Relative importance of the different negative effects of the toxic haptophyte Prymnesium parvum on Rhodomonas salina and Brachionus plicatilis

The aim of this study was to determine the relative importance of the different processes/mechanisms by which the toxic haptophyte Prymnesium parvum, cultured under different nutrient conditions, affects non-toxic phytoplankton competitors and microzooplankton grazers. P. parvum was cultured under steady-state growth in different nutrient conditions: nitrogen depleted (-N), phosphorus depleted (-P) and balanced nitrogen and phosphorus (+NP). Cells from each nutrient condition and culture cell-free filtrates, alone and combined with non-toxic prey (Rhodomonas salina), were used as food for the rotifer Brachionus plicatilis. An additional experiment was carried out to test the effect of P. parvum cells and culture cell-free filtrate on R. salina. The highest haemolytic activity values were achieved by -P F parvum cultures, followed by -N. However, the negative effect of R parvum on R. salina and rotifers did not correlate with haemolytic activity but with the number of P. parvum cells. -N-cultured P. parvum were the most toxic for both R. salina and rotifers, followed by +NP. Therefore, haemolytic activity is not a good indicator of the total potential toxicity of R parvum. The growth rate of R. salina was negatively affected by cell-free filtrates but the effect of P, parvum predation was greater. Rotifers fed on both toxic and non-toxic algae, indicating that they did not select against the toxic alga. The P. parvum cell-free filtrate had an effect on B. plicatilis, although this was weak, B, plicatilis was also indirectly affected by P. parvum due to the negative effects of the toxic alga on their prey (R. salina). However, the greatest negative effect of P. parvum on the rotifers was due to ingestion of the toxic cells. Therefore, the phytoplankton competitor R. salina is more affected by P. parvum predation and the grazer B. plicatilis is more affected by ingestion of the toxic cells, the effects of excreted compounds being secondary.