Effects of dietary fumonisin B1-containing culture material, deoxynivalenol-contaminated wheat, or their combination on growing barrows.

Objective: To examine the toxic effects of fumonisin B1 (FB1)-containing culture material and deoxynivalenol (DON)-contaminated wheat diets on barrows.

Animals: 24, 7-week-old crossbred barrows allotted to 4 equal groups of 3 replicates of 2 barrows/replicate.

Procedure: Barrows were fed diets for 28 days that were formulated as follows: no additional FCM or DON/kg of feed (control); 100 mg FB1/kg of feed; 5 mg DON/kg of feed; or 100 mg FB1 plus 5 mg DON/kg of feed.

Influence of aflatoxin and fumonisin B1-containing culture material on growing barrows.

Aflatoxin (AF)-contaminated and fumonisin B1 (FB1)-contaminated (culture material from Fusarium moniliforme) diets were fed singly and in combination to growing cross-bred barrows. Six barrows (3 replicates of 2 each; mean body weight, 17.5 kg) per group were fed: 0 mg of AF and 0 mg of FB1/kg of feed (control); 2.

Effects of feeding fumonisin B1 present in Fusarium moniliforme culture material and aflatoxin singly and in combination to turkey poults.

Diets containing 200 mg fumonisin B1/kg of feed and .75 mg aflatoxin/kg of feed singly or in combination were fed to female turkey poults (Nicholas Large White) from day of hatch to 21 d of age. When compared with controls, 21-d body weight gains were reduced 10% by fumonisin B1, 39% by aflatoxins, and 47% by the combination.

Influence of the antibiotics lincomycin and tylosin on aflatoxicosis when added to aflatoxin-contaminated diets of growing swine.

Effects of dietary aflatoxin (AF) and the antibiotics lincomycin (L) and tylosin (T) were evaluated in growing crossbred pigs. Six barrows (3 replicates of 2 each, mean body weight 14.0 kg) per group were assigned to 1 of 6 treatment groups (for a total of 36): 0 mg L, 0 mg T, and 0 mg AF/kg of feed (control); 220 mg L/kg of feed (200 g/ton); 110 mg T/kg of feed (100 g/ton); 2.

Influence of fumonisin B1, present in Fusarium moniliforme culture material, and T-2 toxin on turkey poults.

Diets containing 300 mg fumonisin B1 (FB1)/kg of feed and 5 mg T-2 toxin/kg of feed singly or in combination were fed to female turkey poults (Nicholas Large White) from day of hatch to 21 d of age. When compared with controls, 21-d body weight gains were reduced 21% by FB1, 26% by T-2, and 47% by the combination. the efficiency of feed utilization was adversely affected by FB1 and the combination of FB1 and T-2.

Acute hepatic and renal toxicity in lambs dosed with fumonisin-containing culture material.

To examine the effects of acute exposure to fumonisin-containing culture material (FCCM), 15 crossbred wether lambs were dosed intraruminally with FCCM containing 0 (CONTROL, n = 3), 11.1 (LOW, n = 4), 22.2 (MED, n = 4), or 45.

Administration of ochratoxin A and T-2 toxin to growing swine.

Effects of dietary ochratoxin A (OA) and T-2 toxin, fed singly and in combination, were evaluated in growing crossbred pigs. Thirty-six barrows (3 replicates of 3 for each of 4 treatment groups, mean body weight, 18.0 kg) were fed: 0 mg of OA and 0 mg of T-2/kg of feed (control); 2.

Effect of ochratoxin A on Salmonella-challenged broiler chicks.

Poultry products represent a significant reservoir of Salmonella typhimurium. Ochratoxin A, a mycotoxin and natural contaminant of poultry feedstuffs, produces detrimental effects on the immune and other systems of the broiler chick. Because poultry products are possible sources of S.

Influence of vitamin E on aflatoxicosis in growing swine.

Effects of dietary aflatoxin (AF) and supplemental vitamin E (d-alpha-tocopherol) were evaluated in growing crossbred pigs. Nine barrows (3 replicates of 3 each, mean body weight, 14.0 kg) per group were assigned to 1 of 4 treatment groups (for a total of 36 barrows): 0 IU of supplemental vitamin E and 0 mg of AF/kg of feed (control); 2,400 IU of vitamin E divided into equal doses and administered IM on days 1 and 16; 2.

Comparison of two hydrated sodium calcium aluminosilicate compounds to experimentally protect growing barrows from aflatoxicosis.

Two formulations of hydrated sodium calcium aluminosilicate (HSCAS-1 and HSCAS-3), anti-caking agents for mixed feed, were added to the diets of growing barrows and were evaluated for their potential to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 8 barrows (2 replicates of 4 each/treatment) assigned to 1 of the following 6 treatment diets (total of 48): 1) 0 g of HSCAS-1 or HSCAS-3 and 0 mg of aflatoxin (AF)/kg of feed (control); 2) 5 g HSCAS-1/kg of feed; 3) 5 g HSCAS-3/kg of feed; 4) 3 mg AF/kg of feed; 5) 3 mg AF plus 5 g HSCAS-1/kg of feed; or 6) 3 mg AF plus 5 g HSCAS-3/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available for 28 days (from 8 to 12 weeks of age).

Efficacy of zeolitic ore compounds on the toxicity of aflatoxin to growing broiler chickens.

Commercially available zeolitic ore compounds, when incorporated into the diets at 0.5%, were evaluated for their ability to reduce the deleterious effects of 3.5 mg aflatoxin/kg feed on growing broiler chickens from 1 day to 3 weeks of age.

Efficacy of a hydrated sodium calcium aluminosilicate to reduce the toxicity of aflatoxin and diacetoxyscirpenol.

A hydrated sodium calcium aluminosilicate (HSCAS) was incorporated into diets (.5%) containing 3.5 mg/kg aflatoxin (AF) and 5.

Immunotoxicity of ochratoxin A to growing gilts.

Ochratoxin A (OA) was incorporated in the diets of growing gilts (mean body weight, 20.1 kg) at a concentration of 2.5 mg of OA/kg of feed and was fed continuously for 35 days.

Changes in hematological, blood gas, and serum biochemical variables in broilers during exposure to simulated high altitude.

One-day-old broilers were reared until 35 days of age at both natural low (100 m) and simulated high altitude (2133 m) to assess the incidence and development of ascites syndrome. Clinical measurements were conducted at 7, 14, 21, 28, and 35 days of age. Birds reared at 2133 meters exhibited significantly (P less than or equal to 0.

Effects of a hydrated sodium calcium aluminosilicate on growing turkey poults during aflatoxicosis.

Effects of adding .5% of a hydrated sodium calcium aluminosilicate (HSCAS) to diets containing 1 or .5 mg aflatoxin (AF)/kg were determined in male turkey poults from 1 day to 3 wk of age.

Colonization control of lactose-fermenting Salmonella typhimurium in young broiler chickens by use of dietary lactose.

Inclusion of lactose in the diets of chickens has been determined to reduce cecal colonization with Salmonella typhimurium. We hypothesized, therefore, that dietary lactose may be a practical means for reducing the prevalence of Salmonella contamination of chicken products. Because some strains of Salmonella are atypical and ferment lactose, we investigated the effects of dietary lactose on cecal colonization with lactose-fermenting S typhimurium.

The individual and combined toxicity of kojic acid and aflatoxin in broiler chickens.

The individual and combined effects of kojic acid and aflatoxin were studied in male broiler chicks (Peterson x Hubbard). The experiment had a two by two factorial arrangement of treatments with dietary treatments of 0 and 2,500 mg kojic acid/kg feed and 0 and 2.5 mg aflatoxin/kg feed.

Cocontamination of swine diets by aflatoxin and diacetoxyscirpenol.

The effects of dietary aflatoxin (AF) and diacetoxyscirpenol (DAS), singly and in combination, were evaluated in growing crossbred barrows. The experimental design consisted of 4 treatments of 9 barrows each fed diets containing 1) 0 mg AF and 0 mg DAS/kg feed (control), 2) 2.5 mg AF/kg feed, 3) 2.

Toxic effects of kojic acid in the diet of male broilers.

The toxicological effects induced by the administration of kojic acid were characterized in young male broiler chickens (Hubbard x Peterson). The experimental design consisted of six dietary treatments of kojic acid (0, .5, 1, 2, 4, and 8 g/kg feed) and four replicates of 10 broilers per replicate.

Effect of immunosuppression with cyclophosphamide, cyclosporin, or dexamethasone on Salmonella colonization of broiler chicks.

One-day-old broiler chicks were divided into four groups: untreated controls and three groups treated with the immunosuppressive drugs cyclophosphamide, cyclosporin, or dexamethasone on days 1-4 of age. On day 5, all groups were challenged orally with 10(4) Salmonella typhimurium. Suppression of immunocompetency was demonstrated in the treatment groups by significant decrease (P less than 0.

Diminution of aflatoxin toxicity to growing lambs by dietary supplementation with hydrated sodium calcium aluminosilicate.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing wethers (mean body weight, 34.0 kg) and was evaluated for its ability to diminish the clinical signs of aflatoxicosis. The experimental design consisted of 4 treatment groups of 5 wethers each, consuming concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control; group 1); 20 g of HSCAS/kg (2.

Stimulation and release of prostaglandins and thromboxane from macrophages by cotton dust associated lipopolysaccharides.

Decreases in the ventilation capacity of human lungs following the inspiration of cotton dust correlates more closely with the concentration of endotoxin in the dust than with any other parameter measured thus far. A lipopolysaccharide isolated from the endotoxin of Enterobacter agglomerans, a common bacterial contaminant of cotton fiber, stimulated isolated rat macrophages to produce and release prostaglandins 6 keto-PGF1 alpha, PGF2 alpha, PGE2, PGD2, PGA2, and PGB2 and thromboxane B2. If in vivo human pulmonary macrophages respond in a similar fashion by releasing these arachidonic acid metabolites or their immediate precursors in response to stimulation by cotton dust associated lipopolysaccharides, some of the acute pulmonary changes observed in humans following inspiration of cotton dust could be caused by increased release of these biologically active compounds.