Evaluation of XPC and prototypes on aflatoxin-challenged broilers.
Various products and prototypes were added to poultry diets during an aflatoxin challenge on growth and histological parameters. Male broiler chicks were randomly assigned to 8 treatment groups with 8 replicates/treatment and 3 birds/replicate. Treatments were as follows: 1) negative control containing no aflatoxin (NC); 2) positive control containing aflatoxin (PC); 3) 0.1% glucomannan mycotoxin standard industry ameliorator (STD); 4) 0.1% prototype A, a proprietary mixture of a Saccharomyces cerevisiae product and diatomaceous clay; 5) 0.2% prototype A; 6) 0.15% prototype B, a proprietary mixture of a S. cerevisiae product and diatomaceous clay (PB); 7) 0.0625% XPC (S. cerevisiae fermentation product); and 8) 0.125% XPC (XPC2). All treatments except NC contained 2,280 +/- 102 ng/g of aflatoxin and were fed for 28 d. Body weight and feed intake were measured weekly. Livers were collected on d 28, weighed, and used for histopathological evaluation. Beginning weights were similar across treatments, but BW were lower (P </= 0.05) than NC for all treatments except PB and XPC2. Total feed intake was lower (P </= 0.05) only for PC and STD compared with all other groups. Feed efficiency was not significantly (P >/= 0.05) different among the treatment groups. Liver weights relative to BW were higher (P </= 0.05) for all treatments compared with NC. Liver vacuolar lesions were significantly higher (P </= 0.05) than NC for the PC, STD, 0.1% prototype A, and 0.0625% XPC groups. However, vacuolar lesions in the 0.15% prototype B, PB, and XPC2 treatments were not significantly different (P >/= 0.05) compared with NC. Overall, BW gain in treatment groups PB and XPC2 was not different from NC and that corresponded to protective effects against liver lesions. Benefits observed during an aflatoxin challenge when broilers were supplemented with XPC, a fermentation product that does not contain any adsorbents, may be attributed to something other than adsorption as a primary mechanism.
Osweiler
G D
GD
Department of Veterinary Diagnostic and Production Animal Medicine, Iowa State University, Ames, IA, USA. osweiler@iastate.edu
Jagannatha
S
S
Trampel
D W
DW
Imerman
P M
PM
Ensley
S M
SM
Yoon
I
I
Moore
D T
DT
D000348:Aflatoxins / Q000633:toxicity*; D000821:Animal Feed; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy / Q000662:veterinary; D002645:Chickens; D007692:Diatomaceous Earth / Q000494:pharmacology*; D004032:Diet / Q000662:veterinary; D019587:Dietary Supplements; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008297:Male; D009929:Organ Size; D011201:Poultry Diseases / Q000139:chemically induced*; D012441:Saccharomyces cerevisiae / Q000378:metabolism*; D015430:Weight Gain / Q000187:drug effects
D000348:Aflatoxins; D007692:Diatomaceous Earth