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.

Aflatoxins are one of the most dangerous toxic residues in various foods including poultry. This study was conducted to assess the reducing effect of gamma radiation on the levels of aflatoxin B1 in poultry meat, skin, and liver. To this end, a total of 80 poultry samples including meat, skin, and liver were surveyed for the incidence of aflatoxins, where only positive samples (27 samples of muscle, skin, and liver; 9 samples each) were selected for testing the effect of treatment by gamma radiation. The levels of aflatoxins were estimated in the examined samples using High Performance Liquid Chromatography (HPLC) whereas positive samples were exposed to 0 kGy, 5 kGy, or 10 kGy, and the differences in aflatoxin contents before and after exposure were calculated. The obtained results clarified that radiation achieved reduction rates in aflatoxin B1 level in muscle samples with a mean value 99.259±0.741, and 100.00±0.00% when treated with 5 kGy and 10 kGy, respectively. Whereas in skin samples, 98.676±1.324 and 100.00±0.00 % when treated 5 kGy and 10 kGy, respectively. While in liver samples, reduction rates accounted for 84.312±7.406 and 88.249±10.882 were obtained when treated with 5 kGy and 10 kGy, respectively. In conclusion, the exposure of poultry meat, skin, and liver to gamma radiation (5kGy or 10 kGy) has a significant reducing effect (p<0.05) in aflatoxins B1. The results were discussed from the hygienic point of view and compared with the national and international standards to assess their reliability for consumption.

Mycotoxins are considered hidden dangers that threaten the poultry industry globally because they suppress the immunity of birds, reduce their production, and increase their chance of being infected with diseases, which exposes the poultry industry to enormous economic losses. Therefore, this investigation aimed to assess the effectiveness of VemoZyme Detox®, a novel enzymatic detoxifier, in mitigating the detrimental consequences of mycotoxin contamination in broiler chickens. The experiment involved 10,000-day-old, Cobb 500 broiler chicks, which were allotted into two groups of 5000 birds each as follows: T1: received a control basal diet; and T2: birds were provided with a basal diet supplemented with VemoZyme Detox®. The birds underwent comprehensive monitoring, including evaluations of growth performance, blood parameters, mycotoxin levels, hepatic histopathological alterations, and litter bacteriological counts. Broilers receiving dietary VemoZyme Detox® exhibited significant improvements in various aspects, including growth performance, reduced mortality rates, and more favorable feed conversion ratios. Moreover, the enzymatic supplement played a protective role in maintaining hepatic and renal health, as evidenced by reductions in blood aspartate aminotransferase (AST), alanine aminotransferase (ALT), uric acid, and creatinine. Importantly, although there was no significant difference in mycotoxin levels (zearalenone, fumonisin B1, ochratoxin A, aflatoxin B1) within the feed, VemoZyme Detox® had a significant impact on decreasing mycotoxin levels, particularly those of zearalenone and fumonisin B1. Hepatic histological examinations also revealed healthier conditions in T2, and positive impacts extended to litter samples, as indicated by reduced counts of Clostridium perfringens (C. perfringens) and Escherichia coli (E. coli) counts. In conclusion, the use of an enzymatic detoxifier is a promising method for counteracting the negative impacts of mycotoxin contamination in broilers. The results underscore the substantial potential of enzymatic detoxifiers for ensuring the health and productivity of broilers, opening new avenues for safer poultry production.

Forty-nine fresh goat’s milk samples produced by local farmers and sold in market for public consumption as well as raw goat milk in Johor, Malaysia were analysed for total plate count(TPC) , E. coli, Coliform, Brucella melitensis, Brucella abortus,Coxiella burnetii as well as aflatoxin M1 (AFM1) content, as measures for food safety. The mean counts per ml for TPC were 4.90 x 105, 6.50 x 105, 1.60 x 105 and 1.48 x 106 for pasteurised, unpasteurised and unknown (status of pasteurisation) milk sold in the market as well as the raw milk from milkcollection center (MCC), respectively. Among pasteurised samples, only one had TPC count higher than the permitted level whereas the rest were all within the permitted level. The mean counts per ml for E. coli were <1.00 x 102 for pasteurised and unknown milkwhereas 1.67 x 101 for unpasteurised and 1.18 x 102 for raw milk. The mean counts per ml for coliform were 9.53 x 103, 9.76 x103, 1.20 x 102 and 1.16 x 104 for pasteurised, unpasteurised, unknown milk and raw milk, respectively. Overall, no significantdifferences on the bacterial counts in both pasteurised and unpasteurised milk. All milk samples were negative of B. melitensis and B. abortus, but one unknown sample fromthe market and two raw samples from MCC were positive of C. burnetii through the ELISA test. The unknown sample from the market showed the presence of C. burnetii when further analysed microscopically. Meanwhile, no sample exceeded the permitted level of AFM1 in milk.

Enzyme-linked immunosorbent assay screening of antibody produced against aflatoxin was accomplished by a new and simple procedure. To demonstrate the new indirect ELISA technique used, antibody against aflatoxin M1 was produced in female BALB/CJ mice by immunization with an aflatoxin M1-bovine serum albumin conjugate. Instead of coating test-plate wells with purified antibody (direct ELISA) or synthesizing a second protein-aflatoxin conjugate (aflatoxin M1-poly-L-lysine) to coat test-plate wells, wells were coated with the readily available aflatoxin M1-bovine serum albumin and aflatoxin B1-bovine vine serum albumin. This method, applicable for any aflatoxin conjugated by the common cyclopentano-carboxymethoxyl-oxime technique, eliminates the more time-consuming and technically difficult portions of earlier direct and indirect ELISA. The new technique can be valuable in continued efforts toward development of new and improved immunoassays against aflatoxin metabolites.

Newly hatched chickens were treated with the trichothecene mycotoxin, T-2 toxin, during the first day of life. Control chickens were treated with other agents known to cause immunosuppression-cyclosporine, cyclophosphamide, and aflatoxin. Chickens were infected on day 6 (5 days after treatment with T-2 toxin) by intraperitoneal inoculation with Salmonella typhimurium. Blood samples were collected from treated chickens (noninfected) and used to assess the responsiveness of blood lymphocytes to T-cell or B-cell mitogens, phytohemagglutinin, or lipopolysaccharide, respectively. The T-2 toxin had a profound negative effect on the ability of the chickens to resist salmonellosis, as measured by survival. However, the toxin effect in reducing phytohemagglutinin- and lipopolysaccharide-stimulated mitogenesis, though significant (P > 0.05), was not severe. Our data indicate a direct effect of T-2 toxin on native resistance to systemic salmonellosis, which was not accompanied by marked alteration in T- or B-cell responses to mitogenic stimulation.

The effects of dietary aflatoxin and ochratoxin, fed singly and in combination, were evaluated in growing crossbred pigs. Five barrows (7 weeks old at beginning of study) per group were fed either control feed, 2.0 mg of aflatoxin (AF)/kg of feed, 2.0 mg of ochratoxin (OA)/kg of feed, or 2.0 mg of AF and 2.0 mg of OA/kg of feed for 28 days. Production performance, serum biochemical, hematologic, and pathologic evaluations were made. Body weights were reduced by the combination treatment, whereas body weight gain was decreased by all toxin treatments. The effect of AF and OA in combination on body weight gain was additive. Liver weights were increased by the combination treatment, whereas kidney weights were increased only in the OA group. Aflatoxin caused decreases in serum calcium, sodium, phosphorus, urea nitrogen, cholesterol, and glucose concentrations, whereas OA alone caused decreases in serum phosphorus, cholesterol, and hematologic values. The AF-OA treatment induced decreases in mean corpuscular volume, packed cell volume, and in serum concentrations of phosphorus, cholesterol, and urea nitrogen. The AF-OA treatment increased serum alkaline phosphatase activities and triglycerides. It was concluded that AF and OA, singly or in combination, can affect clinical preformance, serum biochemical and hematologic values, and organ weights of barrows. Although values of some measurements were affected more by the combination than by either toxin alone and suggested synergism or antagonism, the toxic interactions could best be described as additive.