Amoebic gill disease (AGD) of maricultured salmonids, turbot, Scophthalmus maximus (L.), European seabass, Dicentrarchus labrax (L.), and sharpsnout seabream, Diplodus puntazzo (Cetti), caused by Neoparamoeba pemaquidensis has been reported from Australia (Tasmania), Ireland, France, Chile, North America (Washington State and California) and Spain. Of the salmonids, Atlantic salmon, Salmo salar L., appears to be the most susceptible with rainbow trout, Oncorhynchus mykiss (Walbaum), also suffering signi®cant disease. Only minor outbreaks have been reported in coho, O. kisutch (Walbaum), and chinook salmon, O. tshawytscha (Walbaum). The disease now accounts for 10±20% of production costs of Atlantic salmon in Tasmania and has lead to temporary abandonment of culture of this species in parts of Spain. It is of lesser, but still signi®cant, importance in other countries. Much is known about the pathology of AGD but the pathophysiology of the disease is poorly understood. There is evidence that non-speci®c immunity is involved in ®sh acquiring resistance to AGD, but no unequivocal evidence exists for protection as a result of speci®c immune responses. To date, for salmonids, the only effective treatment for AGD is a freshwater bath. Control procedures based on modi®cation of management strategies have been minimal and virtually unresearched.

Trials were designed to test the efficacy of freshwater treatments for amoebic gill disease (AGD) of Atlantic salmon, Salmo salar L., and the effect they had on the acquisition of resistance to reinfection with AGD. The first trial involved fish being given an industry-simulated freshwater bath of 2-3 h duration which simulated treatments given on farms. These fish did not display appreciable resistance to reinfection. The second trial involved four groups of fish which had been infected with and treated for AGD in a number of different ways. Once again the fish that had been infected for the first time and given a single 2-3 h freshwater bath and then re-exposed did not exhibit appreciable resistance to reinfection. In contrast, those fish that had been given a second 2-3 h freshwater bath and those that had been maintained in freshwater for 4 weeks displayed high levels of resistance. There is preliminary evidence to suggest that this resistance could be related to stimulation of the non-specific immune system.

No abstract

Levamisole, a known T‐cell stimulator and immunomodulator in mammals, has been demonstrated to enhance resistance to amoebic gill disease in Atlantic salmon, Salmo salar L. When used in fresh water baths, dose rates of 1.25, 2.5 and 5 ppm levamisole stimulated resistance to reinfection with Paramoeba sp. that was evident from 2–3 weeks post‐treatment. It is proposed that this response is related to enhancement of the non‐specific immune system.

Sea water‐adapted Atlantic salmon, Salmo salar L., were given a 2‐h bath in a 2.5 mg L−1 levamisole (as levamisole hydrochloride) solution in fresh‐water. Following bathing, the fish were held in full salinity sea water for 2 weeks before being subjected to a number of immunological assays. Heightened activity of the nonspecific defence system was demonstrated by increases in phagocytic index, phagocytic capacity and phagocytic activity, increased levels of the reactive oxygen intermediate, superoxide anion, and an increased lytic activity of both the mucus and the serum. These results indicate that levamisole is effective in augmenting parts of the nonspecific defence system of Atlantic salmon. This is the first record of the use and efficacy of levamisole as an immunomodulator in Atlantic salmon.