ALGAE Cyanophitas

Medical Toxicologist MIRTA ELENA RYCZEL October 2003

ALGAE Cyanophitas - (cyano = blue) Cyanophyta or blue-green algae
• • • • Prokaryotes (no true nucleus) Unicellular autotrophic isolated monasteri
es or filamentous, flat or globular live humid environments (land) and aquatic (
freshwater or saltwater), very adaptable. Are planktonic. From 1 micron to sever
al microns Its origin dates from 3000 million years (Precambrian) Some species m
ay form sapropels (parent substance of oil) can withstand temperatures up to 85
° C • in eutrophic conditions may develop into large masses called flowers of wa
ter ( Green Nile and Red Sea) produce antibiotic substances (allelopathic) to st
op or reduce the development of other planktonic creatures. Have pigments: Chlor
ophyll, cficocianinas and c-allophycocyanin (green), c-phycoerythrin (red) and b
eta carotene. They form resistant spores commercial importance (fertilizers), ph
armaceuticals (diets for weight loss) and health of humans and animals
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Merismopedia Gleocapsa Mycrocystis Chroococcus Dermocarpa Chamaesiphon Pleurocas
pa Anabaena Nostoc Oscillatoria Spirulina Lyngbya Rivulara Calothrix Scytonema S
tigonem Plectonema
CLASSIFICATION: Cyanophitas:
• 50% of blooms or blooms produce toxins. • Within the same gender may be or may
not produce toxins. The cause of this feature.
BACKGROUND OF POISONING IN HUMAN DRINKING WATER
• • • • • • • 1931: USA - drinking water - Ohio and Potomac Rivers - 5,000 to 8,
000 people affected 1968: Schwimmer: compilation of numerous cases of enf. GI 19
75: Washington - water reservoir - 23 dialysis patients in 1979: Australia (Palm
Island) - drinking water treated with sulphates death of algae and release of
toxins: 141 patients in 1981: Australia (Armidale) - water supply surface - ele
vated liver enzyme levels in the population 1985: USA: Carmichael brings togethe
r case studies: nausea, vomiting, diarrhea, fever, eye infections, ear and throa
t blooms after exposure to 1993: China - Supply with surface water - Increased i
ncidence of liver cancer in people who drink surface water compared to groundwat
er 1993: Australia: 600 000 wages are lost annually because of the toxic cyanoba
cteria 1994: Sweden - Malmo: illegal use of untreated water in the sugar industr
y accidental pollution Drinking Water: 121 people: nausea, vomiting, diarrhea,
muscle cramps. GI disorders was also observed in dogs and cats
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BACKGROUND OF POISONING IN HUMAN IN RECREATIONAL WATER • 1959: Saskatchewan: 13
people: headache, nausea, muscle aches, diarrhea with pain - identification of M
icrocystis spp in stools of a patient • 1989: England: 10 soldiers became ill af
ter practice blooms in aquatic areas: two had pneumonia requiring hospitalizatio
n in Intensive Care • 1995: Australia: retrospective study of 852 people: diarrh
ea, vomiting, flu symptoms, skin rashes, mouth ulcers, fever, irritation of eyes
and ears - time: 2-7 days after exposure -> density of bacteria> longer contact
time> increased symptoms
OTHER ROUTES OF EXPOSURE
• 1996: Brazil - Caruaru - HEMODIALYSIS: 126 patients exposed to microcystin by
water hemodialysis: 108 patients had symptoms, of whom 60 died with symptoms of
acute neurotoxicity (5 February) and subacute hepatotoxicity (55 March to August
) • Presentations: • Gastrointestinal Symptoms and signs: malaise, myalgia, cram
ps, nausea and vomiting, hepatomegaly. Rapidly progressive liver failure and fat
al. Hyperbilirubinemia, increased liver enzymes, hypertriglyceridemia, neurologi
cal symptoms and signs: tinnitus, vertigo, headaches, deafness, blindness and se
izures
Produce toxins that are classified
• neurotoxins: chemically are known more than five different classes: Tetanus
to: produce post synaptic neuromuscular blockade that prevents the degradation o
f acetylcholine (symptoms similar to those of the organophosphates) - LD 50: 200
mg / kg - time: 1 to toxoid to 20 minutes (s): Chemically similar to the prev
ious and with the same action - LD 50: 20 mg / kg PSP "Paralitic Shellfish Poi
soning": Similar to the dinoflagellates Saxitoxin IPM producers. Inhibit nerve c
onduction by blocking cellular sodium channels. Its action is very fast. LD50: 1
0 mg / kg It can be found at: Anabaena Aphanizomenon Lyngbia Cylindrospe
rmopsis
Produce toxins that are classified
• hepatotoxins: These are the most frequent cause of toxicity related to cyanoba
cteria. Chemically they are peptides. Cause necrosis and apoptosis of hepatocyte
s, intrahepatic hemorrhage, with death from shock or severe hepatic insufficienc
y. • Have a more slowly than the neurotoxins (hours to days) • Microcystin: LD50
: 60-70 mg / kg (mouse) is a cyclic heptapeptide. Microcystin YR - Microcystin L
R - RR Microcystin • NODULARINAS: There are more than eight varieties produced b
y: Mycrocistis, Anabaena, Nodularia, Oscillatoria, Nostoc, Cylindrospermopsis -
• LD 50: 30 to 50 mg / kg
Produce toxins that are classified in • Nephrotoxins:
CILINDROSPERMINA: The species producing Cylindrospermopsis raciborskii and Ume
nzaquia natans inhibits protein synthesis, and has proven renal damage in expe
rimental animals. LD50: 2,500 mg / kg / d and 200 mg / kg / 5th 6 days • OTHER A
CTION: ∀ • inhibition of phosphatases type 1 and 2A (PP) (microcystins and nodul
arinas) • CARCINOGENESIS: liver tumors (China
Mechanism of hepatotoxicity
• Microcystin • 1. Absorption by the GI tract • 2. Ac receivers. Bile Join
s Ac. Serine and threonine of the PP: these maintain the balance between the mon
omerización (phosphorylation) / polymerization (desfoforilazión) for the preserv
ation of the cytoskeleton - Maintain phosphorylation • 3. Interacts with the cat
alytic subunit of PP in two steps that are rapidly reversible, but essential for
liver damage • 4. hepatocyte intercellular contact loss by shrinkage of cells
, and between the sinusoids • 5. vacuolar spaces training blood flow to thes
e areas intra parenchymal hemorrhage hepatomegaly Edema
Cyanophitas: Routes of Elimination and Pathology
• Elimination: • conjugated bile endogenous glutathione and thiol (protein) • Th
is process of conjugation and binding to thiol seems to compete with the mechani
sm of action: Union reversible phosphatase
• Autopsy: Loss of architecture liver edema (vacuolization) Anastomosis of b
lood vessels
ROUTE OF EXPOSURE
• • SKIN: Recreation and / or industrial activities in contaminated water or foa
m Bathing or showering with treated water but with blooms or free toxins DRINKIN
G WATER: Accidental ingestion of water and natural water cyanobacteria blooms or
free toxins Water treated with blooms or free toxins • • • • • INHALATION Labou
r practices Shower Water Sports dried cyanobacteria Aspiration FOOD CONSUMPTION:
molluscs or other aquatic products containing toxins Vegetables - if the toxins
accumulated during sprinkler irrigation - HEMODIALYSIS: Using treated water con
taining toxins
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