Harmful Algal Blooms
Quay Dortch, Louisiana Universities Marine Consortium, Chauvin, Louisiana, USA
Harmful algal blooms result from the excessive growth of algae, with deleterious effects on
human or animal health or on ecosystems; many produce biotoxins. The incidence of
harmful algal blooms may be increasing as a result of eutrophication, transport to new
areas by ballast water, or aquaculture/mariculture.
Introduction
Harmful algal blooms (HABs) result from the unusual
growth of a single species of algae, which has some negative
impact. Algae are normal members of both marine and
freshwater flora, forming the base of all aquatic food
chains. Under normal conditions a mixture of species from
many different taxonomic groups is usually present,
although one or more species can predominate. Occasion-
ally, a particular combination of environmental conditions
will result in high algal biomass with an unusual
predominance of one or a few species, and sometimes
those species may be harmful.
In the past, HABs have been described by a number of
other terms, such as toxic and noxious algal blooms, red
tides or brown tides. Some of the organisms considered
HAB species do not fit all of the implied criteria.
Cyanobacteria are no longer considered algae but are still
included. Others are not photosynthetic at all. Finally,
some can be harmful when they are present in very low
abundance and may never form blooms. The single most
important criterion distinguishing HAB species is the harm
they cause.
A wide range of harmful effects is possible. Some HAB
species produce biotoxins that cause human illness or
death after consumption of shellfish or fish that have
accumulated the toxins from their diet. These toxins are
particularly insidious because most are not destroyed by
cooking. Other animals may be susceptible to the same
biotoxins, but there are other HAB species that specifically
cause fish and other animal mortality. These can result in
economic losses and damage to ecosystems. Finally, some
HAB species discolour water, cause water to have a foul
taste or odour, or cause hypoxia or anoxia. This entry will
focus on the species that are a threat to human health, but it
will also mention some of the other problems.
The occurrence of HABs, like the growth of all algae, is
dependent on a species-specific optimal combination of
environmental conditions, such as light, nutrient avail-
ability, temperature, salinity, water column stability,
horizontal water movements and grazing by animals.
Many HAB species have relatively low maximum growth
rates. Consequently, researchers are trying to determine
whether HABs have unique adaptations or requirements
for growth that make it possible for them to outcompete
ENCYCLOPEDIA OF LIFE SCIENCES © 2002, John Wiley & Sons, Ltd. www.els.net
Secondary article
Article Contents
. Introduction
. Marine Harmful Algal Blooms
. Freshwater Harmful Algal Blooms
. Current Global Situation
other algae under some conditions. Some of the possibi-
lities being considered include cyst formation and other life
cycle strategies, vertical migration, development of grazer
avoidance mechanisms or unique nutrient utilization
capabilities. Because HABs are so diverse, it is unlikely
that a single explanation will be found; some possible
adaptations will be mentioned for individual species or
groups.
Marine Harmful Algal Blooms
Human health problems
Paralytic shellfish poisoning
The paralytic shellfish poisoning (PSP) toxins are pro-
duced by some marine dinoflagellates including many
species of Alexandrium, Pyrodinium bahamense var.
compressum and Gymnodinium catenatum (Table 1) and a
few freshwater cyanobacteria; the latter will be discussed in
the next section. The occurrence of similar toxins in such
widely divergent groups of organisms is not readily
explained. Organisms causing PSP are distributed globally
(Table 1) and are thought to be spreading either by natural
mechanisms or in ballast water into waters made more
hospitable by increasing nutrients. The wide distribution of
the causative organisms and the severity of the illness
(Table 2) make PSP one of the most serious HAB problems.
Because new outbreaks often occur in areas with no
monitoring and significant local consumption of fish and
shellfish, much human mortality results.
Most of the PSP-causing dinoflagellates have a moder-
ately complex life cycle. Vegetative cells (usually haploid)
living in the water column form gametes, which fuse to
form a swimming planozygote (usually diploid). Labora-
tory studies with Alexandrium spp. show that this step is
often triggered by depletion of critical nutrients, such as
nitrogen, phosphorus or iron, but the cause is not as clear in
field studies. The planozygote encysts, forming a non-
swimming hypnozygote, which falls to the bottom. After a
period of dormancy, the cyst matures to the point that it
can hatch when environmental conditions, such as
temperature, are right, forming a planomeiocyte (diploid),
1
 Harmful Algal Blooms

Table 1 Selected examples of problems caused by marine harmful algal bloom species
Problem
Human health threats
Paralytic shellfish poisoning
Organism
Alexandrium tamarensea
Alexandrium catenellaa
Alexandrium fundyensea
Alexandrium minutuma
Alexandrium acatenellaa
Alexandrium ostenfeldiia
Gymnodinium catenatuma
Pyrodinium bahamense var.
compressuma
Taxonomic group Locations
Dinoflagellate E & W NA, W Europe, Thailand, Korea,
Japan, Australia, Argentina
Dinoflagellate Cold & temperate: W NA, South Africa,
Japan, Australia, Chile
Dinoflagellate E & W NA
Dinoflagellate Mediterranean, SW Europe, Australia,
New Zealand, Japan
Dinoflagellate W NA, Japan, Argentina, Chile?
Dinoflagellate W Europe Egypt, E & W NA,
Gulf of Mexico, E Asiatic Russia
Dinoflagellate Spain, Portugal, Denmark, Germany,
Mediterranean, Philippines, W NA,
Korea, Japan, Australia, Argentina,
Uruguay, Venezuela
Dinoflagellate Tropical Pacific coastal areas

Amnesic shellfish poisoning/
domoic acid poisoning
Pseudo-nitzschia australis Diatom W NA, W Europe, New Zealand
Pseudo-nitzschia multiseriesa Diatom E & W NA, Gulf of Mexico, W Europe,
Japan, Korea
Pseudo-nitzschia delicatissima Diatom W NA, Gulf of Mexico
Pseudo-nitzschia Diatom E & W NA, Gulf of Mexico
pseudodelicatissimaa
Pseudo-nitzschia pungensa Diatom E & W NA, Gulf of Mexico, New Zealand
Pseudo-nitzschia seriata Diatom W NA, W Europe
Pseudo-nitzschia fraudulenta Diatom New Zealand, Australia
Pseudo-nitzschia turgida Diatom New Zealand

Neurotoxic shellfish poisoning Gymnodinium brevea Dinoflagellate Gulf of Mexico, SE NA

Gymnodinium breve-likea Dinoflagellate New Zealand, Greece, Spain, France,
Israel, Japan, S Africa
Chattonella subsalsaa,b Raphidophyte
Chattonella marinaa,b Raphidophyte Australia
Chattonella antiquaa,b Raphidophyte
Fibrocapsa japonicaa,b Raphidophyte

Ciguatera fish poisoning Gambierdiscus toxicus Dinoflagellate Circumtropical

Ostreopsis lenticularis Dinoflagellate Circumtropical
Ostreopsis siamensis Dinoflagellate Circumtropical
Ostreopsis heptagona Dinoflagellate Circumtropical
Ostreopsis ovata Dinoflagellate Circumtropical
Coolia monotis Dinoflagellate Circumtropical, also temperate
Prorocentrum lima Dinoflagellate Tropical to subpolar
Prorocentrum concavum Dinoflagellate Circumtropical
Prorocentrum mexicanum Dinoflagellate Tropical to temperate
Prorocentrum emarginatum Dinoflagellate Circumtropical
continued

2
 Harmful Algal Blooms

Table 1 – continued
Problem Organism Taxonomic group Locations
Ciguatera fish poisoning Amphidinium carterae Dinoflagellate Circumtropical
Amphidinium klebsii Dinoflagellate Circumtropical

Diarrhoetic shellfish poisoning Dinophysis acuminata Dinoflagellate Widely distributed temperate, eutrophic:
Europe, NE NA, Australia, S Africa
Dinophysis acuta Dinoflagellate Widely distributed, cold temperate:
Europe, New Zealand
Dinophysis caudata Dinoflagellate Widely distributed, tropical to temperate:
Europe, E NA, Gulf of Mexico
Dinophysis fortii Dinoflagellate Widely distributed, temperate:
Mediterranean, Japan, Australia, NW NA
Dinophysis norvegica Dinoflagellate Widely distributed, cold & temperate:
Europe, NE NA
Dinophysis sacculus Dinoflagellate Widely distributed, cold & temperate:
Europe
Dinophysis skagii Dinoflagellate Europe
Dinophysis tripos Dinoflagellate Europe
Prorocentrum lima Dinoflagellate E Canada

Not named Pfiesteria piscicida Dinoflagellate SE NA, Gulf of Mexico

Fish kills and other animal mortalityc

Toxins? Gymnodinium brevea Dinoflagellate Gulf of Mexico
Gymnodinium mikimotoia,d Dinoflagellate ?Australia, W Europe, Japan, Korea,
Gulf of Mexico
Gyrodinium aureoluma,d Dinoflagellate ?Australia, W Europe, Japan, Korea,
Gulf of Mexico, N Africa
Gymnodinium nakasakiensea,d Dinoflagellate ?Japan, S Africa
Gyrodinium pulchellumd Dinoflagellate ?Australia, Gulf of Mexico
Gymnodinium sanguineuma Dinoflagellate Gulf of Mexico
Cochlodinium polykrikioides Dinoflagellate Korea, Japan
Alexandrium monilatuma Dinoflagellate Gulf of Mexico, Pacific coast Ecuador
Prorocentrum minimuma Dinoflagellate Worldwide
Pfiesteria piscicida Dinoflagellate SE NA, Gulf of Mexico
Pfiesteria-like Dinoflagellate SE NA, Gulf of Mexico
Chattonella marinaa Raphidophyte SE Asia, Japan, Australia
Chattonella antiguaa Raphidophyte SE Asia, Japan, Australia
Fibrocapsa japonicaa Raphidophyte Japan
Heterosigma akashiwoa Raphidophyte New Zealand, Chile, British Columbia
Prymnesium parvuum/ Haptophyte Widely distributed, temperate &
patelliferuma subtropical: Europe, Middle East,
Ukraine, China, Australia, USA
Prymnesium calathiferum Haptophyte New Zealand
Prymnesium saltans Haptophyte China
Chryschromulina polylepsisa Haptophyte N Europe
Chryschromulina birgeri Haptophyte Canada, N Europe
Chryschromulina leadbeateri Haptophyte N Europe
continued

3
 Harmful Algal Blooms

Table 1 – continued
Problem Organism Taxonomic group Locations
Toxins? Chryschromulina parva Haptophyte N Europe, New Zealand
(also freshwater)
Aureococcus anophagefferensa Pelagophyte NE coast USA
Aureoumbra lagunensisa Pelagophyte Gulf of Mexico

Mechanical injury Chaetoceros convolutus Diatom W NA, Chile

Chaetoceros concavicornis Diatom W NA, Chile
Leptocylindrus spp.a Diatom Chile
Tabularia affinis Diatom Japan
Dictyocha speculum Silicoflagellate France

Exudates Coscinidiscus centralis Diatom North Sea

Coscinidiscus concinnus Diatom North Sea
Coscinidiscus wailesii Diatom North Sea
Pseudo-nitzschia delicatissima Diatom Adriatic & Tyrrhenian Seas
Thalassiosira mala Diatom Tokyo Bay

Water discoloration (other water-discolouring species have been indicated by: a)

Noctiluca scintillans Dinoflagellate Temperate, subtropical, tropical coastal
waters
Ceratium hircus Dinoflagellate Gulf of Mexico
Katondinium rotundum Dinoflagellate Chesapeake Bay
Mesodinium rubrum Ciliate with crypto- Worldwide
monad symbionts
Phaeocystis spp.e Haptophyte N Europe
Lingulodinium polyedrum Dinoflagellate California, USA, Gulf of Mexico

Low oxygen due to sinking and decomposition of blooms

Ceratium triposa Dinoflagellate NE USA
Ceratium furca Dinoflagellate S Africa
Locations primarily indicate areas where problems have occurred, although for some species their presence is indicative of a problem. NA, North
America; E, east; W, west; N, north; S, south.
a
Species that can form water-discolouring blooms.
b
Japanese and Florida, US isolates produce brevetoxins in culture, but it is unclear if these species contribute to neurotoxic shellfish poisoning in
humans or if brevetoxins are the cause of fish kills.
c
Includes birds, mammals, turtles, invertebrates.
d
Morphologically similar, some consider them the same, others separate them.
e
Causes foam to form on beaches.

which divides to form new vegetative cells (haploid).
Vegetative cells can divide indefinitely, as long as condi-
tions are suitable. Encystment and excystment are often
timed to maximize growth under appropriate conditions.
Finally, all of these species, like many other dinoflagellates,
are motile and capable of vertical migration. This may
allow them to position themselves in the water to optimize
light and nutrients, minimize horizontal transport and thus
maximize growth.
Saxitoxin and a suite of derivatives, which are low-
molecular weight perhydropurine compounds that act as
potent Na 1 -channel blockers, cause PSP. Some deriva-
tives are more toxic than others and additional changes in
the structure and toxicity can occur as the toxins are passed
up the food chain. The exact toxin profile can vary between
different geographic isolates of the same species and is
therefore useful as a marker, for example to establish
transport and introduction to a new area. However, the

4
 Table 2 Major algal toxin groups causing human health problemsa
Syndrome Toxin type Toxins Description of symptoms Duration
Paralytic shellfish poisoning Neurotoxins Saxitoxin and derivatives Tingling/burning of skin and extremities, especially mouth and Starts in 30 min; lasts up to
fingers, loss of muscular coordination, giddiness/staggering, 3 days
drowsiness, dry throat and skin, loss of speech and speech
comprehension, rash, fever, gastrointestinal distress,
respiratory paralysis, death in 2–24 h without immediate
treatment
Amnesic shellfish poisoning/ Neurotoxins Domoic acid Gastrointestinal distress, headache, disorientation, memory Starts in 2–5 h; duration variable
domoic acid poisoning loss, seizures, respiratory difficulty, coma, death
Neurotoxic shellfish Neurotoxins Brevetoxins Tingling and numbness of tongue, throat and lips, muscular Starts in 3–5 h; lasts several days
poisoning aches, gastrointestinal distress, dizziness
Ciguatera fish poisoning Neurotoxins Ciguatoxins, maitotoxin, Gastrointestinal distress, headache, itching, temperature Starts in 12–24 h; usually lasts
gambieric acids, reversal and other abnormal sensations, joint and muscular 1 week, but occasionally
okadaic acid, pain, convulsions/visual hallucinations, dizziness, irregular months to years
prorocentrolid B, pulse/loss blood pressure
haemolysins
Diarrhoetic shellfish Neurotoxins Okadaic acid, Gastrointestinal distress, chills Starts in 30 min to 12 h;
poisoning dinophysitoxins, lasts up to 3 days
pectenotoxins
None Neurotoxins Unknown toxins from Narcosis, sores, reddening of eyes, blurred vision, nausea/ 6 months to 6 years, depending
Pfiesteria piscicida vomiting, sustained difficulty breathing, kidney/liver on exposure
dysfunction, memory loss, cognitive impairment
None Neurotoxins Anatoxin-A and Staggering, gasping, muscle fasciculations, cyanosis, Minutes to hours
homoanatoxin-A respiratory arrest, death
None Neurotoxins Anatoxin-A(S) Hypersalivation, lacrymation, diarrhoea, ataxia, death Minutes to hours
None Hepatotoxins Microcystins and Short-term response to acute exposure: weakness/recumbency, Hours
nodularins pallor, vomiting, diarrhoea, pooling of blood in liver,
respiratory arrest, death
Long-term response to acute exposure: liver failure, death Days
Long-term response to chronic, lower level exposure: Years
liver cancer
None Cytotoxins Cylindrospermopsin Vomiting, headache, abdominal pain, enlarged and tender liver, Days to weeks

Harmful Algal Blooms

diarrhoea, severe electrolyte imbalance
Swimmer’s itch Dermatoxins Aplysiatoxins, Acute dermatitis, asthma-like symptoms Immediate
debromoaplysiatoxins
and oscillatoxin-A
a
Toxin groups may include a single toxin or a suite of derivatives with different toxicity. Symptoms are listed in order of increasing severity and are usually dose-dependent, so most serious
symptoms may not occur frequently. Many less frequently occurring or less well understood toxins are not included.
5
 Harmful Algal Blooms
amount, and sometimes the composition, of toxins can be
determined by environmental factors. Cysts are sometimes
more toxic than vegetative cells and can lead to PSP
outbreaks if they are consumed by shellfish. The role of
bacteria in toxin production is much debated and may be at
the root of the polyphyletic occurrence of toxins.
Amnesic shellfish poisoning or domoic acid poisoning
Amnesic shellfish poisoning (ASP) was first discovered in
1987 when 107 people became sick from eating mussels
from Prince Edward Island, Canada and three died. The
source of the illness was rapidly traced to domoic acid,
produced by a large bloom of the diatom Pseudo-nitzschia
multiseries, which was consumed by the mussels. There
have been no further confirmed reports of human illnesses,
but numerous other incidents have occurred which verify
the seriousness of the problem. Pelicans, cormorants and
elephant seals have died near California and Mexico after
consuming filter-feeding fish contaminated with domoic
acid. Razor clam and Dungeness crab fisheries on the
Pacific coasts of the USA and Canada and mussel and soft-
shell clam harvesting in the Bay of Fundy (Canada) were
closed due to high levels of domoic acid. The illness is called
ASP because permanent loss of short-term memory is one
of the distinguishing symptoms (Table 2), but since
organisms other than shellfish can accumulate and
transmit the toxin it is also called domoic acid poisoning
(DAP).
Domoic acid, an analogue of the neurotransmitter
glutamate, is produced by the only known toxic diatoms,
some members of the genus Pseudo-nitzschia (Table 1) and,
perhaps, Amphora coffeaeformis. Pseudo-nitzschia spp.
have been recognized as abundant members of the
plankton for a long time (Fryxell et al., 1997), but were
not considered toxic. Domoic acid production is enhanced
by factors that limit growth, such as phosphorus or silicate
or low temperature, as long as light and nitrogen
availability is adequate. The presence of bacteria enhances
toxin production, but is not required. The difficulty
distinguishing toxic and nontoxic species and the variable
toxicity within one species enhances the difficulty of
routine monitoring for ASP and necessitates the develop-
ment of new methods.
The life cycle of Pseudo-nitzschia spp. is not yet well
understood. Under good environmental conditions the
cells divide vegetatively and form long chains. The chains,
which can form spirals, remain suspended in the water
(Fryxell et al., 1997). If nutrients become limiting or the
cells become too small, the cells in the chain break apart
and sink to the bottom. Sexual reproduction between
‘male’ and ‘female’ clones has been observed in the
laboratory and may occur on the sea bottom or in
suspended clumps in the natural environment (Fryxell
et al., 1997).
6
Neurotoxic shellfish poisoning
Neurotoxic shellfish poisoning (NSP) is caused by the
dinoflagellate Gymnodinium breve, which occurs primarily
along the western coast of Florida, but can occur
throughout the Gulf of Mexico and as far north as North
Carolina along the eastern US coast (Table 1). G. breve-like
organisms, some of which produce toxins, have recently
been observed worldwide (Table 1). In Florida G. breve
blooms start offshore and can continue there for long
periods of time. Although the life cycle has not been fully
elucidated, G. breve is thought to produce cysts which may
have a role in bloom initiation or transport. Satellite
remote sensing has been used to show that blooms of
vegetative cells can be transported long distances by major
ocean currents, causing problems in widely separated
areas.
Although the toxins are not fatal, the blooms are a major
threat to human health and cause significant ecological and
economic damage when they are transported into shallow
coastal areas. Shellfish become toxic at very low cell
abundance, so harvesting must be closed. Extensive fish
kills occur and dead fish wash up on beaches in areas where
tourism is important. Toxins can be aerosolized in the surf,
causing outbreaks of eye irritation and respiratory
problems in coastal communities. Recently, unusual
numbers of manatee deaths have been attributed to
accumulation of brevetoxins.
Brevetoxins are a suite of polyether toxins, which
activate voltage-sensitive Na1 channels and alter synaptic
transmission. Initially G. breve was thought to be the only
producer of brevetoxins, but several raphidophytes
(Table 1), known to cause fish kills, have recently been
shown to produce brevetoxins. Brevetoxins have chemical
and biosynthetic affinities with toxins causing ciguatera
fish poisoning and diarrhoetic shellfish poisoning, suggest-
ing evolutionary links. The amount and composition of
toxins varies between isolates and is affected by environ-
mental conditions.
Ciguatera fish poisoning
Ciguatera fish poisoning (CFP) results from the consump-
tion of fish harvested from tropical/subtropical reefs.
Herbivorous fish can become toxic from consuming
dinoflagellates, which are epiphytic on macroalgae,
seagrasses or hard substrates, benthic or planktonic, and
higher trophic level fish accumulate the toxin from their
prey. The incidence and severity of CFP is highly variable.
Although it is rarely fatal, it is a severe enough illness to
prevent the use of fish as a protein source in many areas.
Originally, the list of causative dinoflagellate species
included Gambierdiscus toxicus, Ostreopsis lenticularis,
O. siamensis, Coolia monotis, Prorocentrum lima, P.
concavum, P. mexicanum, P. emarginatum, Amphidinium
carterae and A. klebsii. Additional species from these
genera and others have been identified as part of the same

reef communities and some are known to produce toxins.
Variations in species composition between and within reefs
and in response to environmental conditions may explain
some variations in CFP. In addition, the different genera
produce a variety of toxins (Table 2), which have different
effects. Most of the toxins are polyethers, but they differ
considerably in structure and, to the extent that it is known,
mode of action. For example, the two main toxins are
ciguatoxins, which activate voltage-sensitive Na 1 chan-
nels, as do brevetoxins, and maitotoxin, which may
activate voltage-sensitive Ca2 1 channels. Further, toxicity
can be influenced by environmental factors such as
temperature and phosphate availability.
Diarrhoetic shellfish poisoning
Diarrhoetic shellfish poisoning (DSP) is the least serious of
the human health problems caused by algal biotoxins
(Table 2). Because the symptoms are similar to common
viral diseases harboured by shellfish, DSP incidence may
be underestimated. The economic consequences of out-
breaks can be severe, especially in Europe where mussel
mariculture is a major industry and the incidence has
increased.
The primary toxins responsible for DSP, the linear
polyethers okadaic acid and dinophysitoxins, inhibit
protein phosphatases. Some members of the planktonic
dinoflagellate genus, Dinophysis, and some benthic or
epiphytic Prorocentrum spp. (see CFP), produce both
(Table 1). Since the toxins are quite potent, 51000 cells per
litre is enough to cause an outbreak if the cells are toxic.
Most outbreaks of DSP are attributed to Dinophysis spp.
because of their planktonic habit and wider distribution;
however, many planktonic Prorocentrum spp. have never
been tested for toxin production and at least one, P.
minimum, was associated with many human deaths in
Japan (venerupin poisoning; Okaichi and Imatomi, 1979).
No Dinophysis spp. have ever been cultured, seriously
hampering studies of toxin production, life cycles and
environmental conditions favouring growth. From field
data, they are often found when the water is highly
stratified and temperatures are high. They are capable of
vertical migration, which may help them concentrate in
layers of high water stability. Nutrients do not appear to
stimulate their growth, and many are mixotrophic, but
toxin productions seems to be associated with photosynth-
esis. In Prorocentrum spp., which can be cultured, toxin
content increases as cell growth decreases in response to a
variety of environmental factors. Significant proportions
of the most active toxins are excreted, suggesting they may
have a role in interspecific competition.
Pfiesteria piscicida
In 1992 the dinoflagellate Pfiesteria piscicida was first
described because it was responsible for a large number of
massive fish kills in the Pamilico-Albemarle estuary
Harmful Algal Blooms
(Southeast USA) (Burkholder and Glasgow, 1997). As a
generalist toxic ambush predator it has an unusual mode of
action. Subsequently, it was found to be more widely
distributed and other Pfiesteria-like species were discov-
ered (Table 1). Further, it produces toxins with serious
human health impacts (Table 2), although human response
has only been documented in a few cases. The toxins have
not yet been identified, but both water-and lipid-soluble
toxins are produced.
Pfiesteria piscicida is a dinoflagellate with a very complex
life cycle that is not yet well understood. It forms at least 24
flagellated, amoeboid and cyst stages. Some are toxic; they
range in size from 5 to 450 mm. Cysts or amoeboid forms,
which live in sediments, are triggered to form flagellated
zoospore stages and toxins by animal excreta. The toxins
narcotize their prey, cause the skin to slough off, and
induce formation of ulcerative lesions, which allows
further attack. Zoospores can then go through sexual
reproduction and form cysts or nontoxic amoeboid stages.
Amoeboid stages and nontoxic zoospores can stay in the
water, feeding on bacteria, algae and microzooplankton,
until fish are again available. Sometimes nontoxic zoos-
pores acquire chloroplasts from algal prey, which supply
their nutritional needs by photosynthesizing. The diverse
life cycle stages and lack of distinguishing morphological
features in any stage make this taxon difficult to monitor in
the natural environment.
With so many life cycle stages it is difficult to determine
how environmental factors control its growth. Pfiesteria
piscicida has probably always been present in estuaries, but
there has been a big increase in estuarine fish kills,
especially of menhaden which form large schools, in some
highly eutrophic estuaries. Field studies suggest that
zoospore abundance and fish kills are more likely in areas
with high organic loading from sewage or animal wastes
(hog or chicken). Laboratory culture studies confirm that it
is either directly or indirectly stimulated by elevated levels
of organic and inorganic nitrogen or phosphorus, depend-
ing on the stage.
Animal mortality problems
Animals, including invertebrates, fish, birds, turtles and
other mammals, are affected by the HABs that cause
human illness and death and a wide variety of other HAB
species (Table 1). Although massive animal mortality is the
most obvious sign of a problem, much more subtle effects
that are difficult to quantify are also possible. Ecosystem
structure can be radically altered if some organisms
succumb to algal toxins and others do not. Fisheries
recruitment can be severely negatively affected if larval fish
are susceptible to low levels of toxins (Smayda, 1992). The
survival of endangered species can be threatened, as, for
example, the manatees in southern Florida.
The mechanism by which HABs affect animals is often
not known, as most HAB research has been concerned with
7
 Harmful Algal Blooms
the effect on human health. Thus, there are many fish-
killing species (Table 1) that are suspected of producing
toxins, but no toxin has ever been isolated or identified.
HABs can also cause mortality or disease by being
nutritionally unsuitable (perhaps Aureococcus anophagef-
ferens and Aureoumbra lagunensis; Table 1), by having
sharp spines which lacerate gills (mechanical damage,
Table 1), and by producing copious quantities of mucous
and clogging gills (exudates, Table 1).
Both wild and penned animals can suffer the negative
impacts of HABs, but the economic damage is most easily
assessed for mariculture. Fish and shellfish mariculture has
increased substantially in coastal areas. Concomitant
economic losses due to HABs have also increased for two
reasons. The waste products from such operations are high
in nutrients, which may stimulate HABs, and they are often
sited at high densities in areas with poor flushing for
nutrient removal. Simultaneously, there is heightened
vigilance for HABs because of the economic value of the
cultured organisms. Consequently, there is increased
research into fish-killing HABs.
Other harmful effects
Most of the other harmful effects result from the
accumulation of large quantities of biomass. Only a few
well-known species are included as examples in Table 1.
Table 3 Cyanobacterial species and the toxins they produce
Species
a a
Anabaena flos-aquae , circinalis (hassallii), lemmermannii,
planktonica, spiroides, variabilis
Anabaenopsis milleria
Aphanizomenon flos-aquaea
Aphanizomenon ovalisporum
Aphanizomenon spp.
Cylindrospermopsis raciborskii
Cylindrospermum spp.
Leptolyngbya (5Lyngbia) perelegans
Lyngbia gracilis
Lyngbia majusculaa
Lyngbia wolleii
Microcystis aeruginosa, botrys, viridis, wesenbergii
Nodularia spumigenaa
Nostoc spp.
Oscillatoria acutissima, ahardhii, formos, limosa, rubescens
Oscillatoria nigroviridisa
Phormidium abronema, animale
Planktothrix mougeotii
Schizothrix calcicolaa
Trichodesmium thiebuatii a
Umezakia natans
a
Species that may be found in marine or brackish environments.
8
Many species, including many toxic species, form easily
visible coloured or bioluminescent (only some dinoflagel-
lates) blooms. Since it is difficult to distinguish between
harmless and harmful blooms, persistent or large-scale
blooms often result in public outcry. Algae produce
volatile and water-soluble compounds, so a bloom can
have a distinctive smell and impart a taste to the
water, although this is more of a problem with freshwater
HABs. Phaeocystis spp. blooms cause billows of foam to
form on beaches (Table 1). Finally, when blooms end
suddenly the algae may sink to the bottom, decompose,
and deplete the oxygen dissolved in the water at the
bottom, resulting in extensive invertebrate and fish kills.
Almost any alga that reaches very high biomass can cause
hypoxia/anoxia.
Freshwater Harmful Algal Blooms
HABs in freshwater are almost always composed of
colonial cyanobacteria. These organisms are not strictly
speaking algae, because they are prokaryotes, but they are
functionally similar to algae and used to be called blue-
green algae. Although there are many kinds of cyanobac-
teria, the HABs (Table 3) are a much smaller group of
taxonomically diverse species that tend to form large
blooms. Some freshwater cyanobacterial HAB species can
Toxin groups
Microcystins, Anatoxin-A, Anatoxin-A(S), Saxitoxin
derivatives
Microcystins
Saxitoxin derivatives
Cylindrospermopsin
Anatoxin-A
Cylindrospermopsin
Anatoxin-A
Microcystins
Dermatoxins
Dermatoxins, Gastrointestinal toxins
Saxitoxin derivatives
Microcystins
Nodularins
Microcystins
Anatoxin-A, Homoanatoxin, Microcystins
Dermatoxins, Microcystins
Microcystins
Microcystins
Dermatoxins
Similar to anatoxin-A
Cylindrospermopsin

also bloom at low salinities in estuaries, and a few are
strictly marine species, but much less is known about
cyanobacterial HABs in estuarine/marine systems. Blooms
usually occur under conditions of high nutrient avail-
ability, water column stability, temperature and light. The
bloom-forming cyanobacteria tend to have low growth
rates, but have several characteristics that may give them
an advantage. In particular, many are able to produce gas
vesicles that make them positively buoyant, allowing them
to form mats on the water surface in calm weather. This
gives them greater access to light, carbon dioxide, which
may be in short supply in the water during freshwater
blooms but plentiful in the atmosphere, and nitrogen.
Some cyanobacterial bloom species are able to fix atmo-
spheric nitrogen, which makes them independent of
nitrogen availability in the water, although they still need
phosphorus from the water.
Between 40 and 70% of freshwater cyanobacterial
blooms are toxic. At present there are approximately 60
known toxins, including neurotoxins, hepatoxins, cytotox-
ins, dermotoxins and gastrointestinal toxins (Table 1). A
single species can produce toxins from several different
toxin groups, sometimes at the same time (Table 3).
Cyanobacterial blooms have been observed in 44 countries
and all oceans except the Arctic and Antarctic, and many
species may have very wide geographic distribution. The
most common toxic genera are Microcystis, Anabaena,
Oscillatoria, Aphanizomenon and Nodularia from tempe-
rate areas and Cylindrospermopsis from tropical areas.
Toxins are usually produced and stored intracellularly, but
can be released into the water under stress. The greatest
threat to human health is blooms that occur in municipal
water supplies. Toxins can be ingested, come into contact
with skin, or inhaled (during showers). The standard
treatment for public water supplies, chlorination followed
by filtration, tends to release the toxin into the water.
Common treatments to remove blooms may also release
the toxins, so during toxic blooms other, more costly,
treatments are necessary. Human deaths are relatively rare
but livestock deaths due to drinking water with cyano-
bacterial blooms are well known. Illness can also occur
from recreational use of water bodies with blooms if the
toxins are inhaled or ingested or skin contact occurs.
Shellfish and fish can also accumulate toxins, but this is not
a major route for human toxicity. The toxin content and
composition of cyanobacteria is determined by environ-
mental factors and there are toxic and nontoxic strains of
the same species. Thus, knowing the species composition of
a cyanobacterial bloom is not sufficient for determining
whether toxins are being produced.
Cyanobacterial blooms have impacts besides their threat
to human health. They produce compounds that impart a
bad taste and smell to water, even when they are not toxic.
Fish take up some of these compounds, giving fish such a
bad taste that they are inedible. When toxins are
transferred to higher trophic levels they can cause fish kills
Harmful Algal Blooms
and other animal mortalities. Finally, cyanobacterial
blooms produce huge amounts of biomass. As in marine
blooms, the sudden death and sinking of a bloom can cause
hypoxia/anoxia, which can lead to fish and other animal
deaths.
Current Global Situation
HABs are natural phenomena that have always occurred.
Long before the causative agents were identified, red tides
and their effects were noted. Red tides and fish kills due to
G. breve in Tampa Bay, Florida were noted by the Spanish
explorer, Alvar Nuñez Cabeza de Vaca in 1542, and two
crewmembers of Captain George Vancouver’s expedition
to British Columbia (Canada) were killed by PSP in 1793.
In the last 20 or so years there has been an apparent
increase in HABs. The frequency of blooms has increased
(Hong Kong, Seto Inland Sea, Korean coastal waters),
blooms of certain taxa have spread to new areas (G.
catenatum, Pyrodinium bahamense var. compressum) and
new species are suddenly causing problems (Pseudo-
nitzschia spp., Pfiesteria piscicida). Initially, there was
debate as to whether there was a genuine increase, because
the observational effort is much greater now than in the
past, but most accept that the growth is real. Several
hypotheses are given to explain the recent increases,
including escalating coastal eutrophication, ballast water
transport, transport of live shellfish and increasing
mariculture/aquaculture (Anderson, 1995). Some changes
may also be due to natural climatic variation.
Nutrient inputs to rivers, lakes and coastal areas have
increased substantially from a variety of sources. This has
stimulated the growth of all algae and provides a better
environment for HAB species, many of which may need
higher nutrient availability. Further, while nitrogen and
phosphorus availability has increased, silicate, which is
required by diatoms, has stayed the same or decreased.
Since most HAB species do not require silicate, their
growth is favoured over diatoms, which would otherwise
predominate under eutrophic conditions when silicate is
plentiful (Smayda, 1989). The role of increased eutrophi-
cation in causing more frequent cyanobacterial blooms in
freshwater systems is widely understood. In coastal areas
the impact of increased nutrient inputs on increased HABs
has been documented in a few areas, but direct evidence
from other areas is still lacking, in part because of a lack of
long-term data.
Some of the outbreaks of HABs in new areas have been
shown to result from transport in ballast water (Halle-
graeff, 1998). Many HABs form cysts, which allow them to
survive long periods in dark ballast tanks. If ballast water is
taken on during an HAB in one harbour and dumped in an
area with similar environmental conditions, the odds of
introducing a new species are increased. Similarly, live
9
 Harmful Algal Blooms
shellfish can contain cysts or vegetative cells in the water
inside the shell or in the gut, which can be spread to a new
area. In both cases high nutrient inputs in the new area are
likely to increase the chance of survival for the introduced
species.
A number of strategies are being investigated to prevent
or mitigate HAB problems. Efforts are under way to reduce
nutrient inputs to coastal areas. There is growing aware-
ness that site location and density of mariculture/
aquaculture operations is critical in avoiding HABs.
International agreement has been reached that some form
of ballast water treatment is necessary. Safe and economic-
al methods are not yet available, although heat treatment
looks promising (Hallegraeff, 1998). Flocculation of
blooms with clay is being investigated as a short-term
emergency remedy (Anderson, 1997). Finally, there is a
search for species-specific viral (Garry et al., 1998) and
bacterial pathogens that would selectively kill or disable
HAB species.
References
Anderson DM (1995) Toxic red tides and harmful algal blooms: a
practical challenge in coastal oceanography. Reviews of Geophysics 33
(supplement): 1189–1200.
Anderson DM (1997) Turning back the harmful red tide. Nature 388:
513–514.
Burkholder JM and Glasgow Jr HB (1997) Pfiesteria piscicida and
other Pfiesteria-like dinoflagellates: behavior, impacts, and environ-
mental controls. Limnology and Oceanography 42: 1052–1075.
[Supplement 2.]
Fryxell GA, Villac MC and Shapiro LP (1997) The occurrence of the
toxic diatom genus Pseudo-nitzschia (Bacillariophyceae) on the West
Coast of the USA, 1920–1996: a review. Phycologia 36: 419–437.
Garry RT, Hearing PH and Cosper EM (1998) Characterization of a
lytic virus infectious to the bloom-forming microalga Aureococcus
anophagefferens (Pelagophyceae). Journal of Phycology 34: 616–621.
Hallegraeff GM (1998) Review. Transport of toxic dinoflagellates via
ships’ ballast water: bioeconomic risk assessment and efficacy of
possible ballast water management. Marine Ecology Progress Series
168: 297–309.
Okaichi T and Imatomi Y (1979) Toxicity of Prorocentrum minimum var.
Mariae-lebouriae assumed to be causative agent of short-necked clam
poisoning. In: Taylor DL and Seliger HH (eds) Toxic Dinoflagellate
Blooms, pp. 385–388. New York: Elsevier/North Holland.
10
Smayda TJ (1989) Primary production and the global epidemic of
phytoplankton blooms in the sea: a linkage? In: Cosper EM, Carpenter
VM and Bricelj EJ (eds) Novel Phytoplankton Blooms, pp. 449–483.
Berlin: Springer.
Smayda T (1992) Global epidemic of noxious phytoplankton blooms
and food chain consequences in large ecosystems. In: Sherman K (ed.)
Food Chains, Yields, Models, and Management of Large Marine
Ecosystems, pp. 257–307. Boulder, CO: Westview Press.
Further Reading
Anderson DM and Garrison DJ (eds) (1997) The ecology and
oceanography of harmful algal blooms. Limnology and Oceanography
42 (5, part 2).
Anderson DM, Cembella AD and Hallegraeff GM (eds) (1998)
Physiological Ecology of Harmful Algal Blooms. NATO ASI Series
G. Ecological Sciences 41. Berlin: Springer.
Chorus I and Bartram J (eds) (1999) Toxic Cyanobacteria in Water. A
Guide to their Public Health Consequences, Monitoring and Manage-
ment. London: World Health Organization, Routledge.
Hallegraeff GM (1993) Review of harmful algal blooms and their
apparent global increase. Phycologia 32: 79–99.
Hallegraeff GM, Anderson DM, Cembella AD and Enevoldsen H (eds)
(1995) Manual on Harmful Marine Microalgae. UNESCO, Inter-
governmental Oceanographic Commission 33, Paris.
Lassus P, Arzul G, Erard-Le Denn E, Gentien P and Marcaillou-Le Baut
C (eds) (1995) Harmful Marine Algal Blooms. Proceedings of the Sixth
International Conference on Toxic Marine Phytoplankton, October
1993, Nantes, France. Paris: Lavoisier.
Moestrup Ø, Blackburn S, Preisig H, Sivonen K and Kononen K (eds)
(1996) Proceedings of the First International Congress on Toxic
Cyanobacteria (Blue Green Algae) Bornholm 20–24 August 1995, and
First Maj and Tor Nessling Foundation Symposium on Recent
Developments in Cyanobacterial Reserach, Helsinki, 16–18 August
1995. Phycologia 35 (6 supplement).
Reguera B, Blanco J, Fernandez ML and Wyat T (eds) (1998)
Harmful Algae. Proceedings of the VIII International Conference,
Vigo, 1997. Xunta de Galicia and Intergovernmental Oceanographic
Commission of UNESCO. GRAFISANT, Santiago de Compostela,
Spain.
Smayda TJ and Yuzuru Shimizu (eds) (1993) Toxic Phytoplankton
Blooms in the Sea. Proceedings of the Fifth International Conference
on Toxic Marine Phytoplankton, Newport, RI, October 28–Novem-
ber 1 1991. Amsterdam: Elsevier.
Yasumoto T and Murata M (1993) Marine toxins. Chemical Reviews 93:
1897–1909.