Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing wethers (mean body weight, 34.0 kg) and was evaluated for its ability to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 4 treatment groups of 5 wethers each, consuming concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control; group 1); 20 g of HSCAS/kg (2.0%; group 2), 2.6 mg of AF/kg (group 3); or 20 g of HSCAS (2.0%) plus 2.6 mg of AF/kg (group 4). Wethers were maintained in indoor pens, with feed and water available ad libitum for 42 days. Lambs were observed twice daily and weighed weekly, and blood samples were obtained every 2 weeks for hematologic and serum biochemical analyses and for measurement of mitogen-induced lymphocyte-stimulation index. At the termination of the study, wethers were euthanatized and necropsied. Body weight gain was diminished significantly (P less than 0.05) by consumption of 2.6 mg of AF/kg of feed, whereas body weight of lambs consuming HSCAS plus AF did not differ from that of control wethers. The AF-alone treatment increased serum aspartate transaminase and gamma-glutamyltransferase activities, prothrombin time, and cholesterol, uric acid, and triglyceride values and decreased albumin, glucose, and urea nitrogen values, and urea-to-creatine ratio. A 27% decrease in lymphocyte stimulation index, increased spleen weight (as a percentage of body weight), and decreased liver weight were induced by AF-alone treatment. Results indicate that HSCAS may be a high-affinity sorbent for AF, that 2.6 mg of AF/kg of feed induces signs of aflatoxicosis in growing wethers, that lambs may not be as resistant to the effects of AF as previously thought, that 2.0% HSCAS can substantially reduce the toxic effects of 2.6 mg of AF/kg, and that sorbent compounds may offer a novel approach to the preventive management of aflatoxicosis in livestock.

In 2 studies, the effects of dietary aflatoxin (AF) and deoxynivalenol (DON) were evaluated in growing crossbred barrows. The first study consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 2.5 mg of DON/kg of feed, 0.75 mg of AF/kg of feed, and 2.5 mg of DON + 0.75 mg of AF/kg of feed. Pigs were fed their respective diets for 21 days. Treatment with DON caused decreases in weight gains, but no other treatment-related differences could be attributed to diets. In a second study, the experimental design consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 3 mg of DON/kg of feed, 3 mg of AF/kg of feed, and 3 mg of DON + 3 mg of AF/kg of feed fed ad libitum for 28 days. The pigs were observed twice daily for clinical signs, hematologic and serum biochemical measurements were made weekly, and body weights and feed consumption were determined weekly. Body weight gains were significantly depressed by the AF and the AF + DON treatments for days 7, 14, 21, and 28. Body weights and body weight gains were only slightly reduced in the DON treatment. Changes in serum enzymatic activities of alkaline phosphatase, aspartate transaminase, creatine kinase, and gamma-glutamyl transferase were noticed in pigs given treatments with AF alone and those given AF + DON. Total iron binding capacity and serum total protein, albumin, cholesterol, BUN, and glucose concentrations were decreased, whereas prothrombin and activated thromboplastin times were increased by AF and AF + DON treatments. Lesions in the AF-treated groups were compatible with a diagnosis of aflatoxicosis. The control and DON-treated pigs had no abnormalities. These data provide a description of the effects of dietary AF and DON, singly and in combination, in growing barrows.

The relationship of serum complement activity and bacteriostatic activity was investigated in male guinea pigs given aflatoxin and/or rubratoxin. In experiment 1, guinea pigs were given 0.6 mg of aflatoxin/kg of body weight, PO, once. In experiment 2, guinea pigs were given 0.02 mg of aflatoxin/kg, PO, and/or 8 mg of rubratoxin, PO, 11 times. Aflatoxin (0.02 mg/kg) had no effect given alone, but potentiated the effect of rubratoxin. In both experiments, changes in complement activity were accompanied by similar but not always significant (P less than 0.05) changes in bacteriostatic activity of serum. Guinea pigs given 0.06 mg of aflatoxin/kg had significant (P less than 0.05) changes in complement titers and in serum alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase activities. Guinea pigs given repeated oral doses of aflatoxin and/or rubratoxin had changes in complement titers, bacteriostasis, and alkaline phosphatase and aspartate aminotransferase activities, but not in alanine aminotransferase activities. Significant differences were detected only when average values for all guinea pigs given rubratoxin or rubratoxin with aflatoxin were compared with average values for guinea pigs not given rubratoxin.

A study was conducted to determine aflatoxins in tissues and non-tissues of 2 Holstein cows given oral doses of 0.35 mg of purified aflatoxin B1/kg of body weight/day for 3 consecutive days. Cow 1 was slaughtered 24 hours after the 3rd dose, and cow 2, after day 3, was fed aflatoxin-free rations for 7 additional days before slaughter. Tissue samples of brain, gallbladder and bile, heart, intestine, kidney, liver, lung, mammary gland, skeletal muscle, spleen, supramammary lymph nodes, thymus, and tongue, and nontissue samples of blood, feces, milk, rumen content, and urine were examined. Aflatoxins B1 and M1 were found in all samples of cow 1, except the thymus. Kidney, liver, and mammary gland had the highest concentrations of total aflatoxins (57.9, 13.2, and 25.1 ng/g, respectively), with the aflatoxin M1 concentration 40 times more than the aflatoxin B1 level in kidney. Aflatoxin residues were present (0.02 to 0.11 ng/g) only in kidney, liver, and intestine of the tissues from cow 2 (fed aflatoxin-free feed for 7 additional days). Aflatoxin B1 was not present in nontissue samples, but aflatoxin M1 (0.10 and 1.5 ng/ml) was found in the last milk and urine samples from the same cow. Urine assays are a possible way to monitor the presence of aflatoxin residues in meat tissues.

For poultry farmers and quails producers’, one of the biggest challenges is dealing with natural diet contaminants like mycotoxins. Worldwide, mycotoxins are present in all feed sources, primarily in corn, and they significantly reduce the health, immune function, and performance of birds. For this purpose, the effect of citric acid (CA) supplement on contaminated diet with Aflatoxins (AFL) in the liver biochemical, histological, and ultrastructural studies of male Japanese quail (Coturnix coturnix). Influences of experimental diets were assessed in 3 replications of 6 birds each (n = 18 per treatment). Quails two weeks old were assigned into 4 equal groups. The control quails fed only basal diet, AFL group quails were given basal diet contaminated with 2.5 mg AFL/kg diet, citric group quails fed basal diet with 10 g citric acid/Kg, and AFL/citric group quails fed basal diet contaminated with 2.5 mg AFL /Kg and augmented with 10 g/Kg citric acid. After four weeks, feeding AFL to quails induced hepatotoxicity as evidenced by significant decline in body weight, serum albumin and total protein while it significantly increased serum ALT, and AST activities. AFL also induces liver oxidative stress by the elevation of lipid peroxidation and reducing GPx, ADH, SOD and catalase activities. Descriptive hepatic histological and ultrastructural alteration were also noted in the AFL group. Treatment with CA induced an increase in total protein, albumin, SOD, GPx, ADH and significantly decreased ALT and AST activities and MDA level. Moreover, it also improved the histological and ultrastructure alternations induced in the liver of AFL group. It was concluded that supplementation of CA into the AFL polluted diets lessened the adverse influences of AFL on quail’s liver.

This study was conducted to observe the occurrence of aflatoxin in chicken feed from Peninsular Malaysia. A total of 336 samples of chicken feed from Peninsular Malaysia were conveniently collected in this survey. The chicken feed represented the following three categories which are starter, grower and finisher. All samples werecollected from local poultry farms in East Coast Region (Kelantan, Terengganu, and Pahang), Northern Region (Perlis, Kedah, Penang, and Perak), Southern Region (Malacca, Johor) and Central Region (Selangor, Negeri Sembilan) of Peninsular Malaysia for a periodof six months (July-December 2015). Enzymelinked immunosorbent assay (ELISA) was used for screening of total aflatoxin (TA) in the samples. High performance liquid chromatography (HPLC) with fluorescence detector was used for determination of aflatoxin B and G. Moisture content of samples was determined using the hot airoven method (AOAC International, 2011). Overall, the incidence of positive TA >20 µg/kg in chicken feed is 14.9% (50 samples). The average level of TA was found significantly different between different states at p<0.05 for both broiler grower and finisher. Thechromatograph results showed that positive samples were found in broiler finisher from Kedah (94.6 µg/kg and 42.1 µg/kg) and Penang(56.4 µg/kg) with aflatoxin B1. In this study, the range of moisture content were around 6.5-27.3%. About 40% samples have more than12% moisture content. One of the predisposing factors for aflatoxin accumulation in chicken feed is moisture content. The results warrantthe need for surveillance and constant monitoring programmes for the prevention of aflatoxin incidence in poultry farms.

Effects of dietary aflatoxin (AF) and supplemental vitamin E (d-alpha-tocopherol) were evaluated in growing crossbred pigs. Nine barrows (3 replicates of 3 each, mean body weight, 14.0 kg) per group were assigned to 1 of 4 treatment groups (for a total of 36 barrows): 0 IU of supplemental vitamin E and 0 mg of AF/kg of feed (control); 2,400 IU of vitamin E divided into equal doses and administered IM on days 1 and 16; 2.5 mg of AF/kg of feed; or 2.5 mg of AF/kg of feed plus 2,400 IU of vitamin E administered similarly to treatment 2. Barrows were administered their respective treatment for 32 days. Evaluations were made for group production performance and for serum biochemical, immunologic, hematologic, pathologic, serum and tissue tocopherol, and serum retinol variables. Body weight was reduced by AF-alone and AF plus vitamin E treatments, compared with control and vitamin E-alone treatments. Liver weight was increased for the AF alone-treated and the AF plus vitamin E-treated barrows, compared with control barrows. The AF alone-treated barrows had alterations in: serum values of alkaline phosphatase, gamma-glutamyltransferase, albumin, glucose, phosphorus, calcium, cholesterol, total iron, unsaturated iron-binding capacity, total iron-binding capacity, and urea nitrogen; RBC numbers, hematocrit, hemoglobin concentration, and prothrombin time; and mitogen-induced lymphoblastogenic responses. With the exception of some slight ameliorating effects on hematologic measurements, supplemental treatment with vitamin E did not prove beneficial against the toxicosis-associated AF treatment. The AF alone-treated barrows had decreased serum tocopherol and retinol concentrations, compared with control and pretest values, and decreased tocopherol concentration in cardiac tissue. High parenterally administered doses of vitamin E did not have sparing effect on Af-induced reductions of serum tocopherol or retinol concentration; however, compared with pretest values, serum tocopherol concentration was increased by vitamin E-alone treatment. Tocopherol concentration in cardiac tissue of the AF plus vitamin E-treated barrows was increased over that of the AF alone-treated barrows, indicating an ameliorating effect on AF-induced tissue concentrations reductions. These data indicate that vitamin E may not have a sparing effect on AF-induced toxicosis and that AF may reduce serum retinol and serum and tissue tocopherol concentrations.

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire X Landrace X Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time. Treatment with T-2 toxin induced microcytic hypochromic anemia, increased numbers of circulating metarubricytes and decreased absolute numbers of lymphocytes. Hepatocellular lesions in barrows of the AF and the AF plus T-2 groups (2 and 4, respectively) were compatible with aflatoxicosis. When fed in combination, each toxin appeared to have a sparing action on certain effects of the other, and the responses elicited were either additive or less than additive.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCA/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF. Aflatoxin alone induced decreased serum concentrations of urea nitrogen, albumin, total protein, calcium, phosphorus, cholesterol, and glucose, as well as serum total iron-binding capacity, whereas HSCAS or HSCAS plus AF did not induce such effects. Liver weight was increased in barrows of the AF-alone treatment group, compared with control barrows. Hepatic lesions in barrows of the AF-alone treatment group were charaterized as peripheral lobular lipidosis accompanied by periportal and interlobular fibrosis and bile duct hyperplasia. Hepatic lesions were not observed in barrows of the 0.5% HSCAS plus AF or 2.0% HSCAS plus AF treatment groups. These findings suggested that HSCAS can modulate the toxicity of AF in growing barrows (perhaps via sequestration and reduced bioavailability in vivo) and may offer a novel approach to the preventive management of aflatoxicosis in animals.

Two of 3 groups of Holstein-Friesian steers (groups II and III; n = 5 each) were fed a ration containing corn naturally contaminated with 800 ng of aflatoxin/g. The other group of steers (group I; n = 5) was fed a ration containing noncontaminated corn. The respective rations were fed for 17.5 weeks, except the ration given to group III; the latter's first diet (contaminated with aflatoxin) was changed to a noncontaminated diet after 15 weeks, continuing for the remaining 2.5 weeks. All steers were killed and tissues and fluids were obtained for aflatoxin analysis. Although aflatoxin B1 and M1 could be detected in blood and urine at several sampling times during the experimental period in groups II and III steers (given the diets containing aflatoxin), there appeared to be no effects on body weight gains and immune phenomena, such as lymphoblastogenesis and antibody production, but there was a waning of the delayed cutaneous hypersensitivity in steers given aflatoxin-contaminated diets. In group III animals (diet was changed to noncontaminated ration at 15 weeks), aflatoxin B1 and M1 disappeared from urine before they were slaughtered. All tissues and fluids, except the rumen contents from these group III steers, were void of detectable aflatoxins B1 and M1 at necropsy. The concentrations of aflatoxin B1 in the rumen content of the latter steers were low. All tissues collected at necropsy from the group II steers fed the aflatoxin diet throughout the 17.5 weeks had detectable aflatoxins B1 or M1 present.