Biomedical subjects

W E Huff

Publications and source records attributed to W E Huff.

135 records · Page 8Linked to original sources

PubMedDate not supplied

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. II. Ringneck pheasant.

Ringneck pheasants were fed diets containing 1.25, 2.5, or 5 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Severe toxin-induced mortality was seen during the first to third weeks with 2.50 and 5.00 ppm aflatoxin (92.5% and 97.5%, respectively), compared with the mortality in control pheasants fed no toxin (0%). Slight mortality (less than or equal to 5%) was seen with OA and T-2 toxin. Body weights were significantly decreased by the lowest level (1.25 ppm) of aflatoxin by 2 weeks of age, by the two highest levels of aflatoxin by 1 week of age, and by 16 ppm T-2 toxin by 1 week of age. The feed-conversion ratio was increased by 2.50 and 5.00 ppm aflatoxin compared with the feed-conversion ratio in controls, although high mortality may have influenced the results. Aflatoxin had no effect on liver weight, but OA increased kidney weight in 3-week-old pheasants. Mouth lesions were seen in some of the pheasants fed T-2 toxin.

Aflatoxins↗

PubMedDate not supplied

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. III. Bobwhite and Japanese quail.

Bobwhite and Japanese quail were fed diets containing 1.25, 2.50, or 5.00 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Aflatoxin induced mortality in bobwhites during the second and third week with 1.25 ppm (10%), 2.50 ppm (30%), and 5.00 ppm (40%), and during the same period with T-2 toxin at 8 ppm (20%) and 16 ppm (22.5%). Body weights of bobwhite quail were significantly decreased by the two higher levels of aflatoxin by 2 weeks of age, and by the two higher levels of T-2 toxin by 1 week of age. In Japanese quail, only the highest level of aflatoxin and T-2 toxin reduced body weight (by 3 weeks and by 1 week of age, respectively), and even then to a much lesser extent than in bobwhites (less than 10%). Aflatoxin did not affect feed-conversion ratio (FCR) in bobwhite quail, but the two higher levels of T-2 toxin increased FCR. None of the toxins induced mortality or increased the FCR in Japanese quail. Aflatoxin increased liver weight in both bobwhite and Japanese quail. OA increased kidney weight in 3-week-old Japanese quail but had no effect on the kidney weight of bobwhite quail. Mouth lesions were progressively more severe in bobwhite quail fed increasing levels of T-2 toxin, but lesions were far less severe in Japanese quail.

Aflatoxins↗

PubMedDate not supplied

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 0.05) reduced body weights at 7 through 28 days of age. Total serum calcium and biochemical enzyme activities were found to be altered at 35 days of age. In addition, the high-altitude group had significantly (P less than or equal to 0.05) higher erythrocyte counts, hematocrits, and hemoglobin at 14, 21, 28, and 35 days of age and higher serum inorganic phosphorus at each weekly sample time than birds at the low altitude. Total mortality was 20.3% at 2133 meters and 4.6% at 100 meters. The incidence of ascites syndrome in the high-altitude group ranged from 16.6% to 61.1% during the 5-week experimental period.

Altitude↗

PubMedDate not supplied

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. I. Chukar partridge.

Chukar partridges were fed diets containing 1.25, 2.5, or 5 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Toxin-induced mortality was seen during the third week with 4 ppm OA (12.5%) and 16 ppm T-2 toxin (15%), compared with the mortality in control chukars fed no toxin (2.5%). Body weights were significantly decreased by the highest level of aflatoxin at 3 weeks of age, by the highest level of OA by 2 weeks of age, and by 8 and 16 ppm T-2 toxin by 1 week of age. Aflatoxin did not affect liver weight and OA did not increase kidney weight in 3-week-old chukars. There was a slight decrease in kidney weight in chukars fed 4 ppm OA; however, the decrease was related to the decrease in body weight produced by the toxin. Mouth lesions were seen at all levels of T-2 toxin fed.

Aflatoxins↗

PubMedDate not supplied

Identification of transforming growth factor-beta and interleukin-6 in chicken ascites fluid.

Ascites fluids from chickens were analyzed for the occurrence of transforming growth factor-beta (TGF-beta) and interleukin-6 (Il-6) using the mink lung epithelial cell inhibition and B9 hybridoma proliferation assays, respectively. Both of these cytokines were significantly elevated in ascites fluids (TGF-beta, 0.129 +/- 0.017 ng/mg protein; Il-6, 0.054 +/- 0.011 ng/mg protein) relative to serum (TGF-beta, 0.005 +/- 0.003 ng/mg protein; Il-6, < 0.002 ng/mg protein) derived from the same individual birds. TGF-beta occurred in a latent form and required activation by heat or acid (heat, 100%; non-activated, 5.2 +/- 1.1%; acid-activated, 89.5 +/- 12.3%). Heat treatment destroyed Il-6 activity. Both TGF-beta and Il-6 activities could be neutralized by antibodies directed against the recombinant human counterpart of these cytokines. Increasing dilutions of ascites fluid caused proportionate decreases in cytokine activities. Il-6 activity was further characterized by gel filtration using high-pressure liquid chromatography, which yielded a peak of biological activity corresponding to an approximate molecular weight of 35,000. These data suggest that ascites fluid may be an interesting biological model and source for studying avian cytokines and their physiological relevance.

Animals↗

PubMedDate not supplied

A longitudinal study of green-liver osteomyelitis complex in commercial turkeys.

Two flocks of Nicholas tom turkeys from separate farms with histories of above-average condemnations for turkey green-liver osteomyelitis complex (TOC) were studied throughout a 16-week growout. Fifty birds from each farm were necropsied each week for 15 weeks, and birds that had green livers, osteomyelitis in the proximal tibia, or swollen joints were cultured for aerobic bacteria along with an equal number of control birds. At processing, TOC lesions and green livers were obtained for bacterial culture and histopathology. Green-liver-associated TOC was not observed until the turkeys were 9 or 10 weeks of age. The incidence of TOC was higher on one farm, which also had a higher incidence of airsacculitis, higher early and weekly mortality, seroconversion to Newcastle disease virus and Mycoplasma meleagridis, and significantly higher average body weights, relative spleen weights, and relative liver weights. Both farms had a high incidence of intestinal lesions and infestation with Ascaridia dissimilis. Histological evaluation of green livers revealed hyperplasia of bile ducts, dilation of sinusoids, and pigment-containing Kupffer's cells, some of which stained positive for iron. The bacterial isolates most frequently cultured from bones and livers were pleomorphic gram-variable coccobacilli, which grew visible colonies only after a series of subcultures and extended incubation.

Animals↗

PubMedDate not supplied

A survey of two commercial turkey farms experiencing high levels of liver foci.

Two turkey farms that had previously experienced high levels of liver condemnations at slaughter were monitored through one complete growout cycle. Liver foci appeared at both farms by week 2. More than 80% of the liver foci sampled did not have any aerobic or facultative bacteria isolated from the lesions. Low numbers of Ascaridia dissimilis larvae were found on both farms by week 3 in the growout. The patterns for the ascaridiasis at both farms were similar, although one of the farms had a higher number of ascarids earlier than the other. Neither farm had high levels of adult ascarids present, although the average larval burden was high. Piperazine was administered at both farms on multiple occasions, but there were no significant decreases in the level of adult ascarids following administration. There was no apparent development of immunity, since all stages of the life cycle remained stable, even late in the growout. The simultaneous appearance of the liver foci and the A. dissimilis indicate that the ascarids may be responsible for the hepatic pathology.

Animals↗

PubMedDate not supplied

Histologic study of hepatic lesions in two turkey flocks.

Hepatic lesions were studied in two turkey flocks by euthanatizing 50 birds a week from the ages of 1 through 15 wk. Samples of liver that contained lesions and samples of duodenum, pancreas, ileum, and cecal tonsil were examined histologically. Lymphocytic infiltrations made up 82% and 75% of the hepatic lesions, and granulomas occurred in 18% and 25% of the livers. Nematode larvae were present in 12% and 15% of the hepatic lesions.

Aging↗

PubMedDate not supplied

Cell death in avian tibial dyschondroplasia.

Tibial dyschondroplasia (TD) is a local defect of growth plates in fast-growing poultry where the transitional zone cartilage fails to resorb and persists as an avascular plug that prevents endochondral bone formation. We compared the differences in the cartilages from normal and TD-affected growth plates using the reduction of MTS to assess cartilage viability. Chondrocyte apoptosis was determined using biochemical measurement of DNA fragmentation, and in situ labeling of nuclei with fluorescein-dUTP using terminal deoxynucleotide transferase (TdT)-mediated nick end labeling (TUNEL) of isolated chondrocytes and growth plate sections. The TD-affected cartilage showed a significantly lower level of MTS reduction and a decrease in trichloroacetic acid (TCA)-precipitable DNA content. The TD cartilages had a higher percentage of fragmented DNA, which was also evident with agarose gel electrophoresis. A significantly higher number of chondrocytes isolated from TD-affected cartilages had condensed morphology, shrunken nuclei with little cytoplasm, and were TUNEL positive as identified by the incorporation of fluorescein-dUTP into the nuclei. In vivo results similarly showed a significant population of chondrocytes in transition zones undergoing condensation and apoptosis as determined by in situ TUNEL staining of growth plate sections. Normal growth plates, under similar conditions, showed no significant apoptosis of chondrocytes from hypertrophic and chondrolyzing zones. The condensation and apoptotic cell death may be responsible for the reduction of growth plate viability as well as the reduction in DNA content and increased DNA fragmentation. While the cause of the pathogenesis of TD is unknown, it appears that the aberrant death of chondrocytes in hypertrophic regions of growth plates may be responsible for the accumulation of cartilage and the arrest of endochondral bone formation.

Animals↗