Brevetoxin exposure in sea turtles in south Texas (USA) during Karenia brevis red tide.

Five green (Chelonia mydas) and 11 Kemp's ridley (Lepidochelys kempii) sea turtles found dead, or that died soon after stranding, on the southern Texas (USA) coast during 2 Karenia brevis blooms (October 2015, September-October 2016) were tested for exposure to brevetoxins (PbTx). Tissues (liver, kidney) and digesta (stomach and intestinal contents) were analyzed by ELISA. Three green turtles found alive during the 2015 event and 2 Kemp's ridley turtles found alive during the 2016 event exhibited signs of PbTx exposure, including lethargy and/or convulsions of the head and neck. PbTx were detected in 1 or more tissues or digesta in all 16 stranded turtles. Detected PbTx concentrations ranged from 2 to >2000 ng g-1. Necropsy examination and results of PbTx analysis indicated that 10 of the Kemp's ridleys and 2 of the green turtles died from brevetoxicosis via ingestion. This is the first documentation of sea turtle mortality in Texas attributed to brevetoxicosis.

Acute photosensitisation and mortality in a herd of dairy cattle in Tasmania.

CASE HISTORY: A herd of Holstein, Jersey, or Holstein-Jersey cross lactating cattle of mixed ages presented with a sudden drop in milk yield in 94/678 cows on 3 October 2014 (Day 0). The herd was located in Gretna in the Derwent Valley (Tasmania, Australia) and had been grazing dryland pasture. CLINICAL FINDINGS: On Day 0 the cows variably showed recumbency, peracute photosensitisation, inflamed coronary bands, conjunctival erythema, periauricular oedema, distress indicated by kicking at the flank, bruxism, discomfort, weight shifting, vocalisation indicating pain and depression. Blood samples collected on Day 4 from five clinically affected cows showed high activities of aspartate aminotransferase, glutamate dehydrogenase and gamma-glutamyl transferase. Morbidity, based on the number of treated cases within 72 hours of clinical onset, was estimated at 165/678 cows (24.3%). Mortality over the first 30 days was 19/678 cows (2.8%). PATHOLOGICAL FINDINGS: Necropsies of two cows on Day 4 showed marked distension of the gall bladder and extensive icterus. Necropsies of another two cows on Day 5 showed enlarged livers with severe damage and oedema of the distal abomasum. Severe ulcerative abomasal gastritis was present in both cows. Hepatic histopathology was consistent with chronic cholangiohepatitis. MYCOTOXICOLOGY: Fifty-five different mycotoxins were detected from a barley grass (Hordeum murinum) sample from the presumably contaminated pasture. Concentrations of B-trichothecenes, fumonisins, and zearalenone metabolites from this sample were remarkably high. The leaf smut, Jamesdicksonia dactylidis, that has not been previously reported in Tasmania, was identified from the sample of barley grass, but it is not known whether the smut can produce toxins. DIAGNOSIS: Probably an undescribed peracute mycotoxicosis associated with the ingestion of contaminated dryland pasture. CLINICAL RELEVANCE: A definitive diagnosis could not be reached in this case of acute photosensitisation and mortality in dairy cattle grazing possibly contaminated dryland pasture. The findings differed from both facial eczema and acute bovine liver disease, suggesting an undescribed mycotoxicosis.

Protective effects of Urtica dioica seed extract in aflatoxicosis: histopathological and biochemical findings.

The ameliorative potential and antioxidant capacity of an extract of Urtica dioica seeds (UDS) was investigated using histopathological changes in liver and kidney, measuring serum marker enzymes, antioxidant defence systems and lipid peroxidation (malondialdehyde (MDA)) content in various tissues of broilers exposed to aflatoxin (AF). A total of 32 broilers were divided randomly into 4 groups: control, UDS extract-treated, AF-treated and AF+UDS extract-treated. Broilers in control and UDS extract-treated groups were fed on a diet without AF. The AF-treated group and AF+UDS extract-treated groups were treated with an estimated 1 mg total AF/kg feed. The AF+UDS extract groups received in addition 30 ml UDS extract/kg diet for 21 d. The AF-treated group had significantly decreased body weight gain when compared to the other groups. Biochemical analysis showed a small increase in the concentrations of serum aspartate aminotransferase, alanine aminotransferase, gamma glutamyl transpeptidase and lactate dehydrogenase in the AF-treated group compared to that of the control group, whereas concentrations of these enzymes were decreased in the AF+UDS group compared to that of the AF-treated group. Administration of supplementary UDS extract helped restore the AF-induced increase in MDA and reduced the antioxidant system towards normality, particularly in the liver, brain, kidney and heart. Hepatorenal protection by UDS extracts was further supported by the almost normal histology in AF+UDS extract-treated group as compared to the degenerative changes in the AF-treated broilers. It was concluded that UDS extract has a protective hepatorenal effect in broilers affected by aflatoxicosis, probably acting by promoting the antioxidative defence systems.

Deoxynivalenol induces cytotoxicity and genotoxicity in animal primary cell culture.

Deoxynivalenol (DON), a mycotoxin produced by Fusarium graminearum, is widely found as a contaminant of food. DON is responsible for a wide range of toxic activities, including gastro-intestinal, lymphoid, bone-marrow and cardiotoxicity. But, the complete explorations of toxicity in terms of hepatotoxicity, nephrotoxicity, cytotoxicity and genotoxicity as well have not been documented well. Again, the mechanisms through which DON damages the DNA and promotes cellular toxicity are not well established. Considering the above fact, this research article is focused on the effects of DON-induced toxicities on experimental animal model as well as its effects on cellular level via various toxicological investigations. DON treatment showed cytotoxicity and DNA damage. Further, flow cytometric analysis of hepatocytes showed cellular apoptosis, suggesting that DON-induced hepatotoxicity is, may be partly, mediated by apoptosis. Moreover, significant differences were found in each haematology and clinical chemistry value, either (p > 0.05). No abnormality of any organ was found during histopathological examination. Hence, it can be concluded that DON induces oxidative DNA damage and increases the formation of centromere positive micronuclei due to aneugenic activity.

Optic neuropathy in a herd of beef cattle in Alberta associated with consumption of moldy corn.

A group of beef cattle in eastern Alberta was investigated due to sudden onset of blindness after grazing on standing corn in mid-winter. Fumonisin-producing Fusarium spp. were isolated from the corn. Blindness was due to an optic nerve degeneration suspected to be secondary to fumonisin mycotoxin.

Neuropathie optique dans un cheptel de bovins de boucherie en Alberta associée à la consommation de maïs moisi. Un groupe de bovins de boucherie de l'est de l'Alberta a fait l'objet d'une enquête en raison de l'apparition soudaine de cécité après avoir brouté du maïs sur pied vers le milieu de l'hiver. Fusarium spp., qui produit la fumonisine, a été isolé dans le maïs. La cécité a été attribuable à la dégénération du nerf optique ayant pour cause suspectée la mycotoxine fumonisine.(Traduit par Isabelle Vallières).

An overview of mycotoxicoses in rabbits.

Mycotoxicoses are usually a consideration in large animal species but can affect companion animals as well. Due to increasing interest and the ease of using rabbits as laboratory models, a growing number of published experimental studies discuss the effects of various mycotoxins on this species. However, the available evidence is fragmented and heterogeneous, and has not recently been collated in a review, to my knowledge. Although mycotoxicoses in rabbits are typically subclinical, clinical signs can include weight loss, anorexia, gastrointestinal disorders, stunted growth, reproductive abnormalities, and susceptibility to infections. An antemortem diagnosis typically relies on a comprehensive clinical history, and assessment of clinical signs and relevant laboratory findings, with confirmation of exposure achieved through the measurement of mycotoxin concentrations in feed or target organs. My review focuses on the clinicopathologic and histopathologic effects of the mycotoxins most important in rabbits, including fumonisins, ochratoxins, aflatoxins, trichothecenes, and zearalenone. This review offers a thorough overview of the effects of mycotoxins in rabbits, serving as a one-stop resource for veterinary practitioners, diagnosticians, and researchers.

The low doses effect of experimental zearalenone (ZEN) intoxication on the presence of Ca2+ in selected ovarian cells from pre-pubertal bitches.

The objective of this study was to determine the effect of 42-day ZEN intoxication on the presence of Ca2+ in selected ovarian cells from beagle bitches, using the potassium pyroantimonate (PPA) method. Samples were collected from 30 clinically healthy, pre-pubertal, genetically homogeneous animals. The bitches were divided into three groups of 10 animals each: experimental group I--50 microg ZEN/kg BW (100% NOAEL) administered once daily per os; experimental group II--75 microg ZEN/kg BW (150% NOAEL) administered once dailyper os; control group--placebo containing no ZEN administered per os. An electron microscopic analysis revealed that cells died due to apoptosis, depending on the ZEN dose and the type of cells exposed to intoxication. Lower ZEN doses led to apoptosis-like changes in the cells. Cell death was a consequence of excess Ca2+ accumulation in the mitochondria, followed by cell dysfunction and a decrease in or the absence of mitochondrial metabolic activity in oocytes, follicle cells and interstitial cells in experimental bitches.

Aflatoxins in Feed: Types, Metabolism, Health Consequences in Swine and Mitigation Strategies.

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

[Tremorgenic syndrome in a cattle herd after feeding silage contaminated with A. clavatus]. / Tremorgenes Syndrom in einem Rinderbestand nach Verfütterung einer mit A. clavatus befallenen Silage.

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.

Investigation of a Novel Multicomponent Mycotoxin Detoxifying Agent in Amelioration of Mycotoxicosis Induced by Aflatoxin-B1 and Ochratoxin A in Broiler Chicks.

The present study was designed to determine the efficacy of a novel multicomponent mycotoxin detoxifying agent (MMDA) containing modified zeolite (Clinoptilolite), Bacillus subtilis, B. licheniformis, Saccharomyces cerevisiae cell walls and silymarin against the deleterious effects of Aflatoxin B1 (AFB1) and Ochratoxin A (OTA) in broiler chicks. A total of 160 one-day-old Ross 308® broiler chicks were randomly allocated in four treatment groups, with four replicates, according to the following experimental design for 42 days. Group A received a basal diet; Group B received a basal diet contaminated with AFB1 and OTA at 0.1 mg/kg and 1 mg/kg, respectively; Group C received a basal diet contaminated with AFB1 and OTA and MMDA at 1 g/kg feed, and Group D received a basal diet contaminated with AFB1 and OTA and MMDA at 3 g/kg feed. Results showed that ingested mycotoxins led to significant (p ≤ 0.05) reduction in body weight and feed conversion from 25 days of age, induced histopathological changes, increased the pH of the intestinal content, and altered the biochemical profile of birds with significantly (p ≤ 0.05) increased aspartate aminotransferase (AST) values (p ≤ 0.05). On the other hand, the supplementation of MMDA significantly (p ≤ 0.05) improved the feed conversion ratio (FCR) during the second part of the study, diminished biochemical alterations, reduced pH in jejunal and ileal content, and E. coli counts in the caeca of birds (p ≤ 0.05). It may be concluded that the dietary supplementation of the MMDA partially ameliorated the adverse effects of AFB1 and OTA in broilers and could be an efficient tool in a mycotoxin control program.

Spongy Myelinopathy in Newborn Beef Calves Associated with Consumption of Corn Infected with Stenocarpella maydis.

Stillbirth and perinatal mortality with neurological signs and lesions were diagnosed in two calves following ingestion by their dams of corn infected with Stenocarpella maydis during the third trimester of gestation. Grossly, the brain and spinal cord were unremarkable. Microscopically, diffuse severe status spongiosis of the white matter was detected in the cerebral hemispheres, brainstem, spinal cord and cerebellum. To the best of our knowledge this is the first pathological description of congenital disease in calves associated with the consumption of S. maydis-infected corn; the findings resemble those reported for the naturally occurring and experimentally induced disease in lambs.

The effects of astaxanthin on liver histopathology and expression of superoxide dismutase in rat aflatoxicosis.

The metabolism of aflatoxin B1 (AFB1) generates reactive oxygen species (ROS) that destroys hepatocytes. Meanwhile, astaxanthin (AX) is known to have stronger antioxidative activity than other carotenoids. This study aimed to investigate hepatoprotective role of AX from AFB1-induced toxicity in rat by histopathological study and immunohistochemistry of Cu/Zn-SOD (SOD1) which acts as the first enzyme in antioxidative reaction against cell injury from ROS. Twenty Wistar rats were randomly divided into 4 groups. The control and AFB1 groups were gavaged by water for 7 days followed by a single DMSO and 1 mg/kg AFB1, respectively. The AXL+ AFB1 and AXH+ AFB1 groups were given of 5 mg/kg and 100 mg/kg AX for 7 days before 1 mg/kg AFB1 administration. The result showed significantly elevated liver weight per 100 g body weight in AFB1 group. The histopathological finding revealed vacuolar degeneration, necrosis, megalocytosis and binucleation of hepatocytes with bile duct hyperplasia in AFB1 group. The severities of pathological changes were sequentially reduced in AXL+AFB1 and AXH+AFB1 groups. Most rats in AXH+AFB1 group owned hypertrophic hepatocytes and atypical proliferation of cholangiocytes which are adaptive responses to severe hepatocyte damage. The SOD1 expression was also significantly higher in AXH+AFB1 group than solely treated AFB1 and AXL+AFB1 groups. In conclusion, AX alleviated AFB1-induced liver damage in rat by stimulating SOD1 expression and transdifferentiation of cholangiocytes in dose dependent manner.

Lactobacillus bulgaricus or Lactobacillus rhamnosus Suppresses NF-κB Signaling Pathway and Protects against AFB1-Induced Hepatitis: A Novel Potential Preventive Strategy for Aflatoxicosis?

Aflatoxin B1 (AFB1), a mycotoxin found in food and feed, is immunotoxic to animals and poses significant threat to the food industry and animal production. The primary target of AFB1 is the liver. To overcome aflatoxin toxicity, probiotic-mediated detoxification has been proposed. In the present study, to investigate the protective effects and molecular mechanisms of Lactobacillus bulgaricus or Lactobacillus rhamnosus against liver inflammatory responses to AFB1, mice were administered with AFB1 (300 µg/kg) and/or Lactobacillus intragastrically for 8 weeks. AML12 cells were cultured and treated with AFB1, BAY 11-7082 (an NF-κB inhibitor), and different concentrations of L. bulgaricus or L. rhamnosus. The body weight, liver index, histopathological changes, biochemical indices, cytokines, cytotoxicity, and activation of the NF-κB signaling pathway were measured. AFB1 exposure caused changes in liver histopathology and biochemical functions, altered inflammatory response, and activated the NF-κB pathway. Supplementation of L. bulgaricus or L. rhamnosus significantly prevented AFB1-induced liver injury and alleviated histopathological changes and inflammatory response by decreasing NF-κB p65 expression. The results of in vitro experiments revealed that L.rhamnosus evidently protected against AFB1-induced inflammatory response and decreased NF-κB p65 expression when compared with L. bulgaricus. These findings indicated that AFB1 exposure can cause inflammatory response by inducing hepatic injury, and supplementation of L. bulgaricus or L. rhamnosus can produce significant protective effect against AFB1-induced liver damage and inflammatory response by regulating the activation of the NF-κB signaling pathway.

An outbreak of acute aflatoxicosis on a chinchilla (Chinchilla lanigera) farm in Argentina.

Chinchillas (Chinehilla lanigera) are known to be very sensitive to aflatoxins, and often a large number of animals die if toxicosis occurs. An outbreak of acute aflatoxicosis on a chinchilla farm in Argentina is described in the present study. A commercial feed suspected of causing the death of 200 animals was sampled. Livers from 9 dead chinchillas were analyzed for their macroscopic and microscopic characteristics via necropsy and histopathology. Aflatoxins B(1), B(2), G(1), and G(2) were determined, by thin layer chromatography, to be in the feed. Macroscopic inspection of livers revealed general enlargement, pale-yellowish coloration, hypertrophy, rounded borders, and increased friability. Size and color were remarkably different from a healthy organ. Histopathologic analyses of hepatic parenchyma showed severe, diffuse cytoplasmic vacuolation of hepatocytes. Sudan III staining confirmed the presence of lipid within the vacuoles. The feed was positive for aflatoxin B(1) in quantities that exceeded the recommended levels. Histologic lesions were typical of aflatoxin intake. Monitoring feed for mycotoxins is crucial to prevent outbreaks of toxicosis, to improve management practices, and to diminish exposure risk of animals and humans to these harmful toxins.

Ultrastructural changes of ovarian follicle and corpus luteum after experimental zearalenone mycotoxicosis in bitch.

The aim of the study was to determine the influence of experimental zearalenone (ZEA) mycotoxicosis on the ultrastructure of ovaries in bitches receving zearalenone for 100 days per os in the anestrus phase. Experiment has been conducted on 9 sexually mature clinically healthy bitches. The sexually mature animals aged 1-3 years were in anestrus. The dogs have been divided into three groups: EI and EII, receiving ZEAper os in two dosages (25 microg/kg and 50 microg/kg b.w.) and control animals which received placebo per os. On the last day of experiment, ovariohysterectomy was performed in all the bitches and the uterine samples were submitted to ultrastructural analyses. The study has revealed that long lasting administration of higher dose of zearalenone causes ultrastructural changes in the granular layer of ovarian follicles, which showed due to their biological activity decrease. The changes in the granular layer, atrophy of intercellular connections and the appearance of intercellular spaces can stand for reduced activity of this layer. Changes in morphology of mitochondria, rough endoplasmic reticulum and Golgi apparatus sugest ZEA influence on cell metabolism and secretory processes. It seems therefore that in bitches and other monogastric animals, intoxications induced by this mycotoxin causes ultrastructural changes in granular cells of ovarian follicles.

Histopathological examination of ovaries in bitches after experimental zearalenone mycotoxicosis.

The present study deals with the influence of experimental ZEA mycotoxicosis on histopathological lesions in ovaries of bitches, which were administered zearalenone per os during anestrus phase for one hundred days. The experiment was performed on 9 sexually mature, clinically healthy bitches. The animals assigned into two experimental groups received zearalenone per os at two doses, 25 microg/kg b.w. and 50 microg/kg b.w., respectively: the bitches from control group received placebo per os. On the last day of zearalenone intoxication, the bitches were ovariohystorectomized. Histopathology and immunohistochemistry were performed. The study revealed that zearalenone and its metabolites caused profound regressive lesions: granular cells degeneration and atrophy. Numerous edemas and blood extravasations were also found. The intensity of these changes was significantly dose dependent. Furthermore, in ovarian cells and tissues of both experimental groups, no reaction for PCNA antigen was observed. In conclusion, zearalenone and its metabolites exerts unfavorable effects on the morphology of ovaries in bitches.

Pathologic changes in extrahepatic organs and agglutinin response to Salmonella Gallinarum infection in Japanese quail fed Fusarium verticillioides culture material containing known levels of fumonisin B1.

Three hundred 1-day-old Japanese quail (Coturnix coturnix japonica) were divided into two groups of 150 each. One group was maintained on quail mash alone, whereas Fusarium verticillioides culture material (FCM) was added to quail mash in the second group from 5 days of age and supplied 150 mg FB1/kg mash. At day 21, each group was further subdivided into two groups, yielding four groups with 75 birds apiece, which served as the control (group CX), the Salmonella Gallinarum alone group (group CS), the FB1 alone group (group FX), and the group fed FB1 and infected with Salmonella Gallinarum (group FS). An oral challenge with Salmonella Gallinarum organisms (2 x 10(4) colony-forming units [cfu]/ml) was given to groups CS and FS at 21 days of age. Three quail each, were necropsied on day 21 (0 day interval) from groups CX and FX, whereas at subsequent intervals, i.e., 1, 2, 3, 5, 7, 10, 14, and 21 days postinfection (DPI), they were sacrificed from all four groups (CX, CS, FX, and FS) to study the agglutinin response to Salmonella Gallinarum and pathologic changes. The agglutinin titers to Salmonella Gallinarum in the combination group (FS) were generally lower when compared with those in group CS. A reduction in the size of spleen along with depletion of white pulp, thinning of cardiomyocytes, lymphoid cell depletion from bursal follicles, and renal tubular nephrosis were characteristic pathologic changes in group FX. In contrast, there was mild to severe enlargement of spleen accompanied by necrosis and reticuloendothelial cell hyperplasia, pericarditis, myocarditis, and focal interstitial nephritis in groups CS. Similar but more severe lesions were observed in the combination group (FS). In addition, the flabby texture of heart, hydropericardium, and ascites were mainly observed in group FS. It is concluded that continuous presence of fumonisins at 150 mg/kg diet increases the severity of Salmonella Gallinarum infection in young Japanese quail.

Changes in renal gene expression associated with induced ochratoxicosis in chickens: activation and deactivation of transcripts after varying durations of exposure.

Exposure to ochratoxin A (OTA) can lead to changes in global gene expression. This study investigated the individual expression of genes turned on and off in renal cells of chicks after different durations of exposure to dietary OTA. One hundred and eighty day-old male broiler chicks (Ross 308) were randomly assigned to a 3 × 3 factorial arrangement of treatments (3 levels of OTA: 0, 1 and 2 mg OTA/kg diet and 3 time periods: 7, 14 and 21 d). Birds were allocated to 36 pens (4 replicate pens of 5 birds each per treatment). For RNA-Sequencing analysis (RNA-Seq), kidney samples were collected weekly from 3 controls and 3 chicks fed 1 mg OTA/kg. Birds fed 2 mg OTA/kg diet were not chosen for analysis because their reduced feed intake could affect gene expression. The libraries were constructed by Illumina's TruSeq RNA protocol. NextGENe software was used for alignment and transcript quantification. Reads per kilobase of target per million tiled reads (RPKM) were used in the Binary test analysis (P < 0.05). The highest RPKM values were used as criterion for the selection of the genes described. A total of 27,638,976 50-bp RNA-Seq reads were produced over the 3 time periods. Transcripts (40,782) were assembled de novo and annotated by homology to either G. gallus or H. sapiens. The genes activated at 7 d were IL9 and TULP1, at 14 d was GHSR and at 21 d were GRK6 and GAPDH. Unlike all other genes, LOC396365 was activated during all time periods. In contrast, the genes deactivated at 7 d were SPAG4 and LOC100857131, at 14 d were LOC771469, NKX2-1, NKX2-8, FOXO1, MyHC and CLDN18 and at 21 d was XPC. The B-G gene was turned off at 7 and 21 d. All of these genes were involved in kidney toxicity. Therefore, the turning on and off responses of these genes may contribute to carcinogenic and tumorigenic effects of OTA in birds.

Ameliorative Effects of Neutral Electrolyzed Water on Growth Performance, Biochemical Constituents, and Histopathological Changes in Turkey Poults during Aflatoxicosis.

Different in vitro and in silico approaches from our research group have demonstrated that neutral electrolyzed water (NEW) can be used to detoxify aflatoxins. The objective of this investigation was to evaluate the ability of NEW to detoxify B-aflatoxins (AFB1 and AFB2) in contaminated maize and to confirm detoxification in an in vivo experimental model. Batches of aflatoxin-contaminated maize were detoxified with NEW and mixed in commercial feed. A total of 240 6-day-old female large white Nicholas-700 turkey poults were randomly divided into four treatments of six replicates each (10 turkeys per replicate), which were fed ad libitum for two weeks with the following dietary treatments: (1) control feed containing aflatoxin-free maize (CONTROL); (2) feed containing the aflatoxin-contaminated maize (AF); (3) feed containing the aflatoxin-contaminated maize detoxified with NEW (AF + NEW); and (4) control feed containing aflatoxin-free maize treated with NEW (NEW). Compared to the control groups, turkey poults of the AF group significantly reduced body weight gain and increased feed conversion ratio and mortality rate; whereas turkey poults of the AF + NEW group did not present significant differences on productive parameters. In addition, alterations in serum biochemical constituents, enzyme activities, relative organ weight, gross morphological changes and histopathological studies were significantly mitigated by the aflatoxin-detoxification procedure. From these results, it is concluded that the treatment of aflatoxin-contaminated maize with NEW provided reasonable protection against the effects caused by aflatoxins in young turkey poults.

Canine renal failure syndrome in three dogs.

Three dead dogs were brought to the College of Veterinary Medicine, Kyungpook National University for study. Clinically, all the dogs showed emaciation, anorexia, depression, hemorrhagic vomiting and diarrhea for 7-10 days before death. All the clinical signs were first noted for about one month after feeding the dogs with commercial diets. At necropsy, all 3 dogs had severe renal damage with the same green-yellowish colored nephroliths in the renal pelvis. They also showed systemic hemorrhage and calcification of several organs, which might have been induced by uremia. Microscopically, necrosis, calcification and calculi were detected in the renal tubules, and especially in the proximal convoluted tubules and collecting ducts of the kidney. These findings were supportive of a mycotoxic effect, and especially on their kidneys. However, the precise cause of the toxic effect in these cases of canine renal failure could not be determined.