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Background: Mushrooms, an integral component of human diets, range from esteemed delicacies to potentially lethal toxins. The risk of severe poisoning from misidentified species, poses a significant challenge. For clinicians, recognizing mushroom poisoning amidst nonspecific symptoms and determining the specific mushroom ingested are critical yet complex tasks. Additionally, climate change affects the distribution and proliferation of mushroom species, potentially heightening the risk of exposure to toxic varieties. The identification of mushroom intoxication is critical for appropriate treatment. Poisoning with highly toxic species, such as Amanita phalloides (death cap), can result in acute liver and kidney failure. Considering the limited therapeutic options currently available for acute liver failure, we investigated the application of plasmapheresis, a procedure involving the replacement of the patient's plasma with donor plasma, as a potential intervention to improve clinical outcomes in severe cases of mushroom poisoning., Methods: This study aimed to assess the trends and treatment outcomes of mushroom poisoning cases from 2005 to 2022, with a particular focus on the number of incidents and the potential impacts of climate change. We undertook a retrospective monocentric cohort study, evaluating 43 patients with mushroom poisoning. The study focused on identifying the variety of mushrooms involved, including psychotropic, spoiled, inedible, or toxic species, and closely examined patients with elevated transaminases indicative for liver damage. To assess clinical outcomes, we evaluated several aspects, including hepatic encephalopathy and other symptoms. Additionally, we monitored blood analysis results through serial measurements, including transaminases, bilirubin, INR, and creatinine levels. Furthermore, we explored the impact of climate changes on the incidence of mushroom poisoning., Results: While the incidence of mushroom poisonings remained relatively stable during the first eight years of the study period, it nearly doubled over the past nine years. Nine distinct mushroom types were documented. The study showed no change in season patterns of mushroom poisonings. In cases of severe liver damage accompanied by coagulopathy, plasmapheresis was utilized to replace deficient clotting factors and mitigate the inflammatory response. This intervention proved effective in stabilizing coagulation parameters, such as the international normalized ratio (INR) Plasmapheresis was performed until the INR reached stable levels, preventing the occurrence of severe bleeding complications. In instances where liver failure was deemed irreversible, plasmapheresis functioned as a bridging therapy to manage bleeding risks and to stabilize the patient while awaiting liver transplantation., Conclusion: The findings underscore the need for heightened awareness among healthcare professionals regarding mushroom poisoning and emphasize the importance of considering climate change as a factor that may alter mushroom distribution and toxicity. Additionally, this study highlights the potential of plasmapheresis in managing severe cases., Competing Interests: Declarations. Ethics approval and consent to participate: The studies involving human participants were reviewed and approved by Ethics Committee of the University of Regensburg, Regensburg, Germany. Informed consent was obtained from all participants. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests., (© 2024. The Author(s).)

Mycotoxins can be found in many foods consumed by humans and animals. These substances are secondary metabolites of some fungi species and are resistant to technological processes (cooking, frying, baking, distillation, fermentation). They most often contaminate products of animal (beef, pork, poultry, lamb, fish, game meat, milk) and plant origin (cereals, processed cereals, vegetables, nuts). It is estimated that about 25% of the world's harvest may be contaminated with mycotoxins. These substances damage crops and may cause mycotoxicosis. Many mycotoxins can be present in food, together with mold fungi, increasing the exposure of humans and animals to them. In this review we characterized the health risks caused by mycotoxins found in food, pet food and feed. The most important groups of mycotoxins are presented in terms of their toxicity and occurrence.

Diplodiosis is an important neuromycotoxicosis of ruminants in South Africa when grazing on harvested maize fields in winter. It is believed to be caused by mycotoxin(s) synthesised by Stenocarpella (Diplodia) maydis. Although several metabolites have been isolated from S. maydis culture material, none of these have been administered to ruminants to reproduce the disease. The objectives of this study were to isolate diplodiatoxin and to administer it to juvenile goats. Diplodiatoxin, considered as a major metabolite, was purified from S. maydis-infected maize cultures (Coligny 2007 isolate). Following intravenous administration of 2 mg and 4 mg diplodiatoxin/kg body weight for five consecutive days to two juvenile goats, no clinical signs reminiscent of diplodiosis were observed. Based on previous experimental results and if diplodiatoxin was the causative compound, the dosage regimen employed was seemingly appropriate to induce diplodiosis. In addition, intraruminal administration of 2 mg/kg diplodiatoxin to one goat for three consecutive days also did not induce clinical signs. It appears as if diplodiatoxin alone is not the causative compound. Other metabolites and/or mixtures of diplodiatoxin and other mycotoxins, when available in sufficient quantities, should also be evaluated.

Mycotoxins, such as aflatoxin B 1 (AFB 1 ), pose a serious threat as biological weapons due to their high toxicity, environmental stability, easy accessibility and lack of effective therapeutics. This study investigated if blood purification therapy with CytoSorb (CS) porous polymer beads could improve survival after a lethal aflatoxin dose (LD 90 ). The effective treatment window and potential therapeutic mechanisms were also investigated. Sprague Dawley rats received a lethal dose of AFB 1 (0.5-1.0 mg/kg) intravenously and hemoperfusion with a CS or Control device was initiated immediately, or after 30, 90, or 240-minute delays and conducted for 4 hours. The CS device removes AFB 1 from circulation and significantly improves survival when initiated within 90 minutes of toxin administration. Treated subjects exhibited improved liver morphology and health scores. Changes in the levels of cytokines, leukocytes and platelets indicate a moderately-severe inflammatory response to acute toxin exposure. Quantitative proteomic analysis showed significant changes in the level of a broad spectrum of plasma proteins including serine protease/endopeptidase inhibitors, coagulation factors, complement proteins, carbonic anhydrases, and redox enzymes that ostensibly contribute to the therapeutic effect. Together, these results suggest that hemoadsorption with CS could be a viable countermeasure against acute mycotoxin exposure.

Among the array of structurally and toxicologically diverse mycotoxins, aflatoxins have attracted the most interest of scientific research due to their high toxicity and incidence in foods and feeds. Despite the undeniable progress made in various aspects related to aflatoxins, the ultimate goal consisting of reducing the associated public health risks worldwide is far from being reached due to multiplicity of social, political, economic, geographic, climatic, and development factors. However, a reasonable degree of health protection is attained in industrialized countries owing to their scientific, administrative, and financial capacities allowing them to use high-tech agricultural management systems. Less fortunate situations exist in equatorial and sub-equatorial developing countries mainly practicing traditional agriculture managed by smallholders for subsistence, and where the climate is suitable for mould growth and aflatoxin production. This situation worsens due to climatic change producing conditions increasingly suitable for aflatoxigenic mould growth and toxin production. Accordingly, it is difficult to harmonize the regulatory standards of aflatoxins worldwide, which prevents agri-foods of developing countries from accessing the markets of industrialized countries. To tackle the multi-faceted aflatoxin problem, actions should be taken collectively by the international community involving scientific research, technological and social development, environment protection, awareness promotion, etc. International cooperation should foster technology transfer and exchange of pertinent technical information. This review presents the main historical discoveries leading to our present knowledge on aflatoxins and the challenges that should be addressed presently and in the future at various levels to ensure higher health protection for everybody. In short, it aims to elucidate where we come from and where we should go in terms of aflatoxin research/development.

Natural contamination of sorghum grains by aflatoxin B 1 and total fumonisin and their producing toxigenic fungi has been studied. A total of 90 sorghum grain samples were collected from small-scale farmers' threshing floors and 5-6 months later from underground pits during 2013 harvest from three districts of East Hararghe, Ethiopia. Mycotoxin analysis was done using enzyme-linked immunosorbent assay (ELISA). The limits of detection were in the range 0.01-0.03 μg kg -1 . The results revealed that all sorghum grain samples were contaminated with both Aspergillus and Fusarium species. Aflatoxin B 1 was detected at levels ranging from -1 grain. There were marked variations in aflatoxin B 1 concentrations between fresh and stored samples, with much higher levels in the latter. Total fumonisin levels varied between 907 and 2041 µg kg -1 grain across the samples. Lowest total fumonisin was recorded in freshly harvested sorghum grain samples. Sorghum is a main staple cereal in the studied districts and its consumption per day per person is high. Daily intake of low doses of mycotoxin-contaminated food stuff over a period of time could lead to chronic mycotoxicosis.

A young male southern white rhinoceros (Ceratotherium simum), which was resident in a zoo as part of a multi-rhinoceros group, died suddenly. Necropsy and histopathological findings supported a diagnosis of death from acute hepatic necrosis. The microscopic distribution of liver lesions was suggestive of hepatotoxicosis. Further investigation revealed potential exposure to a mycotoxin, sterigmatocystin, present in spoiled lucerne hay contaminated with Aspergillus nidulans. It was concluded that mycotoxicosis was the likely cause of the hepatic necrosis and death in this animal., (© 2016 Australian Veterinary Association.)

Changes in the ecology of macrofungi are poorly understood, not only because much of their life cycle is hidden belowground, but also because experiments often miss real-world complexity and most fruitbody inventories are limited in space and time. The National Poisons Information Centre 'Tox Info Suisse' provides countrywide 24hours/7days medical advice in case of poisonings since 1966. Here, we introduce a total of 12,126 mushroom-related phone calls that were received by Tox Info Suisse between 1966 and 2014. This indirect source of mycological information is dominated by the families of Boletaceae (11%), Agaricaceae (10%) and Amanitaceae (8%), which account for ~30% of all cases. Mushroom fruiting patterns revealed by the Poisons Centre inventory statistically resemble changes in fungal phenology, productivity and diversity as reflected by the Swiss National Data Centre 'SwissFungi'. Although the newly developed Tox Info Suisse dataset provides an innovative basis for timely environmental research, caution is advised when interpreting some of the observed long-term changes and autumnal extremes. Uncertainty of the new record relates to possible data incompleteness, imprecise species description and/or identification, as well as the inclusion of cultivated and non-indigenous mushrooms. Nevertheless, we hope that the Tox Info Suisse inventory will stimulate and enable a variety of ecological-oriented follow-up studies., Competing Interests: The authors have declared that no competing interests exist.

The contamination of food and feed by mycotoxins as toxic metabolites of fungi is a risk not only for consumers resulting in various embarrassment regarding health status and well-being, but also for producers, companies and export market on the ground of economic losses and ruined stability of economic trade. As it is given in historical evidence, the contamination of food by mycotoxins is a topic as old as a history of mankind, finding some evidence even in the ancient books and records. Nowadays, the mycotoxins are used in modern biotechnological laboratories and are considered an agent for targeting the specific cells (e.g., defected cells to eliminate them). However, this promising procedure is only the beginning. More concern is focused on mycotoxins as abiotic hazard agents. The dealing with them, systematic monitoring, and development of techniques for their elimination from agricultural commodities are worldwide issues concerning all countries. They can be found alone or in co-occurrence with other mycotoxins. Thus, this review aims to provide widened information regarding mycotoxins contamination in environment with the consequences on health of animals and humans. The inevitability for more data that correctly determine the risk points linked to mycotoxins occurrence and their specific reactions in the environment is demonstrated. This review includes various symptoms in animals and humans that result from mycotoxin exposure. For better understanding of mycotoxin's impact on animals, the sensitivities of various animal species to various mycotoxins are listed. Strategies for elimination and preventing the risks of mycotoxins contamination as well as economical approach are discussed. To complete the topic, some data from past as historical evidences are presented.

Diplodiosis, a neuromycotoxicosis of cattle and sheep grazing on mouldy cobs infected by Stenocarpella maydis, is considered the last major veterinary mycotoxicosis for which the causative mycotoxin is still unknown. The current study was aimed at characterizing the cell death observed in mouse neuroblastoma (Neuro-2a), Chinese hamster ovary (CHO-K1) and Madin-Darby bovine kidney (MDBK) cell lines exposed to the S. maydis metabolites (i.e. diplodiatoxin and dipmatol) by investigating the roles of necrosis and apoptosis. Necrosis was investigated using the lactate dehydrogenase (LDH) leakage and propidium iodide (PI) flow cytometry assays and apoptosis was evaluated using the caspase-3/7 and Annexin V flow cytometry assays. In addition, transmission electron microscopy (TEM) was used to correlate the cell death pathways observed in this study with their typical morphologies. Both diplodiatoxin and dipmatol (750 μM) induced necrosis and caspase-dependent apoptosis in Neuro-2a, CHO-K1 and MDBK cells. Ultrastructurally, the two mycotoxins induced mitochondrial damage, cytoplasmic vacuolation and nuclear fragmentation in the three cell lines. These findings have laid a foundation for future studies aimed at elucidating in detail the mechanism of action of the S. maydis metabolites., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Background: Aflatoxin contamination of foods is a worldwide problem. Chronic aflatoxin exposure is associated with kidney damage. Curcumin is a herbal agent, used in medicine with a wide range of beneficial therapeutic effects., Objective: to evaluate the effect of curcumin against experimentally induced aflatoxicosis on the renal cortex of adult male albino rats., Materials and Methods: Forty adult male rats were included and they were divided equally into 4 groups (10 rats each): Group I (control group), group II (Curcumin group): The rats received curcumin (200 mg/kg b.w.) orally by gastric tube for 5 days/week, group III (Aflatoxin B1 group): The rats received aflatoxin B1 (250 μg/kg b.w./day) orally by gastric tube 5 days/week for 4 weeks, group IV (Aflatoxin B1 and Curcumin group): The rats received aflatoxin and curcumin orally by gastric tube 5 days/week for 4 weeks. Kidney specimens were prepared and sections were stained with hematoxylin and eosin, Masson's trichrome, Periodic acid Schiff, immunohistochemical detection of desmin and Bcl2., Results: The tubules of group III showed degenerative and necrotic changes with disruption of basal lamina. There was a significant decrease Bcl2 expression in the tubules, but the glomeruli showed an enlargement with dilation of their capillaries lumina in some areas, while the other areas showed glomerular atrophy with obliteration of their capillaries lumina. There was a significant increase in desmin expression in the glomerular cells. The interstitium showed hemorrhage and cellular infiltration. Group IV showed improvement of the histological and immunohistochemical changes described before., Conclusion: Aflatoxin B1 has deleterious effects of on the histological structure of the rat's renal cortex and curcumin minimized these effects as it has antioxidant, anti-inflammatory and antiapoptotic activities. We advise eating nutritious diets that contain sufficient amounts of curcumin and regulation must implement to avoid the presence of aflatoxins in high concentrations in human food.

Mycotoxicoses are acute and chronic poisonings caused by mould toxins called mycotoxins. Although acute mycotoxicoses, caused by high mycotoxin levels in food are rare nowadays, they need to be described in order to inform physicians and other health care workers about their symptoms. Children are more sensitive to mycotoxins because of their lower body mass, higher metabolic rate, and underdeveloped organ functions and detoxication mechanisms. Some mycotoxicoses appear only in children, and some are more pronounced in children than in adults. Acute mycotoxicoses in children are reported poorly, mostly because they occur in the tropical regions with poor healthcare coverage. In developed countries healthcare authorities are more concerned about child exposure to low levels of mycotoxins with immunotoxic, genotoxic or carcinogenic properties.

Aspergillus clavatus intoxication is a highly fatal neuromycotoxicosis of ruminants, especially cattle. It is caused by the ingestion of infected sprouting grain and sorghum beer residue. Locomotor disturbances, tremors and paralysis are observed. Histologically, degeneration and necrosis of larger neurons in the medulla oblongata, the midbrain, the thalamus and the ventral horns of the spinal cord are observed. Although a range of mycotoxins such as patulin, cytochalasin E and pseurotin A have been isolated, there is limited information on which specific mycotoxin or group of mycotoxins are involved during outbreaks of intoxication in livestock. In the present study, two outbreaks of A. clavatus poisoning in cattle are briefly described. Feed samples were collected for fungal identification, and culture and multitoxin analysis. A range of fungal metabolites were detected, and the estimated concentrations (μg/kg) are provided. Both the sprouting barley and brewer's grain were predominantly infected with A. clavatus and, to a lesser extent, Rhizopus arrhizus. The only common Aspergillus secondary metabolite present in all the samples was pseurotin A. Patulin and cytochalasin E were present in the sprouting barley samples, as well as the A. clavatus isolates cultured on malt extract agar for 2 weeks; however, neither of these mycotoxins could be detected in the brewer's grain sample.

The objective of the study was to determine the effect of exposure of pigs to the Fusarium mycotoxins zearalenone (ZEN) and deoxynivalenol (DON), administered together and separately, on the colon microbiota. An experiment was conducted for 42 days on gilts, randomly assigned to four groups and administered either ZEN, DON, ZEN+DON, or a placebo. The number of aerobic mesophilic bacteria, yeasts, molds, anaerobic Clostridium perfringens, fecal streptococci, Enterobacteriaceae, Escherichia coli, and lactic acid bacteria (LAB) were determined in the contents of the ascending colon. The influence of mycotoxins on the functional diversity of the colonic microbiota was assessed using EcoPlate tests (Biolog). Analysis revealed the predominance of LAB in all groups of pigs. Zearalenone, administered separately and together with DON, was found to have an adverse effect on mesophilic aerobic bacteria, but only after long exposure to this mycotoxin. During the six weeks of the experiment, the concentration of C. perfringens, E. coli, and other bacteria in the family Enterobacteriaceae was most considerably reduced in the experimental groups exposed to zearalenone, both separately and together with DON. Mycotoxins also affected the functional biodiversity of microorganisms. Both Shannon's diversity index and the number of catabolized substrates in Biolog plate (the R index) were much higher in the group subjected to mixed mycotoxicosis.

Aflatoxicosis is a cause of economic losses in broiler production. In this study, the effect of one commercial nanocompound, Nanocid (Nano Nasb Pars Co., Iran) was evaluated in reduction of aflatoxin effects on the growth and performance indices in broiler chickens suffering from experimental aflatoxicosis. For this, a total of 300 one-day-old broiler chicks (Ross strain) were randomly divided into 4 groups with 3 replicates of 15 chicks in each separated pen during the 28-day experiment. Treatment groups including group A: chickens fed basal diet, group B: chickens fed 3 ppm productive aflatoxin in basal diet, group C: chickens fed basal diet plus 2500 ppm Nanocid, and group D: chickens fed 3 ppm productive aflatoxin and 2500 ppm Nanocid, in basal diet. Data on body weight, body weight gain (BWG), feed intake, and feed conversion ratio (FCR) were recorded at weekly intervals. Also cumulative data were assessed. Results showed, although supplement of Nanocid to conventional diet had no effect on performance but addition of Nanocid to diet containing 3 ppm aflatoxin increased significantly the cumulative BWG, cumulative feed consumption and decreased FCR in the last 2 weeks of experimental period. The improvement in these performance indices by supplement of Nanocid to diet containing aflatoxin showed the ability of Nanocid to diminish the inhibitory effects of aflatoxin.

A flock of approximately 1,000 sheep were exposed intermittently to food contaminated with T-2 toxin (T-2), a potent type-A trichothecene mycotoxin produced primarily by Fusarium sporotrichioides and Fusarium poae. In the acute stage of the intoxication, affected sheep developed anorexia, decreased water consumption, ruminal atony, soft faeces and apathy. One hundred and ninety of the exposed sheep died. The main gross lesions observed in animals dying during the acute disease were rumenitis and ulcerative abomasitis, depletion of lymphocytes in lymphoid organs, necrosis of the exocrine pancreas, myocarditis and intense oedema of the skin and brain. Sheep developing the chronic stage of disease showed weight loss and reproductive inefficiency and the main pathological features observed in animals dying during this stage were gastrointestinal inflammation, myocardial fibrosis and necrotic and suppurative lesions in the oral cavity. Opportunistic infections (e.g. mycotic mastitis or parasitic pneumonia) were also identified in these animals. Increased serum concentrations of lactate dehydrogenase and creatine kinase were observed, most likely related to heart lesions. T-2 toxins were detected in all samples of the diet of these animals that were analyzed. The changes in the sheep reported here are similar to those described previously in experimental studies. Lesions observed in the present animals suggest an additional cardiotoxic effect of T-2 in sheep., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Mycotoxins have been investigated in relation to a wide range of adverse human health effects, but the evidence for all but a small number of associations is limited. Thus, the full impact on human health of the widespread exposure to mycotoxins remains to be defined. The main exception is for aflatoxins; epidemiological, experimental, and mechanistic studies have contributed to establishing aflatoxins as a cause of human liver cancer, with a particularly elevated risk in people chronically infected with hepatitis B virus. In addition, acute aflatoxicosis after exposure to high dietary toxin levels has been demonstrated. The impairment of child growth by aflatoxin exposure early in life remains an important subject of study. More information is also required on the potential immune effects of aflatoxins, especially in vulnerable populations. For fumonisins, studies indicate a possible role in oesophageal cancer and in neural tube defects, although no definitive conclusions can be drawn at present. For deoxynivalenol and other trichothecenes, exposure has been linked to acute poisoning outbreaks in large numbers of subjects. For ochratoxin A and zearalenone, the human health effects remain undefined. The limited tools available to accurately assess human exposure to mycotoxins and the relative paucity of epidemiological studies need to be addressed if the full extent of the adverse effects of these common dietary contaminants is to be understood and adequate public health measures taken. In this respect, newly established biomarkers of exposure at the individual level are proving valuable in improving exposure assessment in epidemiological studies.

The clinical signs, pathological and laboratory findings of cattle suffering from a tremorgenic syndrome are described. Animals on a farm with a total of 22 cows, 18 heifers and 9 calves were fed mouldy grass and spent malt-grain silage. Five heifers were affected with muscular tremor, hyperexcitability and hypersensitivity. They were ataxic or in sternal recumbency, while their appetite remained normal. Haematology and blood chemistry in two heifers as well as cerebrospinal fluid from one sick animal were unremarkable. The pathological examination of one animal brought no macroscopic changes to light. Histological examination, however, revealed the degeneration of motor neurones in the midbrain, brain stem and spinal cord. Analysis of a silage sample provided evidence of the presence of Aspergillus clavatus, a mould capable of producing neurotoxic tremorgenic mycotoxins. Epidemiology, clinical findings, pathology and microbiological examination suggest that the five cattle were suffering from neuromycotoxicosis.

Spontaneous nephropathy in Bulgaria, which is observed frequently during meat inspection and which differs morphologically from the classical description of mycotoxic porcine/chicken nephropathy as made in Denmark, was found to have a multi-mycotoxic aetiology being mainly provoked by a combined effect of ochratoxin A, penicillic acid and fumonisin B1 in addition to a not-yet-known metabolite. Mean contamination levels of ochratoxin A were consecutively low (188.8 and 376.4 microg kg(-1)) in contrast to high contamination levels of fumonisin B1 (5564.1 and 3254.5 microg kg(-1)) and penicillic acid (838.6 and 904.9 microg kg(-1)) for 2006 and 2007, respectively. Some other mycotoxins with lower importance such as citrinin, penitrem A, etc., may also influence clinicopathological picture of this nephropathy. A heavy contamination with Gibberella fujikuroi var. moniliformis (Fusarium verticillioides) and Penicillium aurantiogriseum complex (mainly Penicillium polonicum) was observed in almost all examined feed samples coming from pig and chick farms with nephropathy problems from Bulgaria. In contrast, low contamination with Aspergillus ochraceus, Penicillium verrucosum and Penicillium citrinum was observed in the same feed samples and these species were isolated as very rare components of the mycobiota.

Fusarium mycotoxin toxicosis has been implicated in the etiology of Keshan disease, an endemic mitochondrial cardiomyopathy prevailing in certain areas of China. Butenolide (4-acetamido-4-hydroxy-2-butenoic acid gamma-lactone) is one of the Fusarium mycotoxins which are frequently detected from cereal grains in endemic areas. A recent study indicates that this mycotoxin induces rat cardiotoxicity, but its effect on the myocardial mitochondria remains unclear. The present study is therefore undertaken to explore the toxic effect potential of butenolide on the myocardial mitochondria. Exposure of cultured cardiac myocytes to 50 microg/ml of butenolide provoked dissipation of mitochondrial membrane potential. Incubation of isolated rat myocardial mitochondria with butenolide of 100 microg/ml for 60 min resulted in mitochondrial swelling, indicating the occurrence of mitochondrial permeability transition. Furthermore, marked oxidative damage in myocardial mitochondria was observed after incubation of isolated myocardial mitochondria with butenolide ranging from 0 to 50 microg/ml for 60 min, as manifested by concentration-dependent increases in the production of thiobarbituric acid reactive substances, the indicator of lipid peroxidation. Contrarily, a representative antioxidant glutathione significantly alleviated this oxidative mitochondrial damage induced by butenolide. In conclusion, these observations clearly show that butenolide can induce dysfunction of myocardial mitochondria, and oxidative damage appears to play a crucial role in these deleterious effects. The present study supports the hypothesis that mycotoxin toxicosis is a probable etiological factor of Keshan disease, the mitochondrial cardiomyopathy.

Disorders related to indoor air quality have become a major concern for primary care physicians, who often are asked to evaluate patients whose symptoms may be caused or aggravated by indoor exposure to mold. In this article, we review the common types of indoor mold and discuss the management of mold exposure and related illnesses.

This study investigates the occurrence of aflatoxins in Ecuador. Early investigators proved the presence of aflatoxins in human and animal food, but the disturbing data lead to the formation of two research teams at Guayaquil University and the Agrarian University of Ecuador to investigate aflaxotins and other mycotoxins in food and their relationship to human health. Because the concept of mycotoxicosis as a result of the secondary metabolites produced by different species of moulds could cause different clinical patterns, the research team includes Aspergillus metabolites found in the urine of a patient with pulmonary aspergilloma. We considered that the body itself could create secondary metabolites. An ELISA method was used to detect mycotoxins with the specific reactive compounds using a company base assay. This allows the detection quantitative of such metabolites in 24 h collected urine. The patient was treated with itraconazole for nine months, after clinical, radiological and aflatoxins testing. We also investigated three other cases in children with a second level of malnutrition and only with vomitoxins results and in three investigated cases of otomycosis caused by Aspergillus niger only in one case traces of aflatoxins were found.

Adverse human health effects from the consumption of mycotoxins have occurred for many centuries. Although mycotoxin contamination of agricultural products still occurs in the developed world, the application of modern agricultural practices and the presence of a legislatively regulated food processing and marketing system have greatly reduced mycotoxin exposure in these populations. At the mycotoxin contamination levels generally found in food products traded in these market economies, adverse human health effects have largely been overcome. However, in the developing world, where climatic and crop storage conditions are frequently conducive to fungal growth and mycotoxin production, much of the population relies on subsistence farming or on unregulated local markets. The extent to which mycotoxins affect human health is difficult to investigate in countries whose health systems lack capacity and in which resources are limited. Aflatoxin B(1), the toxin on which major resources have been expended, has long been linked to liver cancer, yet its other effects, such as immune suppression and growth faltering previously observed in veterinary studies, are only now being investigated and characterized in human populations. The extent to which factors such as immune suppression contribute to the overall burden of infectious disease is difficult to quantify, but is undoubtedly significant. Thus, food safety remains an important opportunity for addressing current health problems in developing countries.

The high prevalence of the Fusarium mycotoxins, deoxynivalenol (DON) and zearalenone (ZON) in animal feeds in mild climatic zones of Europe and North America results in considerable economic losses, as these toxins affect health and productivity particularly of pigs from all age groups. The use of mycotoxin adsorbents as feed additives is one of the most prominent approaches to reduce the risk for mycotoxicoses in farm animals, and to minimise carry-over of mycotoxins from contaminated feeds into foods of animal origin. Successful aflatoxin adsorption by means of different substances (phyllosilicate minerals, zeolites, activated charcoal, synthetic resins or yeast cell-wall-derived products) has been demonstrated in vivo and in vitro. However, attempts to adsorb DON and ZON have been less encouraging. Here we describe the adsorption capacity of a variety of potential binders, including compounds that have not been evaluated before, such as humic acids. All compounds were tested at realistic inclusion levels for their capacity to bind ZON and DON, using an in vitro method that resembles the different pH conditions in the gastro-intestinal tract of pigs. Mycotoxin adsorption was assessed by chemical methods and distinct bioassays, using specific markers of toxicity as endpoints of toxicity in cytological assays. Whereas none of the tested substances was able to bind DON in an appreciable percentage, some of the selected smectite clays, humic substances and yeast-wall derived products efficiently adsorbed ZON (>70%). Binding efficiency was indirectly confirmed by the reduction of toxicity in the in vitro bioassays. In conclusion, the presented test protocol allows the rapid screening of potential mycotoxin binders. Like other in vitro assays, the presented protocol combining chemical and biological assays cannot completely simulate the conditions of the gastro-intestinal tract, and hence in vivo experiments remain mandatory to assess the efficacy of mycotoxin binders under practical conditions.

Zearalenone (ZEA) is a mycotoxin produced mainly by fungi belonging to the genus Fusarium in foods and feeds. It is frequently implicated in reproductive disorders of farm animals and occasionally in hyperoestrogenic syndromes in humans. There is evidence that ZEA and its metabolites possess oestrogenic activity in pigs, cattle and sheep. However, ZEA is of a relatively low acute toxicity after oral or interperitoneal administration in mice, rat and pig. The biotransformation for ZEA in animals involves the formation of two metabolites alpha-zearalenol (alpha-ZEA) and beta-zearalenol (beta-ZEA) which are subsequently conjugated with glucuronic acid. Moreover, ZEA has also been shown to be hepatotoxic, haematotoxic, immunotoxic and genotoxic. The exact mechanism of ZEA toxicity is not completely established. This paper gives an overview about the acute, subacute and chronic toxicity, reproductive and developmental toxicity, carcinogenicity, genotoxicity and immunotoxicity of ZEA and its metabolites. ZEA is commonly found on several foods and feeds in the temperate regions of Europe, Africa, Asia, America and Oceania. Recent data about the worldwide contamination of foods and feeds by ZEA are considered in this review. Due to economic losses engendered by ZEA and its impact on human and animal health, several strategies for detoxifying contaminated foods and feeds have been described in the literature including physical, chemical and biological process. Dietary intakes of ZEA were reported from few countries from the world. The mean dietary intakes for ZEA have been estimated at 20 ng/kgb.w./day for Canada, Denmark and Norway and at 30 ng/kgb.w./day for the USA. The Joint FAO/WHO Expert Committee on Food Additives (JECFA) established a provisional maximum tolerable daily intake (PMTDI) for ZEA of 0.5 microg/kg of body weight.

Background: On 10th May, 2004 food samples suspected to have caused acute poisoning in Makueni district were received at the National Public Health Laboratory Services (NPHLS). On analysis, they were found to be highly contaminated with aflatoxin B1. More cases of poisoning were reported in the district and in neighbouring districts of Kitui, Machakos and Thika. As at 20th July, 2004 the Ministry of Health was aware of 317 cases of which 125 resulted in deaths., Objective: To assess the magnitude of aflatoxin contamination of maize and maize products in the affected areas., Design: Random environmental sampling of maize and maize products and case/control samples of the same in the affected regions and subsequent determination of aflatoxin levels using immunoaffinity coupled with solution fluorometry., Setting: National Public Health Laboratory Services, Ministry of Health, Kenya, from May to August, 2004., Subjects: A total of 480 samples comprising 362 random environmental samples, 26 cases and 92 controls were collected and analysed. The foods analysed included maize grains, maize flour and dehulled dry maize, traditionally known as muthokoi., Results: Forty six point four per cent of the environmental samples, 15% of cases and 29.3% of controls were within the maximum permissible limit of 20 microg implying that over 50% (54.4) of the total did not comply and would be regarded as unfit for human consumption. 6.9% of the environmental samples, 57.7% of cases and 21.7 of controls had levels beyond 1000 microg/Kg. The amount of aflatoxin observed in the food samples had a range of 0-58,000 microg/Kg., Conclusion: The population in the affected region was exposed to high levels of aflatoxin. There is need to address the issue of pre and post harvest handling of grain and establishing monitoring and surveillance for early detection and intervention.

Purpose of Review: Sick building syndrome is a poorly understood condition that can be vexing to clinicians and public health investigators alike. Concerns about possible causes have recently shifted to bioaerosols, especially indoor mold contamination. Recently, controversy over the health effects of indoor bioaerosols has intensified in the media and in medical forums. Allergists and other clinicians are increasingly being asked to evaluate cases of sick building syndrome attributed to bioaerosol exposure. Although allergy may play a role, it is unlikely to fully explain the nonspecific symptoms of the condition. This review of recent literature will attempt to put into context the roles of allergy and nonallergic mechanisms in sick building syndrome., Recent Findings: Epidemiological and toxicological studies have provided further evidence of a possible link between bioaerosol exposure and sick building syndrome, but continue to have methodological limitations. Cross-sectional studies of building occupants have found associations between bioaerosols and symptoms of the condition, but case definitions and exposure assessment remain problematic. Attempts to develop better exposure assessment and biomonitoring methods have made limited progress. Toxicological studies of inhalation of bioaerosols continue to indicate potential toxicity, but at doses that are not comparable to human exposures indoors., Summary: Epidemiological studies suggest an association between bioaerosols and sick building syndrome, and toxicological studies have provided some evidence supporting biological plausibility. However, the extent to which bioaerosol exposure may explain the nonspecific symptoms of the condition is unclear. Nonspecific inflammatory responses to bioaerosols, modified by psychosocial factors such as stress, may be a promising area for continued research.

The presence of toxins or infectious agents combined with environmental factors in combination with a susceptible host can be the cause for neurological disease in groups of horses. During a 5 year observational period outbreaks of neurological diseases among horses were evaluated. Causes of occurring neurological diseases were equine botulism, lolitrem intoxications, equine herpesvirus type 1-associated myelo(encephalo)pathy, and encephalitis caused by (disseminated) Streptococcus equi subspecies equi infection. This article focuses on the first three syndromes because of their predominant influence on locomotion. The pathogenesis of each disease is presented, followed by a description of a general presentation of the diseases as encountered under Dutch circumstances.

Mycotoxins can cause various toxic effects in humans. Acute and chronic respiratory diseases were reported after inhalation of organic dust containing toxigenic moulds and mycotoxins, respectively. To gain first insights into health effects from airborne exposure to these compounds, five toxigenic airborne moulds of the genera Aspergillus and Penicillium collected at composting plants and eight reference mycotoxins were tested for cytotoxicity in four established cell lines as a surrogate of tissues known or suspected to be targets of toxic effects of mycotoxins. The known mycotoxins sterigmatocystin, fumagillin, verruculogen, penitrem A, and roquefortine C were detected in extracts of the moulds. All five extracts caused serious toxic effects in the cell lines. Sterigmatocystin caused a 80-fold higher toxicity in the A-549 lung cell line compared to Hep-G2 liver cells indicating a specific susceptibility of A-549 to this agent. Since only a minor part of the toxic effects of the extracts in A-549 cells and--to a lesser extent--in the other cell lines could be explained by contents of the identified mycotoxins, the presence of additional mycotoxins or other toxic principles is assumed in the mould extracts. However, the detected mycotoxins in the mould extracts and their distinctive cytotoxicity support the hypothesis that mycotoxins may be involved in the aetiology of lung diseases due to the inhalation of organic dust.

Mycotoxins--toxic substances produced by fungi or molds--are ubiquitous in the environment and are capable of damaging multiple biochemical mechanisms, resulting in a variety of human symptoms referred to collectively as "mycotoxicosis." In fact, mycotoxins mimic multiple xenobiotics, not only with respect to their ultimate damage, but also in their routes of detoxification. This suggests potential therapeutic options for the challenging treatment of mycotoxicosis. In this brief review, the author examines the use of lipoic acid as an example of an inexpensive and available nutrient that has been shown to protect against, or reverse, the adverse health effects of mycotoxins.

The authors assessed the psychological, neuropsychological, and electrocortical effects of human exposure to mixed colonies of toxigenic molds. Patients (N = 182) with confirmed mold-exposure history completed clinical interviews, a symptom checklist (SCL-90-R), limited neuropsychological testing, quantitative electroencephalogram (QEEG) with neurometric analysis, and measures of mold exposure. Patients reported high levels of physical, cognitive, and emotional symptoms. Ratings on the SCL-90-R were "moderate" to "severe," with a factor reflecting situational depression accounting for most of the variance. Most of the patients were found to suffer from acute stress, adjustment disorder, or post-traumatic stress. Differential diagnosis confirmed an etiology of a combination of external stressors, along with organic metabolically based dysregulation of emotions and decreased cognitive functioning as a result of toxic or metabolic encephalopathy. Measures of toxic mold exposure predicted QEEG measures and neuropsychological test performance. QEEG results included narrowed frequency bands and increased power in the alpha and theta bands in the frontal areas of the cortex. These findings indicated a hypoactivation of the frontal cortex, possibly due to brainstem involvement and insufficient excitatory input from the reticular activating system. Neuropsychological testing revealed impairments similar to mild traumatic brain injury. In comparison with premorbid estimates of intelligence, findings of impaired functioning on multiple cognitive tasks predominated. A dose-response relationship between measures of mold exposure and abnormal neuropsychological test results and QEEG measures suggested that toxic mold causes significant problems in exposed individuals. Study limitations included lack of a comparison group, patient selection bias, and incomplete data sets that did not allow for comparisons among variables.

Two dogs developed alarming tremorgenic nervous stimulation shortly after ingesting discarded rice that had been forgotten in a refrigerator for an undetermined period and that was covered with a grey-green mould. Both dogs exhibited vomition followed by slight salivation, tremors and ataxia and 1 showed such severe agitation and seizures that it necessitated anaesthesia with thiopentone followed, on recovery, by xylazine. The other dog was only sedated with xylazine. They made an uneventful recovery. The rice vomitus yielded a pure culture of Penicillium crustosum. On chemical analysis it was negative for organochlorine, organophosphor and carbamate insecticides, as well as for strychnine, but contained 2.6 microg/g of the mycotoxins penitrem A as well as 34 microg/g of roquefortine as determined by LC-MS and confirmed by MS-MS. This is the 1st South African case of naturally occurring penitrem A toxicosis and also the 1st case where quantification of the levels of mycotoxins in dog vomitus is reported. The tremorgenicity of roquefortine and its contribution towards this syndrome, is questioned.

The investigations of four Cases involving mold-contaminated buildings and human reaction to exposure, documents tests of extracted urine containing trichothecene mycotoxins confirming exposure and the diagnosis of mycotoxicosis in humans. In each of four Cases, the urine demonstrated antibiotic activity, sulfuric acid charring, and protein release. Urine was extracted using ethyl acetate 40V/60V[EA]. Extracted mycotoxin spotted on (TLC) displayed color and a range of (rf) between 0.2-0.6 using various solvents. Extract was re-suspended using 50% ethanol V/V to inject mycotoxins into weanling female Sprague-Dawley rats. Degeneration and necrosis of the rat's tissue followed. Koch's Postulates conditions were fulfilled by isolation of the causative agent, the trichothecene mycotoxins and the reproduction of disease. Examination of human tissue within the urine extraction group confirms Koch's Postulates and comparative pathology confirms inhalation Mycotoxicosis, with severe necrosis of the central nervous system and severe scarring within the lungs. Extraction of mycotoxins from human patient urine is a very useful confirmatory test to demonstrate exposure and identify mycotoxicosis. Low concentrations (6%) of sodium hypochlorite were ineffective against the activity of trichothecene mycotoxin. The severity or stages of disease directly correlates the level of exposure or poisoning (Patent Pending).

The relevance of many mycotoxins to small animal health is difficult to assess, because available information has not been collated and reviewed. Only aflatoxins, penitrem A, and roquefortine have been confirmed in natural mycotoxicoses in pets. Effects of tricothecene mycotoxins, patulin, and penicillic acid on dogs and cats have only been studied experimentally and have not been confirmed in natural outbreaks. Although they make up only a small portion of the cases presented to veterinarians, mycotoxicoses often require special effort. Establishing an accurate diagnosis is crucial to minimize exposure and provide adequate treatment. In most cases, clinical examination, clinical pathologic testing, and analytical chemistry analysis of suspect feed are necessary to reach a diagnosis.

The most frequent toxigenic fungi in Europe are Aspergillus, Penicillium and Fusarium species. They produce aflatoxin B1 transformed into aflatoxin M1 found in the milk, as well as Ochratoxins and Zearalenone, Fumonisin B1, T-2 toxin, HT-2 toxin and deoxynivalenol (vomitoxin), which are of increasing concern in human health. These mycotoxins are under continuous survey in Europe, but the regulatory aspects still need to be set up and/or harmonised at European level. They are found in foodstuffs and are not destroyed by normal industrial processing or cooking since they are heat-stable. Some of their metabolites are still toxic and may be involved in human diseases. Their toxic effects (liver, kidney and hematopoetic toxicity, immune toxicity, reproduction toxicity, foetal toxicity and teratogenicity, and mainly carcinogenicity) are mostly known in experimental models, the extrapolation to humans being always inaccurate. The inaccuracy of extrapolation to humans may be explained by the lack of adequate food consumption data, lack of knowledge about relative health risks associated with specifically proposed limits and by the possibility of synergism with other mycotoxins present in the same food commodities. Other pathological causes are viral hepatitis, immune or hormonal deficiencies or organ dysfunction. Even when a specific biomarker of a given mycotoxin is identified in humans, it remains difficult to establish the relation with a given illness, because of genetic polymorphism and the possible beneficial influence of diet, and because other environmental toxicants may well interfere. The acceptable daily intake limits are mostly based on animal data and may be too high, due to the differences in the sensitivity of different animal species. The prevention involves first reduction of mycotoxin levels in foodstuffs and further increasing the intake of diet components such as vitamins, antioxidants and substances known to prevent carcinogenesis.

Mycotoxins are low-molecular-weight secondary metabolites of fungi. The most significant mycotoxins are contaminants of agricultural commodities, foods and feeds. Fungi that produce these toxins do so both prior to harvest and during storage. Although contamination of commodities by toxigenic fungi occurs frequently in areas with a hot and humid climate (i.e. conditions favorable for fungal growth), they can also be found in temperate conditions. Production of mycotoxins is dependent upon the type of producing fungus and environmental conditions such as the substrate, water activity (moisture and relative humidity), duration of exposure to stress conditions and microbial, insect or other animal interactions. Although outbreaks of mycotoxicoses in humans have been documented, several of these have not been well characterized, neither has a direct correlation between the mycotoxin and resulting toxic effect been well established in vivo. Even though the specific modes of action of most of the toxins are not well established, acute and chronic effects in prokaryotic and eukaryotic systems, including humans have been reported. The toxicity of the mycotoxins varies considerably with the toxin, the animal species exposed to it, and the extent of exposure, age and nutritional status. Most of the toxic effects of mycotoxins are limited to specific organs, but several mycotoxins affect many organs. Induction of cancer by some mycotoxins is a major concern as a chronic effect of these toxins. It is nearly impossible to eliminate mycotoxins from the foods and feed in spite of the regulatory efforts at the national and international levels to remove the contaminated commodities. This is because mycotoxins are highly stable compounds, the producing fungi are ubiquitous, and food contamination can occur both before and after harvest. Nevertheless, good farm management practices and adequate storage facilities minimize the toxin contamination problems. Current research is designed to develop natural biocontrol competitive fungi and to enhance host resistance against fungal growth or toxin production. These efforts could prevent toxin formation entirely. Rigorous programs for reducing the risk of human and animal exposure to contaminated foods and feed also include economically feasible and safe detoxification processes and dietary modifications. Although risk assessment has been made for some mycotoxins, additional, systematic epidemological data for human exposure is needed for establishing toxicological parameters for mycotoxins and the safe dose for humans. It is unreasonable to expect complete elimination of the mycotoxin problem. But multiple approaches will be needed to minimize the economic impact of the toxins on the entire agriculture industry and their harmfulness to human and animal health.

Inclusion of a biologically active food supplement (BAS) "Rekicen RD" in rat Wistar ration in percentage 5% result in reduction of toxic action of a trichothecene mycotoxin T-2 toxin. The changes of daily increase in body weight of animals, of relative internal weight, of serum enzyme activity, of not sedimentated activity of lysosomal enzymes and of activity of enzymes of a xenobiotic metabolism in a liver were expressed in a lesser degree. It is possible that a protective action of BAS is related with high adsorption capacity of wheat bran in BAS composition and with their possible influence on activity of enzymes participating in detoxification T-2 toxin (UDP-glucuronosyltransferase).

From 1997 to 1999, 29 cases of disorders were detected in cattle and horses that had been fed ryegrass straw imported from the U.S.A. These animals showed symptoms resembling ryegrass staggers and the clinical signs disappeared after removal of the straw. Endophytic hyphae were detected in the seeds of all straw samples that were responsible for the clinical cases. Lolitrem B concentrations in the straw ranged between 972 and 3740 ppb. Ergovaline concentrations were between 355 and 1300 ppb. Even though the concentrations of lolitrem B were lower than the toxic threshold proposed by Oregon State University in better part of the cases, our observations suggest the possibility that lolitrem B lower than the proposed threshold can bring disorders to sensitive individuals.

Mycotoxins are toxic metabolites produced by varous species of fungi. Aflatoxin (AF), a particular type of mycotoxin, can negatively impact many wildlife species in the laboratory; however, the magnitude of the problem in the field environment is unclear. Wild birds generally consume a combination of native foods and agricultural grains. A common practice in which birds, such as northern bobwhite (Colinus virginianus), contact stored agricultural grain is through supplemental feeding. This feeding practice may promote the production of AF. The objectives of this study were to (1) examine AF production in supplemental feeders and (2) examine the relationship between weather and AF production in supplemental feeders. Samples were collected from supplemental feeders from November through February of 1996-97 and 1997-98. Mean monthly AF concentration of samples from feeders ranged from 0.57+/-2.86 to 15.47+/-14.69 ppb. Aflatoxin concentration in supplemental feeders increased from pre-sample to one month after filling the feeders each year. AF production in supplemental feeders was highly variable among months with no real temporal pattern between years. Instead, AF production was related to the highly variable relative humidity of the study area which influences moisture content of grain. Average relative humidity can be used to predict AF production.

Samples of corn available as wildlife feed from retailers throughout Georgia (USA) were collected during April 1997 and analyzed for aflatoxin to determine if levels harmful to wild turkeys (Meleagris gallopavo) were present. Three of 31 (10%) samples collected from a 40-country area were positive. An enzyme-linked immunosorbent assay qualitatively determined that two samples contained from 0 to 20 ppb aflatoxin. A chromatography analysis of a third sample measured 380 ppb total aflatoxin. A small percentage of our sample of wildlife feed collected during one season contained levels of aflatoxin that may cause harm to turkeys, especially poults. However, because aflatoxin levels ranging from 100 to 400 ppb may cause liver dysfunction and immunosuppression in turkey poults and other wildlife, grains known to be contaminated with aflatoxin at levels unacceptable for domestic animal feeds (> or =100 ppb) should not be sold as wildlife feed. Further analyses of grains sold as wildlife feed should be conducted to address this potential problem.

We have used a murine model of subchronic mycotoxicoses produced by ingestion of mycotoxins. The five groups of animals studied were fed for 30, 60 and 90 days, respectively, with commercial diet (CD), experimental control diet (ECD), experimental with fumonisin B1 diet (EFD) and experimental with mixtures of mycotoxins diet (EMD). The animals fed EFD and EMD showed a significant increase in feed consumption/day with respect to the animals fed ECD (P < 0.005 for both groups). The biochemical measurements showed significant differences at 90 days in those animals fed EAD exhibiting a marked decrease in the values of alkaline phosphatase (ALP) and cholesterol (P < 0.05), along with a significant increase in calcium (P < 0.01). Differences in the decrease of the parameters studied were observed in mice fed EFD for triglycerides, cholesterol and calcium (P < 0.05 for all of them). The activity of aspartate transaminase (AST) increased significantly in animals fed EMD (P < 0.01). The tissue specimens at 60 days showed lesions in the livers of the animals fed EAD and EFD. At 90 days, and in those fed EAD, EFD and EMD, the lesions were intensified in the liver at 60 days in 80, 90 and 100% of the animals, respectively.

Perennial ryegrasses are frequently infected with fungal endophyte (Neotyphodium lolii) to increase the resistance of the plant to insect damage. Unfortunately, a side effect of endophyte infection can be the production of alkaloids, including Lolitrem B and ergovaline, that produce toxic effects in animals. A significant 4.6 litre decrease in milk production in a herd of Holstein-Friesian dairy cows was associated with high concentrations of ergovaline in ryegrass silage. Simultaneously, milk SCC increased significantly over a comparable period and reproductive performance declined. Body condition score and coat condition of cows were adversely affected. Unique aspects of this Case report include; very stable production of the herd over a period of years before and after cessation of feeding silage containing high concentrations of ergovaline; the presence of high concentrations of ergovaline in the silage; and a controlled diet that reduced the risks of variation in feed availability and other sources of toxins. Veterinarians and other farm advisors should be aware of the potential for negative effects on animal health and production of fungal endophyte and the potential for Neotyphodium lolii to produce ergovaline.

The effects of grain storage containers on aflatoxin production, and the relationship between the level of aflatoxin and the number and weight of fluorescing kernels were determined in corn (Zea maize) stored in controlled climate regimes. Two hundred and forty 100-g samples were held up to 3 mos using four types of storage containers placed in four climates. Storage containers included corn placed in metal cans, paper bags, plastic bags, and paper bags placed in plastic bags. Climates were constant during the duration of the project and included a combination of temperatures and humidities. Temperatures were 29-32 C and 14-18 C; relative humidities were 85-88% and 35-40%. In addition, corn was exposed to environmental conditions conductive for aflatoxin production and 100 g samples were randomly collected, examined under ultraviolet light for fluorescence, and then quantified for aflatoxin levels. Corn samples tested negative for aflatoxin at the beginning of the project. Main (i.e., container, climate, and month) and interactive effects were not observed. Mean levels of aflatoxin ranged from 0 to 151 microg/kg. Aflatoxin was produced regardless of type of storage container, time of storage, and climatic conditions; however, only 8% of the samples produced aflatoxin levels that exceeded 50 microg/kg. Fluorescing corn ranged from 0 to 19 kernels per sample, while aflatoxin levels ranged from 0 to 1,375 microg/kg for the same samples. No relationships were found between the number and weight of fluorescing kernels of corn and aflatoxin levels. The black light test yielded a false negative rate of 23% when in fact the aflatoxin concentrations exceeded 50 microg/kg. Therefore, quantifying fluorescing grain under UV light should not be considered a feasible alternative for aflatoxin testing of grain intended for wildlife.

Background: Stachybotrys as a fungus has been implicated as a source of mycotoxins. While the toxicity of several well-known mycotoxins (aflatoxins) is well documented, recent studies on Stachybotrys have raised the question that mycotoxins produced by this fungus may be responsible for the health effects of occupants in water-damaged buildings., Methods: Published articles regarding Stachybotrys-related mycotoxins were reviewed with particular focus on human toxicity., Results: A critical review of papers, reports, and studies on Stachybotrys mycotoxins revealed only descriptive reports of suspected animal and human poisoning secondary to consumption of mold-contaminated food products. No studies of good toxicologic and epidemiologic designs answer whether airborne mycotoxins produced by Stachybotrys could produce specific human toxicity., Conclusions: Current data on the toxicology of mycotoxins produced by Stachybotrys demonstrate that this group of mycotoxins is capable of producing immunosuppression and inflammatory insults to gastrointestinal and pulmonary systems. Case control study and case reports have suggested a possible association with environmental exposure to Stachybotrys mycotoxins, although a firm causal relationship has not been firmly established. Additional studies are needed to document that humans with sufficient exposure to these mycotoxins develop compatible clinical and pathologic pictures as demonstrated in animal models.

To evaluate the effectiveness of a superactivated charcoal (SAC) in alleviating mycotoxicosis, two experiments were conducted in which 432 male broiler chicks (216 per experiment) were fed diets containing 4 mg aflatoxin (AF) or 6 mg T-2 toxin/kg of diet, with and without 0.5% SAC, from 1 to 21 d of age. Feeding AF and T-2 toxin significantly decreased BW gain over the 21-d experimental period. Inclusion of SAC in the diet containing AF resulted in BW gains that were intermediate between gains of chicks fed AF and those of controls. No benefits were seen in BW gain when SAC + T-2 toxin was fed. Feeding AF increased relative weights of liver, spleen, and kidney; however, only liver weight in Experiment 1 was similar to controls when SAC was included. Of the blood parameters altered by AF (decreased cholesterol, inorganic phosphorus, total protein, and urea nitrogen, and increased mean corpuscular volume and hematocrit in Experiment 1; decreased albumin and total protein, and increased creatine kinase in Experiment 2) only urea nitrogen, hematocrit, and inorganic phosphorus (Experiment 1) and hematocrit (Experiment 2) were comparable to controls when SAC was included in the diet. Feeding T-2 toxin decreased serum cholesterol, total protein, urea nitrogen, and mean corpuscular volume; however, only cholesterol and mean corpuscular volume were improved with the addition of SAC (Experiment 1). Oral lesions were observed in birds fed T-2 toxin with no difference in severity when SAC was added in Experiment 1, however in Experiment 2, birds fed SAC + T-2 had a significantly lower lesion scores than those fed T-2 alone. Mortality was noted in both experiments but was not influenced by SAC treatment. These findings suggest that the addition of dietary SAC is marginally effective in alleviating some of the toxic affects associated with AF, but was of little benefit when T-2 toxin was fed to growing broiler chicks.