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Efficacy of Graded Levels of p-Ureidobenzenearsonic Acid Against Different Levels of Exposure to Histomoniasis in Turkeys 5 and 13 Weeks Old1,2
450
N. R. GYLES, B. R. STEWART AND C. J. BROWN ceptibility to pseudotypes of Rous sarcoma virus. Virology, 26: 270-276. Vogt, P. K., and R. Ishizaki, 1965. Reciprocal patterns of genetic resistance to avian tumor viruses in two lines of chickens. Virology, 26: 664-672. Waters, N. F., and B. R. Burmester, 1961. Mode of inheritance of resistance to Rous sarcoma virus in chickens. J. Nat'l. Cancer Inst. 27: 656-661. Wood, B. M., and W. H. Garren, 1958. A study of the resistance of Rhode Island Reds to implants of lymphoid tumor strain RPL-12. Poultry Sci. 37: 321-326.
Efficacy of Graded Levels of p-Ureidobenzenearsonic Acid Against Different Levels of Exposure to Histomoniasis in Turkeys 5 and 13 Weeks Old1'2 J. H. WHITMORE 3 , T. W. SULLIVAN3 AND 0. D. GRACE4 University of Nebraska, Lincoln, Nebraska 68503 (Received for publication July 13, 1967)
W
ELTER and Clark (1961) reported that p-ureidobenzenearsonic acid (p-UBAA), administered continuously starting one week before infection, reduced mortality and lesions due to histomoniasis. Similar results were obtained in challenge experiments by Sullivan et al. (1964, 1965), when dietary treatments were initiated five days prior to exposure. Lund (1955) studied histomoniasis mortality as related to the size of the infective dose. He observed a decrease in mortality as the infective dose was decreased. The purpose of this study was to determine the efficacy of graded levels of p-
1 Published with the approval of the Director as paper No. 2151, Journal Series, Nebraska Agricultural Experiment Station. 2 From a thesis submitted by the senior author in partial fulfillment of the requirements for the Ph.D. degree. 3 Department of Poultry Science; J. H. Whitmore's present address: Tyson's Foods,- Inc., Springdale, Arkansas. 4 Department of Veterinary Science.
UBAA against different levels of exposure to histomoniasis in turkeys five and 13 weeks of age. EXPERIMENTAL PROCEDURE
Two challenge experiments were conducted in which turkeys were artificially exposed to embryonated Heterakis gallinae ova containing Histomonas meleagridis. Exposure was accomplished by placing the H. gallinae ova directly into the crop by means of a pipette. The post-challenge periods were 28 and 27 days for experiments 1 and 2, respectively. Turkeys that died during the post-challenge period were examined for hepatic and cecal lesions typical for histomoniasis. All surviving turkeys at the end of post-challenge periods were sacrificed and examined foi lesions. Morbidity reported herein includes all birds (dead birds during the post-challenge period and survivors), which showed hepatic and/or cecal lesions typical for the disease.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
lantoic membrane and of embryonic cells in tissue culture. Virology, 24: 610-616. Prince, A. M., 1958. Quantitative studies on Rous sarcoma virus. II. Mechanism of resistance of chick embryos to chorioallantoic inoculation of Rous sarcoma virus. J. Nat'l. Cancer Inst. 20: 843-850. Rubin, H., A. Cornelius and L. Fanshier, 1961. The pattern of congenital transmission of an avian leukosis virus. Proc. Nat'l. Acad. Sci. U.S. 47: 1058-1060. Rubin, H., 1965. Genetic control of cellular sus-
451
UREIDOBENZENEARSONIC ACID AND HISTOMONIASIS
Experiment 1. Broad Breasted Bronze (B.B.B.) and Broad Breasted White (B.B.W.) poults were fed the same diet from day-old to four weeks of age. One group of eight males (four of each strain) and one group of eight females (four of each strain) were weighed, wingbanded and randomly assigned to each treatment at this age. A four by four factorial arrangement of treatments was employed; all combinations of four dietary levels of p-UBAA and four doses of infective material were evaluated. The p-UBAA levels were 0, 0.025, 0.0375 and 0.05 percent; infective doses were approximately 0, 10, 20 and 40 embryonated H. gallinae ova per poult based on serial dilution. Poults were given doses of infective material four days after dietary treatments were initiated. Experiment 2. All combinations of four dietary levels of p-UBAA and four doses of infective material were evaluated in this experiment. The p-UBAA levels were the same as in experiment 1; infective doses were approximately 0, 20, 40 and 80 embryonated H. gallinae ova per bird based on serial dilution. Seven male and
T A B L E 1.—Mortality, morbidity and body weight gain data from experiment 1 % p-UBAA 0.0
0.025
0.0375
0.05
Average
0.0 25.0 25.0 25.0 19.0b
0.0 0.0 0.0 0.0 0.0a
0.0a 17.2b 32.8bc 42.8c
% Morbidity 1 0.0 0.0 31.2 25.0 50.0 31.2 56.2 31.2 22.2b 34.9bc
0.0 0.0 25.0 0.0 6.2a
0.0a 17.2b 43.8c 43.8c
% Mortalityl
H.
gallinae ova/bird 0 10 20 40 Average
0.0 12.5 56.2 87.5 37.5c
0.0 31.2 50.0 56.2 34.9bc
0 10 20 40 Average
0.0 12.5 68.8 87.5 42.8c
Survivor's av. body wt. gain 0 1,782 1,790 10 1,680 1,844 20 1,722 1,581 40 1,653 1,699 1,687 1,796 Average
(grams) , 2 1,778 1,678 1,565 1,640 1,701
5-9 weeks 1,685 1,753 1,667 1,707 1,556 1,633 1,669 1,674 1,642
1 Each value is the average of 16 birds per treatment group. Values which do not share a letter in common are significantly different from each other (P<0.025) based on Chi-square. 2 Composite main effect means weighted.
seven female poults (B.B.B.) 12 weeks of age were selected at random, weighed, wingbanded and assigned to each of the 16 treatments. The doses of infective material were administered three days later. RESULTS Experiment 1. Graded doses of infective material caused graded levels of mortality and morbidity when 0.0 and 0.025 percent of p-UBAA were present in the diet (Table 1). Mortality was the same when 10, 20 or 40 H. gallinae ova were given per bird with the 0.0375 percent level of pUBAA. No turkeys receiving the 0.05 percent level of p-UBAA died, regardless of the infective dose. When composite averages are considered, mortality and morbidity decreased as the p-UBAA level was increased. Mortality was significantly less with 0.0375 and 0.05 percent of p-UBAA than when p-UBAA was omitted from the diet. The protection afforded by 0.05 percent pUBAA was significantly greater relative to the 0.025 percent level. Morbidity data followed a trend very similar to the mortality data.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
All birds were maintained in electrically heated battery brooders with raised wire floors until they were four weeks of age. Poults were then moved to unheated growing batteries (experiment 1) or floor pens (experiment 2) for the remainder of the experiments. Practical-type diets composed largely of ground yellow corn and soybean meal were used in these studies. The protein levels were 28, 25 and 21 percent, respectively, for the 0-8, 9-12 and 13-16 week periods. All mortality and morbidity data were subjected to a Chi-square test (Snedecor, 1956). In every instance the level of probability used herein to denote significance is 2.5 percent.
452
J. H.
W H I T M O R E , T.
W.
SULLIVAN AND 0 .
TABLE 2.—Mortality, morbidity and body weight gain data from experiment 2 % P - •UBAA 0.0375
0.05
- Average
0.025
H. gallinae ova/bird 0 20 40 80 Average
0.0 57.1 78.6 78.6 53.6a
0.0 0.0 0.0 0.0 0.0b
0.0 0.0 0.0 0.0 0.0b
0.0 0.0 0.0 0.0 0.0b
0.0a 14.3b 19.6b 19.6b
0 20 40 80 Average
0.0 85.7 85.7 85.7 64.3a
% Morbidity! 0.0 0.0 0.0 0.0 0.0 0.0 0.0 7.1 0.0b 1.8b
0.0 0.0 7.1 0.0 1.8b
0.0a 21.4b 23.2b 23.2b
% Mortality*
Survivoi •'s av. body wt. gain 1,628 2,146 0 689 1,932 20 1,270 1,837 40 708 2,114 80 1,266 2,005 Average
(grams) 2 ,, 1,991 1,842 1,991 2,109 1,982
13-17 weeks 2,091 1,964 1,987 1,765 1,792 1,833 2,064 2,005 1,982
GRACE
bidity were significantly less with either 0.025, 0.0375 or 0.05 percent of p-UBAA as compared to 0.0 percent of the compound. Groups receiving 20, 40 and 80 H. gallinae ova per poult showed significantly greater mortality and morbidity than unexposed groups. Based on composite averages, survivor's body weight gain was significantly greater with 0.025, 0.0375 and 0.05 percent than with' 0.0 percent of p-UBAA. There was no apparent trend in survivor's gain relative to doses of infective material. DISCUSSION
As the level of exposure (dose of infective material) was increased, mortality and morbidity increased. This p a t t e r n was established with the two lower levels of p-UBAA, since mortality and morbidity were quite similar with the 0.0375 and 0.05 percent levels. Only small differences were observed among survivor's average body weight gains. Based on composite averages, slightly greater gains occurred with 0.025 percent of p-UBAA and the lower doses of infective material (0 and 10 H. gallinae ova/poult).
When p-UBAA was excluded from the diet in experiments 1 and 2, the percent mortality with 20 H. gallinae ova given per bird was 56.2 and 57.1 respectively. Likewise, when 40 ova were given per bird, the percent mortality was 87.5 and 78.6 percent in experiments 1 and 2, respectively. Therefore, mortality was about the same when like doses of H. gallinae ova were given to turkeys either five or 13 weeks of age and receiving no preventive medication. I t should be mentioned t h a t the embryonated H. gallinae ova used in both experiments were taken from one large supply, which had been obtained for use in several histomoniasis challenge experiments.
Experiment 2. Mortality occurred only in the exposed groups which received no p-UBAA (Table 2). Mortality did not exactly follow parallel to levels of histomoniasis exposure; however, more turkeys died in groups receiving 40 or 80 H. gallinae ova per bird as compared to 20 ova per bird. Morbidity followed about the same p a t t e r n as did mortality relative to treatments. The doses of infective material were inadequate to produce mortality in the presence of any level of p-UBAA in this experiment. Both mortality and mor-
When 0.025 percent of p-UBAA was present in the diet, no mortality occurred in experiment 2 following doses of 20 or 40 H. gallinae ova per turkey. Mortality was 50.0 and 56.2 percent, respectively, in experiment 1 when 20 and 40 ova/poult were given to groups fed the same level of p-UBAA. Thus, 0.025 percent of p-UBAA provided much greater protection against exposure to histomoniasis in older turkeys (13 weeks versus 5 weeks of age). I t is quite interesting to compare mortality and morbidity data from experiment 1 to those d a t a from experiment 2, with ref-
1 Each value is the average of 14 birds per treatment group. Values which do not share a letter in common are significantly different from each other (P<0.025) based on Chi-square. 2 Composite main effect means are weighted.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
0.0
D.
UREIDOBENZENEARSONIC ACID AND HISTOMONIASIS
SUMMARY
Two experiments were conducted to determine the efficacy of graded levels of pureidobenzenearsonic acid (p-UBAA) against different levels of exposure to histomoniasis in five and 13-week old turkeys. Data obtained suggest or indicate the following: 1. When p-UBAA was excluded from the diet, graded doses of infective material (embryonated H. gallinae ova) produced graded levels of histomoniasis mortality and morbidity in five-week old
turkeys, and to a much lesser degree in 13-week old turkeys. 2. The lower levels of p-UBAA were clearly more effective against the same exposure to histomoniasis in 13-week old than in five-week old turkeys. When 0.025 percent of p-UBAA was present in the diet, no mortality occurred in 13-week old turkeys following doses of approximately 20 and 40 embryonated H. gallinae ova/bird. In contrast, mortality was 50.0 and 56.2 percent, respectively, following doses of approximately 20 and 40 H. gallinae ova/bird with five week-old poults receiving the same level of p-UBAA. 3. The influence of dietary drug level, age of bird and infective dosage on histomoniasis prevention is discussed. ACKNOWLEDGEMENT
This study was supported in part by a grant from Whitmoyer Laboratories, Inc., a subsidiary of Rohm and Haas Company, Myerstown, Pa. 17067 REFERENCES Lund, E. L., 1955. The progress of histomoniasis (blackhead) in turkeys as related to size of the infective dose. Poultry Sci. 34:127-130. Snedecor, G. W., 1956. Statistical Methods, 5th ed, The Iowa State College Press, Ames, Iowa. Sullivan, T. W., J. R. Kingan, O. D. Grace and G. W. Kelly, 1964. Evaluation of four compounds for the prevention of blackhead lesions and mortality in young turkeys. Poultry Sci. 43: 1367-1368. Sullivan, T. W., J. H. Whitmore, O. D. Grace and J. R. Kingan, 1965. Effect of certain blackhead preventive compounds on growth and their efficacy against histomoniasis in turkeys. Poultry Sci. 44:1420. Welter, C. J., and D. T. Clark, 1961. The efficacy of p-ureidobenzenearsonic acid as a preventive of histomoniasis in turkey poults. Poultry Sci. 40: 144-147.
AUGUST 22-25. NATIONAL POULTRY AND EGG MARKETING CONFERENCE OF INSTITUTE OF AMERICAN POULTRY INDUSTRIES, CHICAGO, ILLINOIS.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
erence to all three levels of p-UBAA. These results clearly indicate that lower levels of the compound were more effective against the same exposure to histomoniasis in older birds than in younger birds. Why should the same level of a histomonostatic drug be significantly more effective in older than in younger turkeys? One logical explanation could be the ratio of feed and/or drug intake to dose of infective material. Daily feed consumption of turkeys 13 weeks of age is approximately 2.9 times greater than for poults five weeks old. Thus, if the dose of infective material was similar in both five and 13-week old turkeys, the same dietary drug level (i.e. 0.025% p-UBAA) should be about 2.9 times more effective in the older birds. Data reported herein tend to support this line of reasoning. Therefore, it should and might very well be possible to reduce the level of a histomonostatic drug in feed as turkeys age. Drug levels might be reduced at an inverse rate approximately proportional to the increased feed intake with age.
453
N. R. GYLES, B. R. STEWART AND C. J. BROWN ceptibility to pseudotypes of Rous sarcoma virus. Virology, 26: 270-276. Vogt, P. K., and R. Ishizaki, 1965. Reciprocal patterns of genetic resistance to avian tumor viruses in two lines of chickens. Virology, 26: 664-672. Waters, N. F., and B. R. Burmester, 1961. Mode of inheritance of resistance to Rous sarcoma virus in chickens. J. Nat'l. Cancer Inst. 27: 656-661. Wood, B. M., and W. H. Garren, 1958. A study of the resistance of Rhode Island Reds to implants of lymphoid tumor strain RPL-12. Poultry Sci. 37: 321-326.
Efficacy of Graded Levels of p-Ureidobenzenearsonic Acid Against Different Levels of Exposure to Histomoniasis in Turkeys 5 and 13 Weeks Old1'2 J. H. WHITMORE 3 , T. W. SULLIVAN3 AND 0. D. GRACE4 University of Nebraska, Lincoln, Nebraska 68503 (Received for publication July 13, 1967)
W
ELTER and Clark (1961) reported that p-ureidobenzenearsonic acid (p-UBAA), administered continuously starting one week before infection, reduced mortality and lesions due to histomoniasis. Similar results were obtained in challenge experiments by Sullivan et al. (1964, 1965), when dietary treatments were initiated five days prior to exposure. Lund (1955) studied histomoniasis mortality as related to the size of the infective dose. He observed a decrease in mortality as the infective dose was decreased. The purpose of this study was to determine the efficacy of graded levels of p-
1 Published with the approval of the Director as paper No. 2151, Journal Series, Nebraska Agricultural Experiment Station. 2 From a thesis submitted by the senior author in partial fulfillment of the requirements for the Ph.D. degree. 3 Department of Poultry Science; J. H. Whitmore's present address: Tyson's Foods,- Inc., Springdale, Arkansas. 4 Department of Veterinary Science.
UBAA against different levels of exposure to histomoniasis in turkeys five and 13 weeks of age. EXPERIMENTAL PROCEDURE
Two challenge experiments were conducted in which turkeys were artificially exposed to embryonated Heterakis gallinae ova containing Histomonas meleagridis. Exposure was accomplished by placing the H. gallinae ova directly into the crop by means of a pipette. The post-challenge periods were 28 and 27 days for experiments 1 and 2, respectively. Turkeys that died during the post-challenge period were examined for hepatic and cecal lesions typical for histomoniasis. All surviving turkeys at the end of post-challenge periods were sacrificed and examined foi lesions. Morbidity reported herein includes all birds (dead birds during the post-challenge period and survivors), which showed hepatic and/or cecal lesions typical for the disease.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
lantoic membrane and of embryonic cells in tissue culture. Virology, 24: 610-616. Prince, A. M., 1958. Quantitative studies on Rous sarcoma virus. II. Mechanism of resistance of chick embryos to chorioallantoic inoculation of Rous sarcoma virus. J. Nat'l. Cancer Inst. 20: 843-850. Rubin, H., A. Cornelius and L. Fanshier, 1961. The pattern of congenital transmission of an avian leukosis virus. Proc. Nat'l. Acad. Sci. U.S. 47: 1058-1060. Rubin, H., 1965. Genetic control of cellular sus-
451
UREIDOBENZENEARSONIC ACID AND HISTOMONIASIS
Experiment 1. Broad Breasted Bronze (B.B.B.) and Broad Breasted White (B.B.W.) poults were fed the same diet from day-old to four weeks of age. One group of eight males (four of each strain) and one group of eight females (four of each strain) were weighed, wingbanded and randomly assigned to each treatment at this age. A four by four factorial arrangement of treatments was employed; all combinations of four dietary levels of p-UBAA and four doses of infective material were evaluated. The p-UBAA levels were 0, 0.025, 0.0375 and 0.05 percent; infective doses were approximately 0, 10, 20 and 40 embryonated H. gallinae ova per poult based on serial dilution. Poults were given doses of infective material four days after dietary treatments were initiated. Experiment 2. All combinations of four dietary levels of p-UBAA and four doses of infective material were evaluated in this experiment. The p-UBAA levels were the same as in experiment 1; infective doses were approximately 0, 20, 40 and 80 embryonated H. gallinae ova per bird based on serial dilution. Seven male and
T A B L E 1.—Mortality, morbidity and body weight gain data from experiment 1 % p-UBAA 0.0
0.025
0.0375
0.05
Average
0.0 25.0 25.0 25.0 19.0b
0.0 0.0 0.0 0.0 0.0a
0.0a 17.2b 32.8bc 42.8c
% Morbidity 1 0.0 0.0 31.2 25.0 50.0 31.2 56.2 31.2 22.2b 34.9bc
0.0 0.0 25.0 0.0 6.2a
0.0a 17.2b 43.8c 43.8c
% Mortalityl
H.
gallinae ova/bird 0 10 20 40 Average
0.0 12.5 56.2 87.5 37.5c
0.0 31.2 50.0 56.2 34.9bc
0 10 20 40 Average
0.0 12.5 68.8 87.5 42.8c
Survivor's av. body wt. gain 0 1,782 1,790 10 1,680 1,844 20 1,722 1,581 40 1,653 1,699 1,687 1,796 Average
(grams) , 2 1,778 1,678 1,565 1,640 1,701
5-9 weeks 1,685 1,753 1,667 1,707 1,556 1,633 1,669 1,674 1,642
1 Each value is the average of 16 birds per treatment group. Values which do not share a letter in common are significantly different from each other (P<0.025) based on Chi-square. 2 Composite main effect means weighted.
seven female poults (B.B.B.) 12 weeks of age were selected at random, weighed, wingbanded and assigned to each of the 16 treatments. The doses of infective material were administered three days later. RESULTS Experiment 1. Graded doses of infective material caused graded levels of mortality and morbidity when 0.0 and 0.025 percent of p-UBAA were present in the diet (Table 1). Mortality was the same when 10, 20 or 40 H. gallinae ova were given per bird with the 0.0375 percent level of pUBAA. No turkeys receiving the 0.05 percent level of p-UBAA died, regardless of the infective dose. When composite averages are considered, mortality and morbidity decreased as the p-UBAA level was increased. Mortality was significantly less with 0.0375 and 0.05 percent of p-UBAA than when p-UBAA was omitted from the diet. The protection afforded by 0.05 percent pUBAA was significantly greater relative to the 0.025 percent level. Morbidity data followed a trend very similar to the mortality data.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
All birds were maintained in electrically heated battery brooders with raised wire floors until they were four weeks of age. Poults were then moved to unheated growing batteries (experiment 1) or floor pens (experiment 2) for the remainder of the experiments. Practical-type diets composed largely of ground yellow corn and soybean meal were used in these studies. The protein levels were 28, 25 and 21 percent, respectively, for the 0-8, 9-12 and 13-16 week periods. All mortality and morbidity data were subjected to a Chi-square test (Snedecor, 1956). In every instance the level of probability used herein to denote significance is 2.5 percent.
452
J. H.
W H I T M O R E , T.
W.
SULLIVAN AND 0 .
TABLE 2.—Mortality, morbidity and body weight gain data from experiment 2 % P - •UBAA 0.0375
0.05
- Average
0.025
H. gallinae ova/bird 0 20 40 80 Average
0.0 57.1 78.6 78.6 53.6a
0.0 0.0 0.0 0.0 0.0b
0.0 0.0 0.0 0.0 0.0b
0.0 0.0 0.0 0.0 0.0b
0.0a 14.3b 19.6b 19.6b
0 20 40 80 Average
0.0 85.7 85.7 85.7 64.3a
% Morbidity! 0.0 0.0 0.0 0.0 0.0 0.0 0.0 7.1 0.0b 1.8b
0.0 0.0 7.1 0.0 1.8b
0.0a 21.4b 23.2b 23.2b
% Mortality*
Survivoi •'s av. body wt. gain 1,628 2,146 0 689 1,932 20 1,270 1,837 40 708 2,114 80 1,266 2,005 Average
(grams) 2 ,, 1,991 1,842 1,991 2,109 1,982
13-17 weeks 2,091 1,964 1,987 1,765 1,792 1,833 2,064 2,005 1,982
GRACE
bidity were significantly less with either 0.025, 0.0375 or 0.05 percent of p-UBAA as compared to 0.0 percent of the compound. Groups receiving 20, 40 and 80 H. gallinae ova per poult showed significantly greater mortality and morbidity than unexposed groups. Based on composite averages, survivor's body weight gain was significantly greater with 0.025, 0.0375 and 0.05 percent than with' 0.0 percent of p-UBAA. There was no apparent trend in survivor's gain relative to doses of infective material. DISCUSSION
As the level of exposure (dose of infective material) was increased, mortality and morbidity increased. This p a t t e r n was established with the two lower levels of p-UBAA, since mortality and morbidity were quite similar with the 0.0375 and 0.05 percent levels. Only small differences were observed among survivor's average body weight gains. Based on composite averages, slightly greater gains occurred with 0.025 percent of p-UBAA and the lower doses of infective material (0 and 10 H. gallinae ova/poult).
When p-UBAA was excluded from the diet in experiments 1 and 2, the percent mortality with 20 H. gallinae ova given per bird was 56.2 and 57.1 respectively. Likewise, when 40 ova were given per bird, the percent mortality was 87.5 and 78.6 percent in experiments 1 and 2, respectively. Therefore, mortality was about the same when like doses of H. gallinae ova were given to turkeys either five or 13 weeks of age and receiving no preventive medication. I t should be mentioned t h a t the embryonated H. gallinae ova used in both experiments were taken from one large supply, which had been obtained for use in several histomoniasis challenge experiments.
Experiment 2. Mortality occurred only in the exposed groups which received no p-UBAA (Table 2). Mortality did not exactly follow parallel to levels of histomoniasis exposure; however, more turkeys died in groups receiving 40 or 80 H. gallinae ova per bird as compared to 20 ova per bird. Morbidity followed about the same p a t t e r n as did mortality relative to treatments. The doses of infective material were inadequate to produce mortality in the presence of any level of p-UBAA in this experiment. Both mortality and mor-
When 0.025 percent of p-UBAA was present in the diet, no mortality occurred in experiment 2 following doses of 20 or 40 H. gallinae ova per turkey. Mortality was 50.0 and 56.2 percent, respectively, in experiment 1 when 20 and 40 ova/poult were given to groups fed the same level of p-UBAA. Thus, 0.025 percent of p-UBAA provided much greater protection against exposure to histomoniasis in older turkeys (13 weeks versus 5 weeks of age). I t is quite interesting to compare mortality and morbidity data from experiment 1 to those d a t a from experiment 2, with ref-
1 Each value is the average of 14 birds per treatment group. Values which do not share a letter in common are significantly different from each other (P<0.025) based on Chi-square. 2 Composite main effect means are weighted.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
0.0
D.
UREIDOBENZENEARSONIC ACID AND HISTOMONIASIS
SUMMARY
Two experiments were conducted to determine the efficacy of graded levels of pureidobenzenearsonic acid (p-UBAA) against different levels of exposure to histomoniasis in five and 13-week old turkeys. Data obtained suggest or indicate the following: 1. When p-UBAA was excluded from the diet, graded doses of infective material (embryonated H. gallinae ova) produced graded levels of histomoniasis mortality and morbidity in five-week old
turkeys, and to a much lesser degree in 13-week old turkeys. 2. The lower levels of p-UBAA were clearly more effective against the same exposure to histomoniasis in 13-week old than in five-week old turkeys. When 0.025 percent of p-UBAA was present in the diet, no mortality occurred in 13-week old turkeys following doses of approximately 20 and 40 embryonated H. gallinae ova/bird. In contrast, mortality was 50.0 and 56.2 percent, respectively, following doses of approximately 20 and 40 H. gallinae ova/bird with five week-old poults receiving the same level of p-UBAA. 3. The influence of dietary drug level, age of bird and infective dosage on histomoniasis prevention is discussed. ACKNOWLEDGEMENT
This study was supported in part by a grant from Whitmoyer Laboratories, Inc., a subsidiary of Rohm and Haas Company, Myerstown, Pa. 17067 REFERENCES Lund, E. L., 1955. The progress of histomoniasis (blackhead) in turkeys as related to size of the infective dose. Poultry Sci. 34:127-130. Snedecor, G. W., 1956. Statistical Methods, 5th ed, The Iowa State College Press, Ames, Iowa. Sullivan, T. W., J. R. Kingan, O. D. Grace and G. W. Kelly, 1964. Evaluation of four compounds for the prevention of blackhead lesions and mortality in young turkeys. Poultry Sci. 43: 1367-1368. Sullivan, T. W., J. H. Whitmore, O. D. Grace and J. R. Kingan, 1965. Effect of certain blackhead preventive compounds on growth and their efficacy against histomoniasis in turkeys. Poultry Sci. 44:1420. Welter, C. J., and D. T. Clark, 1961. The efficacy of p-ureidobenzenearsonic acid as a preventive of histomoniasis in turkey poults. Poultry Sci. 40: 144-147.
AUGUST 22-25. NATIONAL POULTRY AND EGG MARKETING CONFERENCE OF INSTITUTE OF AMERICAN POULTRY INDUSTRIES, CHICAGO, ILLINOIS.
Downloaded from http://ps.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on June 6, 2016
erence to all three levels of p-UBAA. These results clearly indicate that lower levels of the compound were more effective against the same exposure to histomoniasis in older birds than in younger birds. Why should the same level of a histomonostatic drug be significantly more effective in older than in younger turkeys? One logical explanation could be the ratio of feed and/or drug intake to dose of infective material. Daily feed consumption of turkeys 13 weeks of age is approximately 2.9 times greater than for poults five weeks old. Thus, if the dose of infective material was similar in both five and 13-week old turkeys, the same dietary drug level (i.e. 0.025% p-UBAA) should be about 2.9 times more effective in the older birds. Data reported herein tend to support this line of reasoning. Therefore, it should and might very well be possible to reduce the level of a histomonostatic drug in feed as turkeys age. Drug levels might be reduced at an inverse rate approximately proportional to the increased feed intake with age.
453