An outbreak of field rickets in turkeys prompted studies on the cause. Ln E
xperiment 1, there were four treatments with two replicate pens of 10 poult
s per pen. The treatments consisted of poults fed newly manufactured feed (
control), poults fed a diet containing control feed and 5% clean litter, po
ults fed control feed and 5% litter from the pens of affected poults, and p
oults challenged with an intestinal homogenate by gavage. Field rickets did
not develop with these treatments. The feed was suspect, and, in Experimen
t 2, poults were either fed the suspect feed or newly manufactured feed. Th
ere were four replicate pens of 25 poults per pen. Poults fed the suspect f
eed had a decrease (P less than or equal to 0.05) in BW at 1, 2, 3, and 4 w
k of age; an increase in the relative weight of the liver, pancreas, kidney
, and bursa of Fabricius; acid a decrease in bone ash. There were changes i
n clinical chemistries. Ln the third study, there were five dietary treatme
nts with two replicate pens of 25 poults per treatment. The treatments cons
isted 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% su
spect feed were decreased at 2, 3, and 4 wk as was the relative weight of t
he liver, pancreas, and bursa of Fabricius. The relative weight of the kidn
ey increased. Lameness, a decrease in bone ash, and changes in hematology a
nd blood chemistry were observed in the poults consuming 100% suspect feed.
These data demonstrate that feed from the original outbreak could induce f
ield rickets and was toxic. Because the feed contained adequate vitamin D,
calcium, and phosphorus, the cause of this outbreak of field rickets is tho
ught to be a toxic feed contaminant affecting bone development.