TEMPERATURE AND IMMTTNODEPRESSION cortisone and ACTH-injected birds. J. Immunology, 98: 1076-1084. Haurowitz, F., 1968. Immunochemistry and the Biosynthesis of Antibodies, John Wiley and Sons,N.Y. Kramer, C. Y., 1956. Extension of multiple range tests to group means with unequal numbers of replications. Biometrics, 12: 307-310. Mueller, A. P., H. R. Wolfe and W. P. Cote, 1964. Chapter 20 in: The Thymus in Immunobiology, Ed. R. A. Good and A. E. Gabrielsen, Harper
205
and Row, N. Y. Pressman, D., and A. L. Grossberg, 1968. The Structural Basis of Antibody Specificity, W.A. Benjamin, Inc., N . Y. Selye, H., 1950. The Physiology and Pathology of Exposure to Stress, ACTA, Inc., Montreal. Thaxton, P., C. R. Sadler and B. Glick, 1968. Immune response of chickens following heat exposure or injections with ACTH. Poultry Sci. 47:264-266.
J. F. STEPHENS 2 AND B. D. BARNETT Poultry Science Department, Clemson University, Clemson, South Carolina 29631 (Received for publication September 4, 1969)
T
HE frequent occurrence of coccidiosis in layer flocks has led to speculation that either a program of planned immunization or one of preventative medication throughout the life of the bird will be used in the future to prevent coccidiosis (Reid, 1962). The recent development and use of chemicals which limit coccidial damage to a level below that required to cause the development of immunity have stimulated interest in, and some investigation (Nikolaiczuk, 1966; Stephens et al., 1967) of, the merits of feeding coccidiostats continuously to replacement and layer flocks. This method of coccidiosis control should eliminate the possibility of costly coccidiosis "breaks" in laying flocks. The efficacy of amprolium in preventing coccidiosis in young chickens and turkeys has been demonstrated by several investigators (Cuckler et al., 1960; Bond and
1 Published with the approval of the Director, South Carolina Agricultural Experiment Station as technical contribution no. 921. 2 Present Address: Department of Poultry Science, The Ohio State University, Columbus, Ohio 43210.
Edgar, 1961; Morrison et al., 1961; Peterson and LaBorde, 1962; McLoughlin and Gardiner, 1962; Long, 1963; and others). Polin et al. (1962) reported that feeding diets containing up to 0.07 percent amprolium to laying hens caused no adverse effect upon their productive or reproductive performance. Recently, the continuous feeding of amprolium at a level of 0.0125 percent of the diet to laying hens on an investigational basis was approved by the Food and Drug Administration. This study was conducted to determine whether amprolium, when fed continuously, would affect the performance of laying hens. PROCEDURES
Twenty 14-week-old S.C. White Leghorn pullets reared on a diet containing 0.0187 percent amprolium and 0.0004 percent ethopabate were obtained from a local producer. Challenge-doses of Eimeria tenella, E. necatrix, E. acervulina, and E. maxima oocysts were each administered to five of the 14-week-old pullets 24 hours
Downloaded from http://ps.oxfordjournals.org/ at NERL on April 12, 2015
Effects of Continuous Feeding of Amprolium on Performance of Laying Hens 1
206
J. F. STEPHENS AND B. D. BARNETT
RESULTS AND DISCUSSION
The effects of continuously feeding amprolium to layers are summarized in Table 1. Hens given amprolium required less
feed per dozen eggs produced, but gained less weight during the laying year than did those given no amprolium. The Haugh unit scores of eggs laid by hens given amprolium were significantly lower (P <.01) than those of eggs laid by hens not given amprolium; however, the average scores for eggs laid by both groups were higher than required for classification as Grade AA on the USD A scale. The feeding of amprolium had no significant effect (P = .05) upon percent production, mortality, average egg weight or thickness of egg shells. Symptoms of coccidiosis were seen in none of the birds during the course of this trial. Most of the mortality was caused by visceral lymphomatosis, and mortality rate was not significantly affected by feeding amprolium. SUMMARY
A trial of 60 weeks duration was conducted to study the effects of feeding a diet containing .0125% amprolium continuously to laying hens. S.C.W.L. pullets were reared to 16 weeks of age on a diet containing .0187% amprolium and .0004% ethopabate. One-half of the pullets were subsequently fed a diet containing no coccidiostat. The remaining birds of amprolium on performance of laying hens1
TABLE 1—Effects
% Production (Hen-Day) Kg. feed/doz. eggs Weight gain 16-20 weeks 20-24 weeks 24-76 weeks % Mortality Ave. egg weight (gm.) Ave. shell thickness (mm.) Ave. Haugh units
No amprolium
Amprolium2
72.87 1.98
72.79 1.92*
161.28 186.18 353.82 9.3 59.93 0.337 76.62
169.89 176.57 330.82** 10.7 59.94 0.336 75.51**
1 Means followed by * and ** are significantly different from corresponding mean at P<.05 and P<.01, resepctively. 2 Diet contained .0125% amprolium.
Downloaded from http://ps.oxfordjournals.org/ at NERL on April 12, 2015
after removal of amprolium and ethopabate from the birds' diet. Necropsies performed eight days post-inoculation revealed lesions typical of the species administered in each group of pullets, indicating the flock to be at least moderately susceptible to all four species of Eimeria. Subsequently, additional pullets from the same flock which had continually received amprolium and ethopabate were obtained when they were 16 weeks of age. The birds were leg-banded, weighed individually and placed, 36 per pen, in a house having eight pens with wooden floors covered with about six inches of clean pine shavings. The pullets in four pens were supplied a commercial-type layer ration containing .0125 percent amprolium; the remaining birds were given the same diet without coccidiostat. All birds were reweighed at 20 and 24 weeks of age; ie, four and eight weeks after withdrawal of the coccidiostat from the diet fed to half the birds. Daily egg production was recorded for each pen, and the percent production, feed consumption and feed-egg ratio were determined for 14 consecutive 28-day periods, beginning when the pullets were 20 weeks old. At 56-day intervals, 50 eggs from each pen were weighed individually and the shell thickness and albumen height of each egg was measured. Mortality records were kept throughout the trial and necropsies were performed in an attempt to ascertain the causes of deaths. When the hens were 76 weeks of age, they were again weighed individually and the trial was terminated. Data were statistically analyzed by analysis of variance (Snedecor, 1956).
AMPROLIUM AND PRODUCTION
REFERENCES Bond, D. S., and S. A. Edgar, 1961. Efficacy of a new coccidiostatic drug for the control of coccidiosis in chickens and turkeys. Abstr. So. Ag. Workers Meeting, Jackson, Miss., Feb. 6-8. pp. 1-2. Cuckler, A. C , M. Garzillo, C. Malanga and E. C. McManus, 1960. Amprolium. 1. Efficacy for
coccidia in chickens. Poultry Sci. 39: 1241. Long, P. L., 1963. The chemotherapy of coccidiosis in chickens. Agri. Vet. Chem. 4: 90-92. McLoughlin, B . K., and J. L. Gardiner, 1962. The activity of amprolium in Eimeria tenella infections—Laboratory trials. Avian Dis. 6: 185-190. Morrison, W. D., A. E. Ferguson, M. C. Connell and J. K. McGregor, 1961. The efficacy of certain coccidiostats against mixed avian coccidial infections. Avian Dis. 5: 222-228. Nikolaiczuk, N., 1966. Buquinolate toxicity in growing pullets and laying hens. Poultry Sci. 45: 1110-1111. Peterson, E. H., and J. LaBorde, 1962. A laboratory and field evaluation of amprolium—a new anticoccidial. Poultry Sci. 41: 207-213. Polin, D., C. C. Porter, E. R. Wynosky and W. R. Cobb, 1962. Amprolium. 4. The effect of amprolium on reproduction in chickens. Poultry Sci. 41: 372-380. Reid, M., 1962. Coccidiosis and coccidiostats. Proc. 6th Ann. Poultry Health and Mgt. Short Course, Clemson Univ., Clemson, S. C , Mar. 6-7. pp. 28-35. Snedecor, G. W., 1956. Statistical Methods. Iowa State College Press, Ames. Stephens, J. F., B. D. Barnett and H. E. Butters, 1967. Effects of buquinolate on growth and egg production of White Leghorn pullets. Poultry Sci. 46: 203-206.
Anatoxicosis in the Broiler Chicken1'2 J. W. SMITH AND P. B. HAMILTON Departments of Poultry Science and Microbiology, North Carolina State University, Raleigh, North Carolina 27607 (Received for publication September 4, 1969)
INTRODUCTION
T
H E a n a t o x i n s a r e a g r o u p of h e p a t o toxic c o m p o u n d s p r o d u c e d b y t h e m o l d Aspergillus flavus w h e n growing on
1 Paper Number 2963 of the Journal Series of the North Carolina State University Agricultural Experiment Station, Raleigh, North Carolina. 2 A preliminary report of part of this paper was presented at the 69th Annual Meeting of the American Society for Microbiology, Miami, Florida, 1969.
feedstuffs. They first discovered in 1960 as a result of turkey " X " disease which was responsible for the deaths of over 100,000 turkey poults. Although these toxins were first discovered in poultry diseases, most research efforts were channeled toward public health aspects after it was found that the anatoxins can be responsible for tumor formation in mammalians (Schoental, 1967). The research on avian aflatoxicosis has not kept pace
Downloaded from http://ps.oxfordjournals.org/ at NERL on April 12, 2015
were given the same diet containing .0125% amprolium for the following 60 weeks. Coccidiosis was not observed in any of the birds during this study. Hens given amprolium required less feed per dozen eggs produced, but gained less weight during the laying period, than did hens fed the same diet without amprolium. Total egg production was similar in both groups. The average Haugh unit score of the eggs laid by hens fed amprolium was significantly lower than that of eggs from hens not given amprolium; however, the average scores of eggs from both groups was higher than the minimum value required for classification as Grade AA eggs.
207