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Toxicology course Case presentation Shellfish poisoning

Toxicology course Case presentation Shellfish poisoning. CK Chan UCH. Case 1. Family of three (M/44, F/34, M/10) All develop nausea, dizziness, limbs numbness shortly after taken steamed scallop at 1900 Presented to AED at 2130 with symptoms nearly completely subsided.

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Toxicology course Case presentation Shellfish poisoning

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  1. Toxicology courseCase presentationShellfish poisoning CK Chan UCH

  2. Case 1 • Family of three (M/44, F/34, M/10) • All develop nausea, dizziness, limbs numbness shortly after taken steamed scallop at 1900 • Presented to AED at 2130 with symptoms nearly completely subsided. • All vital signs stable. • All discharged with next day follow up

  3. Case 2 • Family of 3 (F/33, M/11, F/4) • Mother & son c/o dizziness, blurring of vision & difficulty to open up the eyes. Youngest daughter was asymptomatic. • Taken steamed scallop at 6:30pm, developed the symptoms since 8:30pm. • Attended AED at 9:50pm. Complete resolution of symptoms upon assessment at 10:20pm. • Vital signs / electrolyte / ECG all normal

  4. Communicable Disease Watch Mar. 20 – Apr. 2, 2005 Centre of Health Protection, DH • Outbreak of shellfish poisoning associated with consumption of fresh scallops during March 14 - 19, 2005. • 36 incidents, 58 patients involved. • Onset: 10min – 30hrs (median 45min) • Duration: 1-228hrs (median 12hrs) • All presented with mild symptoms. None admitted to hospital.

  5. Investigation performed by the Food and Environmental Hygiene Department (FEHD) • Symptoms compatible with shellfish poisoning by pre-formed toxin. • Predominant neurological symptoms - Neurotoxic (NSP) or low-dose paralytic (PSP) shellfish poisoning • Testing of PSP toxins is conducted by Government laboratory using mouse bioassay • Testing of NSP toxins is conducted by an overseas laboratory using mouse bioassay. • Result: 10 samples tested for NSP & PSP toxin, all negative.

  6. Investigation did not reveal a common source of the suspected scallops. (imported from the Mainland and Vietnam) • Despite the lack of evidence on a common source of scallops for the recent poisoning cases, it seems reasonable to postulate that the poisoning cases were related to the same batch(es) of contaminated scallops distributed through various means to the local market. • Problem unsolved: What is the toxin?

  7. Shellfish poisoning – 4 types • Neurotoxic (NSP – Brevetoxins) • Amnesic (ASP – Domoic acid) (=Encephalopathic shellfish poisoning) • Diarrhetic (DSP – Okadaic acid & its derivatives) • Paralytic (PSP – Saxitoxin) • Related toxins with same mechanism of action & presentation: • NSP Brevetoxins = ciguatoxin • PSP Saxitoxin = tetrodotoxin

  8. Shellfish poisoning – common features • Consequence of toxic algal bloom • Shellfishs feed on algae, & toxins are accumulated in internal organs (major) & flesh. • Toxins are heat & gastric acid stable – not affected by cooking. • Rapid onset of symptoms (pre-formed toxins). Neurological & GI symptoms.

  9. Mechanism of action of shellfish toxins • Marine toxins including brevetoxins (NSP), saxitoxin (PSP), ciguatoxins & tetrodotoxin affect voltage-sensitive Na channel in myelinated & unmyelinated nerve, resulting in peripheral neurological presentation. • Brevetoxin & ciguatoxin cause a persistent opening of the Na channel. • Saxitoxin & tetrodotoxin block the Na channel

  10. SAXITOXINS

  11. Voltage sensitive Na channel • High density at node of Ranvier of myelinated axon. • Together with K channel, responsible for saltatory conduction of action potential

  12. M gate – outer gate • H gate – inner gate • A= Resting state (-70mV transmembrane potential) • B= A threshold depolarization to -50mV leads to conformational change of the Na channel. M gate opens & the influx of Na leads to further depolarization to +50mV. • C=Membrane depolarization also leads to the closure of the H gate, which terminate the depolarization process. • D=Membrane repolarization leads to the closure of M gate. Delayed opening of H gate results in the absolute refractory period.

  13. Mechanism of action of shellfish toxins • Domoic acid (ASP) – structurally similar to the excitatory neurotransmittor glutamic acid. It overstimulates the neurons in the brain hypocampus, causing persistent brain damage. • Okadaic acid (DSP) – causing abnormal sodium secretion in intestinal cells

  14. Management - overview • Clinical diagnosis from history & presentation • Uneaten shellfish sample should be kept for FEHD collection • Supportive treatment • Activated charcoal unlikely useful (∵small quantity of potent toxin with rapid GI absorption) • Significant mortality only associated with PSP.

  15. Management (1)

  16. Management (2)

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