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Maize and its products are most often prone to fungal contamination especially during cultivation and storage by toxigenic fungi. Aflatoxicosis still persist in Ghana despite the numerous education on several ways of its prevention at the farm as well as its adverse health implications which are food safety concerns. A random assessment and human risk analysis was conducted on 90 maize (72 white and 18 colored) samples from markets across all the regions of Ghana. Total aflatoxins (AFtotal) and the constitutive aflatoxins (AFB 1 , AFB 2 , AFG 1 , and AFG 2 ) were analyzed by High-Performance Liquid Chromatography (HPLC). Out of a total of ninety (90) samples investigated, 72 (80%) tested positive for AFB 1 and the contamination levels ranged from 0.78 ± 0.04 to 339.3 ± 8.6 µg kg −1 . Similarly, AFG2 was detected in only 14 (15.5%) samples, and their values ranged between 1.09 ± 0.03 and 5.51 ± 0.26 µg kg −1 while AF total ranged between 0.78 ± 0.04 and 445.01 ± 8.9 µg kg −1 constituting approximately 72 (80%). Limits of AFB 1 and total aflatoxins (AFtotal) for the Ghana Standards Authority (GSA) (5 and 10 µg kg −1 ) and the European Food Safety Authority (EFSA) (2 and 4 µg kg −1 ), were used as checks. A total of 33 (41.25%) samples were above the limits for both. Risk assessments recorded for Estimated Daily Intake (EDI), Hazard Quotient (H.Q), Hazard Index (H.I), Margin of Exposure (MOE), av. Potency, and population risks ranged 0.087–0.38 μg kg −1  bw day −1 , 1.5–6.9, 0.0087–0.38, 3.64–12.09, 0–0.0396 ng Aflatoxins kg −1  bw day −1 and, 3.5 × 10 –1 –0.015 respectively for total aflatoxins. While ranges for aflatoxins B1 (AFB1) recorded were 0.068–0.3 μg Kg bw −1  day −1 , 2.43–10.64, 0.0068–0.030, 4.73–20.51, 0–0.0396 ng Aflatoxins kg −1  bw day −1 and, 2.69 × 10 –3 –0.012 for Estimated Daily Intake (EDI), Hazard Quotient (H.Q), Hazard Index (H.I), Margin of Exposure (MOE), Av. potency, and population risks respectively. It was deduced that although there was some observed contamination of maize across the different ecological zones, the consumption of maize (white and colored) posed no adverse health effects on the population of Ghana since computed H.I was less than 1 (< 1).

Feeding farm animals with aflatoxin-contaminated feed can cause various severe toxic effects, leading to increased susceptibility to infectious diseases and increased mortality, weight loss, poor performance and reduced reproductive capability. Following ingestion of contaminated foodstuffs, aflatoxins are metabolized and biotransformed differently in animals. Swine metabolism is not effective in detoxifying and excreting aflatoxins, meaning the risk of aflatoxicosis is increased. Thus, it is of great importance to elucidate the metabolism and all metabolic pathways associated with this mycotoxin. The damage induced by AFB1 in cells and tissues consists of inhibition of cell proliferation, carcinogenicity, immunosuppression, mutagenicity, oxidative stress, lipid peroxidation and DNA damage, leading to pathological lesions in the liver, spleen, lymph node, kidney, uterus, heart, and lungs of swine. At present, it is a challenging task and of serious concern to completely remove aflatoxins and their metabolites from feedstuff; thus, the aim of this study was a literature review on the deleterious effects of aflatoxins on swine metabolism, as well as alternatives that contribute to the detoxification or amelioration of aflatoxin-induced effects in farm animal feed.

Aflatoxicosis is a grave threat to the poultry industry. Dietary supplementation with antioxidants showed a great potential in enhancing the immune system; hence, protecting animals against aflatoxin B1-induced toxicity. Grape seed proanthocyanidin extract (GSPE) one of the most well-known and powerful antioxidants. Therefore, the purpose of this research was to investigate the effectiveness of GSPE in the detoxification of AFB1 in broilers. A total of 300 one-day-old Cobb chicks were randomly allocated into five treatments of six replicates (10 birds per replicate), fed ad libitum for four weeks with the following dietary treatments: 1. Basal diet (control); 2. Basal diet + 1 mg/kg AFB1 contaminated corn (AFB1); 3. Basal diet + GSPE 250 mg/kg; (GSPE 250 mg/kg) 4. Basal diet + AFB1 (1 mg/kg) + GSPE 250 mg/kg; (AFB1 + GSPE 250 mg/kg) 5. Basal diet + AFB1 (1mg/kg) + GSPE 500 mg/kg, (AFB1 + GSPE 500 mg/kg). When compared with the control group, feeding broilers with AFB1 alone significantly reduced growth performance, serum immunoglobulin contents, negatively altered serum biochemical contents, and enzyme activities, and induced histopathological lesion in the liver. In addition, AFB1 significantly increased malondialdehyde content and decreased total superoxide dismutase, catalase, glutathione peroxide, glutathione-S transferase, glutathione reductase activities, and glutathione concentration within the liver and serum. The supplementation of GSPE (250 and 500 mg/kg) to AFB1 contaminated diet reduced AFB1 residue in the liver and significantly mitigated AFB1 negative effects. From these results, it can be concluded that dietary supplementation of GSPE has protective effects against aflatoxicosis caused by AFB1 in broiler chickens.

Aflatoxin B1 (AFB1), among other aflatoxins of the aflatoxin family, is the most carcinogenic and hazardous mycotoxin to animals and human beings with very high potency leading to aflatoxicosis. Selenium is an essential trace mineral possessing powerful antioxidant functions. Selenium is widely reported as an effective antioxidant against aflatoxicosis. By preventing oxidative liver damage, suppressing pro-apoptotic proteins and improving immune status in AFB1 affected animals; selenium confers specific protection against AFB1 toxicity. Meticulous supplementation of animal feed by elemental selenium in the organic and inorganic forms has proven to be effective to ameliorate AFB1 toxicity. Curcumin is another dietary agent of importance in tackling aflatoxicosis. Curcumin is one of the major active ingredients in the tubers of a spice Curcuma longa L., a widely reported antioxidant, anticarcinogenic agent with reported protective potential against aflatoxin-mediated liver damage. Curcumin restricts the aflatoxigenic potential of Aspergillus flavus. Curcumin inhibits cytochrome P450 isoenzymes, particularly CYP2A6 isoform; thereby reducing the formation of AFB1-8, 9-epoxide and other toxic metabolites causing aflatoxicosis. In this review, we have briefly reviewed important aflatoxicosis symptoms among animals. With the main focus on curcumin and selenium, we have reviewed their underlying protective mechanisms in different animals along with their extraction and production methods for feed applications.

The poultry industry in sub-Saharan Africa (SSA) is faced with feed insecurity, associated with high cost of feeds, and feed safety, associated with locally produced feeds often contaminated with mycotoxins. Mycotoxins, including aflatoxins (AFs), fumonisins (FBs), trichothecenes, and zearalenone (ZEN), are common contaminants of poultry feeds and feed ingredients from SSA. These mycotoxins cause deleterious effects on the health and productivity of chickens and can also be present in poultry food products, thereby posing a health hazard to human consumers of these products. This review summarizes studies of major mycotoxins in poultry feeds, feed ingredients, and poultry food products from SSA as well as aflatoxicosis outbreaks. Additionally reviewed are the worldwide regulation of mycotoxins in poultry feeds, the impact of major mycotoxins in the production of chickens, and the postharvest use of mycotoxin detoxifiers. In most studies, AFs are most commonly quantified, and levels above the European Union regulatory limits of 20 μg/kg are reported. Trichothecenes, FBs, ZEN, and OTA are also reported but are less frequently analyzed. Co-occurrences of mycotoxins, especially AFs and FBs, are reported in some studies. The effects of AFs on chickens’ health and productivity, carryover to their products, as well as use of mycotoxin binders are reported in few studies conducted in SSA. More research should therefore be conducted in SSA to evaluate occurrences, toxicological effects, and mitigation strategies to prevent the toxic effects of mycotoxins.

Evidence about the magnitude of the aflatoxin menace can help policy makers appreciate the importance of the problem and strengthen policies to support aflatoxin mitigation measures. In this study, we estimated aflatoxin-induced liver cancer risk in 2016 for Tanzania and used the information to estimate the health burden due to the aflatoxin exposure in the country. The burden of aflatoxin-induced liver cancer was assessed based on available aflatoxin biomarker data from a previous epidemiology study, hepatitis B virus infection prevalence and population size of Tanzania in 2016. The health burden due to aflatoxin-induced liver cancer was estimated using disability adjusted life years (DALYs). The aflatoxin exposures ranged from 15.0–10,926.0 ng/kg bw/day (median, 105.5 ng/kg bw/day). We estimated that in 2016 there were about 1,480 (2.95 per 100,000 persons) new cases of aflatoxin-induced liver cancer in Tanzania and assumed all of them would die within a year. These morbidity and mortality rates led to a total loss of about 56,247.63 DALYs. These results show, quantitatively, the cases of liver cancer and related deaths that could be avoided, and the healthy life years that could be saved, annually, by strengthening measures to control aflatoxin contamination in Tanzania.

Aflatoxins are endemic in Kenya. The 2004 outbreak of acute aflatoxicosis in the country was one of the unprecedented epidemics of human aflatoxin poisoning recorded in mycotoxin history. In this study, an elaborate review was performed to synthesize Kenya’s major findings in relation to aflatoxins, their prevalence, detection, quantification, exposure assessment, prevention, and management in various matrices. Data retrieved indicate that the toxins are primarily biosynthesized by Aspergillus flavus and A. parasiticus, with the eastern part of the country reportedly more aflatoxin-prone. Aflatoxins have been reported in maize and maize products (Busaa, chan’gaa, githeri, irio, muthokoi, uji, and ugali), peanuts and its products, rice, cassava, sorghum, millet, yams, beers, dried fish, animal feeds, dairy and herbal products, and sometimes in tandem with other mycotoxins. The highest total aflatoxin concentration of 58,000 μg/kg has been reported in maize. At least 500 acute human illnesses and 200 deaths due to aflatoxins have been reported. The causes and prevalence of aflatoxins have been grossly ascribed to poor agronomic practices, low education levels, and inadequate statutory regulation and sensitization. Low diet diversity has aggravated exposure to aflatoxins in Kenya because maize as a dietetic staple is aflatoxin-prone. Detection and surveillance are only barely adequate, though some exposure assessments have been conducted. There is a need to widen diet diversity as a measure of reducing exposure due to consumption of aflatoxin-contaminated foods.

Dietary exposure to aflatoxin B 1 (AFB 1 ) is harmful to the health and performance of domestic animals. The hepatic cytochrome P450s (CYPs), CYP1A1 and CYP2A6, are the primary enzymes responsible for the bioactivation of AFB 1 to the highly toxic exo -AFB 1 -8,9-epoxide (AFBO) in chicks. However, the transcriptional regulation mechanism of these CYP genes in the liver of chicks in AFB 1 metabolism remains unknown. Dual-luciferase reporter assay, bioinformatics and site-directed mutation results indicated that specificity protein 1 (SP1) and activator protein-1 (AP-1) motifs were located in the core region −1,063/−948, −606/−541 of the CYP1A1 promoter as well as −636/−595, −503/−462, −147/−1 of the CYP2A6 promoter. Furthermore, overexpression and decoy oligodeoxynucleotide technologies demonstrated that SP1 and AP-1 were pivotal transcriptional activators regulating the promoter activity of CYP1A1 and CYP2A6 . Moreover, bioactivation of AFB 1 to AFBO could be increased by upregulation of CYP1A1 and CYP2A6 expression, which was trans -activated owing to the upregulalion of AP-1, rather than SP1, stimulated by AFB 1 -induced reactive oxygen species. Additionally, nano-selenium could reduce ROS, downregulate AP-1 expression and then decrease the expression of CYP1A1 and CYP2A6 , thus alleviating the toxicity of AFB 1 . In conclusion, AP-1 and SP1 played important roles in the transactivation of CYP1A1 and CYP2A6 expression and further bioactivated AFB 1 to AFBO in chicken liver, which could provide novel targets for the remediation of aflatoxicosis in chicks.

In April 2004, one of the largest aflatoxicosis outbreaks occurred in rural Kenya, resulting in 317 cases and 125 deaths. Aflatoxin-contaminated homegrown maize was the source of the outbreak, but the extent of regional contamination and status of maize in commercial markets (market maize) were unknown. We conducted a cross-sectional survey to assess the extent of market maize contamination and evaluate the relationship between market maize aflatoxin and the aflatoxicosis outbreak. We surveyed 65 markets and 243 maize vendors and collected 350 maize products in the most affected districts. Fifty-five percent of maize products had aflatoxin levels greater than the Kenyan regulatory limit of 20 ppb, 35% had levels > 100 ppb, and 7% had levels > 1,000 ppb. Makueni, the district with the most aflatoxicosis case-patients, had significantly higher market maize aflatoxin than did Thika, the study district with fewest case-patients (geometric mean aflatoxin = 52.91 ppb vs. 7.52 ppb, p = 0.0004). Maize obtained from local farms in the affected area was significantly more likely to have aflatoxin levels > 20 ppb compared with maize bought from other regions of Kenya or other countries (odds ratio = 2.71; 95% confidence interval, 1.12-6.59). Contaminated homegrown maize bought from local farms in the affected area entered the distribution system, resulting in widespread aflatoxin contamination of market maize. Contaminated market maize, purchased by farmers after their homegrown supplies are exhausted, may represent a source of continued exposure to aflatoxin. Efforts to successfully interrupt exposure to aflatoxin during an outbreak must consider the potential role of the market system in sustaining exposure.

Aflatoxin contamination in feed is a common problem in broiler chickens. The present systematic review and meta-analysis examined the impact of aflatoxin-contaminated feed and the efficacy of various feed additives on the production performance of broiler chickens fed aflatoxin-contaminated feed (AF-feed). A total of 35 studies comprising 53 AF-feed experiments were selected following PRISMA guidelines. Feed additives included in the analyses were toxins binder (TB), mannan-oligosaccharides (MOS), organic acid (OA), probiotics (PRO), protein supplementation (PROT), phytobiotics (PHY), and additive mixture (MIX). Random effects model and a frequentist network meta-analysis (NMA) were performed to rank the efficacy of feed additives, reported as standardized means difference (SMD) at 95% confidence intervals (95% CI). Overall, broiler chickens fed AF-feed had significantly lower final body weight (BW) (SMD = 198; 95% CI = 198 to 238) and higher feed conversion ratio (SMD = 0.17; 95% CI = 0.13 to 0.21) than control. Treatments with TB, MOS, and PHY improved the BW of birds fed AF-feed (P < 0.05) to be comparable with non-contaminated feed or control. Predictions on final BW from the broiler-fed aflatoxin-contaminated diet were 15% lower than the control diet. Including feed additives in the aflatoxins diet could ameliorate the depressive effect. Remarkably, our network meta-analysis highlighted that TB was the highest-performing additive (P-score = 0.797) to remedy aflatoxicosis. Altogether, several additives, especially TB, are promising to ameliorate aflatoxicosis in broiler chickens, although the efficacy was low regarding the severity of the aflatoxicosis.