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Biomedical subjects

W E Huff

Publications and source records attributed to W E Huff.

At least 127 records · Page 7Linked to original sources
PubMed1980

Evaluation of bone strength during aflatoxicosis and ochratoxicosis.

Young chickens were fed graded levels of aflatoxin (0, 0.625, 1.25, 2.5, 5.0, and 10.0 mug/g of diet) or ochratoxin (0, 0.5, 1.0, 2.0, 4.0, and 8.0 mug/g of diet), and the breaking strength, displacement before failure, and diameter of their tibias were determined. Breaking strength was decreased at growth inhibitory levels of aflatoxin (2.5 mug/g) and ochratoxin (2 mug/g), whereas a reduction in diameter required higher levels (5.0 and 4.0 mug/g, respectively). Bones from birds with ochratoxicosis selected to have diameters equal to control bones had lower breaking strength. In an attempt to negate mathematically the effect of decreased diameter and bias in any selection process, stress at time of failure of the bones was calculated and found to be decreased by feeding aflatoxin but not ochratoxin. Total displacement of bones before breaking was increased significantly (P < 0.05) by both toxins at the highest levels administered, but this increase was primarily the result of an increase in displacement from the start of failure to complete failure. Increased displacement associated with both toxicoses was equal in bones selected to be of equal diameter or in bones from the same treatment but of different diameters. However, calculation of modulus of elasticity which is corrected for diameter revealed aflatoxin had no effect whereas ochratoxin tripled the effect. These data indicate that the material properties of bones can be altered during mycotoxicoses and suggest yet another way in which mycotoxins are detrimental to animal health.

Aflatoxins↗
PubMed1980

Evaluation of tibial dyschondroplasia during aflatoxicosis and feed restriction in young broiler chickens.

Graded levels of aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 microgram of toxin per gram of feed) were incorporated into a broiler starter ration that was fed from day-old to 3 weeks of age. Both tibias were removed from the birds, tibial dyschondroplasia lesions were scored, and the incidence of lesions reported. Both the incidence and severity of tibial dyschondroplasia decreased significantly (P less than .05) at the aflatoxin levels of 2.5, 5.0, and 10.0 ppm. In a second experiment, birds received a broiler starter ration either ad libitum or feed restricted by 23% of the feed consumed by the controls. The feed-restricted birds' body weights and the severity and the incidence of tibial dyschondroplasia decreased to values comparable with those of birds receiving 5.0 ppm aflatoxin. These data suggest that either feed consumption or growth rate, or both, plays a major role in the initiation of tibial dyschondroplasia and tibial dyschondroplasia is not a result of direct intervention of aflatoxin in bone development.

Aflatoxins↗
PubMed1980

Evaluation of penicillic acid for toxicity in broiler chickens.

Penicillic acid is a mycotoxin produced by various fungi. It may occur in high concentrations in corn and can also be produced concomitantly with other mycotoxins in poultry feed. This mycotoxin was evaluated for its toxicity in broiler chickens by feeding graded concentrations (0, 100, 200, and 400 microgram/g of diet) to 4 groups of 10 birds per treatment. No significant (P greater than .05) effects were measured on growth rate, feed conversion, relative size of pancreas, spleen, liver, heart, bursa, or kidney or on hemoglobin, packed cell volume, liver lipid, plasma protein, or glucose. The only significant effects were a slight reduction in the size of the proventriculus and gizzard at dose levels of 200 and 400 microgram/g. Neither the salt nor lactone forms of penicillic acid had any detectable effect. The acute oral LD50 for the sodium salt form was 92 +/- 9 mg/kg. These data suggest that penicillic acid by itself has little toxicity (less than 1% of that of aflatoxin) in chickens.

Animals↗
PubMed1980

Discrepancies between bone ash and toe ash during aflatoxicosis.

Graded levels of aflatoxin (0, .625, 1.25, 2.5, 5.0, and 10.0 micrograms/g diet) were incorporated into a broiler-starter ration and fed to chicks from 1 day to 3 weeks of age. The tibias and middle toes were removed, and both bone ash and toe ash were determined. Toe ash significantly (P less than .05) increased at the aflatoxin levels of 2.5 ppm and above, while bone ash significantly (P less than .05) deceased at the same aflatoxin levels (2.5 ppm and above). The increase in toe ash could be partially attributed to a significant (P less than .05) decrease in toe lipid levels at the aflatoxin levels of 2.5 ppm and above. The data indicate that aflatoxin inhibits bone mineralization. The data also show that toe ash does not in all experimental designs reflect bone ash and that data interpreted solely on toe ash determination may not accurately reflect bone mineralization.

Aflatoxins↗
PubMed1979

Decreased glycogen mobilization during ochratoxicosis in broiler chickens.

Graded doses of pure ochratoxin A (0, 0.5, 1.0, 2.0, 4.0, and 8.0 microgram of toxin per g of feed) were incorporated into a commercial diet which was fed to chickens from hatching to 3 weeks of age, at which time the experiments were terminated. Liver glycogen levels were elevated significantly (P less than 0.05) by 4.0 and 8.0 microgram/g but not lower doses. Glucagon stimulation of glycogen mobilization was inhibited at the same concentrations. Histopathological examination revealed cytoplasmic but not nuclear deposits of glycogen in cells at the periphery of liver lobes. These data demonstrated that ochratoxin inhibited glycogenolysis. Impaired ability to generate glucose from glycogen could account for the increased susceptibility to cold stress previously reported to occur in ochratoxicosis. Based on present and prior observations, it seems possible that ochratoxin induces a syndrome which mimics the glycogen storage disease of type X which is caused by a deficiency in the cyclic AMP-dependent enzyme of the glycogenolytic enzymatic cascade.

Animals↗
PubMed1979

Ochratoxin A-induced iron deficiency anemia.

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.

Anemia, Hypochromic↗
PubMed1979

A leucocytopenia induced in chickens by dietary ochratoxin A.

Ochratoxin A was fed (0, .5, 1.0, 2.0, 4.0, and 8.0 microgram/g) to broiler chickens from day-old to three weeks of age when the birds were bled and total leucocyte and differential counts were performed. Ochratoxin A significantly (P less than .05) reduced leucocyte counts at every dose level of ochratoxin A administered. The leucocytopenia was characterized by an increase in the relative concentration of heterophils and decrease in the relative concentration of lymphocytes. From total leucocyte and differential leucocyte counts the number of circulating cells was calculated for each type of leucocyte. The total number of circulating lymphocytes of blood decreased significantly (P less than .05) at every dose level of ochratoxin A administered, and the number of monocytes decreased at 2.0 microgram/g and above. However, the number of circulating heterophils was not altered. These data demonstrated that ochratoxin A induced a severe leucocytopenia (lympocytopenia primarily and monocytopenia to a lesser extent) and implied that the functioning of the immune system might be altered.

Animals↗
PubMed1975

Nephrotoxicity of dietary ochratoxin A in broiler chickens.

Graded doses of pure ochratoxin A (0,0.5,1.0,2.0,4.0, and 8.0 mug of toxin per g of feed) were incorporated into a commercial diet which was fed to chicks from 1 day to 3 weeks of age, at which time the experiments were terminated. Growth was inhibited at 2.0 4,0, and 8.0 mug/g, whereas the kidneys were enlarged at doses of 1.0 mug/g and above. Renal function as measured by clearance of phenol red was decreased 15 and 31% by doses of 4.0 and 8.0 mug/g, respectively. Uric acid was increased 38 and 48% over the control values by doses of 4.0 and 8.0 mug/g, respectively. The plasma electrolytes Na, Cl,Ca, and K were measured; however, only K was significantly ( P smaller than 0.05) altered, showing a decrease at doses of 4.0 and 8.0 mug/g. The percentage dry weight of the kidneys decreased significantly at dose levels of 4.0 and 8.0 mug/g, indicative of edema. Histological examination of kidney sections gave the impression of edema and some tubular necrosis. Pathological changes were observed at all dose levels. These data demonstrate that ochratoxin A is a severe nephrotoxin in young broiler chickens.

Animal Feed↗
PubMed1975

Liver lipid content of twenty varieties of laying hens from three confinement systems.

Average liver lipid values were determined for 20 varieties of 71-week old laying hens managed in 3 confinement systems of the 1972-73 North Carolina Random Sample Laying Test. There were highly significant differences in liver lipid atrributable to variety, to confinement system, and a significant variety X system interaction. Four varieties had consistently high and five had consistently low liver lipid values in all 3 confinement systems. Varietymeans ranged from 25.8 to 49.0% liver lipid on a dry weight basis. Hens confined 2/cage had slight but significantly higher liver lipid than hens 7/cage or in floor pens. Liver lipid was positively correlated with body weight in hens 2/cage and in floor pens. There were no significant correlations of liver lipid with egg production or mortality. A frequency distribution of individual liver lipid values revealed a continuous distribution from 15.4 to 65.4with a pronounced skew to the right of the mean of 38.2%. Neither a fatty liver syndrome nor liver hemorrhage syndrome was reported for any of the flocks during the laying year. The normal range of liver lipid values for hens 71 weeks of age appears to be between 25 and 49 g. of lipid per 100 g. of dry liver weight.

Animals↗
PubMed1975

Decreased plasma carotenoids during ochratoxicosis.

Two field cases of underpigmented broilers were reported; investigation revealed the presence of ochratoxin but not aflatoxin. A laboratory experiment revealed that dietary ochratoxin A at levels of 4.0 and 8.0 mug./g. lowered significantly (P less than 0.05) the concentration of plasma carotenoids which are an accepted indicator of carcass pigmentation.

Animals↗
PubMed1975

The interaction of ochratoxin A with some environmental extremes.

Presently, ochratoxin is the most potent mycotoxin studied in chickens. The possibility that ochratoxin can interact with environmental extremes was investigated by incorporating pure ochratoxin A (0, 0.5, 1.0, 2.0, 4.0, and 8.0 mug./g. feed) into the diet of 4 replicates of 10 birds from hatching until 3 weeks of age. There was a significant (P less than 0.05) decrease in the mean survival times of birds exposed to 4 degrees C. and 90% relative humidity at dose levels of 4.0 and 8.0 mug./g. However, birds exposed to 43 degrees C. and 45% relative humidity had a significantly (P less than 0.05) prolonged mean survival time at 8.0 mug./g. Birds given drinking water containing 2% NaCl had a significant (P less than 0.05) decrease in mean survival time at 8.0 mug./g. These data suggest that ochratoxin like aflatoxin can interact with other agents to produce syndromes not attributable to each alone.

Animals↗
PubMed1975

Effects of dietary aflatoxin on certain egg yolk parameters.

Aflatoxicosis was induced in laying hens by incorporating graded amounts of aflatoxin into a commercial layer ration (0, 1.25, 2.5, 5.0, and 10.0 mug./g. of feed). After four weeks liver size and liver lipid were increased by aflatoxin while egg production and egg size were decreased (P less than 0.05). Total yolk weight and the yolk as percent of total egg weight were lowered (P less than 0.05). The dry weight and lipid content of the yolk were not affected. Yolk and plasma carotenoid concentrations were elevated (P less than 0.05). The data suggest that plasma and yolk lipids respond to the inhibition of lipid synthesis and transport from the liver by aflatoxin, but plasma and yolk carotenoids which are dietary in origin necessarily increase when egg production decreases during aflatoxicosis.

Aflatoxins↗
PubMedDate not supplied

Changes in serum ovotransferrin levels in chickens with experimentally induced inflammation and diseases.

A competitive enzyme immunoassay was developed to measure the changes in serum levels of ovotransferrin (OTF) during inflammation and infectious diseases in chickens. The assay is based on the competition of serum OTF with a fixed concentration of biotin-labeled OTF to bind to a rabbit anti-chicken transferrin antibody immobilized on microtiter wells. After several washing steps, the antibody-bound biotinylated OTF is probed with streptavidin-horseradish peroxidase conjugate (HRP) followed by a colorimetric detection of the HRP activity. The relative changes in the optical density of color are plotted against the competing concentrations of OTF with logarithmic regression to generate a standard curve that is used to determine the concentrations of OTF in unknown samples. Serum had no effect on the measurement of OTE By this method, the time course changes of serum OTF levels in 4-wk-old male broiler chickens that were subjected to inflammation by croton oil injection were measured. The results showed croton oil-induced inflammation elevated serum OTF levels at 16 hr postinjection. OTF levels reached a peak by 72 hr, remained high through 120 hr, and returned to a basal level of olive oil-injected controls by 240 hr. There were no changes in serum OTF levels at any of the above time points in olive oil-injected control chickens. For studies with poultry diseases, specific-pathogen-free (SPF) male chickens were challenged with known bacterial and viral pathogens, and serum was collected at the height of the infection, i.e., 7 days after the challenge. Compared with uninjected controls, the SPF chickens challenged with Escherichia coli, fowl poxvirus, respiratory enteric orphan virus, infectious bursal disease virus, infectious bronchitis virus, or infectious laryngotracheitis virus had higher levels of OTF in serum. Inflammation-induced changes in serum OTF levels were also evident in the changes in the density of a 65-kD band protein corresponding to OTF. These results demonstrate that serum OTF may be a nonspecific clinical marker of inflammation associated with traumatic or infectious avian diseases.

Animals↗
PubMedDate not supplied

Bacteriophage treatment of a severe Escherichia coli respiratory infection in broiler chickens.

A bacteriophage to a serotype 02, nonmotile Escherichia coli was isolated from municipal waste treatment facilities and poultry processing plants. A study was conducted to determine the efficacy of multiple vs. single intramuscular (i.m.) injections of bacteriophage to treat a severe E. coli respiratory infection. The birds were challenged at 7 days of age by injection of 6 x 10(4) colony-forming units (cfu) of E. coli into the thoracic air sac followed by an i.m. injection into the thigh with either heat-killed or active bacteriophage. There were 16 treatments with three replicate pens of 10 birds. There were four control treatments, which included untreated birds, birds injected with either heat-killed or active bacteriophage, and birds challenged only with E. coli. In the remaining treatments, birds were injected with heat-killed or active bacteriophage either once immediately after E. coli challenge or immediately after challenge and at 8 and 9 days of age, once at 8 days of age or at 8, 9, and 10 days of age, and once at 9 days of age or at 9, 10, and 11 days of age. Mortality was significantly decreased from 57% to 13% in the birds given a single i.m. injection of bacteriophage immediately after E. coli challenge, and there was complete recovery in birds treated immediately after challenge and at 8 and 9 days of age, which was a significant improvement from the single injection treatment. There was a significant reduction in mortality from 57% to 10% in the birds treated with bacteriophage once at 8 days of age and those birds treated at 8, 9, and 10 days of age, with no difference between single or multiple treatments. The mortality in the single or multiple phage treated birds that started at 9 days of age was reduced from 57% to 28% and 27%, respectively, but was not statistically different from the control. These data suggest that bacteriophage can be an effective treatment when administered early in this experimental E. coli respiratory disease and that early multiple treatments are better than a single treatment. The efficacy of bacteriophage treatment diminishes as it is delayed, with no difference between single or multiple treatments. Bacteriophage may provide an effective alternative to antibiotics, but like and biotic therapy, the effectiveness of phage to rescue animals decreases the longer treatment is delayed in the disease process.

Analysis of Variance↗
PubMedDate not supplied

The effects of water supplementation with vitamin E and sodium salicylate (Uni-Sol) on the resistance of turkeys to Escherichia coli respiratory infection.

The objective of this study was to determine the prophylactic efficacy of two commercial products, soluble vitamin E and soluble sodium salicylate (Uni-Sol), in an Escherichia coli respiratory challenge. The drinking water of male turkey poults was nonsupplemented or supplemented with either vitamin E or Uni-Sol or a combination of both at dosages recommended by the manufacturer. There were 110 birds in each of the four treatments, housed in four floor pens per treatment. At 5 wk of age, birds in half of the pens were challenged with an air sac inoculation of approximately 50 colony-forming units of E. coli. Water treatment commenced 5 days before challenge and continued for 2 wk after challenge, when birds were necropsied. All water treatments prevented the decrease in body weight due to E. coli challenge; however, either vitamin E or Uni-Sol alone, but not the combination of the two, decreased body weight in nonchallenged controls. Either vitamin E or Uni-Sol treatment alone, but not the combination of the two, significantly decreased mortality and air sacculitis scores of challenged birds, and all treatments decreased the isolation rates of E. coli from the liver. All treatments protected liver, spleen, and bursa weights (relative to body weight) from the effects of E. coli challenge, and Uni-Sol alone or vitamin E with Uni-Sol protected relative heart weights from the effect of challenge. Uni-Sol treatment alone increased the main effect mean total leukocyte counts and the number and percent of lymphocytes. Uni-Sol in combination with vitamin E increased the number of lymphocytes of challenged birds. Uni-Sol alone decreased the main effect mean heterophil/lymphocyte ratio (H/L) ratio, whereas vitamin E alone increased the H/L ratio of challenged birds. These results indicate that treatment of turkey poults with vitamin E or Uni-Sol prior to and during the stressful events that can lead to colisepticema may decrease disease incidence and mortality.

Administration, Oral↗
PubMedDate not supplied

Viral and bacterial agents associated with experimental transmission of infectious proventriculitis of broiler chickens.

Proventriculitis of broilers can be reproduced by oral inoculation of day-old chicks with a proventricular homogenate from affected 3-wk-old broilers. The objective of the following studies was to isolate from this homogenate viral and bacterial isolates that could produce proventriculitis. A monoclonal antibody to infectious bursal disease virus (IBDV) was used to precipitate virus from the homogenate. A primary chicken digestive tract cell culture system was also used to isolate virus from a 0.2-microm filtrate of the homogenate, and a bacterium was also isolated from the homogenate. In trial 1, day-old birds were orally inoculated with either proventriculus homogenate or monoclonal antibody immunoprecipitated IBDV (MAB-IBDV). At 4, 7, 14, and 21 days postinfection (PI), 12 birds from each treatment group were subjected to necropsy. In trial 2, day-old birds were orally inoculated with either infectious proventriculus homogenate, suspect virus isolated in cell culture and propagated in embryo livers and spleens, or a bacterial isolate. Twelve birds from each treatment were subjected to necropsy at days 7, 14, 21, and 28 PI. In trial 3, treatments were maintained in negative pressure isolation chambers, and an additional treatment included virus plus bacterial isolate. Twenty-four birds from each treatment were subjected to necropsy at day 21 PI. In trial 1, infectious homogenate decreased body weight and relative gizzard weights at 4, 7, 14, and 21 days PI. Proventriculus relative weight was increased at days 7, 14, and 21 PI, and proventriculus lesion scores were increased at days 14 and 21 PI. Bursa/spleen weight ratios were decreased at day 14, and feed conversion was increased at days 4 and 21. The MAB-IBDV treatment decreased proventriculus and gizzard relative weights at day 4 PI, increased proventriculus lesion scores and bursa/spleen weight ratios at day 14, and decreased heterophil/lymphocyte ratios at day 21. In trial 2, all infected birds had significantly higher mean relative proventriculus weights at 21 days PI and had higher 4-wk mean proventriculus scores as compared with both control groups. In trial 3, birds treated with homogenate and birds treated with both suspect virus and the bacterial isolate had significantly higher proventriculus lesion scores; higher relative weights of proventriculus, gizzard, liver, and heart; lower body weights; and lower relative bursa weights compared with the saline control group. These studies suggest that infectious proventriculitis has a complex etiology involving both viral and bacterial infection.

Animals↗