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Further development of bithionol therapy as a treatment for amoebic gill disease in Atlantic salmon, Salmo salar L.
Author(s) -
Florent R L,
Becker J,
Powell M D
Publication year - 2009
Publication title -
journal of fish diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.819
H-Index - 85
eISSN - 1365-2761
pISSN - 0140-7775
DOI - 10.1111/j.1365-2761.2008.01001.x
Subject(s) - salmo , biology , zoology , therapeutic effect , physiology , veterinary medicine , medicine , fishery , fish <actinopterygii> , pharmacology
This study examined the efficacy of bithionol as a prophylactic or therapeutic oral treatment for Atlantic salmon (AS), Salmo salar , affected by amoebic gill disease (AGD). Furthermore, it explored the interaction of bithionol oral therapy with the current standard treatment (a freshwater bath for at least 3 h). The efficacy of three medicated feeds was determined in the trial by feeding AGD‐affected AS at 1% body weight (BW) day −1 either oil coated commercial feed (control) or prophylactic and therapeutic bithionol at 25 mg kg −1 feed. Feeding commenced 2 weeks prior to exposure to Neoparamoeba spp. at 300 cells L −1 and continued for 49 days post‐exposure (PE). Bithionol when fed as a 2‐week prophylactic or therapeutic treatment at 25 mg kg −1 feed delayed the onset of AGD pathology and reduced the percentage of gill filaments with lesions. Administration of a 3‐h freshwater bath at 28 days PE significantly reduced amoeba numbers to a similar level across all treatments; in contrast, gross gill score and percent lesioned filaments were reduced to different extents, the control having a significantly higher score than both bithionol treatments. Following the freshwater bath, clinical signs of AGD increased at a similar level across all treatments, albeit controls were significantly higher than the bithionol treatments immediately following freshwater treatment. This study demonstrated that bithionol at 25 mg kg −1 feed, when fed as a 2‐week prophylactic or a therapeutic treatment, delayed and reduced the intensity of AGD pathology and warrants further investigation as a treatment for AGD‐affected AS.