ALGAE

Presented by BSN-2A
Introduction

 Singular alga members of a group of

predominantly aquatic, photosynthetic
organisms of the kingdom Protista.
 They range in size from the tiny flagellate
Micromonas that is 1 micrometre (0.00004
inch) in diameter to giant kelp that reach
60 metres (200 feet) in length
 Algae provide much of the Earth's oxygen,
they are the food base for almost all
aquatic life, they are an original source of
petroleum products, and they provide foods
and industrial products for humans.
 The algae have many types of life cycles,
from simple to complex.

 Their photosynthetic pigments are more

varied than those of plants, and their cells
have features not found among plants and
animals.
 Some algae are ancient, while other groups
have evolved more recently.
 The taxonomy of algae is changing rapidly
because so much new information is being
discovered.

 The study of algae is termed phycology, and

one who studies algae is known as a
phycologist.
Etymology
 The singular alga is the Latin word for a
particular seaweed and retains that meaning
in English.
 The etymology is obscure. Although some
speculate that it is related to Latin algēre,
"be cold"
 A more likely source is alliga, "binding,
entwining."
 The ancient Greek word for seaweed was
φῦκος (fūkos or phykos), which could mean
either the seaweed, probably Red Algae, or
a red dye derived from it.

 The Latinization, fūcus, meant primarily the

cosmetic rouge.
 Biblical ‫( פוך‬pūk), "paint" (if not that word
itself), a cosmetic eye-shadow used by the
ancient Egyptians and other inhabitants of
the eastern Mediterranean.
The lineage of algae according to
Thomas Cavalier-Smith.
Click icon to add picture

Representative algae.
 Images of
Macroscopic Algae
Hormosira banksii
Halimeda discoidea
Laminaria digitata
Fucus serratus
Acetabularia.
 Images of
Microscopic Algae
Drapomaldia
Stauroneis
Hyalotheca
Diatom
Phaeoplaca
Bambosina.
 HUMAN DISEASES
RELATED TO ALGAE
INTOXICATION
Paralytic shellfish poisoning
 numbs the face and extremities for a few days post-
ingestion
 is one of the four recognized syndromes of
shellfish poisoning
 the others being neurotoxic shellfish poisoning,
diarrhetic shellfish poisoning and amnesic shellfish
poisoning.
Epidemiology
 Children are more susceptible
 listed as a ”rare disease" by the Office of Rare
Diseases (ORD) of the National Institutes of Health
(NIH)
 affects less than 200,000 people in the US
population( NIH)
 affects 1 person per 2,000
 The toxins responsible for most shellfish
poisonings are water-soluble, heat and acid-stable,
and ordinary cooking methods do not eliminate the
toxins
 Saxitoxin is probably the most toxic compound
known and is 100,000 times more toxic than
cocaine

 Some shellfish can store this toxin for several

weeks after a harmful algal bloom (HAB) passes,
but others such as butter clams are known to store
the toxin for up to two years.
Causative organisms
 Dinoflagellates (class Dinophyceae) and diatoms,
and cyanobacteria
 Alexandrium tamarense and Gymnodinium
catenatuma
 Patients who are severely immunocompromised
can develop disseminated disease, which is often
fatal. Note the following:
 Localized infection: In immunocompetent
individuals, the infection usually remains confined
to the skin at the site of inoculation. Olecranon
bursitis can develop from protothecosis. Rarely,
tenosynovitis can occur and has been reported
following injection of a sclerosing agent for
varicose vein treatment.4
 Systemic infection: Rare cases of systemic
infection occur almost exclusively in patients who
are severely immunocompromised, as in patients
receiving chemotherapy, or immunosuppressed
patients, such as those on infliximab. Involvement
of the meninges has been reported in a few cases of
patients with AIDS.
 Protothecosis typically affects those older than 30
years or elderly persons, although pediatric cases
have been reported.
Dinoflagellate
Diatom

Highly Magnified
Cyanobacteria
Toxin Induced
 The main toxin responsible saxitoxin,
 neosaxiton and gonyautoxins I to IV
Vessels of toxin

 Bivalve mollusk
Filter feeders and, therefore, accumulate toxins produced by
microscopic algae, such as dinoflagellates and diatoms, and
cyanobacteria.

 Mussels
 Clams
 oysters
 scallops
MUSSELS
CLAMS

(Left) Quahog (Mercenaria); (right) soft-shell clam (Mya)

Oyster

Oyster toadfish (Opsanus tau). European flat oyster (Ostrea edulis)

SCALLOPS
SYMPTOMS
 10-30 minutes after ingestion
 symptoms can include:
nausea, vomiting, diarrhea,
abdominal pain, and tingling
or burning lips, gums,
tongue, face, neck, arms,
legs, and toes. Shortness of
breath, dry mouth, a choking
feeling, confused or slurred
speech, and lack of
coordination are also
possible.
Treatment
 Prehospital Care

 Support and maintenance of the airway are of

crucial importance in PSP
Emergency Department Care
 Therapy for all shellfish poisonings is supportive
and symptom-driven.

 Gastrointestinal decontamination with activated

charcoal is recommended for patients who present
within 4 hours of ingestion. Nasogastric or
orogastric lavage may be performed if the patient
presents within 1 hour of ingestion, but this is often
unnecessary.
 If gastric lavage is performed, the use of isotonic
sodium bicarbonate solution as a lavage irrigant has
been suggested because many of the shellfish
toxins have reduced potency in an alkaline
environment.
 Okadaic acid undergoes enterohepatic recycling
that could be interrupted by delayed or repeat
charcoal administration.
 The greatest danger is respiratory paralysis. Close
monitoring for at least 24 hours and aggressive
airway management at any sign of respiratory
compromise should prevent severe morbidity and
mortality.
 Neostigmine and edrophonium have been used to
improve muscle weakness following tetrodotoxin
intoxication, which is similar to saxitoxin
intoxication. Nonetheless, no clinical trials have
evaluated the use of these drugs for saxitoxin
exposures.
Medication
(Care is primarily symptomatic and
supportive)

GI decontaminant
GI decontaminants are empirically used to minimize
systemic absorption of the toxin. They may only be
beneficial if administered within 1-2 h of ingestion.
 Activated charcoal (Liqui-Char)

Emergency treatment in poisoning. Network of

pores present in activated charcoal adsorbs 100-
1000 mg of drug per gram of charcoal. Does not
dissolve in water. For maximum effect, administer
within 30 min of ingesting poison.
Cathartic not to be used in children <2 y.
Ciguatera
 causes distress and dysfunction in all sorts of
systems including the respiratory system, the
nervous system, and the gastrointestinal system
 most common nonbacterial, fish-borne poisoning in
the United States
 More than 400 species of fish have been implicated
in ciguatera poisoning
Epidemiology
 caused by consumption of reef fish that feed on
certain dinoflagellates (ie, algae) associated with
coral reef systems.
 At least 5 types of ciguatoxin have been identified
and are noted to accumulate in larger and older fish
higher up the food chain.
 Ciguatera poisoning seldom is lethal
 Children appear to be affected more severely and
are involved more often in life-threatening cases.
 Ciguatera poisoning has been a significant concern
in tropical areas for centuries
 generally is believed to be confined to coral reef
fish in water between the latitudes of 35 degrees
north and 35 degrees south
 elevations of sea surface temperatures may expand
the band of concern above and below the 35th
degree parallels
 some areas may become too warm for the
dinoflagellates to flourish
 in the modern era of world travel and rapid
transportation, many warm-water fish are available
commercially in markets throughout the world, and
cases of ciguatera poisoning may be seen in any
location.
Causative Organisms
 Dinoflagellates (Gambierdiscus toxicus /
Ostreopsis.)
Toxins Induced
 ciguatoxin
Vessels of toxin
 groupers, amberjack, red snappers, eel, sea bass,
barracuda, and Spanish mackerel.
 Fish larger than 2 kg contain significant amounts of
toxin and readily produce toxic effects when
ingested
Groupers
Red Snapper
Barracuda
Amberjack
 Greater amberjack(S. dumerili) of the tropical
Atlantic is one of the largest members of the jack
family, often attaining lengths of 1.8 m (6 feet)
Eel

Adult male ribbon eels

(Rhinomuraena quaesita) Moray eel (Gymnothorax javanicus).
Sea Bass

Largemouth black bass (Micropterus

Black sea bass (Centropristis striata) salmoides)
Spanish Mackerel
 any of a number of swift-moving, streamlined food
and sport fishes found in temperate and tropical
seas around the world, allied to tunas in the family
Scombridae (order Perciformes)
Symptoms
 Onset of symptoms may be within 15 minutes or as
late as 24 hours (rarely) after ingestion of the toxin
 Generally, symptoms are noted within 6-12 hours
after ingestion of tropical reef fish
 Symptoms increase in frequency and severity over
the subsequent 4-6 hours
 symptoms are numerous but commonly affect 3
major organ systems: GI, neurologic, and
cardiovascular
 GI symptoms often are the first to appear, may last
1-2 days, and include the following:
 Abdominal pain
 Nausea
 Vomiting
 Diarrhea
 Neurologic symptoms usually are multiple, varied,
and, at times, bizarre. Symptoms may begin within
a few hours to 3 days after the meal and can be
persistent, lasting weeks to several months.
Symptoms may include the following:
 Lingual and circumoral paresthesias
 Painful paresthesias of the extremities
 Paradoxical temperature reversal (eg, cold objects feel hot and hot objects
feel cold) (This is a classic reported finding; however, at least one study
suggests that this perception is likely the result of the exaggerated and
intense nerve depolarization and that gross temperature perception remains
intact).
 Dental pain (teeth feel loose)
 Pruritus
 Arthralgias
 Myalgias
 Weakness
 Ataxia, vertigo
 Respiratory paralysis
 Coma
 Cardiovascular symptoms are less common but can
be severe. They usually resolve within 2-5 days.
Patients may experience weakness and dizziness
from bradycardia and hypotension.
 Other features include
dyspnea, sweating,
salivation, chills, neck
stiffness, and pruritus.
 Physical
 Dehydration from GI losses is a common finding.
 Neurologic findings are extremely variable, from mild to life
threatening.
 Cardiovascular findings include bradycardia and hypotension.
Signs of shock may be observed. Hypotension results from
the following:
 Fluid loss
 Bradycardia
 Peripheral vasodilation
 Myocardial depression
Treatment
 Emergency Department Care
 Treatment of ciguatera poisoning is largely supportive
and symptom driven.
 GI decontamination with activated charcoal may be of
value if performed within 3-4 hours of ingestion.
Avoid syrup of ipecac because of its potential to
worsen fluid losses. Orogastric lavage is not
recommended; it is not of proven benefit for ciguatera
poisoning, and risks of this procedure are likely to
outweigh benefits.
 Antiemetics may control nausea and vomiting.
 Cool showers and antihistamines have been
recommended to relieve pruritus.
 Manage hypotension with volume replacement.
Pressor agents rarely are needed.
 Bradyarrhythmias respond well to atropine.
 Medication
 Medications used to treat ciguatera poisoning include
 neurologic agents
 serotonin-norepinephrine reuptake inhibitors,
 Antihistamines
 Analgesics
 antipyretics
 nti-inflammatories
 Diuretics, osmotic
 These agents are used empirically to treat
neurologic symptoms associated with ciguatera
poisoning.
amnesiac shellfish poisoning
 to a loss of short term
memory---the ultimate
"lost car keys" syndrome
 The toxins responsible for
most shellfish poisonings
are water-soluble, are heat
and acid-stable, and are
not inactivated by ordinary
cooking methods.
Epidemiology
 Toxic outbreaks often are associated with algal
blooms of single-celled dinoflagellates, which can
cause a red-brown discoloration of the water.
 proliferation of toxic dinoflagellates, known as red
tide, is favored by warmer weather
 Most recent cases of PSP have occurred along the
northeast Atlantic coast, northwest Pacific coast, or
Alaska.
 Most cases have involved recreational shellfish
collectors, not commercial vendors.
 Since 1927, a total of 500 cases of PSP and 30
deaths have been reported in California.
 The 2008 Annual Report of the American
Association of Poison Control Centers' National
Poison Data System documented 752 single
exposures to paralytic shellfish; no deaths occurred.
 Sporadic outbreaks have been reported in Europe,
Asia, Africa, and the Pacific Islands.
 The mortality rate in the only known outbreak of
ASP was 3%.
 all the reported deaths from ASP have been in
elderly persons who had more severe neurologic
symptoms.
Causative Organism
 dinoflagellates of the Gonyaulax species (red tide).
 Prototheca wickerhamii
 Less commonly, infection occurs with Prototheca
zopfii.
Toxin Induced
 Domoic acid
Vessel of toxin
 Bivalve mollusks
Symptoms
 Amnestic shellfish poisoning
 The only reported outbreak occurred in 1987 and affected
more than 100 people after eating mussels harvested off
Prince Edward Island, Canada.
 Gastroenteritis followed by headache and short-term
memory loss occurred.
 In a few cases, severe cognitive dysfunction to the point of
interfering with the patient's ability to perform normal daily
activities was noted.
 Seizures, coma, hemiparesis, and ophthalmoplegia were
noted in the most severe cases. The mortality rate is 3%.
 Physical
 Findings vary according to the syndrome involved.
 Gastrointestinal symptoms occur less often in PSP than
in the other syndromes.
 Paresthesias of the face and extremities are noted only in
PSP and NSP.
 ASP is the only shellfish syndrome with cognitive
dysfunction as an early finding.
 Volume depletion from gastrointestinal symptoms is
common to all syndromes.
Protothecosis
 a disease found in dogs, cats, and humans caused
by a type of green alga known as Prothetica that
lacks chlorophyll
 the skin is most commonly involved, resulting from
primary inoculation through a wound or abrasion.
The infection is usually localized to the site of
inoculation; however, in immunocompromised
individuals, it can become widespread.
 Prototheca has been cultured from under the
fingernails and other cutaneous sites in healthy
individuals.
Epidemiology
 Most reported cases have occurred in patients who
are severely immunosuppressed (eg, long-term
immunosuppression for organ transplantation5 ;
autoimmune disease; graft versus host disease; as a
result of chemotherapy or radiation therapy,
Periodic acid-Schiff–stained sections of protothecosis reveal rounded
endospores that form characteristic moruloid structures in the dermis.
Electron photomicrograph of Prototheca wickerhamii shows a central rounded endospore
surrounded by a corona of molded endospores.
Causative organism
 Prototheca
 The classic history is that of trauma (eg, abrasion,
cut) to the skin and subsequent exposure to
contaminated water. In severely
immunocompromised individuals, cutaneous
lesions can be widespread and the algae can be
present in the blood.
 Patients typically present with an isolated plaque or
nodule, with or without ulceration and/or pustules.
However, large eczematous plaques or ulcers have
also been reported. Erythema and pain may occur.
 Patients with protothecosis bursitis present with
painful swelling of the elbow; mild erythema; and,
occasionally, drainage.
Treatment
 Medical Care
 Protothecosis is difficult to eradicate once infection takes hold.
Given that the infection is rare, no defined pharmacologic
protocol is available. All reported patients with disseminated
disease have been treated with intravenous amphotericin B.
Isolated reports describe successful treatment of localized
disease with ketoconazole, itraconazole, and fluconazole.
Sensitivity in vitro has not been shown to be correlated with in
vivo efficacy. Surgical removal of isolated lesions in
combination with antifungal therapy (eg, with azoles) is effective
in immunocompetent individuals. Also reported is dual use of
local thermal application as an adjunct to azole therapy. 9
 Surgical Care
 Surgical excision is the treatment of choice in all cases amenable to
excision.
 Medication
 The goals of pharmacotherapy are to reduce morbidity and to
prevent complications.
 Antifungal agents
 These agents exert a fungicidal effect by altering the permeability of
the fungal cell membrane. The mechanism of action may also
involve an alteration of RNA and DNA metabolism or an
intracellular accumulation of peroxide that is toxic to the fungal cell.
Cyanobacteria
 Harmful cyanobacteria blooms are potential public
health threats in nearly every state in the U.S. due to
their presence in drinking and recreational waters.
 Lyngbya is a toxic marine cyanobacterium (blue-
green algae) which forms clumps or mats of fine
strands that attach to seaweed and rocks
 are the major harmful algal group in freshwater
environments and are recognized as a rapidly
expanding global problem that threatens human and
ecosystem health
Toxin Induced
 Cyanotoxin
 hapatoxins
Causative Organisms
 cyanobacteria
HAB
Symptoms
including skin irritation, stomach cramps, vomiting,
nausea, diarrhoea, fever, sore throat, headache, muscle
and joint pain, blisters of the mouth and liver damage.
Swimmers in water containing cyanobacterial toxins
may suffer allergic reactions, such as asthma, eye
irritation, rashes, and blisters around the mouth and
nose. Animals, birds, and fish can also be poisoned by
high levels of toxin-producing cyanobacteria.
Treatment
 Interventions
 Reducing nutrient build-up (eutrophication) in lakes and
reservoirs, especially by better management of wastewater
disposal systems and control of pollution by fertilizers
(including manure) from agriculture.
 Educating the staff in the health and water supply sectors, as
well as the public, about the risks of drinking, bathing or
water sports in water likely to contain high densities of
cyanobacteria.
 Water treatment to remove the organisms and their toxins
from drinking-water supplies, where appropriate.
Diarrhetic Shellfish Poisoning
 produces gastrointestinal symptoms, usually
beginning within 30 minutes to a few hours after
consumption of toxic shellfish
 caused by the consumption of contaminated
shellfish
Epidemiology
 The first reported cases of DSP were in the
Netherlands in the 1960s, followed by similar
reports in the late 1970s from Japan (Aune &
Yndstad 1993)
 Since then, more than 1300 cases have been
reported from Japan, with the peak season from
April to September.
 Other outbreaks have been reported in Europe and
South America as well as the Far East.
 In Spain, over 5000 cases were reported in 1981; In
France in 1984 and 1986, over 2000 cases were
reported each year and over 300 cases were
reported in Scandinavia in 1984
 Mussels exported from Denmark to France caused
DSP poisoning in over 400 people in 1990
 Finally in 1991 DSP was reported in over 100
people in Chile;
 in 1992, DSP was detected in toxic concentrations
in shellfish beds in Uruguay (Lembeye et al, 1993,
Mendez 1992, Aune & Yndstand 1993).
 Although DSP is reported worldwide, the most
highly affected areas appear to be Europe and
Japan (Aune & Yndstad 1993).
Toxin Induce
 Okadaic acid
Causative Organism
 dinoflagellates Dinophysis
Symptoms
 This is a self-limited diarrheal disease without
known chronic sequelae. There is no evidence of
neurotoxicity and no fatal cases have ever been
reported (Halstead 1988, Viviani 1992).
 usually beginning within 30 minutes to a few hours
after consumption of toxic shellfish (Yasumoto and
Murato, 1990). The illness, which is not fatal, is
characterized by incapacitating diarrhea, nausea,
vomiting, abdominal cramps, and chills. Recovery
occurs within three days, with or without medical
treatment.
Treatment
 Treatment is symptomatic and supportive with
regards to short-term diarrhea and accompanying
fluid and electrolyte losses. In general,
hospitalization is not necessary; fluid and
electrolytes can usually be replaced orally. Other
diarrhetic illnesses associated with shellfish
consumption, such as bacterial or viral
contamination should be ruled out (Aune &
Yndstad 1993).
 As with many of the marine toxin induced diseases,
the initial or index case(s) are often the tip of the
iceberg. Therefore any suspected cases of DSP
should be reported to the appropriate public health
authorities for follow up to ascertain other cases
and to prevent further spread. And every effort
should be made to obtain contaminated materials
and their source.
Neurotoxic Shellfish Poisoning

 milder gastroenteritis
with neurologic
symptoms compared
with paralytic shellfish
poisoning (PSP).
Epidemiology
 produces an  No deaths have been
intoxication syndrome reported and the
nearly identical to that syndrome is less
of ciguatera in which  severe than ciguatera,
gastrointestinal and but nevertheless
neurological debilitating
symptoms
predominate.
 Unlike ciguatera, recovery is generally complete in
a few days. Monitoring programs
Causative Organism
 Karenia brevis
Toxin induced
 Brevetoxin
Vessel of Toxin
 Same as PSP
Symptoms
 gastrointestinal and neurological symptoms
predominate

 formation of toxic aerosols by wave action can

produce respiratory asthma-like symptoms.
Treatment
 In the case of aerosolized Red Tide toxins
respiratory irritation, the use of particle filter masks
or retreat to air conditioned environment will
anecdotally provide relief from the airborne
irritation.
 bronchoconstrictive response; this may have
implications for asthmatics and other susceptible
persons exposed to aerosolized Red Tide toxins