Several nutrient deficiencies have been characterized using semi-purified diets; however, deficiency of a single nutrient is rare in farmed fish (Tables 11, 12, 13). In farmed fish fed commercial feeds, micronutrient deficiencies of specific nutrients are rare. Generally, micronutrients are supplemented above the requirement levels with a safety of margin to offset nutrient losses during processing and storage, poor digestibility, low absorption from gastrointestinal interferences by antinutritional factors and excessive nutrients supplied by certain feed ingredients (e.g. high ash fishmeals). Environmental stress, altered gastrointestinal activity, disease state, higher physiological needs (e.g. iodine during smoltification), drug-induced anorexia, metabolic defects and food contaminants may all lead to malnutrition and nutrient deficiencies. The most well characterized cause of a feed-related intestinal disorder in salmonid fishes is induced by full-fat and extracted soybean meal (Baeverfjord and Krogdahl, 1996; Ingh, Olli and Krogdahl, 1996). It causes a sub-acute inflammatory response in the distal intestine of Atlantic salmon and rainbow trout and is often associated with reduced growth performance and nutrient utilization, as well as diarrhea in a dose-dependent manner.
All salmonids and certain marine fish are susceptible to lipoid liver degeneration when fed rancid feeds containing oxidized lipid. Generally, oxidized lipid affects liver lipid metabolism and leads to several metabolic disorders of the liver, including lipoid degeneration (ceroid accumulation), depigmentation, distention of the bile duct and an anemic, pale, swollen liver. In Atlantic salmon, cataracts develop in certain genetic strains during the smoltification and post-smoltification periods (Bjerkås et al., 1996). Several dietary factors are implicated in the pathogenesis, including histidine deficiency (Breck et al., 2005) and higher growth of smolts fed high energy diet containing high levels of lipid and a low protein content (Waagbø et al., 2003). Deficiencies of eight nutrients have been linked to the pathogenesis of eye disorders: exophthalmia, clouding and severe degeneration of the lens caused by vitamin A deficiency; clouding of the cornea due to thiamin deficiency; degeneration of the cornea and retina caused by riboflavin deficiency; and lenticular opacity with no involvement of other ocular tissues by sulfur amino acids (methionine and cystine), tryptophan, histidine and zinc (Hughes, 1985; Bjerkås, Breck and Waagbø, 2006). Biochemical mechanisms involved in cataract formation are not well understood because multiple nutrients and genetic and environmental factors may be involved. Excessive amounts of minerals (high ash), particularly high levels of calcium and phosphorus, reduce zinc bioavailability and cause cataract formation in salmonid fishes. Skeletal disorders in farmed fish are linked to a complex and poorly understood relationship between nutrition, environment and genetic factors; however, limited information is available on pathogenesis of bone disorders linked to specific nutrient deficiencies in fish (reviewed by Lall and Lewis-McCrea, 2007). Nutrient deficiencies or toxicities of minerals (calcium, phosphorus, zinc, selenium and manganese) and vitamins (A, D, C, E and K), as well as their interactions and lipid peroxidation may cause pathogenesis leading to skeletal deformities. Fin and skin lesions are commonly observed and are often interpreted as unspecific reactions to environmental and mechanical stress factors. However, a number of dietary factors, including deficiencies of lysine, tryptophan, essential fatty acids, zinc, copper, riboflavin, inositol, niacin and vitamin C; toxicities of vitamin A and lead; lipid peroxidation and feed rancidity can cause these lesions (Tacon, 1992; Lall, 2002).
