Microcystin Toxicosis Of Channel Catfish (Ictalurus punctatus)     G. Scott Snyder1, Andrew E. Goodwin2, and Donald W. Freeman3   1USDA, ARS, Aquaculture Systems Research Unit, Aquaculture-Fisheries Center, University of Arkansas at Pine Bluff, Mail Slot 4912, 1200 North University Drive, Pine Bluff, AR 71601; 2           Aquaculture/Fisheries Center, University of Arkansas at Pine Bluff, 1200 N. University, Mail Slot 4912, Pine Bluff, AR 71601; 3H. K. Dupree Stuttgart National Aquaculture Research Center - United States Department of Agriculture, Agricultural Research Service, P.O. Box 860, Stuttgart, AR 72160                 Farmers producing channel catfish in ponds with relatively high salt levels (3-5 ppt) experience sporadic unexplained fish kills. The high mortality and time course of the problem are indicative of exposure to a toxin. Three cases were of particular interest.  Distressed fish swam lethargically at the surface, were covered with an unusually thick layer of mucous, and had red, swollen gills.  Mortality approached 100% within 36 hours of the first signs of distress.  In these cases, and in others, occurrence of the disease is associated with a heavy bloom of Anacystis marina, a halophylic algae species.  Toxicity assays performed with pond water and concentrated algae resulted in no deaths for two cases, and 100% mortality in the third case.  Microcystin levels in the third case were above 1 mgL-1.  Channel catfish fingerlings (15 – 20g) were exposed to purified microcystin-LR by i.p. injections and in static water baths.  Fish were dosed at rates of 1.9, 0.95, and 0.48 mg microcystin-LRkg-1 body weight.  Bath exposure was at 1, 2, and 10 mgL-1. Hepatic serine/threonine protein phosphatase activity differed significantly (p=0.05) between control and experimental fish exposed to microcystin by i.p. injection.  Histology of the liver tissue from the i.p.-injected fish showed that there was shrinkage of the hepatocytes, breakdown in the sinusoidal architecture and pooling of blood.  Histology of the liver tissue from the bath treatments showed focal necrosis of the hepatocytes near portal veins at the 2 mgL-1 level. In order to confirm that Anacystis marina is the cause of this syndrome and to determine if the prophylactic use of algaecides is effective in controlling potentially toxin-producing blooms, we initiated a monitoring and treatment program.  Water samples, secchi depth, and conductivity were collected weekly and bi-weekly (depending on season) from 118 ponds with high salt levels.  There was a seasonal correlation between the presence of Anacystis marina and fish kills.  Preliminary data show that use of algaecides is a promising management technique in preventing the disease.