Atlantic salmon, Salmo salar L., previously infected with Neoparamoeba sp. are not resistant to re‐infection and have suppressed phagocyte function

• Published in: Journal of Fish Diseases
• Main Authors: Gross, K A, Morrison, R N, Butler, R, Nowak, B F
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2004
• Subjects: Atlantic salmon; Salmo salar
• Online Access: http://dx.doi.org/10.1046/j.1365-2761.2003.00514.x; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1046%2Fj.1365-2761.2003.00514.x; https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1365-2761.2003.00514.x

Abstract Previous studies have indicated that Atlantic salmon, Salmo salar L., affected by amoebic gill disease (AGD) are resistant to re‐infection. These observations were based upon a comparison of gross gill lesion abundance between previously infected and naïve control fish. Anecdotal evidence from Atlantic salmon farms in southern Tasmania suggests that previous infection does not protect against AGD as indicated by a lack of temporal change in freshwater bathing intervals. Experiments were conducted to determine if previous infection of Atlantic salmon with Neoparamoeba sp. would provide protection against challenge and elucidate the immunological basis of any protection. Atlantic salmon were infected with Neoparamoeba sp. for 12 days then treated with a 4‐h freshwater bath. Fish were separated into two groups and maintained in either sea water or fresh water for 6 weeks. Fish were then transferred to one tank with a naïve control group and challenged with Neoparamoeba sp. Fish kept in sea water had lower mortality rates compared with first time exposed and freshwater maintained fish, however, these data are believed to be biased by ongoing mortalities during the seawater maintenance phase. Phagocyte function decreased over exposure time and freshwater maintained fish demonstrated an increased ability to mount a specific immune response. These results suggest that under the challenge conditions herein described, antigen exposure via infection does not induce protection to subsequent AGD.