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1.5.3.4 Harmful Algal Blooms
ОглавлениеMicro‐ and macroalgae have been implicated in millions of dollars of loss in aquaculture over the past decade (Hallegraeff et al., 2017) and large numbers of deaths of aquatic animals in the wild and in aquariums. These harmful algal blooms have recently increased in our environment due to increased migration, climate change, CO2 levels, and nutrients in the water. Harmful algal blooms are caused by microalgae species including diatoms, cyanobacteria, raphidophytes, prymnesiophytes, pelagophytes, and silicoflagellates (Landsberg, 2002). The most common freshwater algal blooms are caused by cyanobacteria.
Increased water traffic has allowed for migration of algal blooms from continent to continent, allowing the microalgae to find the most conducive environment for growth. Changes in water temperature, pH, and nutrient upwelling have allowed many of these microalgae species to bloom in new areas where animals are not adapted to their presence (Anderson et al., 2012). Climate change has also affected the percentage of toxic compared with nontoxic strains such as Microcystis and a decreased overwintering period as seen in Cylindrospermopsis (Wood et al., 2015).
The effects of harmful algal blooms are very difficult to anticipate due to the variety of microalgae, the toxins that each species contain, and the sensitivity of aquatic animals to those toxins. Each species of microalgae has a different environmental niche. Some are benthic and require limited sunlight. Others must remain near the surface. There are some microalgae that can adjust their buoyancy to move to the most effective area where both photosynthesis and nutrient absorption are greatest. Many adaptations of microalgae allow for them to have an advantage over other algae. These adaptations also tend to give the nontoxic forms of the species less of an advantage over the toxic forms.
The toxins of algal blooms include hepatotoxins, neurotoxins, and dermatotoxins. Each bloom may occur without the presence of toxins in the water and the toxins may only be found in the water before the mortality is detected. This adds to the difficulty in the diagnosis of algal bloom toxicity. The Centers for Disease Control and Prevention list the majority of toxins that are known at this time (Roberts et al., 2020). A more complete explanation of the individual events that have shown proven effects of the toxins in aquatic animals can be found in Jan Landsberg’s (2002) article “The effects of harmful algal blooms on aquatic organisms”.
Cyanobacteria can cause fresh water algal blooms. They are found in ponds, lakes and estuaries. When fresh water incursion occurs and nutrient levels are high, these blooms can reach marine life on the coast. Cyanobacteria most commonly produce microcystins, anatoxins, and cylindrospermopsin. Most aquatic species appear to be resistant to anatoxins and cylindrospermopsin. There have been bird deaths with anatoxin‐a(s) and a possible alligator mortality with cylindrospermopsin. Microcystins have been shown to cause both acute disease and chronic disease. The route of uptake is through the gastrointestinal tract, gills, and skin. There have been many field observations and laboratory experiments with fish regarding microcystin‐LR. These studies have shown that microcystins affect the leukocytes, liver enzymes, growth rate, and ionic stability. The histopathological changes are dose dependent and include degenerative changes to the kidney, liver, and gills (Malbrouck, 2009).
Fish appear to be more resistant than mammals to many neurotoxins, such as brevetoxins, domoic acid, and saxitoxins. These toxins bioaccumulate in fish and cause high mortality rates in birds and marine mammals. Saxitoxins cause paralytic shellfish poisoning (PSP) in mammals due to sodium channel blockage. There are 21 derivatives of saxitoxins involved with PSP. Recent studies show a direct effect on mollusks causing increased mortality and poor growth. Herring exposed to Alexandrium tamarense show increased mortality due to asphyxiation (Landsberg, 2002). Brevetoxins include nine types of neurotoxins, several of which are found in sea spray and act as a respiratory irritant. The neurotoxins alter membrane properties in the neurologic cells. Manatee deaths caused by brevetoxins is postulated to be caused by the ingestion of tunicates found on the surface of sea grass and through inhalation when traveling through large blooms (Landsberg, 2002).
Domoic acid is an excitatory neurotransmitter binding glutamate receptors. There are some copepods that are very sensitive to domoic acid, others are less sensitive and act as a vector. Domoic acid has not been identified in fish mortality events, but it has caused mortalities in brown pelicans after ingestion of anchovies (Lansberg, 2002).
Harmful algal blooms can also cause a reduction in the available oxygen during respiration, exaggerating the toxic effects. Many of the species involved in these blooms are more tolerant to the low oxygen levels and will thrive on the nutrients created by the increased mortality of other organisms. Harmful algal blooms also contain superoxide radicals, phycotoxins and fatty acids that have been acknowledged to play a role in aquatic species mortality through gill damage (Dorantes‐Aranda, 2015; Hallegraeff et al., 2017). Studies performed by Hallegraeff show that reactive oxygen species do not cause damage to fish independently, but when free fatty acids are present they work in synergy to increase the potency of the fatty acid. This results in damage to the gills and to osmoregulation. Microalgal blooms such as barbed diatoms can also cause damage to the gills through mechanical stress by lodging in fish gills (Hallegraeff et al., 2017).
There is no effective treatment for the toxicity that occurs due to harmful algal blooms. Avoidance of the blooms is best achieved by decreasing runoff of high nutrient materials, planting grasses and other plants near waterways to help reduce nutrient runoff and use the nutrients in the water, and careful monitoring. If a large bloom occurs in an aquaculture facility, there are several considerations that need to be made before action is taken:
Is the toxin present a danger to humans, aquatic species, or both?
Is an early harvest an option?
Will killing the algae cause more toxin to be suddenly released?
With blooms that are specifically ichthyotoxic due to fatty acids and reactive oxygen species, the fish may still be safe for harvest. If so, it is important to prevent histamine build‐up by keeping the fish alive long enough to allow the system to be flushed. This can be accomplished by airlift upwelling and targeted clay applications to remove the ichthyotoxins (such as bentonite clay at 0.05–0.25 g/l for Prymnesium, Karenia, Karlodinium, Chattonella, Heterosigma, and Alexandrium). The last three listed have a lower removal percentage then the first three (Hallegraeff et al., 2017). If an early harvest is not an option, then means for movement of the fish and decreased nutrient load should be considered. The feed should be stopped to decrease nutrient levels. Cages can be moved to unaffected areas if possible. To reduce concentration, surrounding the fish with perimeter skirts and increased aeration or airlift upwelling can be used. Clay flocculation should be carefully considered based on the area the fish are in and the type of algal blooms present. Most clays can cause damage to benthic fauna present, especially mollusks (Hallegraeff et al., 2017)