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Biomedical subjects

W E Huff

Publications and source records attributed to W E Huff.

At least 91 records · Page 5Linked to original sources

Altered renal function in broilers during aflatoxicosis.

Experiments were conducted to determine the effects of aflatoxicosis on acid-base balance, urine flow rate (V), glomerular filtration rate (GFR), clearance of para-aminohippuric acid (CPAH), plasma osmolality, and the renal handling of Na, K, Ca, and P. Three-week-old broilers were gavaged with aflatoxin at a dose of 2 mg/kg of BW per day for 10 consecutive days. Control birds received an equal volume of corn oil, the aflatoxin carrier vehicle. On the eleventh day, the birds were anesthetized and prepared for renal function analysis. A solution containing inulin, para-aminohippuric acid, and mannitol was infused at a low infusion rate (.1 mL/kg of BW per min) and a high infusion rate (.4 mL/kg of BW per min) to determine if aflatoxin affects the renal response to an acute volume load. Aflatoxicosis decreased the fractional excretion of phosphorous (FEP) and plasma Ca concentration but did not significantly alter any other renal function or acid-base variables. The decrease in FEP and plasma Ca may be a direct result of renal tubular damage, decreased Ca absorption from the gut, or a result of altered circulating levels of parathyroid hormone (PTH), and possibly decreased renal sensitivity to PTH.

Animals↗

Effects of treatment of growing swine with aflatoxin and T-2 toxin.

Effects of dietary aflatoxin (AF) and T-2 toxin, singly and in combination, were evaluated in growing crossbred (Yorkshire x Landrace x Hampshire) pigs. The experimental design consisted of 4 treatment groups of 6 barrows each fed diets containing 0 mg of AF and T-2/kg of feed (controls; group 1), 2.5 mg of AF/kg of feed (group 2), 10 mg of T-2/kg of feed (group 3), or 2.5 mg of AF plus 10 mg of T-2/kg of feed (AF + T-2; group 4) ad libitum for 28 days (7 to 11 weeks of age). Production performance, and serum biochemical, and hematologic evaluations were made weekly. Body weight and body weight gain were depressed by all toxin treatments, but the effect of AF and T-2 toxin in combination was less than additive. Liver and kidney weights, as a percentage of body weight, were increased by AF treatment, and heart weight, as a percentage of body weight, was increased by T-2 treatment. Treatment with T-2 toxin induced necrotizing contact dermatitis on the snout, buccal commissures, and prepuce. Consumption of AF resulted in increased serum activities of alkaline phosphatase, aspartate transaminase, cholinesterase, and gamma-glutamyltransferase, and decreased serum concentrations of urea nitrogen, cholesterol, albumin, total protein, calcium, potassium, magnesium, and phosphorus. Consumption of T-2 toxin resulted in increased serum triglyceride concentration and decreased serum iron concentration. Treatment with AF induced lower serum unsaturated iron-binding capacity and high RBC count, PCV, hemoglobin concentration, WBC count, and prothrombin time.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

Individual and combined toxicity of deoxynivalenol and T-2 toxin in broiler chicks.

Effects of feeding diets containing deoxynivalenol (DON)-contaminated wheat (16 mg DON/kg) and purified T-2 toxin at 4 mg/kg singly and in combination were characterized in male broiler chicks from 1 day to 3 wk of age. Total body weight gains and final body weights were significantly reduced by the DON/T-2 toxin combination but were not significantly affected by the toxins singly. The efficiency of feed utilization was reduced in chicks fed either of the diets containing DON-contaminated wheat. The incidence and severity of oral lesions induced by T-2 toxin was increased in the DON/T-2 toxin combination. Several parameters not altered by DON or T-2 toxin singly were significantly affected by the combination, indicating that the combination may pose a potentially greater problem to the poultry industry than either of the mycotoxins individually.

Animal Feed↗

Influence of ochratoxin A and T-2 toxin singly and in combination on broiler chickens.

Effects of feeding diets containing ochratoxin A (OA) at 2.0 mg/kg and T-2 toxin at 4.0 mg/kg singly and in combination were characterized in male broiler chicks from 1 day to 3 wk of age. Body weights were depressed by feeding OA singly, T-2 singly, and the OA/T-2 combination. The efficiency of feed utilization was reduced in the OA and OA/T-2 combination-fed groups. The T-2 toxin caused oral lesions, anemia, and changes in some serum biochemical values. Feeding OA resulted in increases in relative liver, kidney, gizzard, and pancreas weights, a microcytic hypochromic anemia, and changed serum chemistries. The OA/T-2 combination caused increases in relative liver, kidney, proventriculus, and gizzard weights and variable serum biochemistries. The effects of OA and T-2 were additive for reduced body weight gains, mean corpuscular volume, and for reduced serum levels of total protein, and for reduced lactate dehydrogenase activity. A significant interaction occurred between OA and T-2 causing elevated serum triglyceride levels and decreased gamma glutamyl transferase activity and calcium levels. Degenerative renal tubular changes were observed in some OA and OA/T-2 combination-fed chicks. These data indicate that OA and T-2 in combination may be more toxic for some parameters than the individual mycotoxins, and may pose a greater problem for the poultry industry than either of the mycotoxins individually.

Animal Feed↗

Effects of chronic ochratoxin A and citrinin toxicosis on kidney function of single comb White Leghorn pullets.

The objectives of the present study were to examine the effects of repeated or chronic ochratoxin A (OA) and citrinin exposure, and to determine if severe ochratoxicosis permanently alters renal function in pullets. The OA-treated birds were injected intramuscularly (breast muscle) with a 1 mg/mL solution of OA at a dose of .25 mg/kg BW or .5 mg/kg BW. Citrinin-treated birds were injected with a 6 mg/mL solution of citrinin at a dose of 6 mg/kg BW. Control birds received an equal volume injection of the citrinin and OA solvent, 100% ethanol, at a dose of 1 mL/kg BW. Kidney function was evaluated after 10 consecutive days of OA, citrinin, or ethanol injection, and 2 wk following the final injections. Venous blood gas measurements were taken after the seventh day of injection. The OA increased urine flow rate, decreased urine osmolality, increased ion excretion (Na, K, Ca, P), increased water consumption, increased manure moisture, and caused a relative alkalosis when measured immediately after 10 days of OA injection. These effects of OA were not detected 2 wk later. Citrinin increased manure moisture, decreased plasma P, increased the clearance of para-aminohippuric acid, and had no consistent effect on blood acid-base parameters. The results suggest that OA may cause an osmotic diuresis by inhibiting tubular reabsorption of electrolytes. The data also suggests that the effects of OA may be reversible simply by discontinuing toxin administration. Although the citrinin-induced increase in manure moisture indicates that citrinin had an effect on renal function, renal function analysis suggests that even repeated exposure to high doses of citrinin may only have a short duration of diuretic action on the kidneys.

Analysis of Variance↗

Ochratoxin A and dietary protein. 1. Effects on body weight, feed conversion, relative organ weight, and mortality in three-week-old broilers.

An experiment with a completely randomized 3 x 4 factorial design was used to study the effects of ochratoxin A (0, 2, and 4 mg/kg) and protein (14, 18, 22, and 26%) in three-wk-old broilers. The diets were based on ground yellow corn and dehulled soybean meal. Four hundred and eighty Hubbard x Hubbard broilers were randomly placed in battery brooders, with 10 birds per pen. Each treatment was replicated four times. Body weight increased with rising levels of protein, and decreased with rising levels of ochratoxin A (OA). The efficiency of feed utilization was improved in broilers fed 22 and 26% protein, compared with broilers fed 14 and 18% protein. The efficiency of feed utilization was lower for the birds fed 4 mg/kg of OA, compared with broilers fed 0 and 2 mg/kg of OA, respectively. Using OA increased the relative weight of the liver, kidney, spleen, pancreas, proventriculus, gizzard, and heart and also significantly decreased the relative weight of the bursa of fabricius. A significant interaction between OA and protein was seen in terms of the relative weight of the liver, pancreas, and gizzard, indicating that the rising protein levels spared the OA effect on those organs. Mortality was highest among the broilers fed 4 mg/kg of OA. Protein regression coefficients (beta's) were positive with respect to 21-day body weight and were negative for the feed:gain ratio and mortality, suggesting that protein provided beneficial effects.

Animal Feed↗

Ochratoxin A and dietary protein. 2. Effects on hematology and various clinical chemistry measurements.

The health status of broilers fed diets with varying protein contents in the presence of ochratoxin A (OA) were evaluated using clinical-chemistry techniques for blood analysis. A completely randomized, 3 x 4 factorial design was utilized: 14, 18, 22, and 26% of dietary protein and 0, 2, and 4 mg/kg of OA. The broilers were raised to 3 wk of age, at which time blood was collected and various hematological parameters were evaluated. The serum was analyzed for various enzyme activities and for concentrations of metabolites and minerals using an automated, clinical-chemistry analyzer and an atomic-absorption spectrophotometer. Adding OA to the diets of broilers decreased the hemoglobin concentration, corpuscular volume, and the activity of serum alkaline and phosphatase but increased the activity of gamma-glutamyl transferase. Adding protein to the diet increased the activity of the serum aspartate aminotransferase, creatine kinase, and alkaline phosphatase. Adding OA to the diet of broilers decreased the concentrations of serum total protein, as well as the concentrations of albumen and cholesterol and increased the concentrations of serum creatinine and uric acid. The concentrations of serum total protein, albumin, urea nitrogen, and triglyceride were increased by adding protein to the diet. The concentrations of calcium, potassium, and inorganic phosphorus in the serum decreased when OA was added to the diet; but the concentrations of calcium and potassium content in the serum increased along with dietary protein. A regression analysis suggested that dietary protein was synergistic toward OA with regard to the blood levels of cholinesterase, lactate dehydrogenase, and glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗

Prevention of aflatoxicosis by addition of hydrated sodium calcium aluminosilicate to the diets of growing barrows.

Hydrated sodium calcium aluminosilicate (HSCAS), an anticaking agent for mixed feed, was added to the diets of growing barrows and was evaluated for its potential to ameliorate the clinical signs of aflatoxicosis. The experimental design consisted of 6 treatments of 5 barrows each at concentrations of 0 g of HSCAS and 0 g of aflatoxin (AF)/kg of feed (control), 5 g of HSCAS/kg of feed (0.5%), 20 g of HSCAS/kg of feed (2.0%), 3 mg of AF/kg of feed, 5 g of HSCAS (0.5%) plus 3 mg of AF/kg of feed, or 20 g of HSCAS (2.0%) plus 3 mg of AF/kg of feed. Barrows were maintained in indoor concrete-floored pens, with feed and water available ad libitum for 28 days (from the age of 7 to 11 weeks). Barrows were observed twice daily and were weighed weekly, and blood samples were obtained weekly for hematologic and serum biochemical measurements. At the termination of the study, barrows were euthanatized and necropsied. Body weight gains were diminished significantly (P less than 0.05) by consumption of 3 mg of AF/kg of feed, whereas body weight gain in barrows consuming diets containing HSCAS or HSCAS plus AF did not differ from that in control barrows. Serum enzymatic activities of alkaline phosphatase and gamma-glutamyl transferase and prothrombin time were increased in barrows consuming 3 mg of AF/kg of feed, but not in those consuming HSCAS or HSCAS plus AF.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Silicates↗

Effects of aflatoxin, deoxynivalenol, and their combinations in the diets of growing pigs.

In 2 studies, the effects of dietary aflatoxin (AF) and deoxynivalenol (DON) were evaluated in growing crossbred barrows. The first study consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 2.5 mg of DON/kg of feed, 0.75 mg of AF/kg of feed, and 2.5 mg of DON + 0.75 mg of AF/kg of feed. Pigs were fed their respective diets for 21 days. Treatment with DON caused decreases in weight gains, but no other treatment-related differences could be attributed to diets. In a second study, the experimental design consisted of 4 treatments of 5 barrows each (6 weeks old) at dosages of 0 mg of DON and AF (control), 3 mg of DON/kg of feed, 3 mg of AF/kg of feed, and 3 mg of DON + 3 mg of AF/kg of feed fed ad libitum for 28 days. The pigs were observed twice daily for clinical signs, hematologic and serum biochemical measurements were made weekly, and body weights and feed consumption were determined weekly. Body weight gains were significantly depressed by the AF and the AF + DON treatments for days 7, 14, 21, and 28. Body weights and body weight gains were only slightly reduced in the DON treatment. Changes in serum enzymatic activities of alkaline phosphatase, aspartate transaminase, creatine kinase, and gamma-glutamyl transferase were noticed in pigs given treatments with AF alone and those given AF + DON.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

Ultrastructure of hepatic and renal lesions in chickens fed aflatoxin.

Male broiler chicks were given feed and water ad libitum from hatching through 3 weeks of age. The feed contained 0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed. The chicks were killed by cervical dislocation and specimens of liver and kidney were obtained for electron microscopy on days 3, 6, 9, 17, and 21. In chicks fed 5.0 micrograms of aflatoxin, the primary lesions in liver were hepatocellular lipidosis, enlargement of bile canaliculi, reduction in mitochondrial size, mild lymphocytic infiltration, and hepatocellular degeneration and necrosis. Similar lesions were noticed in some chicks fed 2.5 micrograms of aflatoxin, but none was observed in chicks fed at 1.25 micrograms of aflatoxin. At 5 micrograms of aflatoxin, the most consistent lesion in the kidney was thickening of the glomerular basement membrane. Similar glomerular lesions were observed at 2.5 micrograms of aflatoxin, but not at 1.25 micrograms of aflatoxin. Some foot processes of the glomerular epithelial cells were poorly developed. Fusion of foot processes was not observed and fibrous material was not evident in the basement membrane. The pseudopodia of endothelial cells lining the thickened basement membrane were depleted in number or were absent. Degenerative changes also were observed in the cells of the proximal convoluted tubules, but these were less consistent than those of the glomerulus.

Animals↗

Evaluation of diets contaminated with aflatoxin and ochratoxin fed to growing pigs.

The effects of dietary aflatoxin and ochratoxin, fed singly and in combination, were evaluated in growing crossbred pigs. Five barrows (7 weeks old at beginning of study) per group were fed either control feed, 2.0 mg of aflatoxin (AF)/kg of feed, 2.0 mg of ochratoxin (OA/kg of feed, or 2.0 mg of AF and 2.0 mg of OA/kg of feed for 28 days. Production performance, serum biochemical, hematologic, and pathologic evaluations were made. Body weights were reduced by the combination treatment, whereas body weight gain was decreased by all toxin treatments. The effect of AF and OA in combination on body weight gain was additive. Liver weights were increased by the combination treatment, whereas kidney weights were increased only in the OA group. Aflatoxin caused decreases in serum calcium, sodium, phosphorus, urea nitrogen, cholesterol, and glucose concentrations, whereas OA alone caused decreases in serum phosphorus, cholesterol, and hematologic values. The AF-OA treatment induced decreases in mean corpuscular volume, packed cell volume, and in serum concentrations of phosphorus, cholesterol, and urea nitrogen. The AF-OA treatment increased serum alkaline phosphatase activities and triglycerides. It was concluded that AF and OA, singly or in combination, can affect clinical performance, serum biochemical and hematologic values, and organ weights of barrows. Although values of some measurements were affected more by the combination than by either toxin alone and suggested synergism or antagonism, the toxic interactions could best be described as additive.

Aflatoxins↗

Mycotoxin interactions in poultry and swine.

Mycotoxins are toxic compounds produced by fungi. When one mycotoxin is detected, one should suspect that others also are present in a contaminated feed ingredient or finished feeds. The toxicity and clinical signs of observed in animals when more than one mycotoxin is present in feed are complex and diverse. Some mycotoxins, such as the combination of aflatoxin with either ochratoxin A or T-2 toxin, interact to produce synergistic toxicity in broiler chicks. The effects observed during multiple mycotoxin exposure can differ greatly from the effects observed in animals exposed to a single mycotoxin. For example, fatty livers in poultry are used for presumptive diagnostic identification of aflatoxicosis. However, simultaneous presence of ochratoxin A prevents fatty livers. Of the mycotoxin combinations that have been investigated in poultry and swine, the aflatoxin + ochratoxin A and aflatoxin + T-2 toxin interactions appear to be the most toxic.

Aflatoxins↗

Influence of ochratoxin A and deoxynivalenol on growing broiler chicks.

The effects of feeding diets containing ochratoxin A (OA) (2.0 mg/kg) and deoxynivalenol (DON) (16 mg/kg) singly and in combination were characterized in male broiler chicks from 1 to 3 wk of age. Body weight gains and efficiency of feed utilization were significantly reduced by feeding OA singly, DON singly, and the OA/DON combination. Increased relative liver, kidney, and proventriculus weights were observed in the OA and OA-DON groups and blood urea nitrogen (BUN) was increased in the DON group. Serum uric acid, creatinine, and triglycerides were significantly elevated, and total protein, albumin, cholesterol, and aspartate amino transferase (AST) activity were decreased in the OA group. Histopathological examination of the liver, kidney, spleen, proventriculus, gizzard, and bursa revealed that lesions were confined primarily to mild hepatocellular degeneration, with milk diffuse lipidosis of the liver and mild swelling of the renal tubular epithelium of the OA and OA/DON combination groups. For a few parameters such as efficiency of utilization and relative liver, gizzard, and spleen weights. OA and DON appear to interact additively. However, many of the parameters such as body weights, body weight gains, BUN, total protein, and AST show significant interactions that can best be described as less than additive or in some cases antagonistic.

Animals↗

Effects of ochratoxin A alone and in combination with citrinin on kidney function of single comb White Leghorn pullets.

The present study was designed to evaluate the acute effects of ochratoxin A (OA) on pullet renal function, and to determine if the diuretic effects of citrinin are altered by acute ochratoxicosis. Birds were injected intramuscularly with a 1-mg/mL solution of OA at a dose of 5 mg/kg body weight for 2 consecutive days. Control birds received an equal volume injection of the OA carrier vehicle (100% ethanol). On the 3rd day, birds were anesthetized and prepared for renal function studies. Following 30 min of control urine and plasma collection, an intravenous infusion containing 400 ppm citrinin was initiated, and urine and plasma were collected for an additional 70 min. The OA alone caused an increase in manure moisture and increased hematocrits (hemoconcentration), but direct effects on glomerular filtration rate (GFR), urine flow rate/GFR, para-aminohippuric acid clearance (CPAH), free water clearance (FWC), and electrolye excretion (Na, K, Ca, P) were not consistently demonstrated. The OA may cause hemoconcentration by causing a subtle increase in urine flow (diuresis), or by increasing intestinal water loss (diarrhea). Citrinin infusion caused increased urine flow rate, increased urine flow rate/GFR, increased FWC, increased Na excretion, and decreased urine osmolality. Pretreatment with OA attenuated these effects of citrinin, presumably due to renal compensation for the OA-induced hemoconcentration. Citrinin and OA do not appear to have additive diuretic effects during the first 48 h of toxin exposure.

Animals↗

Progression of ochratoxicosis in broiler chickens.

The progression of effects induced by administration of ochratoxin A were characterized in young male broiler chickens (Hubbard x Hubbard). The experimental design consisted of four dietary treatments of ochratoxin A (0, 1.0, 2.0, and 4.0 micrograms ochratoxin A/g feed) and 11 replicates of 10 broilers/replicate. Broilers were housed in electrically heated batteries with feed and water available ad libitum. Broilers were weighed, bled, killed by cervical dislocation, and necropsied at 3, 6, 9, 12, 15, 18, and 21 days of age. Toxicity of ochratoxin A to broilers was evident as early as 6 days of age, when significant (P less than .05) growth depression occurred at 4.0 micrograms dietary ochratoxin A/g feed. Dietary ochratoxin A significantly increased the relative weights of the liver, kidney, spleen, pancreas, and gizzard. Anemia, characterized by a significant decrease in packed-cell volume and hemoglobin levels, was present during ochratoxicosis. Hepatotoxicity of dietary ochratoxin A was evident through an observed significant reduction in serum levels of total protein, albumin, globulin, cholesterol, triglyceride, and blood urea nitrogen, and a significant increase in the serum activities of gamma glutamyl transferase and cholinesterase. A significant increase in serum uric acid and creatinine levels was indicative of nephrotoxicity. These data provide a description of the progression of ochratoxicosis in broilers that should be useful in diagnosis and in improved understanding of ochratoxicosis.

Animals↗

Toxic synergism between aflatoxin and T-2 toxin in broiler chickens.

The individual and combined effects of aflatoxin and T-2 toxin were studied in male broiler chicks (Hubbard X Hubbard). The experimental design was a 2 X 2 factorial design with dietary treatments of 0 and 2.5 micrograms/g aflatoxin and 0 and 4.0 micrograms/g T-2 toxin. The broilers were obtained at 1 day of age and housed in electrically heated batteries with feed and water available ad libitum until they reached 3 wk of age. Aflatoxicosis in this study was characterized by a significant (P less than .05) reduction in body weight, changes in red blood cell counts and serum levels of protein, albumin, glucose, cholesterol, and calcium, and magnesium, activity of the serum enzymes lactic dehydrogenase and alkaline phosphatase, and a significant (P less than .05) increase in relative weights of the liver, kidney, spleen, pancreas, proventriculus, and heart. Dietary T-2 toxin alone caused oral lesions, a significant (P less than .05) decrease in serum protein, albumin, potassium, and magnesium levels, and a significant (P less than .05) decrease in the activity of the serum enzymes lactic dehydrogenase and alkaline phosphatase. In the combination treatment of aflatoxin and T-2 toxin, significant (P less than .05) interactive effects were seen through a decrease in body weights, increase in the relative weights of the kidney, gizzard, and heart, and decrease in mean corpuscular volume and serum levels of potassium. These data indicate that aflatoxin and T-2 toxin can interact to produce synergistic toxicity. This synergism is a threat to poultry production due to the prevalence of these mycotoxins and severity of the interactive toxicity of these mycotoxins.

Aflatoxins↗

Progression of aflatoxicosis in growing barrows.

The progression of aflatoxicosis was evaluated in growing crossbred barrows given 0, 1, 2, 3, or 4 mg of aflatoxin (AF)/kg of feed for 28 days (6 to 10 weeks of age). On day 28, pigs were euthanatized and necropsied, and tissues were removed for histologic examination. Body weight gains were decreased in barrows fed 2 mg of AF/kg after 7 days and in barrows fed 1 mg of AF/Kg after 14 days. By 28 days, all barrows fed AF had decreased body weights and weight gains. Compared with decreased in all barrows fed AF. Neither liver weights nor bone ash values were altered, although liver lipid values were increased in barrows fed AF. Serum aspartate transaminase, gamma-glutamyl transferase, and alkaline phosphatase activities were increased in barrows fed AF, whereas creatine kinase activity was decreased. Aflatoxin diets resulted in decreases in serum concentrations of urea nitrogen, phosphorus, cholesterol, albumin, and total protein. Histologic alterations in liver included interlobular fibrosis, periportal lipidosis, bile duct hyperplasia, and periportal lymphocytic infiltration. Lymphocytes in the thymus were depleted, and numbers of granulocytic cells in the bone marrow were reduced. The frequency and severity of lesions increased with increased doses of AF.

Aflatoxins↗