Eight therapeutants were tested for in vitro inhibition of Perkinsus marinus (Mackin, Owen, and Collier) enlargement and in vivo control of established infections. In addition, acute toxicity of six anticoccidials to oysters was determined. For in vitro experiments 0.2 ml aliquots of infected hemolymph were exposed to 5 concentrations (100 mg/l, 10 mg/l, 1 mg/l, 0.1 mg/l and 0.01 mg/1) of amprolium, arprinocid, cycloheximide, lasalocid, malachite green, monensin, sulfadimethoxine, and a potentiated sulfadimethoxine. Exposure lasted 1 day and was followed by incubation in fluid thioglycollate medium. Lasalocid and malachite green were the most effective compounds, showing significant anti-P. marinus activity at concentrations as low as 10 mg/l. Cycloheximide, monensin, and to a lesser extent sulfadimethoxine, were also effective but only at the highest concentration tested (100 mg/1). At concentrations lower than 10 mg/l, no compound tested had a significant effect on P. marinus. Lasalocid, monensin, and malachite green, were toxic to oysters at concentrations below 10 mg/l. The 96-hr LC50 for lasalocid was 0.59 mg/l. No median lethal dose was obtained for monensin or malachite green, but oyster mortality resulted from exposures ranging from 1 mg/l to 10 mg/l of either compound. In two in vivo experiments, infected oysters were exposed to amprolium, cycloheximide, malachite green, and sulfadimethoxine at various concentrations. Only cycloheximide was effective in reducing P. marinus infections. After 15 days of exposure to 10 mg/l of cycloheximide, weighted prevalence significantly declined from 3.78 in untreated controls to 2. 10 in treated oysters. In addition, infections as measured by repeated hemolymph samples from individual oysters, significantly decreased after treatment. Extension of cycloheximide exposure to 30 days similarly reduced disease prevalence and weighted prevalence. Infections, however, were not completely eliminated even after 30 days of exposure to 10 mg/l of cycloheximide. Furthermore, infections progressed after treatment was discontinued as indicated by an increase in weighted prevalence from 0.71 at the end of treatment to 1.31 one month later
