Microcystins, toxins produced by cyanobacteria, may play a role in fish kills, although their specific contribution remains unclear. A better understanding of the eco-toxicological effects of microcystins is hampered by a lack of analyses at different trophic levels in lake foodwebs. We present 3 years of monitoring data, and directly compare the transfer of microcystin in the foodweb starting with the uptake of (toxic) cyanobacteria by two different filter feeders: the cladoceran Daphnia galeata and the zebra mussel Dreissena polymorpha. Furthermore foodwebs are compared in years in which the colonial cyanobacterium Microcystis aeruginosa or the filamentous cyanobacterium Planktothrix agardhii dominated; there are implications in terms of the types and amount of microcystins produced and in the ingestion of cyanobacteria. Microcystin concentrations in the seston commonly reached levels where harmful effects on zooplankton are to be expected. Likewise, concentrations in zooplankton reached levels where intoxication of fish is likely. The food chain starting with Dreissena (consumed by roach and diving ducks) remained relatively free from microcystins. Liver damage, typical for exposure to microcystins, was observed in a large fraction of the populations of different fish species, although no relation with the amount of microcystin could be established. Microcystin levels were especially high in the livers of planktivorous fish, mainly smelt. This puts piscivorous birds at risk. We found no evidence for biomagnification of microcystins. Concentrations in filter feeders were always much below those in the seston, and yet vectorial transport to higher trophic levels took place. Concentrations of microcystin in smelt liver exceeded those in the diet of these fish, but it is incorrect to compare levels in a selected organ to those in a whole organism (zooplankton). The discussion focuses on the implications of detoxication and covalent binding of microcystin for the transfer of the toxin in the foodweb. It seems likely that microcystins are one, but not the sole, factor involved in fish kills during blooms of cyanobacteria.
1. The effect of phosphorus limitation of the diatom Asierioneila formosa Hass. on growth, survival and epidemic development of its fungal parasite Rhizophydiurn planktonicum Canter emend, was estimated, using measurements of production and infectivity of the zoospores of the chytrid grown on host cultures with different phosphoruslimited growth rates.2. Phosphorus-limited host cells were less susceptible to infection with zoospores of the parasite than non-limited host cells.3. The sporangia on phosphorus-limited algae produced substantially less zoospores, but the development time of these sporangia was only slightly reduced.4. As a result of these effects, Rhizophydium will reach lower growth rates at a given host density, and survival of the parasite will require higher host densities when Asterionella is phosphorus-limited.5. The zoospore production remained high enough to enable the parasite to grow faster than the alga at sufficiently high host densities, both at limiting and non-limiting phosphorus levels.6. In spite of the reduced growth rate of the parasite, phosphorus limitation of Asierioneila was found to facilitate the development of a Rhizophydium epidemic. This was a consequence of the reduced algal growth rate at phosphorus limitation, which makes the host population more easily outgrown by the parasite.7. Phosphorus limitation of the host could reduce the threshold host density required for the development of an epidemic by a factor of 2.5.
A population-dynamic model is formulated to estimale the impact of chytrid and related fungal parasites on phytoplankton populations. The specific loss rate of uninfected host cells due to infection is used as a measure of the impact. Calculating this loss rate requires information about four parameters: prevalence of infection (i.e. the proportion of the host cells infected), development time of the sporangia of the parasite, specific growth rate of the uninfected host, and difference between loss rates of infected and uninfected host cells due to loss factors other than parasitism. When only cell counts of the host population are available instead of growth and loss rate values, the model can be used to calculate a minimum estimate of the impact of the parasite. The impact of the parasite at a given prevalence of infection can vary considerably as a consequence of environmental effects on the latter three parameters. Therefore, prevalence is not a good parameter to judge the severity of fungal epidemics. A phytoplankton population starts to decline when prevalence exceeds a certain threshold value. This critical prevalence of infection can be calculated with the model and is also highly dependent on external conditions.The model is applied to epidemics of the chytrid Rhizophydium planktonicum Canter emend. in ,a population of the diatom Asterionella formosa Hass. in Lake Maarsseveen 1. The end of both the spring and summer 1984 bloom of the diatom was caused by epidemics of tlhe chytrid. Model results suggested also that higher sinking rates, caused by an increasing proportion of dead cells in the colonies, resulted in an additional loss factor due to parasitism for this colcnrial diatom.
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