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

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 sea-water 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.

The expression of immune-regulatory genes in rainbow trout, Oncorhynchus mykiss, during amoebic gill disease (AGD)

“…Interestingly, an apparent down-regulation in the expression level of all the studied genes in the present study, with the exception of IL-1b1, was seen in the anterior kidney at 7 and 14 days p.i. This supports a previous study showing decreased phagocytic and respiratory burst activity in the adherent cell population isolated from the anterior kidney of AGD-infected Atlantic salmon [6]. This finding is not surprising, as parasite-induced immune suppression is a common occurrence during parasitic infections and helps the pathogen to survive host responses [45].…”

“…antibodies [5], and previously infected fish are not protected from reinfection upon subsequent re-exposure to Neoparamoeba sp. [6]. Histological changes associated with infection of the gills with Neoparamoeba sp.…”

Sequential pathology after initial freshwater bath treatment for amoebic gill disease in cultured Atlantic salmon, Salmo salar L.

“…Yet experimentally infected salmon that were bathed and then left in filtered sea water did not display signs of amoebic re‐infection for 3 weeks. The latter fish were not re‐exposed to the pathogen (Gross, Morrison, Butler & Nowak 2004; M B Adams & B F Nowak, unpublished data). This suggests that bath‐tolerant Neoparamoeba sp.…”

Neoparamoeba branchiphila n. sp., and related species of the genus Neoparamoeba Page, 1987: morphological and molecular characterization of selected strains

“…Since the first described outbreaks of amoebic gill disease (AGD) in salmonids (Kent, Sawyer & Hedrick 1988; Roubal, Lester & Foster 1989; Munday, Foster, Roubal & Lester 1990; Munday, Lange, Foster, Lester & Handlinger 1993), a voluminous literature has been accumulated on various aspects of this disease. Many studies have focused on the Atlantic salmon, Salmo salar L., dealing with pathology (Nowak & Munday 1994; Rodger & McArdle 1996; Zilberg & Munday 2000; Adams & Nowak 2001, 2003, 2004a,b; Adams, Ellard & Nowak 2004), epidemiology (Clark & Nowak 1999; Douglas‐Helders, Nowak, Zilberg & Carson 2000; Douglas‐Helders, Saksida, Raverty & Nowak 2001a; Douglas‐Helders, Dawson, Carson & Nowak 2002; Douglas‐Helders, Handlinger, Carson & Nowak 2003a; Douglas‐Helders, O'Brien, McCorkell, Zilberg, Gross, Carson & Nowak 2003b; Douglas‐Helders, Tan, Carson & Nowak 2003c), immunology (Findlay, Helders, Munday & Gurney 1995; Akhlaghi, Munday, Rough & Whittington 1996; Findlay & Munday 1998, 2000; Findlay, Zilberg & Munday 2000; Zilberg & Munday 2001; Bridle, Butler & Nowak 2003; Gross, Carson & Nowak 2004a; Gross, Morrison, Butler & Nowak 2004b), diagnostic procedures (Zilberg, Nowak, Carson & Wagner 1999; Douglas‐Helders, Carson, Howard & Nowak 2001b) and treatment of AGD (Zilberg, Findlay, Girling & Munday 2000; Parsons, Nowak, Fisk & Powell 2001; Clark, Powell & Nowak 2003; Munday & Zilberg 2003; Roberts & Powell 2003). However, our present knowledge of AGD has been derived also from infections of other fish hosts (Dyková, Figueras & Novoa 1995; Dyková, Figueras, Novoa & Casal 1998; Dyková & Novoa 2001).…”