4. DISORDERS IN MINERAL NUTRITION

4.1 Dietary essential mineral deficiency

Table 5 shows the major anatomical deficiency signs which have been reported in fish fed rations deficient in one or more essential minerals. Despite the presence of macro and micro (trace) elements in virtually all raw ingredients commonly used for fish feeding (Tacon & De Silva, 1983) and the ability of fish to absorb certain trace elements from the surrounding water, mineral deficiencies may arise under intensive culture conditions through:

• The absence of a specific macro or trace mineral premix within the diet. For details of specific mineral premix formulations and dietary recommendations see NRC (1983) and Davis & Gatlin (1991).

• Reduced mineral bioavailability through dietary imbalances. The availability and utilization of dietary trace elements in fish is dependent upon the dietary source and form of the element ingested, the adequacy of stores within the body, interactions with other mineral elements present in the gastro-intestinal tract and within the body tissues (antagonisms), and finally by element interactions with other dietary ingredients or their metabolities (ie. vitamins, fibre or phytic acid). For example, Table 6 shows the relative availabilities or apparent absorption efficiency of various forms or sources of dietary phosphorus for channel catfish (I. punctatus), common carp (C.carpio) and rainbow trout (O. mykiss). In general, phosphorus bioavailability has been found to be higher in brown low-ash fish meals than in high-ash white fish meals (Lall & Keith, 1991, Watanabe, Satoh & Takeuchi, 1988).

For certain fish species the availability and absorption of phosphorus and other major elements (calcium) from fish meal and meat and bone meal is further complicated by the absence of an acid-secreting stomach, which is essential for normal bone solubilization. For stomachless fish species soluble monobasic inorganic salts or bioavailable organic salts must therefore be provided in the diet. Conversely, within plant proteins a large proportion of phosphorus is present as organically bound phytates. Not only is phytic acid phosphorus largely biologically unavailable, but phytic acid also has the capacity to chelate other trace elements (ie. iron, copper, zinc, cobalt, molybdenum) and by so doing may render them biologically unavailable to the fish during digestion (Spinelli, 1980; Lovell, 1989; Hossain & Jauncey, 1991). For example, in channel catfish (I. punctatus) dietary phytate has been shown to reduce the bioavailability of zinc, especially in the presence of high dietary calcium (Gatlin & Phillips, 1989). Furthermore, high dietary phytate levels (2.2%) have also been reported to have a negative effect on fish growth and feed efficiency in channel catfish (Satoh, Poe & Wilson, 1989).

Under practical farming conditions mineral deficiency signs often arise from a dietary imbalance of calcium; due to the antagonistic effect of excess dietary calcium on the absorption of phosphorus (Nakamura, 1982) and the trace elements zinc, iron and manganese (Lall, 1979). For example, the bioavailability of zinc and to a lesser extent manganese and magnesium, within white fish meal has been found to be much lower than that contained in brown fish meal (which has a much lower ash and calcium content; Ketola, 1978; Watanabe, Takeuchi & Ogino, 1980; Satoh, Takeuchi & Watanabe, 1987a, 1987b, 1991). Similarly, increasing levels of dietary calcium phosphate (Ca₃(PO₄)₂ and Ca(H₂PO₄)₂) was found to have a inhibitory effect on zinc bioavailability in rainbow trout, inducing short body dwarfism or eye cataracts (Satoh et al. 1987, 1991). It is perhaps not surprising therefore that rainbow trout, chum salmon and common carp fed on diets in which white fish meal was used without a trace element supplement that overt trace element deficiency signs arise, including reduced growth, short body dwarfism and cataracts (Watanabe, Takeuchi & Ogino, 1980; Satoh et al. 1983, 1983a; Yamamoto et al. 1983; Watanabe, Satoh & Takeuchi, 1988). Furthermore, recent trials concerning the dietary zinc requirements of channel catfish (I. punctatus) swim-up fry in soft and hard water appear indicate that environmental calcium interacts with dietary zinc and may also fry growth and survival (Scarpa & Gatlin, 1992). However, the recent trials of Satoh et al. (1991) also suggest that high dietary intakes of phosphorus (1.8% of diet) also has a negative effect on growth and zinc availability, thus indicating the importance of the balance between dietary calcium and phosphorus; the best growth reported for rainbow trout fed calcium and phosphorus in equal proportions.

4.2 Dietary mineral toxicity

A major hazard which may be associated with the use of unconventional dietary feed ingredients is the presence of heavy metal contaminants including the accumulative elements copper, lead, cadmium, mercury, arsenic, fluoride, selenium, molybdenum and vanadium. For example, contamination with copper may arise from products fermented within copper lined vessels (brewery by-products), or within pig and poultry excreta from the use of copper based growth stimulants and anti-fungal agents. Other feed ingredients which may contain metal contaminants include: poultry waste - arsenic; paper pulp waste -lead; fish meals - mercury, selenium, arsenic cadmium and lead; poultry by-product meals - zinc; hydrolysed feather meals - zinc; shellfish - zinc, cadmium; seleniferous accumulating plants of the genera Astragalus and Machaeranthera, or cereals grown in seleniferous soils - selenium; krill meal - fluoride. Table 7 lists the major toxicity signs which have been reported in fish under laboratory conditions.

¹ 1-Ogino & Takeda (1976),
2-Yone & Toshima (1979),
3-Ogino et al. (1979),
4-Takeuchi & Nakazoe (1981),
5-Andrews, Murai & Campbell (1973),
6-Lovell & Li(1978),
7-Sakamoto & Yone (1980),
8-Sakamoto & Yone (1979),
9-Sakamoto &Yone (1978),
10-Arai, Nose & Kawatsu (1974),
11-Ogino & Chiou (1976),
12-Ogino & Takeda (1978),
13-Ketola (1975),
14-Lall & Bishop (1977),
15-Arai et al.(1975),
16-Arai, Nose & Hashimoto (1975),
17-Sakamoto & Yone (1973),
18-Satohet al. (1983),
19-Gatlin et al. (1982),
20-Nose & Arai (1979),
21-Cowey et al(1977),
22-Knox, Cowey & Adron (1981),
23-Ogino, Takashima & Chiou (1978),
24-Knox, Cowey & Adron (1983),
25-Satoh et al. (1983a),
26-Sakamoto & Yone(1978a),
27-Sakamoto & Yone (1978b),
28-Kawatsu (1972),
29-Gatlin & Wilson(1983),
30-Ogino & Yang (1979),
31-Ogino & Yang (1978),
32-Wekell, Shearer &Houle (1983),
33-Ishak & Dollar (1968),
34-Ogino & Yang (1980),
35-Yamamoto etal (1983),
36-Poston, Combs Leibovitz (1976),
37-Bell et al. (1987),
38-Lall(1979),
39-Gatlin & Wilson (1984),
40-Woodall & La Roche (1964),
41-NRC(1983),
42-Shearer (1988),
43-Shim & Ng (1988),
44-Satoh, Takeuchi & Watanabe(1987b)

1 Source: NRC (1983)

¹ 1-Jeng & Sun (1981),
2-Murai, Andrews & Smith (1981),
3-Hilton, Hodson & Slinger (1980),
4-Hicks, Hilton & Ferguson (1984),
5-Hilton & Hodson (1983),
6-Gatlin & Wilson (1984),
7-Koyama& Itazawa (1977),
8-Koyama & Itazawa (1977a),
9-Koyama & Itazawa (1979),
10-Roch & Maly(1979),
11-Johansson-Sjobeck & Larsson (1979), Tacon & Beveridge (1982)