ARS | Publication request: Variation in Susceptibility to Henneguya Ictaluri Infection by Two Species of Catfish and Their Hybrid Cross

Submitted to: Journal of Aquatic Animal Health
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 4, 2009
Publication Date: March 11, 2010
Citation: Griffin, M.J., Camus, A.C., Greenway, T.E., Wise, D.J., Mauel, M.J., Pote, L.M. 2010. Variation In Susceptibility to Henneguya Ictaluri Infection by Two Species of Catfish and Their Hybrid Cross. Journal of Aquatic Animal Health. 22:21-35.

Interpretive Summary: Proliferative gill disease is one of the most prevalent diseases affecting the commercial farm-raised catfish industry. The disease is caused by a parasite (Henneguya ictaluri) that is released by oligochaete worms that live in the bottom muds of catfish ponds. The portal of entry of this parasite into the catfish is through the gills, which in heavy infections can result in extensive gill damage to the fish host. With increased interest in the commercial production of blue x channel catfish hybrids research was conducted to determine the susceptibility of these fish to PGD. Channel and hybrid catfish were shown to be very susceptible to this disease. In comparison blue catfish did not develop clinical symptoms of disease when exposed to the same number of parasites. This data indicates hybridization of channel with blue catfish did not increase resistance of offspring to PGD and that this disease could still cause mortality in hybrid catfish production.

Technical Abstract: Proliferative gill disease (PGD) in channel catfish Ictalurus punctatus is caused by the myxozoan parasite Henneguya ictaluri. There is no effective treatment for PGD, and mortalities can exceed 50% in severe outbreaks. One approach to controlling losses would be to utilize a less susceptible ictalurid species in pond culture; alternatively, one could identify the traits that convey resistance and exploit them in a selective breeding program. Challenge studies have found less severe inflammatory responses in the gill tissue of blue catfish I. furcatus and fewer mortalities than in channel catfish. However, it remains unclear whether infection and subsequent plasmodial development progress the same way in the two species. To investigate this, we compared the dynamics of H. ictaluri infection in blue catfish, channel catfish, and channel catfish blue catfish hybrids in continuous long-term (5–7-d) and short-term (24-h) pond challenges. After long-term challenge, 66.2% of the channel catfish and 63.6% of the hybrid catfish developed characteristic PGD lesions, compared with 3.7% of the blue catfish. Quantitative polymerase chain reaction analysis detected H. ictaluri in larger percentages of channel and hybrid catfish than blue catfish (98.7% and 95.7% versus 45.9%), with significantly greater parasite DNA equivalents in channel and hybrid catfish than blue catfish. Similar findings were obtained in the short-term exposures. Histologically, channel and hybrid catfish developed severe PGD accompanied by large numbers of developing plasmodia. While mild PGD was observed in some blue catfish, the progression of lesions lagged behind that in channel and hybrid catfish. Most importantly, developing plasmodia were not observed in blue catfish, and parasite DNA was not detected 14 d after removal from the source of infection. Our findings indicate that the resistance of blue catfish to H. ictaluri infection can be overcome by large numbers of infective actinospores but that infection appears to be eliminated before plasmodial development occurs.