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Research on the Probable Cause of an Outbreak of Field Rickets in

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									Research on the Probable Cause of an Outbreak of Field Rickets in Turkeys1

             W. E. HUFF,*,2 G. R. HUFF,* F. D. CLARK,† P. A. MOORE, JR.,* N. C. RATH,* J. M. BALOG,*
                                   D. M. BARNES,† G. F. ERF,† and K. W. BEERS†

 *USDA, Agricultural Research Service, Poultry Production and Product Safety Research Unit, Poultry Science Center and
                 †Department of Poultry Science, University of Arkansas, Fayetteville, Arkansas 72701

ABSTRACT An outbreak of field rickets in turkeys                           chemistries. In the third study, there were five dietary
prompted studies on the cause. In Experiment 1, there                     treatments with two replicate pens of 25 poults per treat-
were four treatments with two replicate pens of 10 poults                 ment. The treatments consisted of poults fed newly manu-
per pen. The treatments consisted of poults fed newly                     factured feed; new feed mixed with 25, 50, or 75% suspect
manufactured feed (control), poults fed a diet containing                 feed; or 100% suspect feed. Body weights of poults fed
control feed and 5% clean litter, poults fed control feed                 100% suspect feed were decreased at 2, 3, and 4 wk as
and 5% litter from the pens of affected poults, and poults                was the relative weight of the liver, pancreas, and bursa
challenged with an intestinal homogenate by gavage.                       of Fabricius. The relative weight of the kidney increased.
Field rickets did not develop with these treatments. The                  Lameness, a decrease in bone ash, and changes in hema-
feed was suspect, and, in Experiment 2, poults were either                tology and blood chemistry were observed in the poults
fed the suspect feed or newly manufactured feed. There                    consuming 100% suspect feed. These data demonstrate
were four replicate pens of 25 poults per pen. Poults fed                 that feed from the original outbreak could induce field
the suspect feed had a decrease (P ≤ 0.05) in BW at 1, 2,                 rickets and was toxic. Because the feed contained ade-
3, and 4 wk of age; an increase in the relative weight of                 quate vitamin D, calcium, and phosphorus, the cause of
the liver, pancreas, kidney, and bursa of Fabricius; and                  this outbreak of field rickets is thought to be a toxic feed
a decrease in bone ash. There were changes in clinical                    contaminant affecting bone development.
                                            (Key words: field rickets, turkeys, poults, feed)
                                                                                                 1999 Poultry Science 78:1699–1702


                      INTRODUCTION                                        multiple causes of field rickets seem reasonable. The ob-
                                                                          jective of these studies was to determine the probable
   We experienced a severe outbreak of rickets in our                     cause of this outbreak of field rickets.
facility with over 90% of the poults affected at 2 wk of
age. This outbreak was characterized by lameness, soft                              MATERIALS AND METHODS
and rubbery bones, and beaded ribs, although more than
adequate levels of calcium, phosphorus, and vitamin D                        The original outbreak of field rickets occurred in an
were present in the diet. Field rickets has been defined                   experiment with 240 male and 240 female turkey poults
as a rachitic condition that occurs even though the diets                 (Nicholas 600s) housed in pine litter floor pens with 20
are adequate in calcium, phosphorus, and vitamin D                        turkeys per pen. Over 90% of these poults became lame
(Hurwitz et al., 1973). Field rickets occurs in all turkey-               at 2 wk of age. Upon necropsy, the ribs were beaded and
producing regions and has been studied by a number of                     the bones were found to be soft and rubbery; rickets
researchers (Hurwitz et al., 1973; Walser et al., 1980; Olson             was diagnosed. The feed had been formulated to meet or
et al., 1981; Riddell, 1983; Bar et al. 1987). The etiology of            exceed NRC recommendations (NRC, 1994). The calcium
field rickets remains unknown, and, given the complexity                   and phosphorus levels of the diet were determined with
of mineral and vitamin D utilization and metabolism,                      an inductively coupled argon emission spectrophotome-
                                                                          ter3 following the manufacturer’s procedures, and the
                                                                          levels were found to be consistent with the formulation
                                                                          (1.22 and 0.77%, respectively). The vitamin D level in the
   Received for publication April 19, 1999.                               diet was also found to be as formulated (2,204 IU) using
   Accepted for publication August 11, 1999.
   1
    Mention of a trade name, proprietary product, or specific equipment    the method of Singh and Bradbury (1988).
does not constitute a guarantee or warranty by the USDA and does             This outbreak of field rickets prompted three studies
not imply its approval to the exclusion of other products that may        to determine the probable cause. In Experiment 1, there
be suitable.
   2
    Correspondence should be addressed to: huff@comp.uark.edu             were four treatments with two replicate pens of 10 male
   3
    Model D, Spectro Analytical Instruments, Inc., Fitchburg, MA 01420.   poults (Nicholas 600). The treatments consisted of a con-


                                                                      1699
1700                                                          HUFF ET AL.
                 TABLE 1. The effect of newly manufactured feed and suspect feed on BW,1 the relative weight of the
                    liver1 and kidney,1 bone strength,2,3 bone ash,2 and serum levels of calcium2 and phosphorus2

               Treatment      BW at 28 d    Liver          Kidney         Strength          Ash           Ca            P

                                                     (% BW)               (N/m × 10 )
                                                                               2        6
                                                                                            (%)                  (mg/dL)
               New feed       1,278 ± 14a   2.39 ± 0.04b   0.41 ± 0.01b   28.6 ± 1.1a       47.3 ± 0.4a   10.6 ± 0.2a   7.6 ± 0.2a
               Suspect feed     544 ± 10b   2.84 ± 0.03a   0.46 ± 0.01a    9.0 ± 0.5b       42.4 ± 0.6b    8.9 ± 0.4b   5.5 ± 0.5b
                   Values within a column with different superscripts differ (P ≤ 0.05).
                 a,b
                 1
                  Values represent the means ± SEM of four replicate pens of 25 poults per pen.
                 2
                  Values represent the means ± SEM of four replicate pens of five poults per pen.
                 3
                  Values for bone strength have been corrected for differences in tibia diameter as described by Huff et al.
               (1980).



trol (newly manufactured feed), the new feed containing                   All data presented as percentages were arc sine trans-
5% litter taken from the pens of the affected poults, the                 formed prior to statistical analysis. Significant differences
new feed containing 5% fresh litter, and challenge with                   among treatments were separated using Duncan’s multi-
1 mL of an intestinal homogenate made from the affected                   ple range test (Duncan, 1955). All statements of signifi-
poults delivered by gavage at 1 d of age. The birds were                  cance are based on the probability level of 0.05.
housed in batteries, and feed and water were available
for ad libitum consumption from 1 d to 4 wk of age.                                                       RESULTS
   In Experiment 2, there were two treatments of either
the feed consumed by the poults that developed field                          In the original outbreak of field rickets, over 90% of the
rickets (suspect feed) or newly manufactured feed. There                  poults were affected, characterized by lameness, beaded
were four pens of 25 male poults (Nicholas 600) in each                   ribs, and rubbery bones, despite an adequate amount of
of the two treatments; again, feed and water were avail-                  calcium, phosphorus, and vitamin D in the diets. There
able for ad libitum consumption from 1 d to 4 wk of age.                  were no signs of lameness or rickets in the poults in
When the poults were 4 wk of age, five poults per pen                      Experiment 1. The effects of the treatments in Experiment
were bled by cardiac puncture, and various hematological                  2 on BW, the relative weights of the liver and kidney,
evaluations were performed using a Model 3500 Cell-                       bone strength, bone ash, and serum levels of calcium
Dyn hematology analyzer4 following the manufacturer’s                     and phosphorus are presented in Table 1. There was a
recommendations. Clinical chemistry analysis of serum                     significant decrease in the BW of the poults consuming
was performed using an automated clinical chemistry                       the suspect feed. There was a slight yet significant increase
analyzer5 following manufacturer’s procedures. The                        in the relative weight of the liver and kidney in the poults
poults were killed by cervical dislocation, and various                   consuming the suspect feed. Bone strength was decreased
organs were excised and weighed. The left tibia was re-                   threefold in the birds fed the suspect feed. Bone ash and
moved from five poults per pen, and breaking strength                      serum levels of calcium and phosphorus were also sig-
was determined using an Instron Model 4502 Shear Press6                   nificantly decreased in the poults consuming the sus-
as described by Huff et al. (1980). The bones for bone ash                pect feed.
analysis were fat-extracted in a Soxhlet extractor for 16                    In Experiment 3, the suspect feed was blended with
h with ethanol followed by 16 h with ethyl ether and then                 newly manufactured feed, and the effects of these treat-
ashed at 750 C for 17 h.                                                  ments on BW; the relative weights of the liver and kidney;
   The treatments in Experiment 3 consisted of control                    bone strength; bone ash; and the serum levels of calcium,
feed (newly manufactured) and control feed containing                     phosphorus, and alkaline phosphatase are presented in
25, 50, 75, and 100% suspect feed. There were two pens                    Table 2. There was a significant increase in BW with the
of 25 male poults (Nicholas 600) in each of the treatments,               diet containing 25% suspect feed, and a significant and
and feed and water were available for ad libitum consump-                 substantial decrease in BW with the 100% suspect feed
tion. The poults were bled and necopsied when they were                   diet. The relative weight of the liver was significantly
25 d of age. All other procedures and evaluations were                    decreased with the 100% suspect feed diet, and the rela-
as described for Experiment 2. At the start of Experiment                 tive weight of the kidney was significantly increased with
3, the suspect feed was 8 wk old.                                         the 50 and 100% suspect feed diet. Bone strength was
   A t-test was used to evaluate the data in Experiment                   significantly decreased with the 75 and 100% suspect feed
2. The data in Experiment 3 were anayzed by ANOVA                         diets, and bone ash was significantly decreased only when
(Snedecor and Cochran, 1967) using the General Linear                     the 100% suspect feed diet was fed. There was a significant
Models procedure of SAS software (SAS Institute, 1998).                   decrease in serum calcium levels with the 100% suspect
                                                                          feed diet. The serum phosphorus levels were inconsistent
                                                                          with a significant increase in phosphorus levels in the
  4
                                                                          75% suspect feed diet, and there was a significant increase
  Abbott Diagnostics, Abbott Park, IL 60064.
  5
  Express Plus, Ciba-Corning Diagnostics Corp., Medfield, MA 02052.        in the serum activity of alkaline phosphatase with the
  6
  Instron Corp., Canton, MA 02021.                                        100% suspect feed diet.
                                                                         RESEARCH NOTE                                                                                      1701
                                                                                   1                                        1
 TABLE 2. The effect of diets blended with suspect feed on BW; the relative weight of the liver and kidney; bone strength; bone ash;2       1                   2

                         and the serum levels of calcium,2 phosphorus,2 and alkaline phosphatase (Alk. Phos.)2

Treatment     BW at 25 d       Liver                 Kidney                  Strength                  Ash                Ca                P                  Alk. Phos.

                                             (% BW)                          (N/m × 10 )
                                                                                       2          6
                                                                                                       (%)                             (mg/dL)                 (IU/L)
Control       643   ±   11bc   2.78   ±   0.05a      0.50   ±   0.01b        15.2      ±   0.9a        46.6   ±   0.5ab   11.5   ±   0.3a   6.8   ±   0.5bc     4,676   ±   300b
 25%3         705   ±   14a    2.70   ±   0.04a      0.50   ±   0.01b        18.2      ±   0.8a        48.1   ±   0.4a    11.1   ±   0.2a   8.2   ±   0.2ab     4,670   ±   158b
 50%          684   ±   11ab   2.86   ±   0.06a      0.55   ±   0.01a        15.9      ±   0.9a        47.1   ±   0.6ab   10.8   ±   0.2a   7.4   ±   0.3abc    4,355   ±   323b
 75%          618   ±   19c    2.76   ±   0.04a      0.53   ±   0.01ab        9.5      ±   1.7b        45.7   ±   0.8b    11.8   ±   0.4a   8.6   ±   0.5a      4,972   ±   792b
100%          264   ±   9d     2.48   ±   0.05b      0.56   ±   0.01a         2.8      ±   0.3c        36.6   ±   1.2c     6.3   ±   0.8b   6.0   ±   0.7c     13,099   ±   1,079a
    Values within a column with no common superscript differ (P ≤ 0.05).
  a–d
  1
   Values represent the means ± SEM of two replicate pens of 25 poults per pen.
  2
   Values represent the means ± SEM of two replicate pens of five poults per pen.
  3
   Percentage of suspect feed in diet.



  The effect of these treatments on red blood cell counts,                                    toxic, characterized by a decrease in BW, affecting the
serum levels of cholesterol, triglycerides, uric acid, and                                    relative weights of the liver and kidney, as well as changes
protein are presented in Table 3. Serum levels of choles-                                     in hematology and clinical chemistries. These data clearly
terol and triglycerides were significantly decreased, and                                      indicate that the probable cause of this outbreak of field
red blood cell counts and the serum levels of uric acid                                       rickets was associated with the feed, even though the
and protein were significantly increased with the 100%                                         feed had adequate minerals and vitamin D. The effect of
suspect feed diet.                                                                            this feed on the relative weights of the liver and kidney
                                                                                              suggests that vitamin D metabolism in the liver and kid-
                           DISCUSSION                                                         ney could have been affected.
                                                                                                 In the absence of the isolation and characterization of
   Considering the complexity of bone formation, it is                                        this toxic component of the feed, mycotoxin contamina-
reasonable to suspect that there may be multiple causes                                       tion of the feed would seem to be a reasonable hypothesis.
of field rickets. Infectious agents could disrupt the utiliza-                                 Several mycotoxins have been shown to affect nutrient
tion of minerals and vitamin D through the pathology                                          availability (Hamilton et al., 1974), as well as bone forma-
caused in the liver, kidney, or intestinal tract. Although                                    tion (Huff et al., 1980). In addition, mycotoxins produced
most of the work on field rickets discounts infectious                                         by species of the genus Fusarium have been shown to
agents being involved (Walser et al., 1980; Olson et al.,                                     induce a rachitic-type syndrome in broilers (Gedek et al.,
1981; Riddell, 1983), others suggest that infectious agents                                   1978), and fusarochromanone can cause tibial dyschon-
may be involved (Vertommen et al., 1980a,b). In Experi-                                       droplasia (Chu et al., 1988; Wu et al., 1991, 1993; Chu et
ment 1, we could not induce field rickets either by incor-                                     al., 1995). However, to the authors’ knowledge no specific
porating litter from the pens of affected poults into newly                                   mycotoxin has been shown to cause field rickets, and any
manufactured feed or by challenging turkeys at 1 d with                                       number of other feed contaminants must be considered
an intestinal homogenate from affected poults, which sug-                                     as suspect. Regardless of the identity of the toxic principal
gests that the field rickets we observed was not caused                                        in the feed, it seems that the best approach to the treat-
by an infectious agent.                                                                       ment of field rickets would be to replace or blend the
   Although lameness was not observed in Experiment 2,                                        feed. Massive vitamin D therapy in outbreaks of field
the poults in both Experiments 2 and 3 had rickets, which                                     rickets has not always been successful (Bar et al., 1987;
was characterized by a decrease in bone strength, bone                                        Riddell, 1983). If the cause of field rickets is a yet-to-be
ash, and serum levels of calcium and phosphorus in Ex-                                        identified toxin that affects vitamin D metabolism, the
periment 2 and a decrease in calcium in Experiment 3.                                         toxic affects might be overwhelmed with massive levels
In addition to causing rickets, the suspect feed was also                                     of vitamin D. However, it would seem more reasonable


                    TABLE 3. The effect of diets blended with suspect feed on red blood cell counts (RBC) and the serum
                                          levels of cholesterol, triglycerides, uric acid, and protein1

                Treatment              RBC                        Cholesterol                     Triglycerides           Uric Acid               Protein
                                       (mm   3
                                                 × 10 )
                                                     6
                                                                                                    (mg/dL)                                       (g/dL)
                Control                2.5 ±     0.1b             105    ±   6a                   92 ± 12a                 7.1   ±   0.8b         2.9 ± 0.1b
                 25%2                  2.5 ±     0.1b             103    ±   5a                   71 ± 6ab                 8.1   ±   0.8b         3.0 ± 0.1b
                 50%                   2.5 ±     0.1b              91    ±   5ab                  65 ± 6ab                 8.4   ±   0.8b         3.0 ± 0.1b
                 75%                   2.5 ±     0.1b             100    ±   11a                  77 ± 10a                11.1   ±   1.0b         3.3 ± 0.2b
                100%                   2.9 ±     0.1a              73    ±   9b                   44 ± 10b                30.4   ±   0.8a         4.1 ± 0.3a

                      Values within a column with no common superscript differ (P ≤ 0.05).
                    a,b
                    1
                     Values represent the means ± SEM of two replicate pens of five poults per pen.
                    3
                     Percentage of suspect feed in diet.
1702                                                        HUFF ET AL.

to treat field rickets with the vitamin D metabolites of             Huff, W. E., J. A. Doerr, P. B. Hamilton, D. D. Hamann, R. E.
either 25-hydroxy cholecalciferol or 1, 25 di-hydroxy cho-             Peterson, and A. Ciegler, 1980. Evaluation of bone strength
                                                                       during aflatoxicosis and ochratoxicosis. Appl. Environ. Mi-
lecalciferol. This approach is supported by the work of                crobiol. 40:102–107.
Hurwitz and Bar (1981), which showed that 25-hydroxy                Hurwitz, S., and A. Bar, 1981. Calcium, phosphorus, and vitamin
cholecalciferol was more effective at treating field rickets            D deficiencies in young turkeys: Diagnosis and treatment.
in turkeys than vitamin D.                                             Minnesota Turkey Research. Univ. Minn. Agric. Exp. Stn.
   The complexity of calcium, phosphorus, and vitamin                  Rep. 179:33–41.
D availability and utilization in bone development would            Hurwitz, S., A. Bar, and A. Meshorer, 1973. Field rickets in
                                                                       turkey poults: Plasma and bone chemistry, bone histology,
suggest that field rickets could be caused by a number                  intestinal, calcium-binding protein. Poultry Sci. 52:1370–
of factors. Although the feed was determined to have                   1374.
adequate levels of calcium, phosphorus, and vitamin D,              National Research Council, 1994. Nutrient Requirements of
it was shown to be the probable cause of field rickets in               Poultry. 9th rev. ed. National Academy Press, Washing-
these studies. The fact that the feed was also toxic suggests          ton, DC.
that a contaminating toxin, possibly a mycotoxin, might             Olson, W. G., H. E. Dziuk, M. M. Walser, G. F. Hanlon, P. E.
                                                                       Waibel, J. B. Stevens, and N. A. Jorgensen, 1981. Field rickets
have been responsible for this outbreak of field rickets.
                                                                       in turkey poults: Biochemical findings. Avian Dis. 25:550–
                                                                       554.
               ACKNOWLEDGMENTS                                      Riddell, C., 1983. Rickets in turkey poults. Avian Dis. 27:430–441.
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   The authors gratefully acknowledge the excellent tech-              Cary, NC.
nical assistance of Scott Zornes, Dana Bassi, David Hor-            Singh, U., and J. H. Bradbury, 1988. HPLC determination of
lick, Sonia Tsai, and Chris Taylor.                                    vitamin A and vitamin D2 in south pacific root crops. J. Sci.
                                                                       Food Agric. 45:87–94.
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