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Nutritional disorders and pathology may arise from the presence of specific adventitious toxic factors or contaminants within feedstuffs, including:

  1. Intentional additives

  2. Toxic factors arising from processing

  3. Contaminants of biological origin

  4. Synthetic contaminants

Of the above mentioned adventitious toxic factors probably the most important (from a pathological and economic viewpoint) are the fungal toxins or ‘mycotoxins’. Over 200 different mycotoxins have been identified to date from feed ingredient sources (Jones, 1987). The majority of mycotoxins of pathological importance are produced by filamentous fungi (ie. moulds) belonging to the Aspergillus, Penicillium and Fusarium genera, and include the aflatoxins (aflatoxin B1–2, G1–2), Fusarium toxins (zearalenones, tricothecenes - vomitoxins, T2), ochratoxins (ochratoxin A & B), cyclopiazonic acid, patulin, slaframine, and citrinin (Hendricks & Bailey, 1989; Lovell, 1989, 1991, 1992). Mycotoxins are produced by the moulds within certain feedstuffs either prior to harvesting or during storage prior to animal consumption; feedstuffs which are particularly prone to attack by Aspergillus flavus (producer of the common mycotoxin aflatoxin B1-AFB1) including cottonseed meal, groundnut meal, copra meal, maize (corn) products, and to a lesser extent wheat, rice, barley, sorghum, oats, sunflower, soybean and cassava (Hendricks & Bailey, 1989). For a view of the factors favouring the growth of these contaminating moulds within feedstuffs see Tacon (1988). According to national feed legislation in the USA, maize (corn) and peanut (groundnut) products that are to be used for feeding dairy and immature animals (including fish) cannot contain more than 20 ppb of aflatoxin (Lovell, 1992).

Reported pathological signs of mycotoxin poisoning in fish include: Aflatoxin: Fish general - poor growth, anaemia, impaired blood clotting, sensitivity to bruising, damage to liver and other organs, decreased immune responsiveness, and increased mortality. Prolonged feeding of a low concentration of aflatoxin (B1) to rainbow trout causes liver tumours (Lovell, 1992). Rainbow trout is reported to be one of the most sensitive animals to aflatoxin poisoning; the LD50 (dose causing death in 50% of the subjects) for aflatoxin in a 50g trout being 500–1000 ppb (0.5–1.0 mg/kg), and oral intakes of 0.4–1.0 ppb dietary AFB1 fed continuously for one year producing hepatic tumours (for review see Hendricks & Bailey, 1989). Signs of severe aflatoxicosis in rainbow trout include liver damage, pale gills and reduced red blood cell concentration. However, warm water fish such as channel catfish are reported to be less sensitive to aflatoxin; a dietary concentration of 6600 ppb aflatoxin B1 causing reduced growth rate, haematocrit and haemoglobin concentration in channel catfish over a 10-week trial period (Lovell, 1992). Coho salmon (O. kisutch), chinook salmon (O. tschawytscha) and sockeye salmon (O. nerka) are also reported to be considerably less sensitive to aflatoxin poisoning than rainbow trout (Hendricks & Bailey, 1989).

Ochratoxin A: Rainbow trout - severe necrosis of liver and kidney tissue, pale kidney, light swollen livers and death; LD50 of 4.67mg/kg (Hendricks & Bailey, 1989; Lovell, 1992).

Cyclopiazonic acid (CPA): Channel catfish - a dietary level of 100 ppb CPA significantly reducing growth, and 10,000 ppb causing necrosis of gastric glands. According to the above data CPA is more toxic to channel catfish than aflatoxin (Lovell, 1992).

Vomitoxin: Rainbow trout - a dietary level of 1–12.9 ppm causing reduced growth and feed efficiency (Hendricks & Bailey, 1989)

Apart from the mycotoxins, dietary toxicological studies have not been performed on the majority of the other above mentioned contaminants. For general review see NRC (1983), Hendricks & Bailey (1989) and Roberts & Bullock (1989).

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