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ARS Home » Research » Publications at this Location » Publication #124754


item Snyder, Gregory
item Freeman, Donald

Submitted to: Journal of Fish Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/17/2002
Publication Date: 5/1/2002
Citation: N/A

Interpretive Summary: Farmers growing catfish in regions of the southeast United States, with ground water containing moderate levels of salt, experience sporadic, unexplained fish kills during the spring and fall seasons that have resulted in the death of approximately one million pounds of fish each year. These die offs occurred in a manner inconsistent with any known fish diseases or water quality deterioration. A natural toxin produced by the blue-green algae that inhabit the ponds was suggested as a possible cause of the kills. Microcystin-LR, a toxin produced by several species of blue green algae common to catfish ponds, was identified from samples of catfish pond water during one of these kills. In an effort to solve the problem and develop management techniques that could be implemented by the catfish farmers, a series of experiments was performed to determine the sensitivity of channel catfish to microcystin-LR. An algae monitoring program was established that resulted in the association of the channel catfish kills with one blue-green algae species. The efforts of the work revealed that channel catfish are not sensitive to the toxin, microcystin- LR. There is a positive correlation between one species of blue-green algae that is only present in the catfish ponds during the seasons when the fish kills occur, and the fish kills. The algae monitoring program has provided farmers the ability to kill the deadly algae using a herbicide, copper sulfate, and not kill fish.

Technical Abstract: Catfish farms located in the southeastern U.S. using brackish (3-5 g NaCl/l) well water experience sporadic fish kills with varying degrees of mortality. Investigation of three catastrophic losses occurring in this region has identified no involvement of infectious diseases or traditional water quality problems, including oxygen, ammonia or nitrite. The high mortality and time course of the problem is indicative of exposure to a toxin. Attempts by other workers to explain the cause of this unique syndrome (High Chloride associated Toxicosis of Catfish, H.C.T.C.), suggested that the losses might be due to toxin producing blooms of M. aeruginosa. In our work the liver histology of catfish experimentally exposed to a pure form of the suspect toxin, microcystin-LR is very different from that of catfish sampled during outbreaks of H.C.T.C. Ingestion of massive amounts of microcystin-LR does not cause the acute mortality typical of H.C.T.C. Major hepatic injury to experimental fish from exposure to microcystin-LR did not cause mortality of channel catfish fingerlings within seven days. Outbreaks of H.C.T.C. appear associated with heavy blooms of A. marina, a halophytic cyanobacteria, not with blooms of M. aeruginosa.