nsc-141537 and Poultry-Diseases

The possible protective effect of a feed additive (Mycofix) against the toxic effects of 4,15-diacetoxiscirpenol (DAS) in growing broiler chickens was investigated in a 21-d fully randomized trial consisting of seven dietary treatments (control with no DAS or Mycofix added, 1 ppm DAS alone, 1 ppm DAS supplemented with 0.75 g/kg Mycofix, 1 ppm DAS supplemented with 1.5 g/kg Mycofix, 2 ppm DAS alone, 2 ppm DAS supplemented with 0.75 g/kg Mycofix, and 2 ppm DAS supplemented with 1.5 g/kg Mycofix). When no feed additive was included, both levels of dietary DAS significantly decreased BW and feed intake and caused oral lesions, with the effect of 2 ppm DAS being more severe. When 1 ppm DAS was added to the diet, supplementation of Mycofix protected against the adverse effects of DAS on feed intake and BW at both levels of inclusion (0.75 and 1.5 g/kg); however, no protection against oral lesions was obtained by Mycofix supplementation. This finding suggests that the adverse effect of DAS on performance is not due to the oral lesions per se but it is likely the result of the systemic absorption of the mycotoxin. When 2 ppm dietary DAS was present in the diet, only partial protection on BW and feed intake was obtained by Mycofix supplementation. More studies are required to determine if a higher dose of Mycofix could be capable of counteracting the adverse effects of 2 ppm dietary DAS on chicken performance.

Topics: Animals; Chickens; Diet; Eating; Iodophors; Mouth Diseases; Poultry Diseases; Trichothecenes; Weight Gain

Trichotecene poisoning in poultry can cause oral lesions, haemorrhages, depletion and necrosis in the lymphopoetic organs and death. Spontaneous poisonings with these toxins are rarely described. This paper describes the spontaneous poisoning of two Brahma chickens with T-2 toxin, diacetoxyscirpenol and deoxynivalenol. Two out of 10 chickens died under signs of depression and loss of appetite. Histopathological analysis revealed vacuolar dystrophy of the liver, necrosis and depletion of lymphocyte in the bursa of Fabricius as well as multiple necroses in the glandular stomach and gut. Even though quantities of 0.70 mg/kg T-2 in the food together with 0.50 mg/kg diacetoxyscirpenol significantly differ from the median lethal dose for chickens reported in literature (4.97 mg/kg), parasitological, virological and histopathological results indicate trichotecenes as the causative agents of this pathological condition.

Topics: Animal Feed; Animals; Bursa of Fabricius; Chickens; Fatal Outcome; Fusarium; Liver; Lymphocytes; Necrosis; Poisoning; Poultry Diseases; Stomach; T-2 Toxin; Trichothecenes

The influence of high dietary fat on the toxicity of diacetoxyscirpenol (DAS) was investigated in a 2 x 5 factorial arrangement of treatments (6 and 12% fat, and 0, 1, 2, 4, and 8 micrograms DAS/g diet). The 3-wk body weight was decreased (P less than .0001) by DAS, but fat had no significant (P less than .05) effect. There was a highly significant (P less than .0059) interaction manifested at the higher levels of DAS by a greater decrease in body weight in the high-fat diet than in the low-fat diet. Neither feed conversion nor percentage of fat in fecal material were affected significantly (P less than .05) by DAS. These data were consistent with the high-fat diet promoting lipid micellar absorption of DAS and with DAS, once absorbed, inhibiting protein synthesis at the ribosomal level, a well established mechanism of action for trichothecene toxins such as DAS.

Topics: Animals; Body Weight; Chickens; Dietary Fats; Eating; Male; Mycotoxicosis; Mycotoxins; Poultry Diseases; Trichothecenes

Dietary scirpentriol (STO), triacetoxyscirpenol (TAS), monoacetoxyscirpenol (MAS), and diacetoxyscirpenol (DAS), mycotoxins produced by Fusarium species, were compared for their ability to cause mouth lesions when graded dietary levels (0, 1, 2, 4, and 8 micrograms STO or TAS/g; 0, .5, 1, 2, and 4 micrograms MAS or DAS/g) were fed to male broiler chickens for 21 days after hatching. The mouth lesions provoked by each scirpenol were dose-related. The minimum effective doses (MED) were 4, 2, 1, and .5 micrograms/g for TAS, STO, DAS, and MAS, respectively, whether the number of affected birds or the number of affected mouth parts (angles, upper beak, lower beak, and tongue) was the measured response. Lesion sites in the mouth varied with the toxin. The rank orders from greatest to least affected sites were angles, upper beak, lower beak, and tongue for TAS and STO, upper beak, lower beak, angles, and tongue for MAS, and upper beak, lower beak, tongue, and angles for DAS. Mouth lesions were clearly visible with each toxin after feeding for 1 wk and the numbers of affected mouth parts almost tripled after 2 wk exposure. During Week 3 of exposure, only the increase caused by MAS was significant (P less than .05). The MED for growth inhibition were 2, 2, 2, and 8 micrograms/g for STO, MAS, DAS, and TAS, respectively. Thus, mouth lesions were of equal or greater sensitivity than growth inhibition as an indicator of scirpenol toxicity. It would appear that the discovery of mouth lesions in birds justifies a mold and mycotoxin control program.

Topics: Acetylation; Animal Feed; Animals; Chickens; Food Microbiology; Fusarium; Male; Mouth Diseases; Mycotoxicosis; Mycotoxins; Poultry Diseases; Random Allocation; T-2 Toxin; Trichothecenes; Weight Gain

An episode of suboptimal growth, poor feathering and behavioural abnormalities in broilers in Scotland during the winter of 1980-81 is described. This was considered to be associated with mould-contaminated maize and wheat components of the feed, from which fusaria were isolated in persistently high numbers. Four species, Fusarium culmorum, F tricinctum, F nivale and F moniliforme, were identified. Chloroform extracts of the raw materials and of an artificial medium in which three of the Fusarium species were cultured proved toxic to tissue cultures of a human epithelial cell line (HEp II). Specific identification by thin layer chromatography of the mycotoxins deoxynivalenol, zearalenone and diacetoxyscirpenol was achieved in some extracts. In addition, several other areas of the chromatograms were found to be toxic in the HEp II cell system and these may contain toxins for which standards were not available or, alternatively, previously uncharacterised fungal metabolites. It was concluded that the toxins produced by the fusaria were major contributing factors to the disease symptoms shown by the birds.

Topics: Animal Feed; Animals; Chickens; Food Microbiology; Foodborne Diseases; Fusarium; Mycotoxins; Poultry Diseases; Scotland; Species Specificity; Trichothecenes; Zearalenone

T-2 toxin (3-hydroxy-4,15-diacetoxy-8-[3-methyl-butyrloxy]-12,13-epoxy-delta 9-trichothecene) and diacetoxyscirpenol, structurally similar trichothecene mycotoxins, in dimethylsulfoxide:saline (1:9 v/v) solvent, were given by crop gavage to 7-day-old male broiler chickens. Selected birds were killed at 1, 6, 12, 18, 24, 72, and 168 hours post-treatment. The lesions induced by the two toxins were similar, but were more severe in chicks given T-2 toxin. Necrosis of lymphoid tissue and bone marrow began one hour after treatment with T-2 toxin, and was followed by rapid cell depletion. Cell repletion also was rapid, occurring by hour 24 in mildly injured tissues from birds given diacetoxyscirpenol and by hours 72 and 168 in more severely injured tissues from chickens given T-2 toxin. Hepatic lesions were multiple foci of cell necrosis resolved rapidly and the inflammatory cell reaction was minimal. Necrosis of gall bladder epithelium and secondary cholecystitis followed hepatic cell necrosis. In the alimentary tract, necrosis of the epithelium on the tips of villi in the duodenum was followed by necrosis of the epithelium of villi and crypts in the small and large intestine, and of mucosal epithelium of the proventriculus and ventriculus. Atrophy of intestinal villi and fewer mitotic figures were seen by 18 hours after treatment. The alimentary tract epithelium, however, looked normal by hour 72. Lesions in the integument, including necrosis of feather epidermis and of the follicular epidermis at the neck of the feather follicle, occurred at 12 to 24 hours after treatment.

Topics: Animals; Chickens; Liver; Lymphoid Tissue; Male; Poultry Diseases; Sesquiterpenes; T-2 Toxin; Trichothecenes