Effect of Indomethacin on the Development of Proliferative Gill Disease

Abstract

After parenteral treatment with the cyclooxygenase inhibitor indomethacin, channel catfish Ictalurus punctatus were exposed to mature spores of an Aurantiactinomyxon sp. demonstrated to be the etiological agent of proliferative gill disease (PGD). Fish that received indomethacin at a dose of 2.0 or 5.0 mg/kg body weight within 0.5 h before exposure to the myxozoan and again at 24 h postexposure had significantly (P < 0.05) less severe gill lesions 7 d after exposure than fish that received the drug vehicle alone. Fish that received 0.5 mg indomethacin/kg had moderately severe lesions. All fish were confirmed to be infected with the organism associated with PGD by microscopic examination of gills 4 or 7 d postexposure. These results suggest that products of the cyclooxygenase pathway (e.g., prostaglandins) participate in the pathophysiologic host response to PGD.