Dec 1 Food Toxins

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• Dec 1 Food Toxins
• Some marine algae produce neurotoxins
• Humans consume contaminated fish or shellfish
• May be exposed through water also or ocean spray
• neurotoxic effects from acute exposures are
  established
• concern about chronic, low level exposure is
  growing
• On average, 60,000 acute intoxication
  incidents/year with 1.5 human death rate across
  toxins.
• Also effect marine mammals, birds, and animals
  that eat fish.

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• Origins of Epidemic Exposures
• harmful algal blooms (HABs) originally called
  Red Tide
• only 2 (60-80 species) of blooming algae
  produce harmful toxins
• belong to dinoflagellate and diatom groups
  microscopic
• cause seafood poisoning syndromes

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• Dinoflagellate
• type of marine plankton
• one-celled organisms that have characteristics
  of algae (plant) as well as protozoa (animal)
• under certain conditions, blooms occur
• most produce pigments some are bioluminescent
• Diatom one-celled or colonial plankton that
  have silica-based cell walls

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• Seafood Poisoning Syndromes
• Paralytic Shellfish Poisoning
• Neurotoxic Shellfish Poisoning
• Amnesic Shellfish Poisoning
• Diarrhetic Shellfish Poisoning
• Ciguatera Fish Poisoning
• Most are neurotoxins and require ingestion to do
  harm.
• Cannot be killed through cooking.
• Subset can be harmful through respiratory route.

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Very different from others not due to
seafood consumption
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• Paralytic Shellfish Poisoning
• From mollusks contaminated with saxitoxins
• 2000 human case/yr with 15 death rate
• Also known to kill birds humpback whales
• Saxitoxins believed to have evolved as mollusk
  defense against predators
• Neurotoxic via inhibition of sodium channel that
  blocks neuronal activity

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Symptoms of Paralytic Shellfish
Poisoning Effects primarily on the peripheral
nervous system Toxins found in 3 dinoflagellate
genera - Alexandrium, Gymnodinium, and Pyrodinium
Tingling and numbness around mouth and also in
extremities Loss of motor control Drowsiness Incoh
erence At high doses, respiratory paralysis
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• Neurotoxic Shellfish Poisoning
• Toxins found mainly in mollusks from
  dinoflagellate Gymnodinium breve- known as
  Brevotoxins
• G. Breve red tides cause fish kills (Florida Red
  Tide)
• High affinity for Na channel causes
  persistent activation or opening
• Symptoms of ingestion nausea, tingling ad
  numbness around the mouth, loss of motor control
  severe muscle aches
• In kids seizures and unconsciousness
• Not known to be fatal in humans (manatees have
  died)
• Symptoms of inhalation of aerosolized brevotoxin
  - irritation and burning of the throat and upper
  respiratory tract immunosuppression

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• Ciguatera fish poisoning (CFP)
• From dinoflagellate, Gambierdiscus toxicus -
  grows around coral reefs and reef lagoons
• Human exposure mostly from eating large fish
  from area Baracuda, snapper, grouper (imported
  from contaminated areas)
• Effects 50,000 people/yr
• early onset symptoms (2-6 hr) - gastrointestinal
  disturbance
• later onset symptoms (18-hr) neurologic
  numbness of the perioral area and extremities,
  reversal of temperature sensation, muscle and
  joint aches, headache, itching, increased and
  irregular heart rate, hypertension, blurred
  vision, paralysis
• can be fatal, but rare
• chronic phase may follow - persist for weeks,
  months, or years
• higher binding affinity at Na channel than
  Brevetoxins more toxic

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• Diarrhetic shellfish poisoning (DSP)
• milder than others
• exposure via contaminated shellfish
• From dinoflagellate that produces okadaic acid
• interferes with protein phosphotases important
  in cellular metabolism and neurotransmission
• GI symptoms within 3 hours of ingestion that
  last 2-3 days
• Hyperphosphorylation in GI tract causes fluid
  loss
• Also known to be tumor promoters concern for
  chronic low level in wildlife and humans

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• Amnesic Shellfish Poisoning
• Toxin is domoic acid from diatom
  Pseudo-nitzschia multiseries
• Domoic acid mimics Glutamate, an excitatory
  neurotransmitter binds with certain GLU
  receptors activates Ca channels and causes
  excess Ca and neuronal death
• Exposure mostly from contaminated mussels,
  scallops, and anchovies
• Outbreaks in Canada and CA have killed humans,
  sea lions, pelicans, cormorants

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• Amnesic Shellfish Poisoning
• Acute symptoms - GI plus neurologic - dizziness,
  disorientation, lethargy, seizures, and permanent
  loss of short-term memory
• Sensitive brain areas include CA1 and CA3 of
  hippocampus important in learning and memory
• Lower doses effect memory performance concern
  re chronic, low level effects and
  neurodevelopmental effects
• Most sensitive - the elderly, those with
  impaired kidney function fetus and infants

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• Estuary-Associated Syndrome
• caused by dinoflagellate, Pfiesteria actual
  toxin not known
• different from others re nature of organism and
  of exposure
• T-Rex of the dinoflagellate world
• blooms are invisible no pigments produced
• signs are fish with deep sores and fish kills
• Organisms produce a chemical that stuns fish and
  causes lesions then they feed on the fish
• Human exposure not through fish consumption
  due to exposure to contaminated water
• Exposure through skin contact or inhalation
• Human symptoms include burning sensations on
  contact, skin lesions, fatigue, respiratory
  irritation, headache, disorientation, severe
  cognitive impairment and memory loss

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• Bovine Spongiform Encephalopathy a prion
  disease that is transmitted from a protein in
  infected cattle
• Prion - small proteinaceous infectious particles
  proteins alone that transmit infectious disease
• Prion diseases - spongiform encephalopathies -
  post mortem appearance of the brain has large
  vacuoles in the cortex and cerebellum.
• Mad Cow Disease
• Human form Creutsfeld-Jakobs Disease

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• Unusual in origin and characteristics
• Transmitted by a protein
• Long incubation period during which no symptoms
• For BSE among cattle 3-8 years
• For human - unknown, but at least five years and
  could extend up to 20 years or longer.
• The diseases are fatal - no known treatment or
  cure.
• vCJD believed acquired from eating food
  products containing the BSE agent
• From 1995 - 2000, 88 human cases of vCJD were
  reported in the U.K, 3 in France and 1in Ireland.
  
• Diagnosed by presence in the brain of the prion,
  absence of inflammatory reaction, and a
  neuropathologic feature consisting typically of
  spongiform lesions, astrogliosis, and neuronal
  loss.
• Death within a year of symptom onset