Transcript Algal poisoning

Harmful algal blooms
What are HABs?
Algae that produce toxins
Dinoflagellates
Diatoms
Cyanobacteria (fresh water)
Very potent toxins (few cells per liter can
produce toxic effects)
Adversely affect overall environmental
quality
Environmental impacts
Toxic effects on organisms
Physical impairment of fish
Nuisance conditions from odors or
discoloration of water or habitats
History of HABs
HABs are not a new phenomenon!
Documentation of HABs goes back to
ancient times
Apparent increase of the HAB occurrence
in modern times – real or imaginary?
“Red” Tide
 World-wide
occurrence
 Algae:
Dinoflagellates
Diatoms
“Brown” Tide
 World-wide occurrence
 Algae
 Chrysophyta (“goldenbrown algae”)
 Aureococcus
 Aureoumbra
Algae associated with HABs
 Toxic dinoflagellate blooms
 Ciguatera Fish Poisoning
 Diarrhetic Shellfish Poisoning
 Neurotoxic Shellfish Poisoning
 Paralytic Shellfish Poisoning
 Toxic diatom blooms
 Amnesic Shellfish Poisoning
 Harmful blooms (non-toxic or toxicity not confirmed)
 Fish kills
 Pfiesteria, Chaetoceros, Heterosigma
 Brown tides
 Aureococcus, Aureoumbra
Ciguatera Fish Poisoning
 Gambierdiscus
toxicus (a dinoflagellate)
 Associated with
weeds and coral reefs
 Optimum conditions:
shallow waters, 2534°C, 25-40 ppt
 Ciguatoxin and
maitotoxin
Ciguatera Fish Poisoning
Ciguatoxin
Ciguatera Fish Poisoning
Common cause of food-borne poisoning
~ 50% of US seafood poisoning
90% - Florida and Hawaii
Spring/Summer
Ciguatera Fish Poisoning: Vectors
Usually large fish, bottom dwellers and
reef fish
Red snapper, Grouper, Amber Jack, Sturgeon
Toxins
Bioaccumulate
Stable and heat resistant
Lipid soluble
Highly potent (clinical effects from <1 mg)
Ciguatera Distribution
Ciguatera Fish Poisoning: Symptoms in
humans
 Lag time <12 h
 Acute onset
 Early symptoms (24-48 h): Gastrointestinal
Pain, cramping, diarrhea, vomiting
 Late symptoms
Neurological
 Headache, toothache
 Temperature disturbance (hot-cold sensation reversal)
 Respiratory paralysis and seizure in severe cases
Cardiovascular
 Heart rate abnormalities (rare), usually bradycardia
Ciguatera Fish Poisoning: Treatment and
prevention
 Diagnosis
Biomarkers of exposure not available
 Therapy
Not available
 Prevention
Complicated
 Wide range of susceptible species
 Odorless, colorless, tasteless
 Avoidance
Large reef fish
Avoiding roe, head, viscera
Diarrhetic Shellfish Poisoning
 Dinoflagellates
Dinophysis acuminata,
Dinophysis fortii,
Prorocentrum lima
 Species reported in
the US but associated
illnesses not reported
 Okadaic acids and
dinophysistoxins
Diarrhetic Shellfish Poisoning: Human
Symptoms
Generally mild gastrointestinal illness
Diarrhea, nausea, vomiting
Rapid onset, rapid resolution
No neurotoxic effects
Long-term effects? (Possibly tumorigenic)
FDA level in shellfish – 0.2 ppm okadaic
acid plus 35-methyl-okadaic acid
Neurotoxic Shellfish Poisoning
Karenia brevis
(previously
Gymnodinium
breve)
Florida, Gulf of
Mexico
Brevetoxins
Neurotoxic Shellfish Poisoning: Human
Symptoms
 Similar to ciguatera poisoning
 Early symptoms: Gastrointestinal
Nausea, diarrhea, vomiting
 Late symptoms
Neurological
 Tingling
 Numbness
 Loss of motor control
 Usually not associated with human mortality
 FDA level in fish – 0.8 ppm brevitoxin-2
equivalent
Brevetoxins: Ecological Impacts
 Massive fish kills
 Harmful to birds
(pelican, seagulls,
cormorants) and
manatees
Brevetoxins: Economical Impacts
Human health-associated impacts
Closure of shellfish beds
Skin and respiratory irritation to humans at
the seashore
Losses in commercial catch and tourism
Paralytic Shellfish Poisoning
Dinoflagellates
Alexandrium spp.
Gymnodinium spp.
Pyrodinium spp.
Northern Atlantic and
Pacific coasts
Temperate and tropical
Saxitoxins
Paralytic Shellfish Poisoning: Human
Symptoms
 Rapid onset (~30 min)
 Absence of gastrointestinal symptoms
 Neurological symptoms
Numbness
Headache
Ataxia
Weakness
Cranial nerve dysfunction
Diaphragmatic paralysis
Death by asphyxiation
 Weakness can persist for weeks
Paralytic Shellfish Poisoning: Therapy
and Prevention
Therapy
Not available (supportive only)
FDA limit in fish 0.8 ppm
Saxitoxins: Ecological Impacts
Mass bivalve mortality (1980- 5,000,000
mussels, 1980; 1997- 50,000, Eland Bay,
South Africa)
Lobster mortality (Eland Bay, South Africa)
Humpback whales (Cape Cod, MA)
1997 South Africa
Amnesic Shellfish Poisoning
 Pseudo-nitzschia spp.
(diatoms)
 Discovered in 1987
(Price Edward Isl.,
Canada)
 Domoic acid
Amnesic Shellfish Poisoning: Human
Symptoms
 Early symptoms: Gastrointestinal
Nausea, vomiting, diarrhea
 CNS symptoms
Dizziness
Cognitive effects
Disorientation
Memory loss
Delirium
Seizures
Agitation
 Highly variable course
10% with permanent neurological damage
Domoic acid: Ecological Effects
1991 Monterey Bay CA - >100 pelicans
and cormorants were found dead or
suffering from unusual neurological
symptoms
Pseudo-nitzschia australis
Vector: Northern Anchovie
Pfiesteria piscicida:
fish kills
 Unknown
substances
secreted by finfish
and shellfish
stimulate Pfiesteria
to transform from
benthic cysts or
amoebae or nontoxic flagellated
cells, to toxic
zoospores
Pfiesteria in humans
Rare
Narcosis
Sores
Nausea/vomiting
Acute short-term memory loss
Severe cognitive impairment
Recovery in 6-8 weeks, but may re-occur
Most cases – Chesapeake fishermen and
algal researchers (aerosol!)
HABs: Distribution in the US
HABs: What can we do about it?
Prevention
Complicated
Public awareness (=negative publicity for fish
and shellfish industry)
Prediction
Satellite tracking of red and brown tides
Mathematical models predicting blooms
Satellite images: Karenia brevis in NC,
1987
Staellite images: Red tide in FL, 1978
Freshwater HABITATS:
A new “Silent Spring”?
Over 100 bald eagles found dead
around man-made lakes in South
Carolina, North Carolina, Texas,
Arkansas and Georgia since 1995
Due to fast decay and scavengers,
this may be only 10-15% of the total
bald eagle deaths – therefore,
estimated death toll may be as high
as 1000 birds since 1995
The cause of the deaths was
unknown until recently.
Disease:
Avian vacuolar myelinopathy (AVM)
Hydrilla verticillata
Native to Africa, Australia, and the warmer parts of Asia.
Brought to Florida in 1959 to sell as a plant for aquariums.
Hydrilla verticillata
This abundant source of biomas is a
known hyperaccumulator of Mercury,
Cadmium, Chromium and Lead, and as
such can be used in phytoremediation
Good or bad
Recorded cases of AVM in southeastern United States
Avian Vacuolar Myelinopathy
(AVM)
Normal brain
AVM
Why Hydrilla?
Hydrilla verticillata
 Hydrilla verticillata and an associated epiphytic
cyanobacterial species are cause of AVM.
 Cyanobacteria produce the neurotoxic amino
acid BMAA,
 Biomagnification of BMAA occurs in wetland
ecosystems
 The consumption of fish and waterfowl (e.g.
Canada geese and mallards) from AVMconfirmed reservoirs in Arkansas, Texas,
Georgia, North Carolina and South Carolina
could represent a significant human health risk.
Hapalosiphon fontinalis
Indole alkaloids
vinblastine
d-tubocurarin