|Straus, David - Dave|
|MEINELT, THOMAS - Leibniz Institute Of Freshwater Ecology And Inland Fisheries|
Submitted to: Aquaculture
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/23/2012
Publication Date: 3/3/2012
Citation: Straus, D.L., Meinelt, T., Farmer, B.D., Beck, B.H. 2012. Acute toxicity and histopathology of channel catfish fry exposed to peracetic acid. Aquaculture. 342-343(1):134-138.
Interpretive Summary: Research has demonstrated that peracetic acid (PAA) can be used as a disease treatment for fish and it can prevent fungus on catfish eggs. This study shows how much PAA is toxic to hatching catfish fry. We found it was more toxic to swim-up fry (approximately 7 days old) than to yolk-sac fry (approximately 1 day old). A safe treatment rate was 2.2 parts per million PAA for yolk-sac fry and 1.7 parts per million PAA for swim-up fry. Advantages to using PAA are that it does not produce any residues that would harm fry or the environment and it degrades to harmless residues rapidly. Research like this is important information that is needed by the catfish industry to fight fungus problems on eggs.
Technical Abstract: Channel catfish Ictalurus punctatus yolk-sac fry and swim-up fry were exposed to peracetic acid (PAA) for 48h in static toxicity bioassays at 23C. The test water was 217 and 126 mg/L (as CaCO3) total alkalinity and total hardness, respectively. Probit LC50 values were estimated with the trimmed Spearman-Karber method using nominal PAA concentrations (1.0, 1.3, 1.7, 2.2, 2.8, 3.7, 4.8, 6.3, 8.2 mg/L PAA). The mean 24 and 48-h LC50 values for yolk-sac fry and swim-up fry was 2.6 mg/L PAA and 1.6 mg/L PAA, respectively. Catfish yolk-sac fry were more tolerant of PAA than catfish swim-up fry by about 1.6-fold, and no additional mortality was observed after 24h in swim-up fry. Peracetic acid-related histopathology were analyzed in whole body serial sections of swim-up fry at two selected doses of PAA; 2.2 mg/L (1 h post-treatment) and 1.7 mg/L (48 h post-treatment). Lesions consisted of severe gill damage in fish treated with 2.2 mg/L PAA, and a moderate degeneration of the renal tubule epithelium within the posterior kidney in fish treated with 1.7 mg/L PAA.