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In this paper we have reviewed dermatotoxins produced by blue-green algae. Dermatotoxins are harmful compounds that target human skin. Blue-green algae ( Cyanobacteria ) are prokaryotic microorganisms, mainly found in the water environment – marine and freshwater. A number of species are able to synthesize several toxic substances that affect human health upon exposure to lyngbya-, aplysia- and debromoaplysiatoxin. Lipopolysaccharides present in cyanobacteria cell walls can be irritating to human skin. Therefore, surface waters for recreational use should be monitored for the presence of toxic species of blue-green algae.
Postępy Dermatologii i Alergologii XXIX; 2012/1 47
Address for correspondence: Piotr Rzymski MD, PhD, Department of Biology and Environmental Protection, Poznan University of Medical
Sciences, 1/2 Długa, 61-848 Poznan, Poland, e-mail:
Dermatotoxins synthesized by blue-green algae
Piotr Rzymski, Barbara Poniedziałek
Department of Biology and Environmental Protection, Poznan University of Medical Sciences, Poland
Head: Prof. Krzysztof Wiktorowicz MD, PhD
Post Dermatol Alergol 2012; XXIX, 1: 47–50
Review paper
In this paper we have reviewed dermatotoxins produced by blue-green algae. Dermatotoxins are harmful com-
pounds that target human skin. Blue-green algae (Cyanobacteria) are prokaryotic microorganisms, mainly found in
the water environment – marine and freshwater. A number of species are able to synthesize several toxic substances
that affect human health upon exposure to lyngbya-, aplysia- and debromoaplysiatoxin. Lipopolysaccharides pre-
sent in cyanobacteria cell walls can be irritating to human skin. Therefore, surface waters for recreational use should
be monitored for the presence of toxic species of blue-green algae.
Key words: blue-green algae, cyanotoxins, dermatotoxins, lyngbyatoxin, aplysiatoxin, debromoaplysiatoxin.
Blue-green algae (Cyanobacteria) are a group of
prokaryotic, autotrophic microorganisms that contain the
photosynthetic pigments (chlorophyll and phycocyanin).
So far over 2,500 species have been identified, mainly
related to ecosystems of surface waters, both marine and
freshwater [1, 2]. Almost 80 species were recognized as
able to synthesize toxic metabolites showing activity espe-
cially against the warm-blooded vertebrates [3, 4]. These
chemical compounds include alkaloids, cyclic peptides
and lipopolysaccharides with a wide spectrum of health
effects: hepatotoxic, neurotoxic, cytotoxic as well as der-
matotoxic [5]. Cyanotoxins are released mainly during the
rapid growth phase called blue-green algae blooms. This
phenomenon is based on the mass reproduction of a par-
ticular type of Cyanobacteria species for a period of sev-
eral days and is manifested by the appearance of blue-
green color of water and foam, scum, or mats floating on
the water surface. In the temperate climate, blooms are
formed during high availability of nutrients (mineral nitro-
gen and phosphorus), elevated temperature and limited
water waving. The problem of the direct exposure to cyan-
otoxins exists primarily in the summer and early autumn
[6, 7]. Because of the tendency of these compounds to
accumulate in the invertebrate tissues (shrimps, clams,
snails) and fish, there is a risk of health complications as
a result of consumption of food of unknown origin [5, 8,
9]. A new Regulation of the Minister of Health dated
8 April 2011 on the supervision over the quality of bathing
water and the areas used for swimming provides for,
among others, the necessity of monitoring of water used
for recreation for dangerous algal blooms [10].
This study aims to characterize the dermatotoxic
group of chemical compounds produced by Cyanobacte-
ria and to determine their potential impact on human
Lyngbyatoxins (LA) are indole alkaloids, their name
was taken from a cyanobacteria genus Lyngbya (order:
Oscillatoria) [11]. The main producers are filamentous
cyanobacteria: marine L. majuscule and freshwater
L. wollei – both able to form significant colonies that reveal
as green mats floating on the water surface. Three iso-
forms of lyngbyatoxin were identified: a, b and c; their
molecular mass is 437 Da [12, 13]. The structure of lyng-
byatoxin-a is identical to an isomer of teleocidin A, iso-
lated from mycelium of several species of Streptomyces
[14]. LD50 for mice (oral route) is 250 μg/kg [15].
Massive occurrence of Lyngbya majuscula was found
in almost 100 locations around the world including trop-
Postępy Dermatologii i Alergologii XXIX; 2012/1
ical, subtropical as well as temperate zones [12]. So far
L. majuscula has not been identified on the Polish coast
of the Baltic Sea. However, there is a risk of expansion in
this area, due to the confirmed presence in the region of
Kattegat Strait, Cape Arkona and the Gulf of Riga [16].
Lyngbyatoxin-a has a skin tumour promoting activ-
ity similar to 12-O-tetradecanoylphorbol-13-acetate (TPA)
basing on the activation of protein kinase C (PKC) as
a result of replacing endogenous activator of this
enzyme – 1,2 diacyloglycerol. The observed damages of
nexus junctions are most likely induced by connexin
phosphorylation of PKC [17, 18]. Lyngbyatoxin-b and lyn-
gbyatoxin-c have 1/200th and 1/20th the activity of lyn-
gbyatoxin-a, respectively [12]. Lyngbyatoxins are slight-
ly lipophilic, penetration through human skin after 1 h
of exposure to 26 μg/cm2was estimated as 6% of the
dose [19].
Medical literature described several confirmed cases
of significant lyngbyatoxins effects on humans having
contact with water resources with high occurrence of Lyn-
gbya. The most common symptoms involve skin and are
usually defined as “seaweed dermatitis” [20]. Osbourne
et al. examined a group of 5000 marine recreational users
in northern Moreton Bay (Queensland, Australia) during
a period of L. majuscula occurrence. The most frequently
observed symptoms were: skin itching (23%), skin red-
ness (10.5%), skin burning (10.5%), skin blistering (2.2%)
and skin swelling (0.8%) [21]. These symptoms were most
intense in genital, perineum and perianal areas [12, 22].
The irritant properties of lyngbyatoxin also affected ears
(sore, discharge) and eyes (sore). The most frequent gen-
eral symptoms were headache, nausea, vomiting and diar-
rhea probably resulting from simultaneous ingestion of
intact cyanobacterium with water [23]. Young adults (18-
29 years of age) had the highest sensitivity to lyngbya-
toxin. First symptoms occurred within a few minutes to
a few hours after exposure. Visible dermatitis with red-
ness began to occur after 3-20 h and lasted for 2-12 days.
No connection between the type of symptoms and their
intensity with duration of bathing was found. Similar
symptoms were observed for people staying in water from
2 min to 4 h [24, 25].
Histopathologic examination of human skin exposed
to L. majuscule (topical application) found acute, vesicu-
lar dermatitis. Superficial desquamation and edema of
the epidermis was apparent in the microscope image.
Within the epidermis (stratum malpighii) numerous vesi-
cles of various size were observed. Some vesicles con-
tained red blood cells and polymorphonuclear leukocytes
which were also present in the deepest part of epidermis.
The superficial dermis showed the infiltration of chronic
and acute inflammatory cells including mononuclear cells,
eosinophils and neutrophils [24].
Lyngbyatoxins can also be carried by wind in an
aerosolized form and cause a health risk for people not
exposed to water. L. majuscula dermatitis was diagnosed
in subjects walking on the beach during strong winds.
Most common symptoms included facial rash, groin and
torso skin itching, conjunctivitis, inflamed eyes and
lacrimation [26, 27]. Fishers cleaning fish nets and crab
pots from L. majuscula also reported skin and eye irrita-
tion [28].
Osbourne et al. [27] listed treatment methods for
Lyngbya-induced dermatitis that included: ice packs,
loratadine (10 mg/day) and 1% hydrocortisone cream
(topically four times daily).
Another issue associated with Cyanobacteria able to
synthesize lyngbyatoxins is their accumulation in tissues
of aquatic organisms being a source of food as sea tur-
tles Chelonia mydas [29]. Consumption of such products,
as well as ingestion of water containing lyngbyatoxin
leads to inflammation of the esophagus and digestive
tract [17].
Aplysiatoxin and debromoaplysiatoxin
Aplysiatoxin (AT) and debromoaplysiatoxin (DAT)
belong to phenolic bislactones. Their molecular mass is
671 Da and 592 Da, respectively [30]. They were first iso-
lated from marine mollusks belonging to Stylocheilus
genus [31], feeding upon Cyanobacteria species from Lyn-
gbya, Schizothrix and Planktothrix genus that have an abil-
ity of AT and DAT synthesis [17]. Chemically the only dif-
ference between aplysiatoxin and debromoaplysiatoxin
is that the phenolic structure of AT is replaced with single
bromine atom in DAT [32].
Several experimental studies showed the potential
negative impact of aplysiatoxin and debromoaplysiatox-
in on mammals’ health. In mice, both toxins caused severe
ear irritation [33]. Inhibition of epidermal growth factor
(EGF) (10 times higher for aplysiatoxin) [34] and activa-
tion of ornithine decarboxylase in human skin cells was
observed [35]. Both substances are considered to have
tumorigenic properties and are activators of protein kinase
C [36]. Aplysiatoxin and debromoaplysiatoxin caused dif-
ferentiation of HL-60 cells into macrophages [37]. Applied
topically, debromoaplysiatoxin was found to cause an irri-
tant pustular folliculitis in humans and severe cutaneous
inflammatory reaction in the rabbits and in hairless mice
[25]. Direct contact with aplysia- and debromoaplysiatox-
in contaminated water caused acute skin irritation,
rashes and blisters [12, 38, 39]. There is also a risk of
inhalation of aplysia- and debromoaplysiatoxin from
aerosols transported by the wind along the coasts. Wil-
ley et al. [40] suggested that both toxins induce terminal
squamous differentiation in normal human bronchial
epithelial cells.
Bioaccumulation in aquatic organisms and potential
biomagnification of AT and DAT are still poorly understood
[41]. However, the tendency of some benthic snails to
accumulate these toxins in different parts of the body was
demonstrated [42]. Further analyses are necessary to esti-
Piotr Rzymski, Barbara Poniedziałek
Postępy Dermatologii i Alergologii XXIX; 2012/1 49
mate the exposure possibility to AT and DAT by con-
sumption of organisms obtained from water.
Lipopolysaccharide (LPS) is commonly present in
cyanobacterium cell wall, forming complexes with pro-
teins and phospholipids. Its structure is made of lipid A,
R-type core oligosaccharide and O-specific polysaccharide
chains [43]. Toxicity of cyanobacterium LPS is lower than
LPS of Enterobacteriaceae, although it differs between
species. Orally, LD50 for mice varies from 40 mg/kg to
425 mg/kg. In most common blue-green algae Microcys-
tis aeruginosa LD50 was 50 mg/kg [32, 44]. There are only
few publications on impact of cyanobacterium LPS on
human health and its mechanism of action remains
unclear [33]. This is due to the difficulties in distinguish-
ing the symptoms caused only by LPS and caused by sec-
ondary metabolites synthesized by blue-green algae.
Therefore, the whole range of symptoms were attributed
to LPS such as: skin [45, 46] and eye [47, 48] irritation, hay
fever [49], respiratory problems [50], headaches and dizzi-
ness [51], blistering of mucous membranes and fever [52].
It must be assumed that contact with any water charac-
terized by high concentration of Cyanobacteria can lead
to human health complication, including dermatitis.
The role of dermatotoxic metabolites synthesized by
blue-green algae in human health is still not clear. A few
papers on this subject have been published due to der-
matologic complications not being connected with
cyanobacterium occurrence and production of a wide
range of toxic compounds. Therefore, knowledge of the
above substances is based mainly on studies of animal
models. Described cases clearly reveal negative impact of
lyngbya-, aplysia- and debromoaplysiatoxin on human
skin, even during a short-term exposure. Health hazard
concerns also people not directly using water resources
but residing or walking near the coasts, especially in windy
weather. Cyanobacterium toxins can be spread with
aerosols from water surface causing dermatitis and aller-
gic reactions. Prolonged exposure can lead to promotion
of carcinogenesis. In the case of massive occurrence of
blue-green algae (even species not producing toxic
metabolites) there is a risk of exposure to lipopolysac-
charide which in a few reports seems to have an irritant
effect on human skin.
Climate change and water pollution can have a sig-
nificant role in expansion of toxic Cyanobacteria [53, 54].
New locations of dermatotoxic species may occur and
raise human health concern. Water resources used recre-
ationally should be regularly monitored. Dermatologists
should consider diagnosis of water-linked dermatitis for
exposed patients.
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... In parallel to the environmental impact, cyanobacterial blooms engender serious economic losses that would have different social aspects. In the USA only, yearly losses due to the consequences of cyanobacterial blooms are estimated for 2 billion dollars and are increasing every year [73]. ...
... It is mainly secreted by the filamentous cyanobacteria Lyngbya creating important green blooms that could happen anywhere in the world but might be more considerable in sub-tropical and temperate regions. It has three lipophilic variants called a, b and c [73]. ...
... There is a lack of data and knowledge about the main effect of this toxin, due to the difficulties in differentiating the illness caused only by LPS and from the symptoms caused by the cyanotoxins. But some symptoms were attributed to LPS as fever, headaches, dizziness, eye and skin irritation, respiratory complications and blistering of the mucous respiratory membrane [73]. ...
Karaoun artificial lake (1965) is the largest water body in Lebanon and undergoes successive blooms of two potentially toxic cyanobacteria: Microcystis aeruginosa and Aphanizomenon ovalisporum. Apart from lake Kinneret, middle-eastern lakes are poorly studied and documented. Hydropower, irrigation and future water supply to the capital Beirut were the main purposes of the reservoir back in the 60ties when the water quality was outstanding. Since then, untreated industrial water, sewage and agricultural activities (excessive use of fertilizers) have resulted in the degradation of the water quality and lake eutrophication. At present, several activities are prohibited due to the degraded state of the lake and due to the occasional environmental disasters (massive death of fish and goat, the blockage of the river flow by hyper- scums and the bad odor emissions). This thesis addresses the question of assessment of the effects of such blooms and to facilitate the implementation of the adequate future monitoring of the reservoir. The literature part gives a general overview on cyanobacterial blooms, their driving factors and their potential risks and impacts. It also summarizes the latest techniques implemented in the detection of cyanobacteria and the quantitation of their secondary metabolites. It also describes the site of the Lebanese reservoir Karaoun in the context of its environmental problems.Nearly monthly field campaigns were conducted between August 2019 and October 2020. Water specimens were directly examined for taxonomic identifications and then processed together with fish samples with adequate preliminary pre-treatments. Molecular examinations using q-PCR, biochemical techniques (ELISA and PPIA), and mass spectrometry (LC-MS/MS, LC-HRMS and HS-SPME-GC-MS) were implemented for a holistic and complementary approach.Results not only confirmed the dominance of cyanobacteria because of nutrient enrichment in the lake, but also proved its contamination with high levels of cyanotoxins (almost 200 times higher than the WHO guidelines). Microcystins were the most abundant toxins, mainly in October and December with concentrations up to 200 µg/L. Other toxins were also detected (anabaenopeptins), together with some bioactive compounds (microginins, Aeruginosin and Balgacyclamide).In parallel, a variety of bio-organic taste and odor compounds, e.g. dimethyl disulfide, dimethyl trisulfide, dimethyl tetrasulfide, dihydro 6-ionone, β-cyclocitral, 3 methyl-indole, dihydro β-ionone, β-ionone) were detected in water samples. Samples with sulfur compounds had distinctive “septic”/“cabbage” odors, degrading the quality of water intended for human consumption. Other anthropogenic compounds, such as toluene and trichloromethane, reflecting the various sources of pollution along the stream and the reservoir were also detected. The results of all the applied methods converged, with mass spectrometry techniques showing the possibility of the identification of the individual species not possible to be obtained by the other techniques.
... While lyngbyatoxin-A is an indole alkaloid produced by marine benthic cyanobacteria (L. majuscule and freshwater L. wollei), it can cause dermatitis and inflammation of oral and gastrointestinal tissues (41). Among cyanotoxins, dermatotoxins are the least examined toxins, accounting for less than 2% of all studies on cyanotoxins in 2013 (2); therefore, information on these toxins is limited and further studies are required. ...
... Cyanobacteria from Oscillatoriales, Nostocales, and Chroococcales species are the main cyanobacteria found in freshwater environments. Meanwhile, L. majuscule is a potentially toxic marine cyanobacterium (41). ...
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... Certain secondary metabolites synthesized by cyanobacteria, known as cyanotoxins, are some of the most dangerous compounds produced in nature. Based on their effect on vertebrates, these compounds can be divided into four groups: hepatotoxins, neurotoxins, cytotoxins and dermatotoxins [1][2][3][4][5]. ...
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Cyanobacteria produce a range of toxic secondary metabolites that affect many processes in human, animal and also plant cells. In recent years, some efforts have concentrated on deepening the understanding of their effect on living cells in the context of the disruption of antioxidant systems. Many results suggest that cyanotoxins interfere with glutathione (GSH) metabolism, which often leads to oxidative stress and, in many cases, cell death. Knowledge about the influence of cyanotoxins on enzymes involved in GSH synthesis or during its antioxidant action is relatively broad. However, to date, there is no information about the antioxidant properties of GSH after its direct interaction with cyanotoxins. In this paper, we investigated the effect of four cyanotoxins belonging to the groups of hepatotoxins (microcystin-LR and nodularin) or neurotoxins (anatoxin-a and β-N-methylamino-L-alanine) on the in vitro antioxidant properties of GSH. Moreover, the same study was performed for domoic acid (DA) produced by some diatoms. The obtained results showed that none of the studied compounds had an effect on GSH antioxidant potential. The results presented in this paper are, to the best of our knowledge, the first description of the kinetics of scavenging radicals by GSH reactions under the influence of these cyanotoxins and DA. This work provides new and valuable data that broadens the knowledge of the impact of cyanotoxins and DA on GSH metabolism and complements currently available information. Future studies should focus on the effects of the studied compounds on antioxidant systems in vivo.
... *Significant difference from the control at P < 0.05. produced by cyanobacteria (Dittmann and Wiegand, 2006;Rzymski and Poniedziałek, 2012). It should be noted that their harmful effects should not be underestimated. ...
Toxins produced by cyanobacteria (cyanotoxins) are among the most dangerous natural compounds. In recent years, there have been many published papers related to the toxic alkaloids cylindrospermopsin (CYN) and anatoxin-a (ANTX-a), which are synthesized by several freshwater species of cyanobacteria (i.e. Raphidiopsis raciborskii and Anabaena flos-aquae) and are some of the most common cyanotoxins in aquatic reservoirs. The harmful properties of CYN are wide and primarily include cytotoxicity. To date, several analogs and decomposition products of CYN have been described, which can potentially increase its toxic effects in living organisms. The mode of action of ANTX-a is different than that observed after CYN exposure and involves structures in the nervous system. One of the most frequent situations in which cyanotoxins are introduced into the human body is by skin contact with contaminated water, i.e., during water sports, fishing or agriculture. Unfortunately, to date, knowledge on the influence of CYN, its decomposition products, and ANTX-a on human skin is limited. In this paper, we investigated the impact of CYN, its decomposition products, and ANTX-a on the proliferation of human keratinocytes, which provide a protective barrier on the skin. Moreover, we described the cytotoxic effects developed in the selected cell type and estimated the ability of the keratinocytes to migrate under the influence of the studied cyanotoxins. The obtained results suggest that CYN and its decomposition products at concentrations corresponding to that determined for CYN in nature (1 μg·mL⁻¹) are strong inhibitors of keratinocyte proliferation (70% inhibition within 24 h for pure CYN). The cytotoxic effects of CYN and the CYN decomposition products on keratinocytes was also significant, and the pure toxin (1 μg·mL⁻¹) was estimated to be 35% after 24 h of exposure. Similarly, harmful effects caused by CYN and its byproducts were observed during keratinocyte migration, and the initial form of the toxin (1 μg·mL⁻¹) showed 40% inhibition within 16 h. Different results were obtained for ANTX-a. The toxic effects of this compound on human keratinocytes estimated by the applied tests was observed only at the highest tested concentration (10 μg·mL⁻¹) and after a long period of exposure. The results presented in this paper are, to the best of our knowledge, the first description of the influence of CYN, CYN decomposition products, and ANTX-a on human epidermal cells. Clearly, CYN and its decomposition products are serious threats not only when acting on internal organs but also during the skin contact stage. Further studies on cyanotoxins should focus on the determination of their decomposition products and ecotoxicology in natural aquatic environments.
... In the marine environment, Lyngbya mujuscula is the major cyanobacterial species producing toxic compounds. Lyngbyatoxins, aplysiatoxin, debromoaplysiatoxin and lipopolysaccharides (LPS) from Lyngbya were known to be potent skin irritants causing dermatitis on human skin (Rzymski and Poniedziałek, 2012). Werner et al. (2012) have reported that Lyngbya mujuscula induced clusters of reddish-brown vesicles, papules, and a blistering rash in the abdomen of 13-year-old girl after swimming in south shore of Oahu, Hawaii, upon direct contact. ...
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The brine shrimp toxic marine cyanobacterium, Lyngbya sordida, was collected from the littoral rocks of Mandapam Coast, Tamil Nadu, India. Its organic extract exhibited brine shrimp toxicity against Artemia salina at LC50 of 7 μg mL–1 and rodent toxicity against Swiss albino male mice at LD50 of 45.49 mg kg–1 bw. Fractionation of the extract of L. sordida based on brine shrimp toxicity lead to the isolation of new terminal vinyl carbons containing toxic alkenoic fatty acid derivative, octacosa‐1,27‐diene. The configuration of the isolated compound was assigned based on NMR, FT‐IR, and ESI‐HRMS spectroscopic analysis bearing the molecular formula of C28H54 and mass of [M+H]+ 391.2910 m/z. Isolated compound displayed toxicity against brine shrimp at LC50 value of 4.8 μg mL–1. Toxic fraction containing octacosa‐1,27‐diene was administered (IP) to mice at 1 and 2 mg kg–1 bw daily for 4 days and 8 days, and showed reduction in bodyweight, feed intake, and organ weight when compared to PBS received control mice. Histopathological studies revealed severe tissue injuries in liver, kidney, spleen, and testes of treated mice. Hepatic tissues revealed hydropic degeneration, collapse in hepatic architecture, inflammation, pycnosis, karyolysis, and focal coagulative necrosis, while renal tissues displayed glomerular rupture, infiltration of inflammatory cells in glomerulus and interstitial space, rapid progressive glomerulonephritis, and segmental glomerulosclerosis. Moreover, aggregates of macrophage with hemosiderin pigments, decreased cellularity in splenic tissue and exfoliation of germ cells, impaired spermiation, depopulation of matured sperms, and cell disruption in testicular tissue were observed. Computational analysis disclosed that isolated compound efficiently docked with mitochondrial respiratory chain complex cytochrome C oxidase, antioxidant enzyme catalase, and major phase I cytochrome P450 detoxification enzymes CYP3A4.
... They can cause inflammation and severe dermatitis to people in contact with the filaments. These toxins are found in marine blue-green algae such as Planktothrix and Oscillatoria [48,49]. They are potent tumour promoters and protein kinase C activators [50]. ...
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Purpose of Review Cyanobacteria, commonly known as blue-green algae, are often seen as a problem. Their accumulation (bloom) in surface water can cause toxicity and aesthetic concerns. Efforts have been made in preventing and managing cyanobacterial blooms. By contrast, purposeful cultivation of cyanobacteria can create great opportunities in food, chemical and biofuel applications. This review summarises the current stage of research and the socio-economic impacts associated with both the problems and opportunities induced from the presence of cyanobacteria in surface water. Recent Findings Insightful knowledge of factors that trigger cyanobacterial blooms has allowed for the development of prevention and control strategies. Advanced technologies are utilised to detect, quantify and treat cyanobacterial biomass and cyanotoxins in a timely manner. Additionally, understanding of cyanobacterial biochemical properties enables their applications in food and health industry, agriculture and biofuel production. Researchers have been able to genetically modify several cyanobacterial strains to obtain a direct pathway for ethanol and hydrogen production. Summary Cyanobacterial blooms have been effectively addressed with advances technologies and cyanobacterial research. However, this review identified a knowledge gap regarding cyanotoxin synthesis and the relevant environmental triggers. This information is essential for developing measures to prevent cyanobacterial blooms. Additionally, this review affirms the promising opportunities that cyanobacteria offer in the food, cosmetics, pigments and agriculture. Biofuel production from cyanobacterial biomass presents an immense potential but is currently constrained by the cultivation process. Thus, future research should strive to achieve effective mass harvesting of cyanobacterial biomass and obtain a profound understanding of cyanotoxin production.
... Other health problems were respiratory and eye problems. According to Rzymski and Poniedziałek (2012), cyanobacteria in the genus Lyngbya produce lyngbyatoxins, which are indole alkaloids causing skin problems such as itching, redness, burning, blistering and swelling of genital, perineum and perianal areas, ears (sores, discharge) and eyes (sores). Other health problems farmers faced included headache due to high fever as well as digestive problems which includes stomach ache, nausea, vomiting and diarrhoea and sometimes death cases due to eating the sea turtle that was contaminated by some cyanotoxins. ...
Technical Report
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This guidance is focused on strategies that you may use in response to cyanobacterial blooms that are found in freshwater aquatic environments, including lakes, streams, rivers, reservoirs, ponds, and freshwater-influenced estuaries. It is intended to help you select monitoring, excess nutrient reduction, in-lake management, and communication approaches that may be suitable for use in your water body. We provide interactive tools to help you explore options in monitoring, management, and nutrient reduction. Our Visual Guide will help you recognize cyanobacteria and other common aquatic phenomena that can be confused with them. Interactive features available at:
Cyanobacteria are ancient photosynthetic microorganisms that shaped today's atmosphere. Anthropocentric and irresponsible activities are changing the atmosphere which favor the frequent occurrence and mass development of cyanobacteria. Extensive cyanobacterial blooming causes numerous problems, including negative effects on human skin. Climate change, depletion of ozone layer, and the increased ultraviolet radiation also affect the skin and lead to more frequent occurrence of skin cancer. This research, for the first time, attempts to establish a connection between these two factors, or whether, in addition to ultraviolet radiation, cyanobacteria can influence the incidence of melanoma.With this objective in mind, an epidemiological investigation was conducted in Vojvodina, Serbia. It was observed that the incidence of melanoma was higher in municipalities where water bodies used for recreation, irrigation and fishing are blooming; however, results could be considered as inconclusive, because of the restrictions in the cancer database. Nevertheless, results gathered from the reviewed literature support the hypothesis that cyanobacteria could be a new potential risk factor for melanoma, while climate change could be a catalyst that converts these potential risk factors into cofactors, which act synergistically with the main risk factor – ultraviolet radiation – and induce an increase of melanoma incidence.
Cyanobacteria are a group of phytoplankton of marine and freshwaters. The accelerated eutrophicationof water sources by agricultural and industrial run-off has increased the occurrence and intensity ofcyanobacterial blooms. They are of particular concern because of their production for potent hepato-,neuro-, and dermatoxins, being hazardous to human health. Dissemination of knowledge about cyanobacteriaand their cyanotoxins assists water supply authorities in developing monitoring and managementplans, and provides the public with appropriate information to avoid exposure to these toxins. Thischapter provides a broad overview and up-to-date information on cyanobacteria and their toxins interms of their occurrence, chemical and toxicological characteristics, fate in the environment, guidelinelimits, and effective treatment techniques to remove these toxins from drinking water. Future researchdirections were also suggested to fill knowledge and research gaps, and advance the abilities of utilitiesand water treatment plant designers to deal with these toxins.
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Cyanobacteria are the Earth's oldest known oxygen-evolving photosynthetic microorganisms, and they have had major impacts on shaping our current atmosphere and biosphere. Their long evolutionary history has enabled cyanobacteria to develop survival strategies and persist as important primary producers during numerous geochemical and climatic changes that have taken place on Earth during the past 3.5 billion years. Today, some cyanobacterial species form massive surface growths or 'blooms' that produce toxins, cause oxygen depletion and alter food webs, posing a major threat to drinking and irrigation water supplies, fishing and recreational use of surface waters worldwide. These harmful cyanobacteria can take advantage of anthropogenically induced nutrient over-enrichment (eutrophication), and hydrologic modifications (water withdrawal, reservoir construction). Here, we review recent studies revealing that regional and global climatic change may benefit various species of harmful cyanobacteria by increasing their growth rates, dominance, persistence, geographic distributions and activity. Future climatic change scenarios predict rising temperatures, enhanced vertical stratification of aquatic ecosystems, and alterations in seasonal and interannual weather patterns (including droughts, storms, floods); these changes all favour harmful cyanobacterial blooms in eutrophic waters. Therefore, current mitigation and water management strategies, which are largely based on nutrient input and hydrologic controls, must also accommodate the environmental effects of global warming.
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Anecdotal evidence reported an outbreak of symptoms on Fraser Island during the late 1990 s similar to those expected from exposure to dermotoxins found in the cyanobacterium L. majuscula. This coincided with the presence of a bloom of L. majuscula. Records from the Fraser Island National Parks First aid station were examined. Information on cyanobacterial blooms at Fraser Island were obtained from Queensland National Parks rangers. Examination of first aid records from Fraser Island revealed an outbreak of symptoms predominantly in January and February 1998. During a bloom of L. majuscula there were numerous reports of symptoms that could be attributed to dermotoxins found in L. majuscula. The other four years examined had no L. majuscula blooms and the number of L. majuscula symptoms was much reduced. These cases comprised a high percentage of the cases treated at the first aid station.
We report on the emergence of the potentially toxic filamentous cyanobacterium, Lyngbya wollei as a nuisance species in western Lake Erie. The first indication of heavy L. wollei growth along the lake bottom occurred in September 2006, when a storm deposited large mats of L. wollei in coves along the south shore of Maumee Bay. These mats remained intact over winter and new growth was observed along the margins in April 2007. Mats ranged in thickness from 0.2 to 1.2 m and we estimated that one 100-m stretch of shoreline along the southern shore of Maumee Bay was covered with approximately 200 metric tons of L. wollei. Nearshore surveys conducted in July 2008 revealed greatest benthic L. wollei biomass (591 g/m2±361 g/m2 fresh weight) in Maumee Bay at depth contours between 1.5 and 3.5 m corresponding to benthic irradiance of approximately 4.0–0.05% of surface irradiance and sand/crushed dreissenid mussel shell-type substrate. A shoreline survey indicated a generally decreasing prevalence of shoreline L. wollei mats with distance from Maumee Bay. Surveys of nearshore benthic areas outside of Maumee Bay revealed substantial L. wollei beds north along the Michigan shoreline, but very little L wollei growth to the east along the Ohio shoreline.
Marine animals1-6 have long been known to produce acute dermatitis on contact with the human skin. The eruption described herewith, however, is the first (to our knowledge) to be due to contact with a marine plant, a seaweed. This dermatitis has been proven experimentally by one of us (Col. Grauer) by patch testing to be produced by contact with a marine blue-green alga7,8 which has tentatively been identified as Lyngbya majuscula Gomont9 (Fig. 1). During July and August, 1958, an acute dermatitis, previously not reported in Hawaii, occurred in swimmers frequenting windward beaches on the island of Oahu. During this period more than 125 cases received treatment for this disorder and hundreds of mild, unreported cases were suspected. Cases occurred at beaches from Laie and Kaaawa to Lanikai and possibly Waimanalo, with no instances of occurrence in Kaneohe Bay (Fig. 2). In the experience of one of
Blue–Green algae (cyanobacteria) have long been recognized as a source of objectionable taste and odors in drinking water. In recent years, there has been increasing concern regarding toxic metabolites produced by some species. The species of most concern in Australia are Microcystis aeruginosa and Nodularia spumigena, which produce hepatotoxic peptides, Anabaena circinalis, which produces the same neurotoxins that cause paralytic shellfish poisoning, and Cylindrospermopsis raciborskii, which produces an alkaloid toxin associated with liver and kidney damage. There is also some concern that lipopolysaccharides, which may be produced by a number of blue–green algae, may be involved in human illness. Management strategies for water supplies should include measures in the catchments, source waters, and the distribution systems. An ability to monitor the organisms and their toxins in the source waters and the distribution systems is essential to determine the need for control measures and to determine their effectiveness. This article discusses the management approaches currently used in Australia and the areas of potential future development. ©1999 John Wiley & Sons, Inc. Environ Toxicol 14: 183–195, 1999
The absolute configuration of lyngbyatoxin A (teleocidin A-1) and teleocidin A-2, potent tumor promoters on mouse skin, has been determined by chemical degradation including ozonolysis.
A survey of residents in an area subject to annual toxic cyanobacterial blooms was undertaken to examine potential health effects of cyanobacteria toxins. The survey assessed the health of marine recreational water users in Deception Bay/Bribie Island area in northern Moreton Bay, Queensland, which is exposed to blooms of the nuisance and potentially harmful cyanobacterium Lyngbya majuscula. A postal survey was mailed to 5000 residents with a response rate of 27%. High numbers of people (78%) responding to the survey reported recreational water activity in Moreton Bay. Of those having marine recreational water activity, 34% reported at least one symptom after exposure to marine waters, with skin itching the most reported (23%). Younger participants had greater water exposure and symptoms than older participants. Participants with greater exposures were more likely to have skin and eye symptoms than less exposed groups, suggesting agents in the marine environment may have contributed to these symptoms. Of those entering Moreton Bay waters 29 (2.7%) reported severe skin symptoms, 12 of whom attended a health professional. Six (0.6%) reported the classic symptoms of recreational water exposure to L. majuscula, severe skin symptoms in the inguinal region. Participants with knowledge of L. majuscula were less likely to report less skin, gastrointestinal and fever and headache symptoms. In conclusion, high numbers of participants reported symptoms after exposure to waters subject to L. majuscula blooms but only a small number appeared to be serious in nature suggesting limited exposure to toxins. (c) 2006 Elsevier Ltd. All rights reserved.