Van Peteghem C. Biological risks associated with consumption of reptile products. Int J Food Microbiol. 2009 Sep 15;134(3):163-75. Epub 2009 Aug 12.)
URL [略]
– Mod.MPP]

Archive Number 20101105.4008
Published Date 05-NOV-2010
Subject PRO/AH/EDR> Prion disease update 2010 (10)
[Mod. CP氏解説:
variant Creutzfeldt-Jakob disease 新変異型クロイツフェルト・ヤコブ病 [ProMED-mail では、かつて vCJD or CJD (new var.)と略称使用]の患者数が減少し続けているので、不定期のアップデートでは、他の[異常]プリオン関連疾患を含むように範囲を広げる決定を行っている。また、vCJD に加えて、クロイツフェルト・ヤコブ病の他病型: sporadic 散発性, iatrogenic 医原性, familial 家族性, GSS (Gerstmann-Straussler-Scheinker disease) も( vCJD の発生や病因に多少関連する可能性があるので、) occasional ProMED-mail updates に含めている。
]

ProMED-mail Archive Number 20100405.1091
Published Date 05-APR-2010
Subject PRO/AH/EDR> Prion disease update 1010 (04)
Google Buzz
[Mod. CP氏解説:
variant Creutzfeldt-Jakob disease [変異型クロイツフェルト・ヤコブ病 以前の略称 vCJD or CJD (new var.)]のヒト症例数は引き続き減少しているので、ProMED-mail の不定期アップデートの範囲を他のプリオン関連疾患 other prion-related diseasesを含めるよう拡大することに決定した。vCJDに加えて、CJDの他の病型である 孤発性[散発性] sporadic, 医原性 iatrogenic, 家族性 familial, and GSS (Gerstmann-Straussler-Scheinker disease) も(これら病型は、vCJD の発生頻度、病因にいくらかの関係があるので)含まれている。]

Facebook ページ http://www.facebook.com/permalink.php?story_fbid=110430565646610&id=189856398106
ProMED-mailによる不定期アップデートの中に、変異型クロイツフェルト・ヤコブ病 [variant Creutzfeldt-Jakob disease, vCJD, CJD (new var.)、他のプリオン関連疾患の記事が含まれています。ヒト vCJD 患者数は継続的に減少しています。これらプリオン病の概要(日本語)配信は、症例増加時に記事を抽出して行います。
2010年4月5日19:33