The consequences of mycotoxins in aquaculture

//01 Oct 2006

By Pedro Encarnação
The contamination of feeds and raw materials by mycotoxins is increasing on a global basis. While the effect of mycotoxins is well known in most terrestrial farm animals the effect of mycotoxins on aquaculture species has not been studied extensively. Nevertheless, several studies reported pathological signs of mycotoxin poisoning in fish and shrimp species which can cause economic losses to the industry. By Pedro Encarnação.
Dr. Pedro Encarnação has an extensive background in aquaculture and nutrition, and conducted several research projects focusing on the improvement of feed formulations for aquaculture species. He has an Honors Degree in Marine Biology and Fisheries and an MSc in Aquaculture from the University of Algarve (Portugal), and obtained is PhD in Animal Nutrition from the University of Guelph (Canada). He currently works as aquaculture specialist at Biomin.
Most of the mycotoxins that have the potential to reduce growth and health status of fish and other farmed animals consuming contaminated feed are produced by Aspergillus, Penicillium and Fusarium sp. The major classes of mycotoxins include the aflatoxins, trichothecenes, fumonisins, zearalenone and ochratoxins1.

Aflatoxins in fish

Aflatoxins are produced by Aspergillus fungi, which can infect many potential feedstuffs as corn, peanuts, rice, fish meal, shrimp and meat meals2. Aflatoxin B1 (AFB1) is one of the most potent, naturally occurring, cancer-causing agents in animals. Initial findings associated with aflatoxicosis in fish include pale gills, impaired blood clotting, anemia, poor growth rates or lack of weight gain.
The extent of disease, caused by consumption of aflatoxins, depends upon the age and species of the fish. Fry are more susceptible to aflatoxicosis than adults and some species of fish are more sensitive to aflatoxins than others3. 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 AFB1 in a 50g trout being 500–1000 ppb (0.5–1.0 mg/kg)4. The carcinogenic or toxic effects of aflatoxins in fish seem to be species specific. While Rainbow trout are extremely sensitive to AFB1, warm water fish such as channel catfish (Ictalurus punctatus) are reported to be less sensitive to aflatoxins5.
Although less sensitive, warm water species are still affected by aflatoxin contamination. Feeding a diet containing 10 ppm AFB1/kg diet to channel catfish caused reduced growth rate and moderate internal lesions over a 10-week trial period6. In carp, it was reported that aflatoxins are potential immuno-suppressors7. A recent study 8 indicated that feeding diets containing aflatoxins from moldy corn does not seem to affect channel catfish weight gain, feed consumption, feed efficiency, and survival. Studies on the Nile tilapia (Oreochromis niloticus) showed reduced growth rates when tilapias were fed diets containing 1880 ppb AFB19. In addition, tissue abnormality or lesions in the livers of these tilapias showed the beginnings of cancer development. In another study, Nile tilapia fed diets with 0.1 ppm AFB1 for 10 weeks had reduced growth, and fish fed diet with 0.2 ppm AFB1 had 17% mortality10. A more recent study11 showed that acute and sub-chronic effects of AFB1 to Nile tilapia are unlikely if dietary concentrations are 0.25 ppm or less. However, diets containing levels of AFB1 higher than 0.25 ppm had lower weight gain and haematocrit count compared to a control diet. Diets containing 100 ppm AFB1 caused weight loss and severe hepatic necrosis in Nile tilapia12. Other studies have shown that tolerance levels for tilapia can vary with the production system. In green water and flow-through systems, the presence of aflatoxins at 25 to 30 ppb in the water decreased growth without any noticeable signs of mortality. However, in cage culture, concentrations of aflatoxins above 5 ppb caused an increase in mortality rates13.

Aflatoxins in shrimp

In marine shrimp, several studies showed that AFB1 can cause abnormalities such as poor growth, low apparent digestibility, physiological disorders and histological changes, principally in the hepatopancreatic tissue14,15,16,17.
Nevertheless, reports on the effect of AFB1 on shrimp are inconsistent. A study in 200318 reported that after just 7 or 10 days of consumption of diets with AFB1 levels below 20 ppb, mortality rate was slightly higher in AFB1-treated groups than in the control group.
Histopathological findings indicated hepatopancreatic damage by AFB1 with biochemical changes of the haemolymph. In another study, AFB1 at 50–100 ppb showed no effect on growth in juvenile shrimps19. However, growth was reduced when AFB1 concentrations were elevated to 500–2500 ppb. Survival dropped to 26.32% when 2500 ppb AFB1 was given, whereas concentrations of 50–1000 ppb had no effect on survival20. There were marked histological changes in the hepatopancreas of shrimp fed diet containing AFB1 at a concentration of 100–2500 ppb for 8 weeks, as noted by atrophic changes, followed by necrosis of the tubular epithelial cells. Severe degeneration of hepatopancreatic tubules was common in shrimp fed high concentrations of AFB121. According to a study in 200522, the effect of AFB1 toxicity to shrimp results in the modification of digestive processes and abnormal development of the hepatopancreas due to exposure to mycotoxins.


Ochratoxins are a group of secondary metabolites produced by fungal organisms belonging to Aspergillus and Penicillium genera. Ochratoxin A (OA) is the most abundant of this group and is more toxic than other ochratoxins. Very few studies have been conducted to determine the effect of ochratoxins in fish species. In juvenile channel catfish, diets containing levels of 1 to 8 ppm of OA resulted in the development of toxic responses. Significant reduction in body weight gain were observed after only 2 weeks in fish fed diets containing 2 ppm of ochratoxin A or above23. After 8 weeks body weight gain was significantly reduced for fish fed diets containing 1 ppm OA or above. Additional toxic responses included poorer FCR for fish fed diets with 4 or 8 ppm OA, and lower survival and hematocrit count for fish fed the 8 ppm OA diet. Severe histopathological lesions of liver and posterior kidney were observed after 8 weeks for catfish fed diets containing levels of OA of 4 and 8 ppm24. In growing rainbow trout the oral LD50 of ochratoxin A has been determined to be 4.67 ppm.

Cyclopiazonic acid (CPA)

Cyclopiazonic acid (CPA) is a mould toxin produced by several species of Aspergillus and Penicillium fungi. CPA, a neurotoxin frequently found in association with aflatoxins, has been found to be more toxic to channel catfish than aflatoxins and is more frequently found than aflatoxins in feedstuffs in the southern United States25. A dietary level of 100 ppb CPA significantly reduced growth, and 10,000 ppb caused necrosis of gastric glands.
The minimum dietary concentration that caused a reduction in growth rate was 100 ppb for CPA as compared with 10,000 ppb for AFB126.


The fumonisins represent a group of mycotoxins produced predominantly by Fusarium moniliforme species. The toxic effects in fish remains still poorly understood. In one study, channel catfish fed F. moniliforme culture material containing 313 ppm of fumonisin B1 (FB1) for 5 weeks revealed minimal adverse effects27. Conversely, another study28 reported that dietary levels of FB1 of 20 ppm or above are toxic to year-1 and year-2 channel catfish. After 10 and 14 weeks, respectively, year-1 and year-2 catfish fed 20 ppm or more of FB1 in the diet had lower weight gain compared to the control, and those fish fed diets with levels of 80 ppm and above showed significantly lower hematocrits and red and white blood cells than those fed lower doses29. In 2000 it was found that in channel catfish, diets containing 20 ppm of moniliformin (MON) or FB1 significantly reduced body weight gain after 2 weeks30, where FB1 is more toxic than MON to channel catfish. Adverse effects of fumonisin contaminated diets have also been reported in tilapia. Results presented in 200331 demonstrated that feeding MON and FB1 at 70 and 40 ppm, respectively, adversely affected growth performance of Nile tilapia fingerlings. FB1 is slightly more toxic than MON to tilapia fingerlings as toxic symptoms appear earlier in fish exposed to FB1. Nevertheless, neither MON nor FB1 caused mortality or histopathological lesions in Nile tilapia fingerlings. Compared to channel catfish, Nile tilapia appears to be more resistant to these two mycotoxins in the diet32.Although research studies revealed that FB1 is toxic to tilapia and channel catfish by suppressing growth and/or causing histopathological lesions, this fish survived mycotoxins levels up to 150 ppm. Reduction on the percentage of survival of channel catfish was observed for diets containing 240 ppm FB133.
Studies on the effect of FB1 in carp indicated that long-term exposure to 0.5 and 5.0 mg per kg body weight is not lethal to young carp, but can produce adverse physiological effects. The primary target organs of FB1 in the carp are kidney and liver34. Other changes subsequent to fumonisin exposure that have been reported for carp include scattered lesions in the exocrine and endocrine pancreas, and inter-renal tissue, probably due to ischemia and/or increased endothelial permeability35.


Trichothecenes are a group of mycotoxins produced by certain fungi of the genus Fusarium that infect the grains, wheat by-products and oilseed meals used in the production of animal feeds.
The type A-trichothecene T2-toxin produced by the fungus Fusarium tricintum proved lethal to rainbow trout at a dietary concentration near 6 mg/kg body weight36,37, however, fed rainbow trout T2-toxin at 15 ppm of diet and found that the main effects were reduced feed consumption, reduced growth, lower hematocrit, and lower blood hemoglobin.
Results from 200338 demonstrated that T2-toxin is toxic to juvenile channel catfish. Reductions in growth rate were observed after 8 weeks for fish fed diets containing levels of T2-toxin ranging from 0.625-5.0 ppm, compared to a control diet. Significantly poorer feed conversion ratio was found only for the highest level of T2-toxin (5 ppm). The survival of fish fed T2-toxin at 2.5 and 5 ppm was significantly lower than that of the control fish39.
A recent study with channel catfish indicate that disease resistance of juvenile channel catfish was reduced when fed feedborne T-2 toxin, resulting in significantly greater mortality when challenged with Edwardsiella ictaluri compared to a control group40.
In carp, the injection of T-2 toxin did not significantly change the activity of enzymes in carp liver, although a tendency for reduction was noted41.
Deoxynivalenol (DON), also known as vomitoxin, and other type B trichothecenes are produced by Fusarium sp. and can be an important contaminant of wheat. Deoxynivalenol levels of 0.2, 0.5, and 1.0 ppm in the diet significantly reduced body weight and growth rate in white shrimp Litopenaeus vannamei42. However, the effects of 0.2 and 0.5 ppm DON were manifested at later stages of growth, and 0.2 ppm DON affected only growth rate and not body weight. Feed conversion ratio and survival of shrimp fed diets containing 0.2, 0.5, and 1.0 ppm DON were not significantly different from those of shrimp fed the control diet (0.0 ppm DON)43.
Reduced weight gain has also been noted in rainbow trout fed DON-contaminated feeds and feed refusal has been found to occur in fish fed with diets containing more than 20 ppm DON. For rainbow trout, a dietary level of 1–12.9 ppm resulted in reduced growth and feed efficiency44,45 showed that rainbow trout had sensitive taste acuity for DON and reduced their feed intake as the concentration of DON increased from 1 to 13 ppm of diet; the fish refused to consume the diet with a DON concentration of 20 ppm.

References 1-45 are available on request


Binders or adsorbents have been used to neutralize the effects of mycotoxins by preventing their absorption from the animal's digestive tract. Unfortunately, different mycotoxin groups are completely different in their chemical structure and therefore it is impossible to equally deactivate all mycotoxins by using only one single strategy. Adsorption works perfectly for aflatoxin but less- or non-adsorbable mycotoxins (like ochratoxins, zearalenone and the whole group of trichothecenes) have to be deactivated by using a different approach. Furthermore, all mycotoxins are known to influence detrimentally toward the liver and cause immunosuppression in animals. The addition of plant and algae extracts to the animals' diet helps to overcome these negative influences.
A new approach to combat mycotoxins is using bio-inactivation or biotransformation. This innovative approach uses microorganisms or enzymes to break down functional groups of mycotoxins such as trichothecenes, ochratoxin A and zearalenone, to degrade the toxic structures to non-toxic metabolites.