Abstract

This study examined serum complement levels in channel catfish from two commercial ponds over a period extending from the winter through the summer months. The fish from one pond (6B) experienced significant fungal associated mortality in the month of January. In March, there was also notable mortality of fish in the same pond; moribund fish exhibited external fungal as well as systemic Aeromonas infections. In July, all fish collected were apparently healthy in that there was no observed mortality. In contrast, the fish from the second pond (16A) were apparently healthy at all sample times except March when there was amild incidence of fungal associated mortality. The results of analyses of haemolytic complement activity showed that representative fish from both ponds had severe complement deficiences during January and March. The haemolytic complement activity continued to be monitored from fish from these ponds into the summer months and the CH 50 values were found to increase to within the normal range. To determine if low water temperature alone induced complement deficiencies, labolatory-acclimated catfish were subjected to a rapid down-shift in water temperature from 23°-11° C during a 24-h period, and the serum CH 50 values were monitored over the following 5 weeks. The results showed that low temperature can significantly affect the ability of catfish to maintain normal levels of haemolytic complement activity; however, these results do not appear to solely explain the abnormally low levels of haemolytic complement found in the serum of catfish during January and March. These results suggest that other factors, in addition to low temperature may have contributed to low CH values observed in the catfish during the winter and spring months. These analyses, in conjunction with other studies, suggest that fungal associated winter mortality and perhaps the subsequent bacterial infections associated with channel catfish during the following spring, are likely manifestations of a severe multifaceted immunodeficiency syndrome wherein complement as well as the humoral and cell-mediated immune systems are compromised.

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