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Biomedical subjects

W E Huff

Publications and source records attributed to W E Huff.

At least 109 records · Page 6Linked to original sources
PubMed1987

Hepatic fatty acid profiles in aflatoxin-exposed broiler chickens.

This study was initiated to determine whether a specific fatty acid marker from hepatic lipids could be identified to confirm aflatoxin exposure in chickens. Male broiler chicks (240) were reared to 21 days of age on diets containing 0, 625, 1.25, 5.0, and 10.0 ppm aflatoxin. Live weights and organ weights differed significantly among the dietary groups. Total liver lipids increased significantly (P less than .001) with increasing aflatoxin levels. Separation of extracted lipids into neutral and polar fractions established that this increase in hepatic lipid was accounted for almost entirely by increases in neutral lipid fractions. A gain of 117% occurred in the weight of neutral lipids as aflatoxin increased from 0 to 10 ppm. In both neutral and polar lipid fractions subsequent chromatographic analysis of fatty acid methyl esters (FAME) showed linear increases in the monoenoic fatty acids with increasing aflatoxin. No single FAME from either lipid fraction was suitable for confirming aflatoxin exposure.

Aflatoxins↗
PubMed1987

Effects of feeding deoxynivalenol (DON, vomitoxin)-contaminated wheat to female White Leghorn chickens from day old through egg production.

White Leghorn chickens one day of age were fed starter and grower diets containing either a control (noncontaminated) wheat diet or a naturally contaminated deoxynivalenol (DON) wheat diet (18 mg DON/kg) from 1 day of age to the onset of egg production. The hens were then placed on their respective layer diets of control wheat or DON-contaminated wheat (18 mg DON/kg) for six 28-day egg production periods. Feeding the DON-contaminated diet did not significantly influence body weights during the growing or the laying phases. Overall, hen-day egg production and egg weights were significantly higher for hens receiving the DON diet. Feeding DON contaminated wheat caused no significant changes in percent shell, albumen height, percent fertility, percent hatch of fertile eggs, percent hatch of eggs set, or weight of chicks at hatch. There were slight, although significant, changes in shell weight and shell thickness and in some serum chemistry values. There were no significant differences in the hematology parameters measured or in prothrombin times. None of the eggs collected from hens fed the control and the DON-contaminated wheat diet contained detectable quantities of DON. Microscopic examination of sections of the liver, kidney, and proventriculus of control and treated hens revealed no unusual histopathology. The results indicate that feeding DON at relatively high levels beginning at 1 day of age and continuing through six egg production periods had only slight effects on the parameters measured.

Animal Feed↗
PubMed1987

Increased sensitivity to staphylococcal beta hemolysins of erythrocytes from chickens during aflatoxicosis.

The size of the zones of beta-hemolysis surrounding staphylococcal colonies on blood agar was found to be related to the level of dietary aflatoxin consumed by the chickens donating the blood. Zone sizes on blood from chickens fed the highest level of aflatoxin (10 micrograms/g of diet) were about six-fold larger than those on blood from control birds. The percentage of staphylococcal isolates displaying beta-hemolysis was increased from about 15% in normal blood to about 90% in blood from chickens fed aflatoxin (10 micrograms/g) whereas the time required for detection of beta-hemolysis was decreased by about one-half. The hemolytic activity of purified staphylococcal beta-hemolysin against suspensions of washed erythrocytes increased as the level of aflatoxin consumed by the donor chickens increased. These data imply a new mechanism for enhanced susceptibility of animals to infectious agents during mycotoxicoses whereby the animal is made more sensitive to the virulence factors of pathogens.

Animals↗
PubMed1986

Individual and combined effects of aflatoxin and deoxynivalenol (DON, vomitoxin) in broiler chickens.

The individual and combined effects of aflatoxin and deoxynivalenol (DON) were evaluated in young broiler chickens (Hubbard X Hubbard). The experimental design was a 2 X 2 factorial with treatments of 0 and 2.5 micrograms of aflatoxin/g of feed (ppm) and 0 and 16 micrograms of DON/g of feed. The broilers were maintained on these dietary treatments from hatching to 3 weeks of age in electrically heated batteries with feed and water available ad libitum. The aflatoxin treatment significantly (P less than .05) decreased body weight; weight gain; increased the relative weight of the spleen, liver, and kidney; induced hepatic hyperlipemia; decreased activity of lactic dehydrogenase; and decreased serum levels of protein, albumin, and phosphorus. The toxicity of DON was expressed through reduced growth rate, increased feed conversion; increased relative weight of the gizzard, anemia, decreased activity of lactic dehydrogenase, and decreased serum triglycerides. The interaction between aflatoxin and DON was characterized by reduced growth rates; increased feed conversion, increased relative weight of the proventriculus, gizzard, spleen, liver, and kidney, anemia, hepatic hyperlipemia, decreased activity of alkaline phosphatase, glutamic oxalacetic transaminase, and lactic dehydrogenase, and decreased serum levels of protein, albumin, uric acid, cholesterol, triglycerides, and calcium. These data demonstrate that both aflatoxin and DON can limit broiler performance and adversely effect broiler health. The effects of the combination of aflatoxin and DON on broiler performance and health was more severe than the individual effects of these mycotoxins; however, the interaction was not severe enough to represent toxic synergy and can best be characterized as additive toxicity.

Aflatoxins↗
PubMed1986

Progression of aflatoxicosis in broiler chickens.

The progression of aflatoxicosis was evaluated in young broiler chickens (Hubbard X Hubbard). The experimental design consisted of four dietary treatments of aflatoxin (0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed, ppm) and 11 replicates of 10 broilers/replicate. The broilers were maintained in electrically heated batteries with feed and water available ad libitum from hatching to 3 weeks of age. The broilers were weighed, bled, killed by cervical dislocation, and necropzied at 3, 6, 9, 12, 15, 17, and 21 days of age. Body weights were significantly decreased by 5.0 ppm aflatoxin at 6 days of age and by 2.5 ppm at 17 days of age. Aflatoxin induced a significant increase in the relative weight of the proventriculus, gizzard, spleen, and kidney. Liver atrophy was indicated in the early stages of aflatoxicosis by a decrease in the relative weight of this organ. As aflatoxicosis progressed, hepatomegaly became apparent due to lipid accumulation in the liver. Packed-cell volume and hemoglobin levels were significantly decreased by 5.0 ppm aflatoxin at 12 days and by 2.5 ppm aflatoxin at 21 days of age. Serum levels of albumin and total protein were significantly reduced at 5.0 and 2.5 ppm aflatoxin by 3 and 6 days of age, respectively. Serum levels of uric acid, triglycerides, and cholesterol were significantly decreased from control values from 12 through 21 days of age by 5.0 ppm aflatoxin and, to a lesser extent, by 2.5 ppm aflatoxin. The activity of serum lactic dehydrogenase was significantly decreased at all aflatoxin treatment levels from 12 through 21 days of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMed1984

The individual and combined effects of aflatoxin and ochratoxin A on various processing parameters of broiler chickens.

Male broilers (Hubbard X Hubbard) were placed at hatching into a completely randomized 2 X 2 X 2 factorial experimental design with the treatments consisting of 0 and 2.5 micrograms aflatoxin/g of feed (ppm) and 0 and 2.0 ppm ochratoxin A. In Trial 1, there were four replicate pens of 10 broilers per replicate at each treatment level. At 3 weeks of age two replicate pens were randomly selected and placed on control feed (0 to 3 weeks), the remaining two replicate pens were maintained on treatment (full-term). In Trial 2, there were three replicates of 38 broilers per replicate at each treatment level. At 3 weeks of age 13 broilers from each replicate pen were randomly selected and placed in separate housing and fed control diets (0 to 3 weeks). The remaining 25 broilers were kept on mycytoxin treatments until the conclusion of this trial (full-term). Data collected in these trials indicate that body weights of broilers were significantly (P less than .05) decreased by aflatoxin, ochratoxin A, and the combination treatments of the full term feeding regimen. Broilers partially recovered body weight in the 0 to 3-week feeding regimen; however, recovery was less rapid during ochratoxicosis compared to aflatoxicosis. Body weights of broilers in the combination treatment remained significantly (P less than .05) depressed throughout the trials. As body weight decreased, parts weights decreased accordingly. Carcass yield was significantly (P less than .05) decreased by all treatments, primarily by a decrease in breast yield.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMed1984

Effect of litter treatment on broiler performance and certain litter quality parameters.

Litter-Aid, a product consisting primarily of ferrous sulfate but also containing propionic acid and magnesium and copper sulfate was incorporated into litter at three application rates (0, .73, and 1.46 kg/m2) to determine its effects on broiler chicken performance and various aspects of litter quality. In Trial 1, litter treatments were applied to litter used for two previous flocks with a 10-week layout period. In Trial 1, there were 10 replicate pens of 175 birds per treatment. In Trial 2, litter used in Trial 1 was retreated, after a 26-week layout period, at the same application rates as Trial 1 with five replicate pens of 175 birds per treatment. This product in Trial 1 at .73 kg/m2 and in Trial 2 at 1.46 kg/m2 significantly (P less than .05) increased body weight without affecting feed conversion or mortality. The product did not significantly (P less than .05) affect litter moisture or litter nitrogen levels, but significantly (P less than .05) decreased litter pH. However, even at the application rate of 1.46 kg/m2, litter pH values rose above 8 as the birds reached 7 weeks of age. This product had no effect on bacteria counts and significantly (P less than .05) increased mold counts. These data indicate that Litter-Aid can be used without detrimental effects on broiler performance or litter quality.

Air Pollution↗
PubMed1983

Individual and combined effects of aflatoxin and ochratoxin A on bruising in broiler chickens.

A 2 x 2 factorial design with treatments of 0 and 2.5 microgram/g aflatoxin and 0 and 2.0 microgram/g ochratoxin A was used to evaluate the individual and combined effects of these mycotoxins on bruising and blood thigh syndrome in broiler chickens. Trial 1 consisted of four replicate pens of 10 broilers per replicate, which were maintained on these dietary treatments from 0 to 3 weeks of age. At 3 weeks of age two replicate pens per treatment were randomly selected and placed on toxin-free feed with two replicate pens remaining on toxin feed until they were 6 weeks of age when the trial was concluded. In Trial 2 three replicate pens of 38 broilers per treatment were maintained on toxin feed from 0 to 3 weeks of age. At 3 weeks of age 13 broilers per replicate were placed on toxin-free feed with 25 broilers per replicate remaining on toxin until they reached 7 weeks of age when Trial 2 was concluded. These data indicate that a synergistic toxicity exists between aflatoxin and ochratoxin A to significantly (P less than .05) decrease body weight. Body weights of broilers on aflatoxin or ochratoxin A diets for only 3 weeks partially recovered by 6 or 7 weeks of age; however, the body weights of broilers on the interaction treatments for only 3 weeks remained significantly (P less than .05) depressed at 6 and 7 weeks of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMed1983

Effects of low level chronic aflatoxicosis in broiler chickens.

A completely random design consisting of three replicates of 25 broiler chickens (Hubbard x Hubbard) at each of four treatments was used to evaluate the effects of low level, chronic aflatoxicosis on performance and various processing parameters. The treatments in Trial 1 were control, .075, .225, and .675 and in Trial 2 control, .3, .9, and 2.7 micrograms/g toxin in feed (ppm). The chickens were maintained on these treatments from day-old to 7 weeks of age with feed and water available ad libitum. All aflatoxin dose levels in Trial 1 significantly (P less than .05) decreased live, dressed, and chilled eviscerated weight, whereas only 2.7 ppm significantly (P less than .05) decreased live and dressed weight in Trial 2, with chilled eviscerated weight being significantly (P less than .05) decreased at .3 and 2.7 ppm in Trial 2. Parts weights and dimension measurements reflected the aflatoxin-induced decrease in dressed weight. Breast yield (%) was significantly (P less than .05) decreased by aflatoxin while back, wing, drum, and thigh yields were significantly increased by aflatoxin. No effect of aflatoxin was seen on the incidence of crooked keel, feather follicle infection, breast blisters, or conformation. A hypocarotenoidemia and hepatic hyperlipemia were clearly a result of chronic aflatoxicosis in these broiler chickens. These data demonstrate that the toxicity of aflatoxin is dependent on the environment in which broiler chickens are exposed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Evaluation of immunity of young broiler chickens during simultaneous aflatoxicosis and ochratoxicosis.

A 2 X 2 factorial experimental design consisting of the treatments 0 and 2.5 micrograms/g aflatoxin and 0 and 2.0 micrograms/g ochratoxin A with 12 replicates of 10 birds per treatment level was used to evaluate the effects of these mycotoxins on various aspects of immunity. Male chicks (Hubbard X Hubbard) were maintained on these treatments from one day of age to 3 weeks of age at which time six replicate pens per treatment were sacrificed and various parameters measured. The additional six replicate pens per treatment were maintained on toxin feed beyond 3 weeks of age, and at 4 weeks of age, three replicate pens were immunized with sheep red blood cells (SRBC) and Brucella abortus. Antibody titers were measured up to 10 days postimmunization. Aflatoxin and ochratoxin A, individually, significantly (P less than .05) decreased body weight, and a synergistic toxicity was evident by a significant (P less than .05) decrease in body weight. Antibody titers and phagocytic activity of heterophils were not significantly (P less than .05) altered by any treatments. The relative weight of the bursa of Fabricius and the number of follicles for a given area of the folds of the bursa of Fabricius were significantly (P less than .05) decreased only by the interaction treatment. Complement activity was significantly (P less than .05) decreased by aflatoxin and the combination of aflatoxin and ochratoxin A and depressed, although not significantly (P less than .05), by ochratoxin A.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of acute ochratoxicosis on blood pressure and heart rate of broiler chickens.

Male broiler chickens (Hubbard X Hubbard) were placed at hatching into electrically heated batteries with feed and water available ad libitum and maintained to 3 weeks of age under continuous lighting. In Trial 1, two replicate pens of 10 broilers per replicate were fed ochratoxin A from day-old to 3 weeks of age with treatments of 0, 2.0, and 4.0 micrograms/g ochratoxin A in feed (ppm). Trial 2 was identical to Trial 1 except that when the broilers reached 3 weeks of age they were administered an additional intravenous dose of either ochratoxin A, methoxamine, or isoproterenol. Trial 3 broiler chickens were maintained on control feed until they reached 3 weeks of age at which time they were taken off of feed for 2.5 hr and then placed on either control feed or feed containing 4.0 ppm ochratoxin A, and heart rate and blood pressure were measured every half hour through 7 hr. In Trial 1, no effect of ochratoxin A was seen in any treatment on heart rate or diastolic, systolic, or mean blood pressure. However, when an intravenous dose of ochratoxin A was administered to these broilers, a significant (P less than .05) decrease in heart rate and diastolic, systolic, and mean blood pressure occurred. The severity and duration of intravenous ochratoxin A administration were significantly (P less than .05) enhanced as the level of dietary ochratoxin A increased. The response of broilers to isoproterenol was significantly (P less than .05) altered by dietary ochratoxin A, whereas the broilers responded in a predictable manner to methoxamine without significant (P less than .05) ochratoxin A treatment effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1982

The effect of floor type on the development of breast blisters and feather follicle infections in broilers.

The effect of floor types on the incidence of feather follicle infection and breast blisters in caged broilers was investigated in two trials. Broilers were reared on corn-soybean meal diets with warm-room brooding. Floor types included litter (control), wire, wire covered with various types of plastic mats, and wire woven with surgical tubing. In trial 1, the effect of a coccidiostat (Monensin, 120 mg/kg of feed) was investigated for broilers not on litter, and in trial 2, the effect of supplemental zinc was investigated. Broilers were processed in the laboratory processing plant when they were 51 (trial 1) and 53 days old (trial 2). Carcasses were evaluated for the occurrence of fleshing downgrades, crooked keels, feather follicle infection, and breast blisters. Incidence of feather follicle infection was low for broilers on litter or wire floor and high for broiler reared on plastic mats. Breast blisters incidence was low for broilers on litter and plastic mats and was high for broilers on the wire floor. Overall carcass quality for litter (control) was superior to any of the cage treatments. Neither the coccidiostat nor supplemental zinc affected the incidence of breast blisters or feather follicle infection.

Animals↗
PubMed1982

Eimeria acervulina and Eimeria tenella infections in ochratoxin A-compromised broiler chickens.

A 2 x 6 factorial experimental design was used to evaluate the effects of coccidial infections in ochratoxin A-compromised chicks. Ochratoxin A was incorporated into the feed at the dose levels of 0, .5, 1.0, 2.0, 4.0, and 8.0 micrograms/g toxin in feed (ppm), and fed to the birds from 1 day of age. Birds from each treatment were inoculated with either Eimeria acervulina or Eimeria tenella at 14 days of age. Ochratoxin A decreased the severity of lesions caused by both E. acervulina and E. tenella but did not prevent infection. Packed cell volume, hemoglobin concentration, relative weight of the kidney, and plasma protein levels were altered in a manner consistent with the independent effects of ochratoxicosis and coccidiosis. A combination of ochratoxin A and either species of coccidia produced a greater decrease in body weights, increase in feed conversions, and decrease in plasma carotenoid levels than either disease alone. The relative weight of the liver and level of plasma uric acid were altered in a manner that was dependent on the species of coccidia used. These data indicate that ochratoxin A and coccidial infections can interact to limit broiler performance and that some responses are directly related to the species of coccidia.

Animals↗
PubMed1982

Comparison of ochratoxin, aflatoxin, and T-2 toxin for their effects on selected parameters related to digestion and evidence for specific metabolism of carotenoids in chickens.

Aflatoxicosis, ochratoxicosis, and T-2 toxicosis were produced by feeding diets containing graded concentration of the appropriate toxin to broiler chicks from hatching unit 3 weeks of age. Aflatoxin, even at levels not growth inhibitory, produced a malabsorption syndrome characterized by steatorrhea, hypocarotenoidemia, and decreased concentrations of bile salts and pancreatic lipase, trypsin, amylase, and RNase. The T-2 toxin at concentrations higher than required to inhibit growth produced a mild malabsorption syndrome characterized by steatorrhea and decreased levels of pancreatic lipase, trypsin, amylase, and RNase. The only suggestion of malabsorption during ochratoxicosis was a severe hypocarotenoidemia. The following observations indicated a lack of correlation between lipid malabsorption and hypocarotenoidemia. The T-2 toxicosis exhibited lipid malabsorption in the absence of hypocarotenoidemia, ochratoxicosis exhibited hypocarotenoidemia in the absence of lipid malabsorption, and aflatoxicosis exhibited both symptoms. These findings imply that carotenoids are physiologically active compounds with specific metabolic processes and are not inert substances swept along with lipids as is commonly assumed from the ability to grow apparently healthy birds free of carotenoids. The current findings also indicate that great specificities exist in mycotoxicoses despite superficial similarities.

Aflatoxins↗
PubMed1982

Natural occurrences of ochratoxicosis in poultry.

Five independent episodes of ochratoxicosis in about 970,000 turkeys, two episodes in about 70,000 laying hens, and two episodes in about 12,000,000 broiler chickens were investigated. Ochratoxin A concentrations in suspect feed and ingredients ranged from less than .2 to 16 ppm. Feed samples tested for T-2 toxin, F-2 toxin, heavy metals, and polychlorinated biphenyls were negative. Minor amounts of aflatoxin (less than 60 ppb) were found in suspect feed from two episodes. The main symptoms in turkeys were mortality (up to 59%), nephrotoxicity (pale, swollen kidneys that became tan colored in the sequel to acute toxicity), decreased feed consumption (as little as 20% of the normal feed intake) prior to death, and secondary air sacculitis. Histopathology revealed edema and necrosis of the proximal tubules of the kidneys and no changes in the liver or other organs. Suspect feed containing 2 ppm ochratoxin A increased uric acid levels in serum when fed to poults in the laboratory. The episodes in laying hens were characterized by reduced egg production, poor egg shell quality, and nephropathy. The episodes in broiler chickens were characterized by poor growth rate, poor feed conversion efficiency, poor pigmentation, nephropathy, and increased incidence of air sacculitis. Obtaining feed and ingredients free of ochratoxin, cleaning the feed and ingredient handling equipment, and adding antifungal agents to the feed proved beneficial. Eight of the 9 episodes were traced to the corn supply and the ninth episode was traced to corn gluten meal that became contaminated during storage after manufacture. Evidence was obtained that the ochratoxin was unstable and declined in concentration during storage. Aqueous acetone was a better solvent for extracting ochratoxin than was the recommended phosphoric acid: chloroform. The ochratoxin extracted from high potency samples consisted of ochratoxins A, B, and C in ratios of about 90:8:2.

Animals↗
PubMed1981

Synergism between aflatoxin and ochratoxin A in broiler chickens.

A 2 X 2 factorial experimental design consisting of four treatments (0, 2.5 microgram/g aflatoxin, 2.0 microgram/g ochratoxin A, and 2.5 microgram/g aflatoxin + 2.0 microgram/g ochratoxin A) with six replicates of 10 birds each was used to evaluate the synergism between aflatoxin and ochratoxin A. The chicks (Hubbard X Hubbard) were maintained on these dietary treatments from hatching until they reached 3 weeks of age, when the experiment was terminated. The size of the liver, spleen, pancreas, and proventriculus was significantly (P less than .05) altered by the individual toxins; however, a synergistic effect on the size of these organs was not observed. The kidney and gizzard were sensitive to the coincident exposure to these mycotoxins and were significantly (P less than .05) enlarged. The kidney was the most sensitive organ to the combined toxicity of aflatoxin and ochratoxin A, and nephropathy was the most important characteristic of this interaction. The synergism between aflatoxin and ochratoxin A significantly (P less than .05) decreased growth rate and numerically increased mortality, demonstrating the enhanced toxicity of cocontaminated feed. Liver lipid levels were significantly (P less than .05) increased by aflatoxin and decreased by ochratoxin A. The interaction of both mycotoxins on this parameter was significant (P less than .05) and the combined effect demonstrates that ochratoxin A inhibited lipid accumulation normally induced by aflatoxin. The data show that toxicity-enhancing synergisms exist between mycotoxins and that symptom patterns are altered during multiple mycotoxicoses. The data also demonstrate that nephropathy is the primary effect of this interaction and, thus, is of diagnostic importance.

Aflatoxins↗