| pubmed-article:10626644 | pubmed:abstractText | An outbreak of field rickets in turkeys prompted studies on the cause. In Experiment 1, there were four treatments with two replicate pens of 10 poults per pen. The treatments consisted of poults fed newly manufactured feed (control), poults fed a diet containing control feed and 5% clean litter, poults fed control feed and 5% litter from the pens of affected poults, and poults challenged with an intestinal homogenate by gavage. Field rickets did not develop with these treatments. The feed was suspect, and, in Experiment 2, poults were either fed the suspect feed or newly manufactured feed. There were four replicate pens of 25 poults per pen. Poults fed the suspect feed had a decrease (P < or = 0.05) in BW at 1, 2, 3, and 4 wk of age; an increase in the relative weight of the liver, pancreas, kidney, and bursa of Fabricius; and a decrease in bone ash. There were changes in clinical chemistries. In the third study, there were five dietary treatments with two replicate pens of 25 poults per treatment. The treatments consisted of poults fed newly manufactured feed; new feed mixed with 25, 50, or 75% suspect feed; or 100% suspect feed. Body weights of poults fed 100% suspect feed were decreased at 2, 3, and 4 wk as was the relative weight of the liver, pancreas, and bursa of Fabricius. The relative weight of the kidney increased. Lameness, a decrease in bone ash, and changes in hematology and blood chemistry were observed in the poults consuming 100% suspect feed. These data demonstrate that feed from the original outbreak could induce field rickets and was toxic. Because the feed contained adequate vitamin D, calcium, and phosphorus, the cause of this outbreak of field rickets is thought to be a toxic feed contaminant affecting bone development. | lld:pubmed |
