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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.

A tremorgenic syndrome occurs in dogs following ingestion of moldy walnuts, and Penicillium crustosum has been implicated as the offending fungus. This is the first report of suspected moldy walnut toxicosis in man. An adult male ingested approximately eight fungal-infected walnut kernels and after 12 h experienced tremors, generalized pain, incoordination, confusion, anxiety, and diaphoresis. Following symptomatic and supportive treatment at a local hospital, the man made an uneventful recovery. A batch of walnuts (approximately 20) was submitted for mycological culturing and identification as well as for mycotoxin analysis. Penicillium crustosum Thom was the most abundant fungus present on walnut samples, often occurring as monocultures on isolation plates. Identifications were confirmed with DNA sequences. The kernels and shells of the moldy walnuts as well as P. crustosum isolates plated on yeast extract sucrose (YES) and Czapek yeast autolysate (CYA) agars and incubated in the dark at 25 °C for 7 days were screened for tremorgenic mycotoxins and known P. crustosum metabolites using a liquid chromatography-tandem mass spectrometric (LC-MS/MS) method. A relatively low penitrem A concentration of only 1.9 ng/g was detected on the walnut kernels when compared to roquefortine C concentrations of 21.7 μg/g. A similar result was obtained from P. crustosum isolates cultured on YES and CYA, with penitrem A concentrations much lower (0.6-6.4 μg per g mycelium/agar) compared to roquefortine C concentrations (172-1225 μg/g). The authors surmised that besides penitrem A, roquefortine C might also play an additive or synergistic role in intoxication of man.

Acute bovine liver disease (ABLD) is a hepatotoxicity principally of cattle which occurs in southern regions of Australia. Severely affected animals undergo rapid clinical progression with mortalities often occurring prior to the recognition of clinical signs. Less severely affected animals develop photosensitization and a proportion can develop liver failure. The characteristic histopathological lesion in acute fatal cases is severe, with acute necrosis of periportal hepatocytes with hemorrhage into the necrotic areas. Currently there are a small number of toxins that are known to cause periportal necrosis in cattle, although none of these have so far been linked to ABLD. Furthermore, ABLD has frequently been associated with the presence of rough dog's tail grass ( Cynosurus echinatus ) and Drechslera spp. fungi in the pasture system, but it is currently unknown if these are etiological factors. Much of the knowledge about ABLD is contained within case reports, with very little experimental research investigating the specific cause(s). This review provides an overview of the current and most recently published knowledge of ABLD. It also draws on wider research and unpublished reports to suggest possible fungi and mycotoxins that may give rise to ABLD., Competing Interests: The authors declare no conflict of interest.

Concentrations of zearalenone (ZEN), deoxynivalenol (DON) and their metabolites α-zearalenol (α-ZEL), β-zearalenol (β-ZEL), zearalanone (ZAN), α-zearalanol (α-ZAL), β-zearalanol (β-ZAL) and de-epoxy-deoxynivalenol (de-DON) in serum, liquor and urine of female piglets fed diets containing 0.01, 0.05, 0.08, 0.17 and 0.29 mg ZEN/kg and 0.03, 0.59, 1.27, 2.01 and 4.52 mg DON/kg during 29 days of treatment were analysed. After 1, 3, 8, 15, 22 and 29 days, four piglets per group were slaughtered. The simultaneous determination of all analytes was carried out using a sensitive and selective in-house-validated liquid chromatography tandem mass spectrometry (LC-MS/MS) method after sample preparation with Oasis™ HLB columns. ZEN, α-ZEL, DON and de-DON were detected in serum, whereas in liquor only ZEN, DON and de-DON were found at lower concentrations. In urine, all analytes were detected in considerably higher concentrations as in serum and liquor, whereby α- and β-ZAL could only be detected sporadically. Apart from ZEN in liquor and α- and β-ZAL in urine, the mycotoxin concentrations increased with increasing concentrations of Fusarium toxins in the diet. The toxin intake per kg body weight 3-4 h prior to slaughtering correlated well with the DON and the sum of DON and de-DON concentrations in all three specimens as well as with the ZEN, α-ZEL and the sum of ZEN and metabolite concentrations in urine. Due to the high correlation between the dietary DON concentration and the DON (r = 0.855) and the sum of DON and de-DON (r = 0.870) concentration in serum, the exposure to DON can be evaluated. Moreover, serum levels of these toxins indicative of an exceeding of the guidance value in feed can be established using the corresponding regression equations. Strictly speaking, these relationships are only valid for the experimental conditions of the underlying experiment. For practical application of these relationships, the individual variation needs to be additionally considered. Effects of the duration of toxin exposure within the feeding groups were observed for ZEN, DON and de-DON in all specimens as well as for α-ZEL, β-ZEL and ZAN in urine.

Ingestion of tremorgenic mycotoxins formed in spoiled food can cause an acute tremor syndrome, the severity of which can range from mild to life-threatening. Swift recognition of the likely cause is required for accurate prognostication and rapid institution of appropriate therapy, which leads to complete resolution in most cases.

Humans and animals can be simultaneously exposed through the diet to different mycotoxins, including aflatoxins, ochratoxin A, deoxynivalenol, zearalenone, and fumonisins, which are the most important. Evaluation of the frequency and levels of human and animal exposure to these mycotoxins can be performed by measuring the levels of the relevant biomarkers in urine. Available data on the toxicokinetics of these mycotoxins in animals suggest that aflatoxin M(1) (AFM(1)), ochratoxin A (OTA), deoxynivalenol (DON)/de-epoxydeoxynivalenol (DOM-1), alpha-zearalenol (α-ZOL)/beta-zearalenol (β-ZOL), and fumonisin B(1) (FB(1)) can be used as urinary biomarkers. A liquid chromatographic-tandem mass spectrometric method has been developed for simultaneous determination of these mycotoxin biomarkers in human or animal urine. Urine samples were purified and concentrated by a double cleanup approach, using a multitoxin immunoaffinity column and a reversed-phase SPE Oasis HLB column. Separation of the biomarkers was performed by reversed-phase chromatography using a multi-step linear methanol-water gradient containing 0.5% acetic acid as mobile phase. Detection and quantification of the biomarkers were performed by triple quadrupole mass spectrometry (LC-ESI-MS/MS). The clean-up conditions were optimised to obtain maximum analyte recovery and high sensitivity. Recovery from spiked samples was performed at four levels in the range 0.03-12 ng mL(-1), using matrix-matched calibration curves for quantification. Mean recoveries of the biomarkers tested ranged from 62 to 96% with relative standard deviations of 3-20%. Enzymatic digestion with β-glucuronidase/sulfatase resulted in increased concentrations of the biomarkers, in both human and pig urine, in most samples containing measurable concentrations of DON, DOM-1, OTA, α-ZOL, or β-ZOL. A highly variable increase was observed between individuals. Co-occurrence of OTA and DON in human urine is reported herein for the first time.

Invasion of the flowering heads of grasses by Claviceps spp. can produce sclerotia (ergots) containing several toxins. Ingestion of these toxins, through the consumption of paspalum (Paspalum dilatatum), can induce a range of clinical symptoms, including staggers. Cattle are the most commonly affected species, but although sheep and horses have been reported affected there are no published descriptions of paspalum staggers in horses. We describe two occurrences of paspalum staggers, the first in three Australian Stockhorse foals and the second in mature Standardbred horses. All three foals presented with ataxia in all limbs after consuming infected paspalum. One foal died from misadventure and the other two recovered within 1 week of removal from the infected paddock. In the second case, two of eight mares and geldings grazing in an irrigation channel developed hindquarter paresis. After removal of all horses from the area, one of the affected horses continued to deteriorate. Both horses were treated with antibiotics. The more severely affected horse was also treated with fluids and electrolytes, but had to be euthanased. The second affected horse recovered after 2 days. Paspalum pastures should inspected for Claviceps paspali infection before the introduction of horses., (© 2010 The Authors. Australian Veterinary Journal © 2010 Australian Veterinary Association.)

Twenty-eight incapacitated individuals (average 43 years old, 7 males, 21 females, range 12-70) exposed to molds and mycotoxins were studied and treated with a protocol of cleaning up or changing their environment to be mold free. Injections of the optimum dose of antigens were given as part of the treatment protocol as was oral and intravenous (i.v.) antioxidants; heat depuration (sauna); physical therapy with massage and exercise under environmentally controlled conditions; oxygen therapy at 4-8 L/min for 2 hours with a special wood-grade cellophane reservoir and a glass oxygen container. Many patients were sensitive to plastics; therefore, exposures to these were kept to a minimum. Autogenous lymphocytic factor was given as an immune modulator. Of 28 patients, 27 did well and returned to work. One patient improved but did not return to work during the period of study.

Case History: A 1-year-old, intact male Labrador-cross dog vomited after eating walnuts that had been on the ground for 5 months. The dog then developed tremors, ataxia, increased salivation, and hyperaesthesia., Clinical Findings: The dog had marked generalised tremors, ataxia and a temperature of 39.9 degrees C. Both pupils were of normal size and normally responsive to light. Vomiting was induced, and walnut shell was visible in the vomitus., Diagnosis: Due to the sudden onset of tremors, lack of exposure to other convulsive toxins, and the evidence of ingestion of walnuts, the provisional diagnosis was tremorgenic mycotoxicosis. The dog was treated symptomatically, and made a full recovery over 18 hours. Tremorgenic mycotoxins were detected within walnuts collected from the dog's environment., Clinical Relevance: Fungi that produce tremorgenic mycotoxins are present in New Zealand. Intoxication should be suspected in dogs that suddenly develop muscle tremors, especially if there is a history of ingestion of mouldy food 2-3 hours prior to the development of tremors.

Mycotoxins likely have existed for as long as crops have been grown but recognition of the true chemical nature of such entities of fungal metabolism was not known until recent times. Conjecturally, there is historical evidence of their presence back as far as the time reported in the Dead Sea Scrolls. Evidence of their periodic, historical occurrence exists until the recognition of aflatoxins in the early 1960s. At that time mycotoxins were considered as a storage phenomenon whereby grains becoming moldy during storage allowed for the production of these secondary metabolites proven to be toxic when consumed by man and other animals. Subsequently, aflatoxins and mycotoxins of several kinds were found to be formed during development of crop plants in the field. The determination of which of the many known mycotoxins are significant can be based upon their frequency of occurrence and/or the severity of the disease that they produce, especially if they are known to be carcinogenic. Among the mycotoxins fitting into this major group would be the aflatoxins, deoxynivalenol, fumonisins, zearalenone, T-2 toxin, ochratoxin and certain ergot alkaloids. The diseases (mycotoxicoses) caused by these mycotoxins are quite varied and involve a wide range of susceptible animal species including humans. Most of these diseases occur after consumption of mycotoxin contaminated grain or products made from such grains but other routes of exposure exist. The diagnosis of mycotoxicoses may prove to be difficult because of the similarity of signs of disease to those caused by other agents. Therefore, diagnosis of a mycotoxicoses is dependent upon adequate testing for mycotoxins involving sampling, sample preparation and analysis.

Disease associated with exposure to mycotoxins is known as the "Great Masquerader" of the 21st century because of its complex natural history involving different tissues and resembling different diseases at each stage in its evolution. It can present with a variety of nonspecific clinical signs and symptoms such as rash, conjunctivitis, epistaxis, apnea, cough, wheezing, nausea, and vomiting. Some cases of vomiting illness, bone marrow failure, acute pulmonary hemorrhage, and recurrent apnea and/or "pneumonia" are associated with exposure to mycotoxins. Familiarity with the symptoms of exposure to the major classes of mycotoxins enables the clinician to ask pertinent questions about possible fungal exposures and to remove the infant or child from the source of exposure, which could be contaminated food(s), clothing and furniture, or the indoor air of the home. Failure to prevent recurrent exposure often results in recurrent illness. A variety of other conditions, including hepatocellular and esophageal cancer and neural tube defects, are associated with consumption of foods contaminated with mycotoxins. Awareness of the short- and long-term consequences of exposures to these natural toxins helps pediatricians to serve as better advocates for children and families.

One hundred fifty 1-d-old quail chicks (Coturnix coturnix japonica) were divided into 2 groups. The 2 groups were designated as controls (CX) and fumonisin-fed birds (FX) with each containing 50 and 100 chicks, respectively. The birds in group CX were maintained on quail mash alone, whereas the birds in group FX were maintained on diets supplemented with 300 ppm of fumonisin B1 from Fusarium verticillioides (formerly Fusarium moniliforme) culture material from 1 d. Quail chicks in both groups were examined daily for clinical signs and mortality. Five randomly selected quail from each group were individually weighed on 0, 7, 14, 21, and 28 d post-feeding (DPF). After weighing, blood was collected from these birds at 7, 14, 21, and 28 DPF for hematological studies and at 14, 21, and 28 DPF for biochemical studies. Fumonisin B1-fed birds (FX) had ruffled feathers, reduced feed and water intake, poor body growth, and greenish mucus diarrhea with 59% mortality. Nearly 30% of the fumonisin B1-fed birds showed nervous signs during the 4-wk experimental period. From 7 DPF onward, BW in group FX were significantly lower than those in group CX. Fumonisin feeding significantly increased hemoglobin, packed cell volume, total erythrocyte count, and total leukocyte count. There was also a significant increase in aspartate transaminase and alanine transaminase in the fumonisin-fed group. Fumonisins significantly increased concentrations of total serum protein and albumin on 14 and 21 DPF, serum calcium and cholesterol levels from 14 DPF onward, and creatinine from 21 DPF onward. This study revealed that the addition of F. verticillioides culture material supplying a level of 300 ppm of FB1/kg of diet is highly toxic to quail chicks, resulting in heavy mortality, decreased growth rate, and significant alterations in hemato-biochemical parameters.

The objective of this presentation is to document the salient clinical findings in a case of aflatoxicosis and to review the literature on the same so as to increase the index of suspicion, enhance early diagnosis and improve management. The case was a 17-year-old schoolboy presenting with vomiting, features of infection and gastrointestinal tract symptoms. Examination revealed a very ill looking pale patient with abdominal distension, tenderness and rectal bleeding and easy bruisability. Investigations showed abnormal liver function tests, pancytopenia and elevated serum levels of aflatoxins. Management consisted of supportive care including antibiotics and antifungal therapy, transfusion of red blood cells and fresh frozen plasma. His recovery was uneventful. The literature on human aflatoxicosis shows that the presentation may be acute, subacute and chronic. The degree of emanating clinical events also conforms to status of the aflatoxicosis. Overall, the features are protean and may masquerade many other forms of toxaemias. In conclusion, the diagnosis of aflatoxicosis takes cognisance of geographical location, past events, staple diet and clinical features to exclude other infections. Also required are high index of suspicion and importantly serum levels of aflatoxin. Treatment strategies involved use of antimicrobials and supporting the damaged multi-organs.

Twenty young female adult one-humped racing camels (Camelus dromedarius) kept in camps scattered outside Al Ain city and aged between 3- and 6-years-old, died after a short clinical illness. Affected camels were dull, inappetant and pyrexic, with submandibular oedema and enlargement of submandibular lymph nodes. Of 100 camels within the camps, 31 showed clinical signs. At necropsy examination, the liver of dead animals appeared yellowish, enlarged, congested and friable. The main hepatic histological findings were centrolobular necrosis, haemorrhages and cellular vacuolation. Aflatoxins were detected in sera, liver, ruminal contents and in feed ingested by affected animals. Sera of symptomatic and recovered camels also showed increased levels of glutamic oxaloacetic transaminases, glutamic pyruvic transaminases, aspartate transaminases, gamma glutamyl transaminases, glucose, urea nitrogen, phosphorus and total iron. Decreased levels of albumin, calcium, cholesterol and triglycerides were also observed. It was probable that aflatoxicosis was responsible for clinical signs and subsequent death of the camels. The need for suitable and appropriate storage conditions of animal feed to prevent fungal growth and aflatoxin contamination is highlighted.

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.

In this report, we describe the natural intoxication of 2 dogs that consumed moldy dairy products found in the household garbage and the procedures used to identify and quantify the tremorgenic mycotoxins, roquefortine and penitrem A, in the remaining portions of ingested materials. Following the ingestion of mycotoxins, the dogs of our report developed muscle tremors or seizures that resembled clinical signs of strychnine poisoning. Roquefortine was the predominant mycotoxin in a moldy cream cheese wrapper that was found among scattered garbage consumed by the first dog. Penitrem A was the only mycotoxin detected in discarded moldy macaroni and cheese that was consumed by the second dog. Treatment of dogs with tremorgenic mycotoxin intoxication involves supportive care. Close monitoring is important because the development of aspiration pneumonia is common and has been reported as the cause of death. Clinical signs of intoxication gradually resolve within 24 to 48 hours.

Well-known plant poisonings such as 'dunsiekte' (seneciosis) and 'jaagsiekte' (crotalariosis) of horses in southern Africa are briefly reviewed. Relatively unfamiliar mycotoxicoses such as stachybotryotoxicosis and perennial rye grass staggers and potentially occurring exotic intoxications such as equine nigropallidal encephalomalacia and ergot alkaloid poisoning are also discussed. This article is aimed at informing the southern African equine practitioner about probable poisonings that might occur locally in horses.

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).

Penitrem A and roquefortine poisonings were diagnosed in a Laborador retriever following garbage consumption. Clinical signs of mycotoxicosis included polypnea, tachycardia, and ataxia that quickly progressed to lateral recumbency and seizures. Removal of the mycotoxins from the stomach soon after ingestion allowed the dog to recover within 72-96 hours.

Since October 3, 2001, the Centers for Disease Control and Prevention and other organizations have been investigating potential bioterrorist-related anthrax cases. The pediatrician may be faced with complex issues related to diagnosis and treatment of illnesses caused by intentionally released biological agents. The agents that pose a major potential bioterrorist threat are reviewed by the clinical syndromes they produce: acute respiratory distress with fever, influenza-like illnesses, acute rash with fever, neurologic syndromes, and blistering syndromes. Specific and detailed diagnostic, treatment, and prophylaxis information is provided for anthrax, plague, tularemia, smallpox, botulism, viral hemorrhagic fevers, and other diseases. In cases of suspected bioterrorism, the pediatrician must be able to obtain diagnostic and treatment information efficiently and expeditiously. The system controlling the interaction between public and nonpublic health laboratories in suspected cases of bioterrorism is described. Finally, information regarding emergency contacts and links to educational resources is provided.

Horses consume feed grains and forages that can produce a range of mycotoxins resulting from mold invasion. Toxicosis of horses often occurs from fumonisins or aflatoxin in grains, from the tremorgenic mycotoxins in dallis grass, or from slaframine in red clover. Fumonisin toxicosis often is severe and fatal, and aflatoxin can be acute or chronic and debilitating. Other mycotoxins reported in horses may cause moderate to mild signs that regress when the contaminated feedstuff is removed. Overall, horses appear to have a relatively low prevalence of reported mycotoxicoses among domestic animals, but they are extremely sensitive to the fumonisins. Since there are no good therapies for mycotoxin poisoning, attention to providing high quality grains and forages to prevent mycotoxicoses is the most effective means for reducing the risk of mycotoxins in horses.

Maps are provided showing the national and provincial distributions of many plant poisonings and mycotoxicoses in South Africa. The various poisonings are briefly described and criteria for their diagnoses are given. The annual mortalities of cattle from plant poisonings/mycotoxicoses in South Africa were calculated as c. 37 665 head with a current cash value of c. R57 627 450, and that of small stock as c. 264851 head with a value of c. R46 878 627. The annual total cost of plant poisonings/mycotoxicoses to the livestock industry of South Africa is conservatively estimated at R104 506 077. These figures do not include hidden losses such as diminished production, reproductive failure, the cost of not utilizing toxic pastures and the fall in price of infested land.

Sixty-three male sprague Dawley rats were randomly assigned to dietary treatments containing 1) N-formylloline alkaloid (NFL), 2) N-acetylloline alkaloid (NAL), 3) NFL + NAL, 4) NFL + a mixture of ergot alkaloids, 5) NAL + a mixture of ergot alkaloids, 6) NFL + NAL + a mixture of ergot alkaloids, 7) a mixture of ergot alkaloids, 8) endophyte-free tall fescue seed (EFTF), and 9) endophyte-infected tall fescue (EITF) seed (negative control). All diets were prepared by mixing the prepared treatments and Laboratory Chow (1:1 ratio) and were fed at a maximum of 15 g per rat per day. All rats were killed at termination (d 18). Rats fed the EITF consumed less (P < .05) than those fed all other treatments. Feed intake for rats fed the NFL + ergot alkaloids was lower than for those fed NAL, NAL + ergot alkaloids, NFL + NAL + ergot alkaloids, ergot alkaloids, and EFTF treatments. Average daily weight gains (ADG) followed a trend similar to feed intake with some exceptions. Rats fed the NFL + NAL treatments had higher (P < .05) ADG than those fed all other treatments except the NFL + NAL + ergot alkaloid treatment. Rats fed the EITF had lower (P < .05) ADG than those fed all other treatments except those fed ergot alkaloids and NAL + ergot alkaloids. Epididymides, testes, hypothalamus, corpus striatum weights, prolactin and alkaline phosphatase content were not altered by dietary treatments. Results suggest that loline alkaloids may have a slight depressing effect on feed intake.

The role of bioassay in the diagnosis of mycotoxicoses in farm animals is discussed. Methods for detecting mycotoxin contamination of animal feeds using biological species (aquatic and terrestrial animals and plants but excluding bacteria and yeast) are reviewed. Factors that need to be considered when choosing and using particular bioassay procedures in a feed-screening programme are discussed in relation to the occurrence of false positives and false negatives.

Experiments with topically applied T-2 trichothecene mycotoxin were undertaken to determine whether lesions caused by this toxin could be differentiated from autolysis. Two pathologists, who had previously seen lesions caused by T-2 toxin, graded lesions without knowledge of treatment group and stated whether the animal had received the toxin or not. Both pathologists differentiated T-2 toxin-treated mice up to 6 h post-mortem. Failure to distinguish between treated and control mice resulted in false-negative diagnoses only. It was concluded that the diagnosis of trichothecene mycotoxicosis would probably be missed more than 6 h post-mortem.

Mycotoxins have been named "agents in search of a disease," and the considerable progress in analytical methodology over the last 10 years has not changed this very much. The following are factors that contribute to the difficulty of making a diagnosis: (1) nonspecificity of lesions; (2) masking of mycotoxic effects by secondary effects, e.g., through immunosuppression; (3) late appearance of a lesion, e.g., bone marrow damage or neoplasia; (4) interaction of several mycotoxins or presence of other toxicants or deficiency states; (5) species variation in the response to the mycotoxin(s); (6) difficulty of linking a late appearing effect with a demonstrable cause; (7) low doses of mycotoxins may cause stimulating effects; and (8) not being aware of the potential of a mycotoxin as a causative factor in disease. The mycotoxins of major importance in Canada are trichothecenes, ochratoxin, zearalenone, and ergot. It is concluded that the significance of mycotoxins for animals in Canada is likely generally underestimated.