Cyanobacterial blooms

This is the principal linkage between cyanobacterial blooms and eutrophication. Avoidance of cyanobacterial production does not necessarily depend upon eliminating all phosphorus inputs, but upon ensuring that optimum physical and chemical conditions for these organisms do not coincide. It is easy to understand why the biggest blooms in the UK have been in fertile lakes and reservoirs after prolonged spells of warm, dry weather in summer. 

In the Slimmer of 1989, Rutland Water, the largest man-made lake in Western Europe and which supplies potable water to approximately 500 000 people in the East of England, contained a heavy bloom of Microcystis aeruginosa. By the end of the summer, a number of sheep and dogs had died after drinking from the bloom and concentrated scum. Analysis revealed that the cyanobacterial bloom material was toxic to laboratory mice, and that rumen contents from a poisoned sheep contained fivemicrocystin variants.Microcystins were detected in waters used for recreation in Australia at concentrations greater than 1 mg per... 

Daphnia assay, the brine shrimps are exposed to different concentrations of toxicant, and the toxicity is expressed as the LCjo value. Extracts of cyanobacterial blooms and laboratory cultures, containing microcystins or anatoxin-a, have been found to be toxic towards brine shrimp," and fractionation of such extracts resulted in brine shrimp fatalities only with fractions containing microcystins." " ... 

Not all cyanobacterial blooms and scums contain detectable levels of toxins. Indeed, the incidence of toxicity detection by mouse bioassay, and toxin detection by HPLC among environmental samples, ranges from about 40% to However, in view of this high occurrence, it is the policy of regulatory authorities and water supply operators in some countries to assume that blooms of cyanobacteria are toxic until tested and found to be otherwise. In the absence of available analytical facilities or expertise or for logistical reasons, this precautionary principle should be regarded as sensible and prudent. 

The final article, by S. G. Bell and G. A. Codd of the University of Dundee Department of Biological Services, is concerned with detection, analysis, and risk assessment of cyanobacterial toxins. These can be responsible for animal, fish, and bird deaths and for ill-health in humans. The occurrence of toxic cyanobacterial blooms and scums on nutrient-rich waters is a world-wide phenomenon and cases are cited from Australia, the USA, and China, as well as throughout Europe. The causes, indentification and assessment of risk, and establishment of criteria for controlling risk are discussed. 

Paul VJ, Thacker RW, Banks K, Golubic S (2005) Benthic cyanobacterial bloom impacts the reefs of South Florida (Broward County, USA). Coral Reefs 24 693-697 Paul VJ, Puglisi MP, Ritson-Williams R (2006) Marine chemical ecology. Nat Prod Rep 23 153-180... 

Hepatotoxins include microcystins, which are cyclic heptapeptides (Fig. 5.1a) and cylindrospermopsin, a sulfated guanidinium alkaloid (Fig. 5. lb). Microcystins bind to certain protein phosphatases responsible for regulating the distribution of cytoskeletal proteins (Zurawell et al. 2005 Leflaive and Ten-Hage 2007). Hepatocytes exposed to microcystins eventually undergo cellular deformation, resulting in intra-hepatic bleeding and, ultimately, death (Carmichael 2001 Batista et al. 2003). In contrast, cylindrospermopsin appears to have a different mode of activity, possibly involving inhibition of protein or nucleotide synthesis (Codd et al. 1999 Froscio et al. 2003 Reisner et al. 2004). Nevertheless, microcystins are the most common cyanotoxins isolated from cyanobacterial blooms (Sivonen and Jones 1999). 

Giovannardi S, Pollegioni L, Pomati F, Rossetti C, Sacchi S, Sessa L, Calamari D (1999) Toxic cyanobacterial blooms in Lake Varese (Italy) a multidisciplinary approach. Environ Toxicol 14 127-134... 

T.S. Bianchi, E. Engelhaupt, P. Westman, T. Andre, C. Rolff and R. Elmgren, Cyanobacterial blooms in the Baltic Sea natural or human-induced Limnol. Oceanogr. 45 (2000) 716-726. 

There is a peak of N2 fixation coincident with the early cyanobacterial bloom, shown by the increase in acetylene reducing activity in the figure. Nitrogen fixation by the colonial cyanobacteria is slower but lasts longer. 

The cosmopolitan cyanobacterium Microcystis aeruginosa is frequently the major component of freshwater cyanobacterial blooms. These blooms can cause serious water management problems and are occasionally associated with animal poisoning. The aeruginosa toxins are potent lethal peptides which contain three invariant D-amino acids (Ala, erythro-3-methyl Asp, and Glu), two variant L-amino acids, N-methyl dehydroalanine, and a 3 amino acid (1-3). Multiple toxins have been purified from clonal isolates (1,4). The toxic peptide described in this chapter is denoted toxin-LR using the standard one-letter abbreviations for its two variant amino acids, leucine and arginine. 

Slater, G.P. Blok, V.C. (1983) Isolation and identification of odorous compounds from a lake subject to cyanobacterial blooms. Water Sci. Technol., 15, 229-40. 

Cyanobacteria - the Jekyll and Hyde of marine organisms - are a novel source of potential new pharmaceutical compounds (2618-2620, 2662). On the other hand, toxic cyanobacterial blooms in lakes, rivers, and water storage reservoirs have occurred worldwide (2621, 2663, 2664). For example, 60 patients in a Brazil hemodialysis unit died after drinking water from a lake contaminated with cyanobacterial microcystins (2622), not unlike the toxicity of red tides (2623). Cyanobacteria also produce the highly toxic neurotoxin, p-N-methylamino-L-alanine, which may be produced by all cyanobacteria (2624, 2665). 

The developed biosensor was applied to the analysis of cyanobacterial bloom samples from freshwater lakes of Spain, Greece, France, Scotland and Denmark. Two samples from Scotland and one from Denmark irreversibly inhibit the acetylcholinesterase. The estimated concentrations were between 1.5 and 30nmol/g of dry weight, values extremely high when compared to the intraperitoneal 50% lethal dose of anatoxin-a(s) in mice (121 nmol/kg). 

A.R. Humpage, J. Rositano, A.H. Bretag, R. Brown, P.D. Baler, B.C. Nicholson and D.A. Steffensen, Paralytic shellfish poisons from Australian cyanobacterial blooms, Aust. J. Mar. Freshwater Res., 45 (1994) 761-771. 

Tarczynska, M., Nalecz-Jawecki, G., Brzychcy, B., Zalewski, M. and Sawicki, J. (2000) The toxicity of cyanobacterial blooms as determined by microbiotests and mouse assays, in G. Persoone, C. Janssen and W.M. De Coen (eds.), New Microbiotests for Routine Toxicity Screening and Biomonitoring, Kluwer Academic/Plenum Publishers, New York, pp. 527-532. 

It is believed that the presence of secondary metabolites impacts on the survivorship of a cyanobacterial strain in reef habitats that are subject to intense herbivory. Under suitable environmental conditions, cyanobacteria undergo rapid increases in population size, generating large cyanobacterial mats which are not calcified or of tough texture and which therefore present a potential source of food for herbivorous fish and other generalist predators. By restricting predation, potent cyanobacterial toxins facilitate the formation of cyanobacterial blooms.48... 

Cyanobacterial blooms pose a public health risk and may have adverse effects on marine life (fish, turtles) that accidentally consumes them. The production of toxins or of antifeedant compounds, particularly in cyanobacterial strains that are slow growing can lead to rapid bloom production in areas of high herbivory, for example on tropical coral reefs.8... 

Health hazards from algal toxins are primarily associated with overgrowth (bloom) events, Algal blooms may develop rapidly and be of short duration they are generally seasonal and are frequently associated with the presence of nutrients, particularly phosphate. Levels of nutrients are often increased by human activity (see also Chapters 5, 6 and 7), increasing the likelihood of cyanobacterial blooms. 

In Scotland, during 1981-1982, cyanobacteria from several lakes were found to be toxic by mouse bioassay (i.p.) (Richard et al. 1983), but the first case of AN intoxication due to benthic cyanobacteria was reported 10 years later (Edwards et al. 1992). The neurotoxic bloom consisted mainly of Planktothrix species and was associated with three canine fatalities AN was identified in the stomach contents of one of the dogs (Gunn et al. 1992). In Finland, the first survey of cyanobacterial blooms during 1985-1987 revealed that 13 out of 30 bloom samples contained AN (Sivonen etal. 1989). Toxin content was in the range 12 360 pg AN/g lyophilized material. During this... 

Cyanobacterial culture studies and reported observations of natnral blooms have shown that differences in cyanobacterial composition and toxicity are dependent on a number of environmental factors including, light, temperature, pH, and nutrients and physical factors such as buoyancy of the algae, prevailing weather conditions, and water currents (Rapala et al. 1993 Gupta et al. 2002). These variables, along with the age of the cells, their tendency to lyse and release toxins, decomposition and detoxification mechanisms (Rapala et al. 1994), help to explain why poisonons cyanobacterial blooms tend to occur in such an erratic and unpredictable fashion (Carmichael and Gorham 1980). 

Park, H.-D, Kim, B., Kim, E., and Okino, T. 1998. Hepatotoxic microcystins and neurotoxic anatoxin-a in cyanobacterial blooms from Korean lakes. Environ Toxicol Water Qual 13, 225-234. 

Pawlik-Skowronska, B., Skowronski, T, Pirszel, I, and Adamczyk, A. 2004. Relationship between cyanobacterial bloom composition and anatoxin-a and microcystin occurrence in the eutrophic dam reservoir (SE Poland). Polish J Ecol 52, 479-490. 

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