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.

Male broiler chicks were given feed and water ad libitum from hatching through 3 weeks of age. The feed contained 0, 1.25, 2.5, and 5.0 microgram of aflatoxin/g of feed. The chicks were killed by cervical dislocation and specimens of liver and kidney were obtained for electron microscopy on days 3, 6, 9, 17, and 21. In chicks fed 5.0 microgram of alfatoxin, the primary lesions in liver were hepatocellular lipidosis, enlargement of bile canaliculi, reduction in mitochondrial size, mild lymphocytic infiltration, and hepatocellular degeneration and necrosis. Similar lesions were noticed in some chicks fed 2.5 microgram of aflatoxin, but none was observed in chicks fed at 1.25 microgram of aflatoxin. At 5 microgram of aflatoxin, the most consistent lesion in the kidney was thickening of the glomerular basement membrane. Similar glomerular lesions were observed at 2.5 microgram of aflatoxin, but not at 1.25 microgram of alfatoxin. Some foot processes of the glomerular epithelial cells were poorly developed. Fusion of foot processes was not observed and fibrous material was not evident in the basement membrane. The pseudopodia of endothelial cells lining the thickened basement membrane were depleted in number or were absent. Degenerative changes also were observed in the cells of the proximal convoluted tubules, but these were less consistent than those of the glomerulus.

Aflatoxins are produced mainly by Aspergillus flavus and Aspergillus parasiticus that grow in improperly stored cereals. Aflatoxin B₁ (AFB₁) is a potent hepatocarcinogen in a variety of experimental animals including human beings. In spite of a high attention to the hepatocarcinogenecity of AFB₁, the relative toxicity of aflatoxins (AFB₂ and AFG₁) is not fully clarified. Sprague-Dawley male rats were orally administered with AFB₁, AFB₂, and AFG₁ at the dose of 250 μg/kg (additionally including a dose of 1250 μg/kg for AFB₁) body weight.

The mycotoxin test data base (2005–2009) of the Veterinary PublicHealth Laboratory (VPHL), Department of Veterinary Services, Malaysia (DVS) showed that there was a significant increase (51%) of overall aflatoxin occurrences in various types of animal feed samples, especially those formulated from agricultural by-product, for the year 2008. A study was thus conducted to investigate if there could be some sources of mycotoxin contamination during theperiod of sample handling. Three different laboratory storage conditions were chosen for the study within a period of fourteendays i.e 4 °C, room temperature (in light) with mean relative humidity of 62.5%, and room temperature (in dark) with mean relative humidity of 55.7%. The observations showed that there were nosignificant differences in total aflatoxin, zearalenone, and fumonisin detections in all storage conditions as screened by the ELISA technique. However 11– 50% inconsistencies of the mycotoxinconcentrations detected were observed within the samples.