Harmful algal blooms & phycotoxins Flashcards

1
Q

How widespread is the production of toxins in marine organisms?

A
  • Very, and had evolved many time simultaneously
  • 1,000+ marine families containing poisons & toxins.
  • Maybe x500 more venomous species in tropics that temperate regions.
  • Mostly contain proteins, peptides & other pharmacologically active

substances.

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2
Q

What is a poison?

A
  • An umbrealla term, can be any substance that produces a detrimental biological response in another/same organism.
  • They are very stable.
  • They exhibit a very wide range of toxicities.
  • Their efficiency and effectiveness is very variable but include some of the most toxic substances known.
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3
Q

What is venom?

A

Venom, unlike toxins which are chemically and biologically very stable, are the reverse and break down very easily.

But they are also incredibly highly evolved and efficient at what they do.

Holocrine venom

  • Really are not true venom.
  • Venomous, posinous subtances
  • For example spines that you brush against, cause physical harm and release a poisonous substance. Not intentional but more incidental.

Stings / Bites

  • True venom requires a direct and deliberate mode of venom transfer, generally a bite or a sting.
  • Generally unstable
  • Generally very efficient and effective
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4
Q

Why is it hard to pick up trends from medical history?

A
  • Effects on humans are perceptive i.e. one person’s pain is another’s discomfort.
  • Much information is historical, and therefore dubious in terms of accuracy.
  • Symptoms – heart & respiratory failure – 50 yrs ago would not be distinguished from other conditions.
    • Trends may suggest that the number of cases in increasing, which may be explained this
  • Know less about marine toxins now than was known about medicine in dark ages.
  • Sediment cores show toxic algal blooms from 2000 BC.
    *
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5
Q

How do harmfull macroalgal blooms fit into the food web?

A
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6
Q

How many marien alage are there (10 yeras ago)

A
  • Over 5,000 spp marine microalgae described to date.
      • new molecular techniques = reclassification e.g. Skeletonema
  • Approx 300 sp. develop into ‘algal blooms’
  • Defined as can discolour the water – so called ‘red tides’ & ‘brown tides’.
  • Cell densities can exceed millions of cells per litre.
  • Duration can last from hours to months
  • Algal cell density is also affected by oceanographic forcing e.g. upwelling, wind drive circulation etc.
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7
Q

Do all harmful algal blooms produce toxins?

A
  • Of the 300 blooming species, over 100 produce potent toxins which are harmful to plants, animals and humans these are termed ‘Harmful Algal Blooms’.
  • Nuisance Algal Blooms’ (branch within algal blooms) = don’t produce toxins but cause major problems e.g. reduced O2 concentration or damage (when they die they deoxygenate the water) to fish gills.
  • Chaetoceros sp. Long, sharp spines can penetrate fish gills resulting in excess mucus production & death by asphyxiation. May also result in secondary infections.
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8
Q

Incidences of HABS are increasing globally, why is this?

A

Possible reasons include:

    • Increased scientific awareness of toxic species.
      1. More people listening to scientists
      2. More goverments taking notice
      3. More monitoring equipment
      4. Better diagnosis assays
    • Increased utilisation of coastal waters for aquaculture.
      1. Utilise more of our inshore waters for food production
      2. Harvesting for bivalves, crustaceans ect
    • Stimulation of plankton blooms by cultural eutrophication &/or unusual climatological conditions.
      1. Fueling the system by adding nutrients
  1. -Transport of dinoflagellates as resting cysts either in ships’ ballast water or associated with translocation of shellfish stocks from one area to another.
    1. Ballast water
    2. Aquaculture moving broodstock
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9
Q

What types of algae produce toxins?

A
  • 5 main algal classes identified as toxin producers**:
    1) Dinoflagellates – 90 species
    2) Diatoms – 10 species
    3) Haptophytes – 9 species
    4) Raphidophyceans– 7 species
    5) Cyanobacteria / blue-green algae – **not true algae** - 10 species
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10
Q

Dinoflagellates

A

Dinoflagellates:

Saxitoxins, neosaxitoxins, gonyautoxins, okadaic acid, yessoensis toxins, azaspiracids, ciguatoxins, maitotoxins, brevetoxins, Pfiesteria toxin (plus several other less frequently occurring compounds).

  • Huge range of toxins produced by dinoflagellates (many in each group)
  • Chemically and toxiologicaloly diverse
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11
Q

Diatoms:

A

Domoic acid; oxylipins

Primarily talking about domoic acid, as a neurotoxin.

The most potent toxins are neurotoxins, which attack the central nervous system.

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12
Q

Haptophytes:

A

Prymnesin & prymnesin-like toxins

A range of neuro and cycotoxins

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13
Q

Cyanobacteria: (says interesting things are happening - exam)

A

Cyanobacteria:

Anatoxins, saxitoxins, microcystins, nodularins, cylindrospermopsins,

β-N-methylamino-L-alanine, debromoaplisiatoxin, lyngbyatoxin,

lipopolysaccharides.

  • Alot of toxins, alot of overlap with dinoflagelllates, but also alot of toxins unique to themselves.
  • Some of them are contact skin toxins
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14
Q

Paralytic shellfish poisoning (PSP)

A

Causative organisms –Alexandrium, Gymnodinium, Gyrodinium,

Gonyaulax & Pyrodinium.

  • The life cycle has the hypnocyst (resting stage.) - is transportable e.g. ballast water & therefore may increase biogeographic range & frequency of PSP incidents.
  • Saxitoxin one of only 2 natural toxins on UN agreement on biological weapons (Schedule 1 Chemical Warfare Agents – other is ricin.)
  • Dose of only 0.2 mg can be fatal.
  • 2 main groups of PSP toxins – saxitoxins (STX) & neosaxitoxins.
  • STX first isolated from Saxidoma mollusc.
  • Change in R- groups radically change the toxicity.
    • 14 structural forms of STX & 9 for neosaxitoxins. It also includes the gonyautoxins. The degree of toxicity varies with each structural form.
    • Epimerization is an isomer change of H & S groups which alters potency.
    • This change in chemistry can happen within the algae, the animal that digests or within us.
    • The acid in the stomach will make saxitoxin around six times as toxic. This makes regulatory control and guidance in terms of fisheries and public health very very difficult.
    • You can freeze, cook or extract it out.

Gyrodinium aureolum – annual North Sea bloom. Caused PSP incident in Newcastle in 1968 (mussels) also notable fatalities among the sea bird population of Farne Islands. (yearly bloom around UK shores from cysts in the firthe of fourth - monitoring for this unlike developing countries)

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15
Q

How does saxitoxin work?

A
  • Very fast-acting, and works by sitting in the sodium channels in your nervous system and stop the movement of sodium ions across your nerves.
    • Saxitoxins are specific & potent sodium channel blockers preventing propagation of action potentials.
  • STX found in widely differing groups e.g. pufferfish, Californian newt, red alga Jania sp. & blue-ringed octopus.
    • STX not produced by these organisms, but rather bacteria living in/on the organisms.
  • Also, evidence that it is not in fact the dinoflagellate which produces PSP toxins, but bacteria.
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16
Q

What other factors have an effect on the amount of toxin produced?

PSP concentrations in algal cells are influenced by

A
  • Algal clone
  • Environmental temperature – often down to the growth rate. Cells that grow slower have more time to build up saxitoxin per cell. It could be a true biochemical effect or slower growth resulting in greater accumulation per cell.
  • The more nitrogen you have, The more toxin you have in total in a bloom but the less you have in each individual cell.
  • Phosphorus – tends to be the reverse. When you get less phosphorous you get more toxin, slows cell division down so you get more build up in a cell.
  • ‘Age; of bloom – most toxic during the middle of the exponential phase.
  • Saxitoxin, when the cells are young, fit and vibrant you get toxin production. When the growth rate slows down you should get more toxin per cell, but the rate of toxin produced per unit cell decreases.
    *
17
Q

Concentrations of PSP toxins in shellfish will depend upon:

A
  • Algal concentrations in the water (bloom size & patchiness)
    • If the toxic algae is the dominant species filter feeders will not be able to be selective.
  • Avoidance of algae by shellfish (Mytilus, Saxidoma & Pecten are toxin-sensitive)
  • Toxin concentration in algal cells
  • Feeding rate of shellfish
  • Transformation of consumed toxin +/- toxic byproducts (epimerization)
  • Selective retention & excretion of toxins – called depuration. Is species & temperature specific?
    • Can the animal get rid/avoid some of the toxins
18
Q

What body parts of scallops contain the highest levels of PSP?

A

Toxin concentrations in shellfish tissues: (Patinopecten sp.)

The muscle contains very little toxin, but things like the gonad, viscera, and gills contain high levels.

Adductor muscle – 54 μg /100g tissue

Viscera – 4945 μg /100g tissue

Gills – 504 μg /100g tissue

Gonads – 1361 μg /100g tissue

Maximum permitted level is

80 μg /100g tissue

19
Q

Diarrhetic Shellfish Poisoning (DSP)

What organisms cause it?

A

Causative organisms: Dinophysis sp., Prorocentrum lima, P. maculosum, Protoceratium reticulatum, Coolia sp.

20
Q

Diarrhetic Shellfish Poisoning (DSP)

A

Toxins produced: Okadaic acid, Dinophysistoxins, Yessotoxins & Pectenotoxins. 31 known structural forms of DSP toxins.

21
Q

DSP - risk from okadaic acid.

A
  • Okadaic acid (OA) is a potent protein phosphatase inhibitor.
  • Has become an extremely useful tool for studying cellular processes regulated by reversible phosphorylation of proteins such as signal transduction, memory, cell division & apoptosis.
  • Carcinogenic (stomach cancers), greater exposure to okadaic acid increases long term risk o cancer.
  • All types of shellfish can become contaminated by DSP toxins.
  • Don’t have to present in large numbers to be toxic. In Ireland shellfish harvesting suspended at cell densities of 1 cell per L.
  • It could be massively under-represented in this country, as it is not tested for, and symptoms come under food poisoning.
22
Q

Neurotoxic Shellfish Poisoning

causative organisms

A

Causative organisms: Karenia brevis cf Gymnodinium breve

23
Q

Neurotoxic Shellfish Poisoning

Toxins produced

A

Toxins produced: Brevetoxins (8 forms).

24
Q

NSP How does it work?

A

Brevetoxins (BTXs) target voltage-sensitive sodium channels.

Fragile cells break in onshore waves and are pushed ashore by prevailing winds.

The formation of toxic aerosols by wave action can produce respiratory asthma-like symptoms.

No deaths yet reported. Recovery is generally complete in a few days

25
Q

Azaspiracid Poisoning (AZA)

A

Recently discovered, azaspiracids are polyethers with unprecedented structural features.

Produced by microalgae of the genus Azadinium spinosum.

  • Toxic syndrome first identified following a severe gastrointestinal illness from consumption of contaminated mussels in Ireland - now confirmed throughout the western coastline of Europe.
  • Azaspiracids can induce widespread organ damage in mice (frontline ways to monitor these toxins).
    • Liquified mice organs.
  • Probably more dangerous than previously known classes of shellfish toxins.
26
Q

Ciguatera fish poisoning

A
  • Sub tropical / tropical
  • Skip invertebrate part of the food chain, can get this from fish just eating on seaweed.
  • Causative organisms: Gambierdiscus toxicus & members of genus Prorocentrum.
  • Toxins: Ciguatoxins, Maitotoxin, Gambiatoxin, Scaritoxin, Okadaic acid
  • Humans intoxicated from consumption of fish which have fed on
  • CTX producing algae – normally herbivorous fish, e.g. parrotfish.
  • In doing so, CTX has ‘jumped’ the invertebrate food chain.
  • CTX accumulates efficiently along food chain, i.e. predatory fish
  • e.g. snapper, barracuda & moray eels will contain highest toxin
  • concentration.
  • CTX found in 425 species of fish at each stage along food chain.
  • CTX is a Na+ and Ca2+ channel activator.
27
Q

Algae that eats you alive

A

Pfiesteria poisoning (last year exam paper)

  • Estuarine dinoflagellate (prefers 15 ppt) with extremely resistant cyst stage.
  • Produces potent neurotoxins against fish – also affects humans
  • Fish mucus & urine are triggers
  • Causes ulceration (now linked with possible Aphanomyces invadans fungal infection)
  • Linked to eutrophication, especially pig farming effluents
  • Highly controversial: Burkholder & Marshall 2012 Harmful Algae 14: 196-230
  • Now invaded North Sea (thankfully not the poisonous form!)
  • Metal-containing organic toxin identified.
  • High toxicity due to free radical production.
  • Very unstable – degraded by white light,
  • pH variations & prolonged heat.