Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/11/1999
Publication Date: N/A
Interpretive Summary: An outbreak of rickets occurred in our facility and prompted studies on the cause. Turkey poults became lame at 2 weeks of age and were diagnosed as having rickets, with soft and rubbery bones and beaded ribs. The feed contained adequate levels of minerals and vitamin D, therefore, this outbreak of rickets was characterized as field rickets. To determine if an infectious agent was the cause, the litter in the pens of affected poults was added to new feed, and an intestinal homogenate made from affected poults was used to challenge poults. These poults did not develop field rickets. In another study, the feed that was eaten by the poults that developed field rickets (suspect feed) was feed to new poults as well as new feed. The poults consuming the suspect feed developed field rickets, and the suspect feed was found to be toxic. The toxicity of the suspect feed was characterized by decreasing body weight, and affecting the liver, pancreas, kidney, and bursa of Fabricius. A third study was conducted where the suspect feed was diluted with new feed. This study confirmed that high concentrations of the suspect feed caused field rickets and was toxic to the poults. These data demonstrated that the suspect feed, although adequate in mineral and vitamin D levels, was the cause of this outbreak of field rickets. The suspect feed was also toxic to the poults. These data support the hypothesis that field rickets can be caused by toxic contaminants in feed, which are thought to be mycotoxins. Because of the demonstrated toxicity of this suspect feed to the liver and kidney, where vitamin D is activated, it is likely that field rickets developed in these poults through the inhibition of vitamin D activation.
Technical Abstract: An outbreak of field rickets in turkeys prompted studies on the cause. To determine if this condition was caused by an infectious agent an experiment with 4 treatments and 2 replicate pens of 10 poults was conducted. The poults were fed newly manufactured feed, a diet containing control feed and 5% clean litter, a diet containing 5% litter from pens of affected poults, and poults challenged with an intestinal homogenate from poults with field rickets. Field rickets did not develop. The feed in the original outbreak had adequate vitamin D, calcium, and phosphorus but was suspect. A second study with 4 replicate pens of 25 poults fed the suspect feed or new feed was conducted. Poults fed the suspect feed had a decrease in body weights, and an increase in the relative weight of the liver, pancreas, kidney, and bursa of Fabricius, bone ash was decreased, and there were changes in clinical chemistries. In the third study, there were 5 dietary treatments with 2 replicate pens of 25 poults fed new feed, new feed mixed with 25, 50, and 75% suspect feed, or 100% suspect feed. Body weights of the poults consuming 100% suspect feed were decreased, as was the relative weight of the liver, pancreas, and bursa of Fabricius, the relative weight of the kidney increased. Overt field rickets, a decrease in bone ash, and changes in hematology and blood chemistry were observed in the poults consuming 100% of the suspect feed. Feed from the original outbreak of field rickets could induce field rickets, since this feed contained adequate vitamin D, calcium, and phosphorus, the cause of this outbreak is thought to be a feed contaminant that affects vitamin D, calcium, or phosphorus utilization.