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The influence of diet composition and tissue taurine content on the incidence of sudden death syndrome… Jacob, Jacqueline Patricia 1989

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THE INFLUENCE OF DIET COMPOSITION AND TISSUE TAURINE CONTENT ON THE INCIDENCE OF SUDDEN DEATH SYNDROME B.Sc., The U n i v e r s i t y of B r i t i s h Columbia, 1981 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE in THE FACULTY OF GRADUATE STUDIES (Department of Animal Science) We accept t h i s t h e s i s as conforming IN MALE BROILER CHICKENS by JACQUELINE PATRICIA JACOB to the r e q u i r e d standard THE UNIVERSITY OF BRITISH COLUMBIA A p r i l 1989 J a c q u e l i n e P a t r i c i a Jacob, 1989 In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission. Department of flr»(wved Sci€y>'ca_ The University of British Columbia Vancouver, Canada Date A r , l j i ^ i q f t q DE-6 (2/88) ABSTRACT Five experiments were conducted with male broiler chickens to study the influence of diet composition on the incidence of Sudden Death Syndrome (SDS). In Experiment 1, the effects of 4 levels of dietary lactate ( 0 , 2.5, 5.0 and 7.5% calcium lactate) and 4 levels of dietary glucose (0, 15, 30 and 45% cerelose) were studied in a factorial experiment with 1280 chicks reared in battery brooder cages to 4 weeks of age. There were no significant differences in either total mortality or mortality due to SDS. In Experiments 2, 3 and 4, the chicks were fed isocaloric and isonitrogenous diets with either corn or wheat as the grain type and meat meal or soybean meal as the main protein source. In Experiments 2 and 3, the chicks (6000 and 9600, respectively) were raised in floor pens to 6 weeks of age while in Experiment 4, the chicks (640) were reared in battery brooder cages to 4 weeks of age. SDS mortality was affected by both cereal type and protein source. Broilers fed wheat based diets had a higher incidence of SDS mortality than those fed corn based diets. The incidence of SDS was higher when meat meal was excluded from the diet. In Experiment 5, the chicks were fed diets supplemented with guanidinoethy1 sulfonate (GES), a taurine transport inhibitor in rats. At 4 weeks of age broilers receiving 1.50% dietary GES had significantly lower (p<.05) cardiac taurine concentrations, but significantly higher (p<.05) brain taurine concentrations than controls. There was no effect of GES supplementation on total mortality or the incidence of SDS. iii TABLE OF CONTENTS page Abstract ii Table of Contents iii List of Tables vi List of Figures viii Acknowledgements ix 1.0 Introduction 1 2.0 Literature Review - Sudden death syndrome 4 2.1 Cause of death 4 2.2 Predisposing factors 5 2.2.1 Sex 5 2.2.2 Genet ics 6 2.2.3 Growth rate 6 2.2.4 Time of year 7 2.2.5 Stress 7 2.2.6 Lighting 8 2.2.7 Nutrition 10 2.2.7.1 Minerals 10 2.2.7.2 Vitamins 11 2.2.7.3 Protein 12 2.2.7.4 Energy 12 2.2.7.5 Fat 12 2.2.7.6 Fatty acids 13 2.2.7.7 Cereal type 15 2.2.8 Pelleting 15 2.2.9 Acid-base balance 16 2.2.10 Feed Additives 17 iv 3.0 Literature Review - Taurine 18 3 . 1 Introduction 18 3.2 Functions of taurine 19 3.3 Sources of taurine 20 3.4 Taurine and the heart 23 3.5 Taurine and cardiomyopathy in poultry 24 3.6 Reducing tissue taurine content 25 3.7 Taurine supplementation in broiler diets 26 4.0 The effect of dietary lactate and glucose content on the incidence of SDS in male broiler chickens 27 4 . 1 Abstract 2 7 4 . 2 Introduct ion 28 4.3 Materials and Methods 29 4.3.1 Design and Treatments 29 4.3.2 Management 30 4.3.3 Statistical analysis 30 4.4 Results 32 4.5 Discussion ... 41 5.0 The effect of dietary protein source and cereal type on the incidence of SDS in male broiler chickens .. 42 5 . 1 Abstract 42 5.2 Introduction 43 5.3 Materials and Methods 45 5.3.1 Experiments 2 and 3 - Design and Treat-ments 45 5.3.2 Experiments 2 and 3 - Management 46 5.3.3 Experiment 4 - Design and Treatments . . . . 48 5.3.4 Experiment 4 - Management 48 V 5.3.5 Statistical analysis 49 5.4 Results 49 5.4.1 Experiment 2 49 5.4.2 Experiment 3 . . 54 5.4.3 Experiment 4 60 5.5 Discussion 60 5.5.1 Effect of cereal type 60 5.5.1.1 Mortality 60 5.5.1.2 Mean body weight and feed c onve rsion 61 5.5.2 Effect of dietary protein source 62 5.5.2.1 Mortality 62 5.5.2.2 Mean body weight and feed c onve rsion 64 6.0 The effect of tissue taurine depletion on the incidence of SDS in male broiler chickens 65 6 . 1 Abstract 65 6.2 Introduction 66 6.3 Materials and Methods 69 6.3.1 Design and Treatments 69 6.3.2 Management 71 6.3.3 GES synthesis 72 6.3.4 Taurine analysis 72 6.3.5 Statistical analysis 73 6.4 Results 74 6.5 Discussion 80 7.0 Conclusions 83 8.0 Literature Cited 8 6 vi LIST OF TABLES Table Page 4.1 Composition and calculated analysis of diets,used in Experiment 1 31 4.2 Effect of dietary lactate and glucose on total mortality (Experiment 1): Results at 4 weeks of age .. 33 4.3 Effect of dietary lactate and glucose on SDS mortality as a percent of broilers housed (Experiment 1): Results at 4 weeks of age 34 4.4 Effect of dietary lactate and glucose on SDS mortality as a percent of total mortality (Experiment 1): Results at 4 weeks of age 35 4.5 Effect of dietary lactate and glucose on feed consumption (g/broiler) (Experiment 1): Results at 4 weeks of age 36 4.6 Effect of dietary lactate and glucose on mean body weight (g/broiler) at 4 weeks of age (Experiment 1) .. 37 4.7 Effect of dietary lactate and glucose on feed conversion (g/feed/ g body weight gain) from 0 to 4 weeks of age (Experiment 1) . 38 5.1 Composition and calculated analysis of diets used in Experiments 2, 3 and 4 47 5.2 Effect of diet on final body weight, feed conversion and mortality (Experiment 2): Results at 21 days of age 50 5.3 Effect of diet on final body weight, feed conversion and mortality (Experiment 2): Results at 40 days of age 51 v i i 5.4 Effect of diet on final body weight, feed conversion and mortality (Experiment 3): Results at 21 days of age 55 5.5 Effect of diet on final body weight, feed conversion and mortality (Experiment 3): Results at 40 days of age 56 5.6 Effect of diet on final body weight, feed conversion and mortality (Experiment 4): Results at 28 days of age 59 6.1 Composition and calculated analysis of diets used in Expe r iment 5 70 6.2 Effect of GES supplementation on final body weight (g), feed consumption (g/broiler) and feed conversion (g feed/g body weight gain) (Experiment 5): Results at 4 weeks of age 75 6.3 Effect of GES supplementation on cardiac taurine concentration (umol/g wet weight) (Experiment 5) 76 6.4 Effect of GES supplementation on brain taurine concentration (umol/g wet weight) (Experiment 5) 78 v i i i LIST OF FIGURES Figure Page 3.1 Metabolic pathways r e l a t e d to t a u r i n e b i o s y n t h e s i s .. 22 4.1 E f f e c t of d i e t a r y l a c t a t e , at d i f f e r e n t l e v e l s of d i e t a r y glucose; on mean body weight at 4 weeks of age (Experiment 1) 39 4.2 E f f e c t of d i e t a r y g l u c o s e , at d i f f e r e n t l e v e l s of d i e t a r y l a c t a t e , on mean body weight at 4 weeks of age (Experiment 1) 40 5.1 E f f e c t of d i e t a r y c e r e a l type on feed conversion (g feed/g body weight gain) at 40 days of age (Experiment 2) 52 5.2 E f f e c t of d i e t a r y p r o t e i n source on feed conversion (g feed/g body weight gain) at 40 days of age (Experiment 2) 53 5.3 E f f e c t of d i e t a r y c e r e a l type on feed c o n v e r s i o n (g feed/g body weight gain) at 40 days of age (Experiment 3) 57 5.4 E f f e c t of d i e t a r y p r o t e i n source on feed conversion (g feed/g body weight gain) at 40 days of age (Experiment 3) 58 6.1 E f f e c t of GES supplementation on c a r d i a c t a u r i n e c o n c e n t r a t i o n (Experiment 5) 77 6.2 E f f e c t of GES supplementation on b r a i n t a u r i n e c o n c e n t r a t i o n (Experiment 5) 79 A C K N O W L E D G E M E N T S This research was made possible by funding from the Alberta Farming For the Future Fund and I am grateful for their financial support. There are many other people I would like to ( thank, and without whose assistance this thesis could never have been completed. I would like to thank my graduate supervisor, Dr. Blair, and the other members of my graduate committee, Drs. Hart, Owen and Gardiner, for their patience, comments and guidance. I would also like to thank the farm staff of the UBC Poultry Unit and of the Poultry Section of Agriculture Canada Research Station in Agassiz, B.C. and "the department laboratory technicians for their contributions in time and labour. THE INFLUENCE OF DIET COMPOSITION AND TISSUE TAURINE CONTENT ON THE INCIDENCE OF SUDDEN DEATH SYNDROME IN MALE BROILER CHICKENS 1.0 INTRODUCTION: Sudden Death Syndrome (SDS) refers to the condition in which apparently healthy, fast-growing broiler chicks die suddenly from no apparent cause. There is usually a short, wing-beating convulsion prior to death so that the majority of affected broilers are found dead lying on their backs. As a result, the condition is often referred to as "Flip-Over disease". SDS has also been referred to as "Acute Death Syndrome", "heart attack" and "fatal syncope" (Merck, 1986). Broilers of all ages are affected starting as early as two days of age and continuing through to market age (6 1/2 weeks for broilers and 9 weeks for roasters). Peak mortality usually occurs between 3 and 4 weeks of age (Brigden and Riddell, 1975; Ononiwu et al., 1979b; Gardiner et al., 1988b). In Ontario, however, the period of peak mortality appears to be occurring at a younger age and in 1986 was reported to be between 8 and 20 days of age (Bowes and Julian, 1986). With most of the major disease problems under control, the economic importance of SDS has become more apparent. Since death occurs principally from 3 weeks of age on, the economic loss incurred involves not only the initial cost of the chick, but also the cost of the feed consumed prior to the chicken's death. SDS is recognized as a major cause of mortality in broiler flocks throughout Canada. Cassidy et al. (1975) reported incidences of 2 - 16% in experimental broiler flocks at the Agriculture Canada Research Station in Kentville, Nova Scotia in Eastern Canada. The average incidence in Western Canada that same year appeared to be somewhat lower. Brigden and Riddell (1975) reported an average incidence of 1.13% in 4 broiler flocks in Alberta and Saskatchewan. By 1985 the average level of SDS in Alberta and Saskatchewan appeared to have increased. In a survey of 51 broiler flocks, the average incidence of SDS was 1.95% (Riddell and Springer, 1985). Levels in individual flocks, however, varied from .71 to 4.07%. In Ontario, SDS was reported to affect 1.05% of the broilers housed, representing more than 30% of total mortality (Bowes and Julian, 1986). The SDS reported in Canada appears to be the same as the conditions referred to as "lung edema" in England (Hemsley, 1965) and "died in good condition" in Australia (Jackson et al., 19 7 2). The incidence of SDS reported in Canadian broiler flocks is somewhat higher than those reported for flocks in England and Australia. Hemsley (1965) reported an average incidence of .46% in 14 broiler flocks in England. This represented 23% of total mortality. The survey was done at least 10 years prior to those done in Canada. It is possible the levels of SDS in England have increased to the levels recently reported in Canada. Jackson et al. (1972) surveyed nine flocks on four broiler farms in New South Wales, Australia and an average of .65% of broilers housed (or 15.6% of total mortality) were classified as having "died in good condition". This included SDS affected broilers as well as broilers that died from known panics. When only SDS affected broilers are considered, the average is reduced to .46% of broilers housed (or 11% of total mortality). In 1982, however, Steele and Edgar, also from Australia, reported an average incidence of 2.4%, or 36% of total mortality. . This was, however, in a single broiler flock and in Western Australia rather than in New South Wales. SDS is difficult to study because of its relatively low rate of occurrence and because no particular behavioral or environmental event has been identified as preceding death (Newberry et al., 1987). Various dietary and management practices, as well as a variety of chemicals, have been studied to try and alter the occurrence, but the results have been inconsistent from study to study. The objective of this series of experiments was to find a dietary regime which would increase the incidence of SDS so that its cause could more easily be studied. The following hypotheses were tested: 1. Supplementation with lactate in the diet will induce SDS. 2. Glucose fed broilers are more susceptible to SDS than corn starch fed broilers. 3. The incidence of SDS is higher for wheat fed than corn fed broilers. 4. Exclusion of meat meal from the diet of male broilers will increase the incidence of SDS. 5. Supplementation with guanidinoethy1 sulfonate, a taurine transport inhibitor, will reduce tissue taurine levels and induce SDS. 2.0 LITERATURE REVIEW - SUDDEN DEATH SYNDROME: 2.1 Cause of death: The actual cause of death in SDS cases is unclear and no specific diagnostic lesions are associated with the syndrome. Well fleshed, otherwise healthy broilers, found dead on their backs are usually assumed to have died of SDS since that position is rare in death from other causes (Merck, 1986). SDS affected broilers cannot, however, be diagnosed solely on the basis of their being found on their backs. Newberry et al. (1985) noted that some SDS affected broilers were found dead lying on their sternums while other broilers not diagnosed as having died of SDS were observed to have a sudden attack and were found dead lying on their backs. Affected broilers are well fleshed and were eating normally as indicated by a full or partially full crop containing normal ingesta, feed in the gizzard, distended intestines filled with semi-solid digesta and mucus, and a small or empty gall bladder. The ventricles of the heart are usually contracted and the auricles dilated and filled with blood. No particular bacterial or viral agent has been identified in broilers that died from SDS (Jackson et al., 1972; Bridgen and Riddell, 1975). Some researchers have found lung congestion and edema and have proposed that the lung congestion was a result of heart failure and that the broilers suffocated (Brigden and Riddell, 19 7 5; Ononiwu et al., 1979a). Further studies have shown that lung congestion is not a consistent feature and that freshly dead broilers diagnosed as dying from SDS had no lung congestion (Riddell and Orr, 1980). This suggests that lung congestion is a postmortem change probably 5 related to position at death. Cassidy et al. (1975) observed "blood structures" in the heart chambers of broilers dying from SDS. The structures were found in all four heart chambers with gross appearance unaffected by age or sex. They had a shiny, smooth appearance and were molded to the shape of the chamber. Since these structures are common in broilers affected by SDS, it was thought that they were the cause of death. Histological examination of these structures, however, showed that they were composed of erythrocytes, leucocytes, fibrin and serum with no fibroblasts, collagen fibers or thrombocyte agglutination present. This composition would indicate that the structures were postmortem blood clots. SDS death appears to involve heart damage. Microscopic examination of cardiac muscle from SDS affected broilers showed degeneration of the fibers, separation of the fibers by edema, and infiltration of heterophils (Ononiwu et al., 1979a). Julian and Bowes (1987) have suggested that death is due to left ventricular fibrillation, but there is still no conclusive evidence as to the cause of this fibrillation. 2.2 Predisposing factors: Several factors have been investigated for possible involvement in the etiology of SDS. In many cases the results have been inconsistent from study to study. 2.2.1 Sex: The incidence of SDS is clearly influenced by the sex of the broiler since more than 70% of SDS affected broilers are male (Hemsley, 1965; Brigden and Riddell, 1975; Steele and Edgar, 1982; Riddell and Springer, 1985). It is not 6 c l e a r whether t h i s i s due to t h e i r f a s t e r growth rate or to some e n d o c r i n o l o g i c a l e f f e c t on metabolism. Gardiner et a l . ( 1988a) i n j e c t e d e s t r a d i o 1 - 17g-monop almitate i n t o male b r o i l e r c h i c k s to t r y and a l t e r the i n c i d e n c e of SDS. The e s t r a d i o l treatment i n h i b i t e d e a r l y male sexual development so that at 9 weeks of age combs and t e s t i c l e s from the t r e a t e d b r o i l e r s were 1/4 the weight of those from the c o n t r o l s . There was no e f f e c t of the e s t r a d i o l treatment on the inciden c e of SDS. 2.2.2 G e n e t i c s : Hemsley (1965) observed that SDS m o r t a l i t y was lower with b r o i l e r s of slower growing breeds, such as the L i g h t Sussex c r o s s e s , than with b r o i l e r s of three White Rock s t r a i n s (Arbor Acre, Cobb and P i l c h ) . When females of four d i f f e r e n t maternal breed types were mated to c o r n i s h males, the progeny of the "Cobb" female had twice the i n c i d e n c e of SDS as the progeny of any of the other breeds. Newberry et a l . (1985) noted d i f f e r e n c e s i n the incidence of SDS between b r o i l e r s of two s t r a i n s used in a study on the e f f e c t of a l t e r n a t i n g l i g h t . It would appear that there may be a genetic b a s i s f o r the i n c i d e n c e of SDS. Chambers (unpublished d a t a ) , however, stated that the h e r i t a b i l i t y of SDS was low and concluded that non-g e n e t i c methods should be considered f o r reducing SDS m o r t a l i t y . 2.2.3 Growth r a t e : The i n f l u e n c e of sex and genetics on the i n c i d e n c e of SDS has o f t e n been a t t r i b u t e d to d i f f e r e n c e s in growth rate (Cassidy et a l . , 1975). Ononuwi et a l . (1979b) observed that b r o i l e r s dying from SDS were the heavier b r o i l e r s in the f l o c k . In a d d i t i o n , Gardiner et a l . (1988b) demonstrated that the i n c i d e n c e of SDS increased with body weight of the flock. Brigden and Riddell (1975), however, indicated that SDS affected broilers were of average weight. Mollison et al. (1984) reported that feed restriction, and thus slower growth rate, did not decrease the incidence of SDS. A 13% feed restriction was used and a 15% reduction in mean bod weight obtained. Bowes et al. (19 88), using a 25% feed restriction, reported a 41% reduction in mean body weight and obtained no SDS mortality out of the 300 broilers housed. Although the number of broilers used in the study was low, this would appear to support the hypothesis of relationship between growth rate and the incidence of SDS. A feed restriction of greater than 13%, or a mean body weight reduction of greater than 15%, would appear to be required to reduce the incidence o SDS . Newberry et al. (1985) noted that one strain of male broile chickens had a significantly lower SDS mortality but a higher mean body weight than a second strain used in the same trial. This would suggest that genetics, and not growth rate, is a major predisposing factor in the etiology of SDS. It also suggests that it is possible to use genetic manipulation to reduce the incidence of SDS without depressing growth rate. 2.2.4 Time of year: Gardiner et al. (1988b) observed seasonal fluctuations in the incidence of SDS in male broiler flocks. Those broiler flocks started in the winter months had a higher incidence of SDS than those started in the summer. No reasons for this relationship were proposed. 2.2.5 Stress: Environmental stressors such as noise, social interaction, stocking density and sudden operation of 8 feed auger motors, have been implicated in the etiology of SDS (Ononiwu et al., 1979b; Steele and Edgar, 1982). Using continuous video tape recordings of individually marked male broiler chickens, Newberry et al. (1987) demonstrated that no particular behavioral or environmental event occurred prior to death by SDS. None of the SDS affected broilers died following a sudden loud noise, agonistic interaction, cannabalism or piling up of broilers. Rotter et al. (1985) showed that 2 stocking density (.09 vs .08 m /broiler or 11.1 vs 12.5 2 broilers/m ) had no effect on SDS mortality. It is therefore unlikely that stress plays a major role in the etiology of SDS. Gardiner and Hunt (1984) studied the possibility of reducing the incidence of SDS by inclusion of the compound reserpine (3,4,5-trimethoxy-benzoy1 methyl reserpate) at low levels (0 to 3 mg/kg) in the diet. Resperine is an anti-hypertensive and tranqui1izing agent that has been included in poultry diets as an anti-stress compound. They concluded that neither total mortality nor mortality due to SDS was affected by dietary reserpine. 2.2.6 Lighting: Ononiwu et al. (1979b) reported that the incidence of SDS in mixed-sex flocks could be reduced by using intermittent (1 h light: 3 h dark per 4 hour period phased in over a 14 day period after 10 days of age) rather than continous lighting. Total mortality was not affected indicating that mortality due to causes other than SDS increased. Carcass fatness was reduced and there was improved feed efficiency. The effect of intermittent lighting on mean body weight was not reported. Cave (1981) indicated that mortality, including SDS, was not s i g n i f i c a n t l y d i f f e r e n t between b r o i l e r s of both sexes r e c e i v i n g i n t e r m i t t e n t l i g h t (1 h l i g h t : 3 h dark per 4 hour p e r i o d from day old) and those r e c e i v i n g continuous l i g h t . Again carcass f a t n e s s was reduced and there was improved feed e f f i c i e n c y . There was no e f f e c t of l i g h t i n g program on weight g a i n . Newberry et a i . (1985) st u d i e d the e f f e c t s of r e a r i n g male b r o i l e r s to r o a s t e r weight under a program of a l t e r n a t i n g b r i g h t l i g h t from s i d e - t o - s i d e w i t h i n pens at r e g u l a r i n t e r v a l s , versus continuous l i g h t i n g . The l i g h t treatment had no e f f e c t on SDS m o r t a l i t y , mean 70-day body weight or feed to gain r a t i o s . L i g h t i n t e n s i t y has been shown to a f f e c t b r o i l e r perform-ance. Skoglund and Palmer (1962) i n d i c a t e d that b r o i l e r s were heavier when reared under i n t e n s i t i e s of 22 or 54 lux than when reared under very high i n t e n s i t y (1292 lux) l i g h t . Ononiwu et a l . (1979b) proposed that i f l i g h t i n t e n s i t y was above optimum i t would induce c a n n i b a l i s m , excitement, f i g h t i n g and p i l i n g . Such a c t i v i t i e s would add to the s t r e s s of the b r o i l e r s . Newberry et a l . (1985) observed that b r o i l e r s were more l i k e l y to be a f f e c t e d by SDS i n the l i g h t e d areas (6 or 12 lux) than in the darker areas of the pen (.5 l u x ) . L i g h t i n t e n s i t y was, t h e r e f o r e , i n v e s t i g a t e d f o r p o s s i b l e e f f e c t on the occurrence of SDS. R i d d e l l and Springer (1985) f a i l e d to f i n d a c o r r e l a t i o n between m o r t a l i t y due to SDS and l i g h t i n t e n s i t y w i t h i n the range of .1 to 13.2 l u x . Newberry et a l . (1986), using l i g h t i n t e n s i t i e s v a r y i n g from .1 to 100 l u x , reported that l i g h t i n t e n s i t y had no e f f e c t on t o t a l m o r t a l i t y or m o r t a l i t y due to SDS. It i s t h e r e f o r e u n l i k e l y that l i g h t i n t e n s i t y i s a contributing factor in the incidence of SDS. 2.2.7 Nutrition: Several dietary factors have been investigated for their involvement in the incidence of SDS including levels of minerals, vitamins, protein, energy and fat. 2.2.7.1 Minerals: A condition similar to SDS in broilers has been identified in broiler breeders and commercial hens at onset of egg production (Hopkinson et al., 1983; Pass, 1983). The condition was shown to be due to a dietary potassium deficiency. Supplementation with potassium bicarbonate in the water (.62 g/layer) or potassium carbonate in the feed (.36%) prevented the syndrome. Hunt and Gardiner (1982) demonstrated that supplementation with .1, .2 or .3% potassium carbonate to a wheat-soy diet did not influence total mortality or the incidence of SDS in male broiler chickens. Dietary fat forms calcium and magnesium soaps in the digestive tract of chickens making these minerals unavailable for absorption. Julian (1986) proposed that SDS was caused by acute hypomagnesemic tetany as a result of magnesium lost in the faeces. Supplementation with .2% calcium, .2% phosphorus and .2% magnesium, however, had no effect on the incidence of SDS. Bowes et al. (1989) compared the serum biochemical profiles of male broilers with female broilers and male White Leghorn chickens. (SDS has not been identified in White Leghorn chickens). There were no significant differences in serum potassium, phosphorus or magnesium levels. Serum calcium levels in male White Leghorns were, however, found to be significantly higher than those found in male broilers at 9 days of age. There were no significant differences at 20, 30 or 42 days of 11 age. Riddell and Orr (1980) compared the potassium, magnesium, sodium and glucose levels of blood and hearts from broilers dying from SDS with those of normal healthy broilers. They observed no consistent differences. Rotter et al. (1985) reported that the calcium in the heart tissue of SDS broilers was significantly higher than in culled broilers. In subsequent studies, however, Rotter et al. (1987) and Rotter et al. (1988) observed no significant differences in cardiac calcium levels between these two groups. 2.2.7.2 Vitamins: Hulan et al. (1980) studied the effects of biotin, pyridoxine and thiamin supplementation, singly or in combination, on the incidence of SDS. The B vitamins function principally as coenzymes. For example, biotin is involved in carboxy1 ation reactions, pyridoxine in protein metabolism and thiamin in decarboxylation of <*-keto acids and in the transketo1 ation reaction in the monophosphate shunt pathway of glucose metabolism. Inclusion of biotin alone, at 300 ug/kg diet (2 times NRC requirements), significantly reduced total mortality (p<.005) and the incidence of SDS (p<.05). Inclusion of biotin at the same level, but combined with 5 mg pyridoxine per kg diet (1.7 times NRC requirment) and 3 mg thiamin per kg diet (1.7 times NRC requirment) did not significantly affect SDS mortality. No reasons for this interaction were proposed. Steele et al. (1982) reported that the occurrence of SDS was unaffected by supplementation of high levels (1.2 to 25 times NRC require-ments for different stages of growth) of biotin in the water. Uptake was confirmed by radioisotopic analysis of liver biotin. Whitehead and Randall (1982), Hunt and Gardiner (1982), and M o l l i s o n et a l . (1984) also f a i l e d to f i n d any e f f e c t of b i o t i n supplementation on the incidence of SDS. It i s t h e r e f o r e u n l i k e l y that d i e t a r y b i o t i n i s inv o l v e d i n the e t i o l o g y of SDS. 2.2.7.3 P r o t e i n : The e f f e c t of d i e t a r y p r o t e i n l e v e l on the incidence of SDS i s u n c l e a r . M o l l i s o n et a l . (1984) observed that the incidence of SDS was s i g n i f i c a n t l y reduced by feeding a 24% p r o t e i n f i n i s h e r d i e t as compared to feeding a 19% f i n i s h e r d i e t . The d i e t s were i s o c a l o r i c (3100 k c a l AME/kg). J u l i a n and Bowes (1987), however, reported no s i g n i f i c a n t d i f f e r e n c e s in the incidence of SDS among b r o i l e r s fed i s o c a l o r i c (3100 k c a l AME/kg) d i e t s with high ( 3 1 % ) , medium (24%) or low (17%) p r o t e i n content. 2.2.7.4 Energy: J u l i a n and Bowes (1987) st u d i e d three d i e t a r y energy sources and t h e i r e f f e c t on the incidence of SDS. In f l o c k s fed d i e t s with s i m i l a r energy (3100 kc a l AME/kg) and p r o t e i n (24%) content, the occurrence of SDS was higher when glucose monohydrate was the energy source as compared to t a l l o w or cor n . They hypothesized that SDS i s r e l a t e d to a problem with carbohydrate metabolism. There may be a p r o t e i n x c e r e a l i n t e r a c t i o n a f f e c t i n g the inci d e n c e of SDS. J u l i a n and Bowes (1987) reported that the inci d e n c e of SDS was s i g n i f i c a n t l y higher in b r o i l e r s reared on a high p r o t e i n ( 2 8 % ) , high c a l o r i c (3100 k c a l AME/kg) d i e t than those reared on a low p r o t e i n ( 1 8 % ) , low c a l o r i c (2400 k c a l AME/kg) d i e t . 2.2.7.5 Fat: Rotter et a l . (1985) proposed that f a t metabolism may be in v o l v e d i n the e t i o l o g y of SDS and that d i e t a r y f a t type may play a r o l e in pr e v e n t i o n of i t s occurrence. They reported that the incidence of SDS, but not total mortality, was lower when a wheat-soy diet was supplemented with sunflower oil (an unsaturated fat) than when the same diet was supplemented with tallow (a saturated fat). In a later study (Rotter e t ' a 1 .", 1988), the effects of hydrogenated coconut oil (HCO), tallow, sunflower oil (SFO) and tallow/SFO on the incidence of SDS were investigated. There was no effect of dietary fat type on overall mortality. SDS mortality between 0 and 4 weeks of age, however, was significantly lower for the broilers receiving the HCO (a saturated fat) diet as compared to those receiving the SFO (an unsaturated fat) diet. This contradicts the earlier findings that feeding an unsaturated fat resulted in a lower incidence of SDS than feeding a saturated fat. 2.2.7.6 Fatty Acids: Rotter et al. (1985) analyzed the fatty acid composition of heart and liver tissues from SDS affected broilers in comparison with those from culled broilers. In the heart, palmitic (16:0') and oleic (18:1) acids were higher in the tissues from the SDS affected broilers while the linoleic (18:2) and arachidonic (20:4) acids were lower. In the liver, oleic acid levels were higher in SDS affected broilers while linoleic and arachidonic acids were lower. Linoleic acid is converted to arachidonic acid which in turn is a precursor of prostaglandins. Prostaglandins have a wide variety of roles including modulating and regulating myocardial contractile force, heart rate, and cardiac rhythms. Rotter et al. (1985) proposed that a deficiency of arachidonic acid would reduce the amount of prostaglandins that would be synthesized so that heart f u n c t i o n would be d i s r u p t e d l e a d i n g to f i b r i l l a t i o n or arrhythmia. Since b i o t i n plays a r o l e in the conversion of l i n o l e i c a c i d to a r a c h i d o n i c a c i d , Rotter et a l . (1985) also hypothesized on the r o l e of b i o t i n s t a t u s in the e t i o l o g y of SDS. In a subsequent study, Rotter et a l . (1987) f a i l e d to f i n d a n - e f f e c t of d i e t a r y l i n o l e i c a c id c o n c e n t r a t i o n on the inci d e n c e of SDS. T h e r e f o r e , the r o l e of l i n o l e i c a c i d i n the e t i o l o g y of SDS remains q u e s t i o n a b l e . As p r e v i o u s l y s t a t e d , Rotter et a l . (1985) reported that c a r d i a c and he p a t i c a r a c h i d o n i c a c i d l e v e l s were lower in SDS a f f e c t e d b r o i l e r s than i n c u l l s . In a subsequent study, however, Rotter et a l . (1988) compared the f a t t y a c i d composition of heart and l i v e r t i s s u e s from SDS a f f e c t e d and normal, healthy b r o i l e r s . They observed s i g n i f i c a n t l y reduced a r a c h i d o n i c l e v e l s i n hearts from the SDS b r o i l e r s but no d i f f e r e n c e s in l i v e r l e v e l s . Wu and Nakue (1987), however, reported decreased a r a c h i d o n i c a c i d l e v e l s in the l i v e r of SDS a f f e c t e d b r o i l e r s when compared to l e v e l s in c o n t r o l s . Contrary to the r e s u l t s already presented, Buckley et a l . (1987) reported that heart and l i v e r t i s s u e a r a c h i d o n i c acid l e v e l s were g e n e r a l l y higher i n SDS than i n c o n t r o l c h i c k e n s . Buckley et a l . (1987) observed s i g n i f i c a n t l y higher l e v e l s of unsaturated f a t t y a c i d s , as i n d i c a t e d by the double bond in d e x : s a t u r a t e d f a t t y a c i d r a t i o , i n the hepa t i c triacy1g1ycero1 f r a c t i o n of SDS b r o i l e r s and hypothesized that t h i s may increase membrane f l u i d i t y d i s r u p t i n g the a c t i v i t y of membrane bound enzymes. A r e d u c t i o n i n p r o s t a g l a n d i n s y n t h e s i s cannot, t h e r e f o r e , be r u l e d out as a cause of SDS. 15 2.2.7.7 Cereal Type: The involvement o f . c e r e a l type on the e t i o l o g y of SDS i s u n c l e a r . Hunt and Gardiner (1982) s t a t e d that there were no d i f f e r e n c e s in t o t a l m o r t a l i t y or m o r t a l i t y a t t r i b u t e d to SDS between b r o i l e r s fed wheat-soy or corn-soy based d i e t s . On the other hand, M o l l i s o n (1983) reported that b r o i l e r s fed wheat-soy d i e t s had higher incidences of SDS than those fed corn-soy d i e t s . In a l a t e r study, however, M o l l i s o n et a l . (1984) showed that corn-fed b r o i l e r s had s i g n i f i c a n t l y b e t t e r weight gains and feed to gain r a t i o s than wheat-fed groups, but t o t a l and SDS m o r t a l i t y were not a f f e c t e d . In a survey of m o r t a l i t y i n 51 b r o i l e r f l o c k s in A l b e r t a and Saskatchewan, R i d d e l l and Springer (1985) noted a r e l a t i o n s h i p between the incidence of SDS and the type of d i e t a r y c e r e a l used. The incidence of SDS was higher i n f l o c k s s u p p l i e d by a feed company which used l e s s c o r n , and more wheat, than the other feed companies used by the b r o i l e r farms surveyed. 2.2.8 P e l l e t i n g : Proudfoot and Hulan (1982) and Hulan and Proudfoot (1987) observed higher SDS m o r t a l i t y in male b r o i l e r chickens fed a crumb1ed-pe11et d i e t versus those fed an all-mash d i e t . Since the b r o i l e r s r a i s e d on the crumb1ed-pe11et d i e t a l s o had i n c r e a s e d body weights, i t was unclear whether the i n c r e a s e i n SDS m o r t a l i t y was due to the p e l l e t i n g or to i n c r e a s e d growth r a t e . Proudfoot et a l . (1982) reported no s i g n i f i c a n t d i f f e r e n c e s i n growth r a t e s of b r o i l e r s fed ground crumb1ed-pe11et d i e t s as compared with those fed all-mash d i e t s yet the i n c i d e n c e of SDS was higher i n b r o i l e r s fed the former. They t h e r e f o r e concluded that the higher i n c i d e n c e of SDS 1 6 a s s o c i a t e d with crumb1ed-pe11et d i e t s was due to some f a c t o r ( s ) in the p e l l e t i n g process r a t h e r than the increased growth rate r e s u l t i n g from the higher d e n s i t y of p e l l e t e d f e e d s . Proudfoot et a l . (1984) demonstrated that the incidence of SDS was s i g n i f i c a n t l y reduced when the d i e t a r y p r o t e i n supplements of soybean meal, canola meal and fishmeal bypassed the p e l l e t i n g p r o c e s s . There was no r e d u c t i o n in SDS m o r t a l i t y when e i t h e r the m i c r o n u t r i e n t or f a t components bypassed the p e l l e t i n g p r o c e s s . They hypothesized that a t o x i c f a c t o r ( s ) was produced when p r o t e i n supplements are subjected to p e l l e t i n g , which may be inv o l v e d in causing SDS. 2.2.9 Acid-base balance: Summers et a l . (1987) have shown that l a c t i c a c id and/or a d i s r u p t i o n of acid-base balance may be i n v o l v e d in the e t i o l o g y of SDS. L a c t i c a c i d i s produced in the chicken as a waste product of anaerobic o x i d a t i o n and i s produced in large q u a n t i t i e s when white muscles are a c t i v e . L a c t i c a c i d i s also a fermentation product which i s produced in the crop. The l e v e l of l a c t i c a c id i n the crop depends upon the amount and type of feed present and the length of time the feed remains i n the crop. Chickens fed mash d i e t s have been shown to have a crop l a c t i c a c id c o n c e n t r a t i o n three times higher than that of b i r d s maintained on a p e l l e t e d d i e t . The l a c t i c acid produced i n the crop i s absorbed i n t o the blood system ( B o l t o n , 1965). Summers et a l . (1987) p i p e t t e d 5 ml of a 20% l a c t i c acid s o l u t i o n i n t o the crop of 2 week old male b r o i l e r chickens maintained on a r e g u l a r b r o i l e r s t a r t e r d i e t . Within a few minutes the b r o i l e r s f l i p p e d in a manner s i m i l a r to those 1 7 diagnosed as being a f f e c t e d by SDS. B r o i l e r s fed glucose supplemented d i e t s were more prone to f l i p on l a c t i c a c i d dosing than those fed a s t a r c h or f a t supplemented d i e t . J u l i a n and, Bowes (1987), however, observed that blood l a c t a t e l e v e l s were high i n some b r o i l e r s not a f f e c t e d by SDS, but were not el e v a t e d in b r o i l e r s that had died from SDS. 2.2.10 D i e t a r y a d d i t i v e s : Proudfoot and Hulan (1983) evaluated the e f f e c t s of a s p i r i n (ASA) as a p r o p h y l a c t i c drug to reduce the incidence of SDS in b r o i l e r s . No b e n e f i c i a l e f f e c t on the i n c i d e n c e of SDS was observed and t o t a l m o r t a l i t y was i n c r e a s e d . The a d d i t i o n of ASA at .16% of the d i e t r e s u l t e d in decreased body weights. 18 3.0 L I T E R A T U R E REVIEW - T A U R I N E : 3.1 I n t r o d u c t i o n : Taurine was f i r s t i s o l a t e d from ox b i l e in 1827 (Tiedemann and Gmelin, 1827) and f o r many years was b e l i e v e d to be s o l e l y an exc r e t o r y product of s u l f u r amino acid metabolism. It has since been shown to be a major component of the free amino a c i d pool in animal body t i s s u e s (Jacobsen and Smith, 1968). S t r u c t u r a l l y t a u r i n e (t^N-CI^-CI^-SO^H) i s a g - s u l p h o n i c acid while the more common amino acids are a- c a r b o x y 1ic a c i d s . The sulphonic a c i d (pK = 1.5) and ammonium (pK = 8.7) f u n c t i o n s of t a u r i n e are more a c i d i c than the c a r b o x y l i c a c i d (pK = 2) and ammonium (pK - 9) f u n c t i o n s of c-amino a c i d s . As a r e s u l t , t a u r i n e forms l e s s s t a b l e complexes with the v a r i o u s t r a n s i t i o n -a l metals (Wright et a l . , 1986). The a b i l i t y of amino acids to form metal complexes i s an important f e a t u r e of t h e i r b i o l o g i c a l a c t i v i t y . Muscle c o n t a i n s the bulk of body t a u r i n e , e s p e c i a l l y red muscle which, i n the c h i c k e n , has c o n c e n t r a t i o n s twenty times those found i n white muscle (21.3 _+ 3.7 and 1.1 _+ .3 umole/g wet weight, r e s p e c t i v e l y ) (Airaksenen and Partanen, 1985). The c o n c e n t r a t i o n s found i n animal t i s s u e s vary between organs and between s p e c i e s . For example, l e v e l s of t a u r i n e i n the heart vary from 40 umoles per gram wet weight f o r the adult rat to 4 umoles per gram wet weight f o r the cow,(Huxtable, 1978). In g e n e r a l , the heart has the highest t a u r i n e c o n c e n t r a t i o n s and the l i v e r shows the g r e a t e s t amount of v a r i a t i o n (Awapara et al , . 1950 ) . Although t a u r i n e i s widespread in animals, i t has a very l i m i t e d d i s t r i b u t i o n i n p l a n t s (Jacobsen and Smith, 1968; Kataoka and O h n i s h i , 1986). T a u r i n e , or t a u r i n e d e r i v a t i v e s , have been i d e n t i f i e d in some marine species of algae and some f u n g i . In the higher p l a n t s , t a u r i n e was i d e n t i f i e d i n the p o l l e n of some d i c o t y l e d o n s while no t a u r i n e has been detected in others (Jacobsen and Smith, 1968). When t a u r i n e i s present in p l a n t s i t i s at c o n c e n t r a t i o n s about 1% of those found in animal t i s s u e s (Kataoka and O n h i s h i , 1986). 3.2 Functions of Taurine: The f i r s t c l e a r l y recognized f u n c t i o n of t a u r i n e was b i l e a c i d c o n j u g a t i o n . G l y c i n e and t a u r i n e b i l e s a l t s aid i n the e m u 1 s i f i c a t i o n of d i e t a r y l i p i d s This i n c r e a s e s the surface area a v a i l a b l e f o r attack by the d i g e s t i v e enzymes and f a c i l i t a t e s a b s o r p t i o n of the f r e e f a t t y a c i d s . Taurine b i l e s a l t s have two advantages over g l y c i n e b i l s a l t s i n that they are more r e s i s t a n t to m i c r o b i a l degradation and they aid i n the a b s o r p t i o n of long chain s a t u r a t e d f a t t y a c ids (anonymous, 1988). There i s c o n s i d e r a b l e species d i f f e r e n c e s i n regard to which of the two amino acids ( g l y c i n e or t a u r i n e ) i s used f o r b i l e a c i d c o n j u g a t i o n (Sturman and Hayes, 1980). In g e n e r a l , h e r b i v o r e s use predominantly g l y c i n e while c a r n i v o r e s used mainly t a u r i n e . The b i l e of the domestic f o w l , an omnivore, con t a i n s both t a u r i n e and g l y c i n e b i l e s a l t s (Duke, 1988). Taurine a l s o appears to play a r o l e in r e g u l a t i n g i n t r a -c e l l u l a r osmotic p r e s s u r e . This i s p a r t i c u l a r l y evident i n marine i n v e r t e b r a t e s . Surveys on the amino a c i d content of marine, b r a c k i s h - and f r e s h - water crustaceans have shown that t a u r i n e c o n c e n t r a t i o n s are higher i n the marine species ( A l l e n 20 and G a r r e t t , 1971). Taurine a l s o appears to play a r o l e i n r e g u l a t i n g i n t r a c e l l u l a r osmotic pressure in the higher animals (van Gelder and Barbeau, 1985). I n t e r e s t i n t a u r i n e increased when i t was shown to be an e s s e n t i a l n u t r i e n t f o r c a t s . Cats r a i s e d on a t a u r i n e - f r e e d i e t developed r e t i n a l degeneration lead i n g to b l i n d n e s s (Berson et a l . , 1976). It now appears that t a u r i n e i s e s s e n t i a l f o r ma i n t a i n i n g the s t r u c t u r a l and f u n c t i o n a l i n t e g r i t y of photo-r e c e p t o r s , outer segments and tapetum lucidum of the eye (Huxtable and Se b r i n g , 1976). Taurine has r e c e n t l y been shown to be i n v o l v e d i n a wide v a r i e t y of phenomena. For example, t a u r i n e has been shown to act as an anti-convu1sant and has been b e n e f i c i a l i n the treatment of e p i l e p s y ( K o i v i s t o et a l . , 1986). It i s b e l i e v e d to act as a neuromodulator by s t a b i l i z i n g e x c i t a b l e membranes and by suppressing the r e l e a s e of n e u r o t r a n s m i t t e r s at synapses (Kuriyama, 1980). Taurine also appears to p o t e n t i a t e the e f f e c t s of i n s u l i n s i n c e , i n the presence of i n s u l i n , i t st i m u l a t e d g l y c o l y s i s and gl y c o g e n e s i s (Lampson et a l . , 1983). 3.3 Sources of t a u r i n e : Tissue t a u r i n e i s d e r i v e d from e i t h e r exogenous or endogenous sources. The r e l a t i v e importance of the two sources v a r i e s between species and appears to be r e l a t e d to d i e t . In g e n e r a l , c a r n i v o r e s , which have a large d a i l y supply of d i e t a r y t a u r i n e , have l i t t l e or no c a p a c i t y f o r t a u r i n e b i o s y n t h e s i s while h e r b i v o r e s , which r e c e i v e l i t t l e or no t a u r i n e i n the d i e t , are presumably able to syn t h e s i z e a l l t h e i r own t a u r i n e (Huxtable and L i p p i n c o t t , 1982). Species d i f f e r i n t h e i r a b i l i t y to s y n t h e s i z e t a u r i n e from 2 1 v a r i o u s p r e c u r s o r s . Five main pathways have been i d e n t i f i e d (see f i g u r e 3.1). They are summarized as f o l l o w s : Pathway I: methionine-cysteine-cysteine sulfinic acid-hypotaurine-taurine Pathway II: methionine-cysteine-cysteine sulfinic acid-cysteic acid-taurine Pathway III: cysteamine/cystamine-inteni^iates-hypotaurine-taurine Pathway IV: sulfate-sulfite-intermediates-cysteic acid-taurine Pathway V: cystine-cystine disulfoxide-cystamine disulfoxide-hypotaurine-taurine In the domestic fowl t a u r i n e i s s y n t h e s i z e d by at l e a s t three d i f f e r e n t pathways (Jacobsen and Smith, 1968). The chick embryo l i v e r i s capable of producing t a u r i n e from methionine and c y s t i n e with c y s t e i n e s u l f i n i c a c id (CSA) and c y s t e i c a c i d (CA) as i n t e r m e d i a t e s . No hypotaurine formation was observed, i n d i c a t i n g that CA was decarboxy1 ated while CSA was not. It was thus concluded that in the embryonic l i v e r t a u r i n e i s s y n t h e s i z e d v i a pathway II and that pathway I does not operate. The posthatch c h i c k l i v e r decarboxylase a l s o has a higher a f f i n i t y f o r CA than CSA i n d i c a t i n g that t a u r i n e s y n t h e s i s proceeds v i a pathway I I . There i s , however, s l i g h t but d e f i n i t e CSA-decarboxy1 ase a c t i v i t y i n d i c a t i n g that pathway I also o p e r a t e s , but to a l i m i t e d e x t e n t . It was not c l e a r whether the c h i c k l i v e r contained CSA s p e c i f i c decarboxylases not present in the embryonic l i v e r , in a d d i t i o n to a C A - s p e c i f i c decarboxylase, or whether i t was one enzyme which p r e f e r e n t i a l l y acts on CA but which can decarboxy 1 ate CSA to a l i m i t e d e x t e n t . In the chicken b r a i n a d i f f e r e n t s i t u a t i o n has been observed i n that there appears to be a higher a c t i v i t y of CSA decarboxyl-a t i o n (to hypotaurine) than CA d e c a r b o x y l a t i o n (Jacobsen et a l . , 1964). Thus, in the chicken b r a i n , b i o s y n t h e s i s of t a u r i n e 22 Figure 3.1 Metabolic pathways related to taurine biosynthesis METHIONINE HOMOCYSTEINE « = * HOMOCYSTINE serine CYSTATHIONINE homoserine^ CYSTEINE — •» CYSTEAMINE^CYSTAMINE CYSTINE CYSTEINE DISULFOXIDE K c o 2 CYSTAMINE DISULFOXIDE CYSTEINE SULFINIC ACID—r-HYPOTAURINE CYSTEIC ACID TAURINE SULFITE SULFATE serine 23 appears to f o l l o w pathway I. Chicken t i s s u e s have also been shown to s y n t h e s i z e t a u r i n e from i n o r g a n i c s u l f a t e f o l l o w i n g pathway IV (Machlin et a l . , 1955; M a r t i n , 1972). The s u l f a t e i s reduced to s u l f i t e which is then used together with L - s e r i n e i n the p r o d u c t i o n of L - c y s t e i c a c i d . Pathway IV may be important in t a u r i n e p r o d u c t i o n in the h e a r t . In the s t r e s s e d heart t r a n s p o r t appears to be more important than b i o s y n t h e s i s i n the r e g u l a t i o n of c a r d i a c t a u r i n e l e v e l s . The rate of b i o s y n t h e s i s of t a u r i n e in the rat i s c o n s t a n t . With i n c r e a s i n g d i e t a r y t a u r i n e content the h a l f - l i f e of endogenous t a u r i n e decreases (Huxtable and L i p p i n c o t t , 1982). The i n c r e a s e i n t a u r i n e content a s s o c i a t e d with congestive heart f a i l u r e appears to be due to an increase i n t a u r i n e i n f l u x with no a l t e r a t i o n i n t a u r i n e b i o s y n t h e s i s (Huxtable, 1980). 3.4 Taurine and the heart: Taurine appears to play a r o l e in r e g u l a t i n g heart f u n c t i o n but i t i s u n c l e a r what that f u n c t i o n i s . It i s present in large c o n c e n t r a t i o n s i n heart muscle and may represent more than 50% of the f r e e amino a c i d pool ( K o c s i s et a l . , 1976). Myocardial metabolism of r a t s was found to be s i g n i f i c a n t l y a l t e r e d by a d e p l e t i o n of c a r d i a c t a u r i n e ( M o z a f f a r i et a l . , 1986) and t a u r i n e d e f i c i e n t cats have been shown to s u f f e r from myocardial f a i l u r e (Pion et a l . , 1987). Taurine has also been shown to have pharmacological value in the treatment of congestive heart f a i l u r e (Azuma et a l . , 1 985 ) . Read and Wetly (1963) showed that t a u r i n e a d m i n i s t r a t i o n (.5 mmol/kg body weight) prevented the development of 24 epinephrine and d i g o x i n induced arrhythmias i n dogs. Higher doses (2 to 10 mmole/kg body weight) reversed e x i s t i n g a r rhyt hm i a s . Kramer et a l . (1978) noted that t a u r i n e p r o t e c t e d the rat heart against calcium paradox. Calcium paradox r e f e r s to the phenomenon that occurs when a heart i s perfused with calcium-f r e e medium and then reexposed to p h y s i o l o g i c a l calcium c o n c e n t r a t i o n s . The zero calcium p e r f u s i o n r e s u l t s i n changes to membrane u l t r a s t r u c t u r e and p e r m e a b i l i t y so that reexposure to calcium leads to calcium o v e r l o a d . Extensive c e l l u l a r and f u n c t i o n a l damage r e s u l t . The presence of t a u r i n e i n the c a l c i u m - f r e e medium prevents the l o s s of p e r m e a b i l i t y and, thus the calcium overload and c e l l u l a r damage that occurs on reexposure. Taurine appears to be a c t i n g as a membrane s t a b i l i z e r (Huxtable and B r e s s l e r , 1973) and may be modulating ion f l u x e s (Hayes, 197 6; Huxtable and S e b r i n g , 1986). 3.5 Taurine and cardiomyopathy in p o u l t r y : F u r a z o l i d o n e (CgH^N^^) ^s a n a n t i b a c t e r i a l and a n t i p r o t o z o a n agent added to p o u l t r y feeds (recommended dose i s 110 mg/kg) to t r e a t a number of d i s e a s e s . In turkey p o u l t s the incidence of cardiomyopathy has been shown to increase with f u r a z o l i d o n e dose (Czarnecki et a l . , 1974). The f u r a z o l i d o n e induced cardiomyopathies resembled the spontaneous round-heart syndrome and i n v o l v e d damage to the myocardial c e l l s ( C z a r n e c k i , 1980) and a l t e r a t i o n of glycogen metabolism (Czarnecki and Evanson, 1980). F u r a z o l i d o n e t r e a t e d p o u l t s had s i g n i f i c a n t l y (p<.001) reduced c a r d i a c t a u r i n e content but b r a i n and muscle l e v e l s were u n a f f e c t e d ( S c h a f f e r et a l . , 1982). Oral a d m i n i s t r a t i o n of t a u r i n e to turkeys not t r e a t e d with f u r a z o l i d o n e s i g n i f i c a n t l y (p<.001) increased t a u r i n e l e v e l s of the b r a i n , muscle and h e a r t . Oral administra-t i o n of t a u r i n e to f u r a z o l i d o n e t r e a t e d turkeys r e s t o r e d myocardial, t a u r i n e to normal l e v e l s but did not a l t e r . t h e i n c i d e n c e of f u r a z o l i d o n e induced cardiomyopathies ( S c h a f f e r et a l . , 1982). 3.6 Reducing t i s s u e t a u r i n e content: Taurine i s taken up be a s a t u r a b l e a c t i v e t r a n p o r t system. Hypotaurine, g - a l a n i n e , and guandinoethy1 s u l f o n a t e (GES) are s t r u c t u r a l anologs of t a u r i n e and have been shown, in v i t r o , to'be com p e t i t i v e i n h i b i t o r s of t a u r i n e t r a n s p o r t ( A z a r i et a l . , 1979). Hypo-t a u r i n e e x i s t s n a t u r a l l y i n c e l l s as an intermediate in t a u r i n e s y n t h e s i s and would not be expected to be an e f f e c t i v e t a u r i n e t r a n s p o r t i n h i b i t o r in v i v o . Transport of g-alanine i n t o the heart has both a s a t u r a b l e and a nonsaturable component while GES i s t r a n s p o r t e d by a s a t u r a b l e process only (Huxtable et a l . 1981) GES i s a n a t u r a l l y o c c u r r i n g substance found in the muscle t i s s u e and g a s t r o i n t e s t i n a l t r a c t of some i n v e r t e b r a t e s . GES was not detected i n the b r a i n , blood or heart of r a t s , but was detected at low l e v e l s in the l i v e r , kidney and muscles ( G u i d i t t o and C o s t a g l i , 1970). A marked decrease in i n v i v o t i s s u e t a u r i n e content in r a t s can be achieved by supplementing the d r i n k i n g water with 1% GES (Huxtable et a l . , 1979). Cardiac t a u r i n e l e v e l s were reduced t 20-30% of normal while the l e v e l s of the other amino acids remained u n a f f e c t e d . The i r r e d u c i b l e p o r t i o n of the c a r d i a c t a u r i n e content was due to b i o s y n t h e s i s w i t h i n the h e a r t . This i r r e d u c i b l e p o r t i o n w i l l vary between species depending upon the c a p a c i t y f o r t a u r i n e s y n t h e s i s . The a b i l i t y of GES to deplete t i s s u e t a u r i n e content shows c o n s i d e r a b l e species v a r i a t i o n (Huxtable and L i p p i n c o t t , 1981). Rats and mice do not metabolize GES so that a d m i n i s t r a t i o n of 1% GES i n the d r i n k i n g water of r a t s or mice fed t a u r i n e f r e e d i e t s causes l a r g e decreases in t i s s u e t a u r i n e c o n c e n t r a t i o n s w i t h i n a few days. GES a d m i n i s t r a t i o n has no e f f e c t on t a u r i n e l e v e l s in the guinea pig since t h i s animal i s herbivorous and would, presumably, not be dependent on the d i e t as a source of t a u r i n e . Cats fed t a u r i n e f r e e d i e t s and given 1% GES in the water do not have a decrease in t i s s u e t a u r i n e l e v e l s since they are able to metabolize GES to t a u r i n e . 3.7 Taurine supplementation i n b r o i l e r d i e t s : M i l l e r et a l . (1987) supplemented the d i e t of male b r o i l e r chickens with t a u r i n e (0 to .6%) and reported that t a u r i n e supplementation had no e f f e c t on growth rate or feed e f f i c i e n c y . Any e f f e c t s on m o r t a l i t y were not r e p o r t e d . Campbell and Classen (unpublished data) a l s o supplemented the d i e t s of male b r o i l e r chickens with t a u r i n e (0 to . 2 % ) . They found that t a u r i n e supplementation did not a f f e c t growth rate but improved feed e f f i c i e n c y . There was a l s o some evidence that t o t a l m o r t a l i t y and m o r t a l i t y due to SDS were reduced by t a u r i n e supplementation. 27 4.0 EFFECT OF DIETARY LACTATE AND GLUCOSE CONTENT ON THE INCIDENCE OF SDS IN MALE BROILER CHICKENS 4.1 ABSTRACT: A f a c t o r i a l experiment using 4 l e v e l s of d i e t a r y l a c t a t e (0, 2.5, 5.0, 7.5% calcium l a c t a t e ) and and 4 l e v e l s of d i e t a r y glucose (0, 15, 30 and 45% c e r e l o s e ) was conducted to determine the e f f e c t of these compounds on the incidence of Sudden Death Syndrome (SDS) in male b r o i l e r c h i c k e n s . A t o t a l of 1280 male b r o i l e r s were reared in b a t t e r y brooder cages to four weeks of age. Mean body weights and feed consumption were measured at two and four .weeks of age. M o r t a l i t y was recorded d a i l y and any SDS a f f e c t e d b i r d s i d e n t i f i e d by necropsy. O v e r a l l m o r t a l i t y was 6.64% of which 32.9% (2.19% of b r o i l e r s housed) was a t t r i b u t e d to SDS. There were no s i g n i f -i c a n t d i f f e r e n c e s between treatments in e i t h e r t o t a l m o r t a l i t y or m o r t a l i t y due to SDS. Feed consumption was i n f l u e n c e d by the d i e t a r y l e v e l of both l a c t a t e and g l u c o s e . I n c l u s i o n of g r e a t e r than 2.5% l a c t a t e in the d i e t reduced feed consumption while the i n c l u s i o n of d i e t a r y glucose at 15% or higher increased feed consumption. There was a s i g n i f i c a n t l a c t a t e x glucose i n t e r a c t i o n a f f e c t i n g 4 week mean body weights (p<.05). In g e n e r a l , as d i e t a r y l a c t a t e c o n c e n t r a t i o n s increased mean body weight was depressed. C o n v e r s e l y , mean body weights were higher as glucose content was i n c r e a s e d . The depressing e f f e c t of d i e t a r y l a c t a t e was g r e a t e s t when glucose was absent from the d i e t . Feed to gain r a t i o s were s i g n i f i c a n t l y (p<.05) reduced by d i e t a r y l a c t a t e l e v e l s of 5.0 and 7.5% and increased by d i e t a r y glucose l e v e l s of 30 and 45%. 28 4.2 INTRODUCTION: Sudden Death Syndrome (SDS) i s a c o n d i t i o n i n which apparently h e a l t h y , f a s t growing b r o i l e r c h i c k s die suddenly from no apparent cause. There i s u s u a l l y a short wing-beating c o n v u l s i o n p r i o r to death so that the m a j o r i t y of a f f e c t e d b r o i l e r s are found dead l y i n g on t h e i r backs. As a r e s u l t , the c o n d i t i o n i s o f t e n r e f e r r e d to as " F l i p - O v e r d i s e a s e " . It has a l s o been c a l l e d "Acute Death Syndrome", "heart a t t a c k " , "lung edema" and "died i n good c o n d i t i o n " (Merck, 1986). SDS i s a major cause of m o r t a l i t y i n Canadian b r o i l e r f l o c k s with i n d i v i d u a l i n c i d e n c e s ranging from .71 to 4.07% of b r o i l e r s housed ( R i d d e l l and S p r i n g , 1985). B r o i l e r s of a l l ages are a f f e c t e d s t a r t i n g as e a r l y as two days of age and c o n t i n u i n g through to market age. Peak m o r t a l i t y u s u a l l y occurs between three and four weeks of age (Bridgen and R i d d e l l , 1975; Ononiwu et a l . , 1979b; Gardiner et a l . , 1988b). The c o n d i t i o n appears to be i n f l u e n c e d by the sex of the chickens since more than 70% of SDS a f f e c t e d b r o i l e r s are male (Hemsley, 1965; Brigden and R i d d e l l , 1975; Steele and Edgar, 1982; R i d d e l l and S p r i n g e r , 1985). The e t i o l o g y of SDS i s unknown, but i t i s g e n e r a l l y b e l i e v e d to be a metabolic d i s o r d e r ( J u l i a n and Bowes, 1987). Death i s b e l i e v e d to be due to l e f t v e n t r i c u l a r f i b r i l l a t i o n ( J u l i a n and Bowes, 1987), but i t i s unc l e a r as to what causes t h i s f i b r i l l a t i o n to occur. J u l i a n and Leeson (1985) reported that the i n c i d e n c e of SDS was doubled i n b r o i l e r s fed glucose monohydrate based d i e t s as compared to b r o i l e r s fed corn or t a l l o w based d i e t s . They 29 hypothesized that SDS i s r e l a t e d to a problem in carbohydrate me t a b o l i s m . Summers et a l . (1987) noted that an SDS type death could be induced by i n j e c t i n g a 20% l a c t i c a c i d s o l u t i o n i n t o the wing v e i n of male b r o i l e r c h i c k s . P i p e t t i n g 5 ml of the same 20% l a c t i c a c i d s o l u t i o n i n t o the crop of male b r o i l e r s had v a r i a b l e r e s u l t s . B r o i l e r s r e c e i v i n g d i e t s high i n glucose " f l i p p e d " w i t h i n 30 minutes of dosing with l a c t i c a c i d while those b r o i l e r s r e c e i v i n g a d i e t high in corn s t a r c h took over an hour and a h a l f to " f l i p " . It was t h e r e f o r e hypothesized that l a c t i c a c i d or acid-base balance i s i n v o l v e d in the e t i o l o g y of SDS. J u l i a n and Bowes (1987), however, found that blood l a c t a t e l e v e l s were high i n some b r o i l e r s u n a f f e c t e d by SDS, but were not e l e v a t e d i n b r o i l e r s that died from SDS. The purpose of t h i s experiment was t w o - f o l d . F i r s t , to t e s t the hypothesis that l a c t i c a c i d i s i n v o l v e d i n the e t i o l o g y of SDS and, second, to determine whether the l e v e l of d i e t a r y glucose would modify the e f f e c t s of the l a c t i c a c i d . 4.3 MATERIALS AND METHODS: 4.3.1 Design and treatments: Day-old commercial male b r o i l e r c h i c k s (Hubbard) v a c c i n a t e d against Marek's disease were placed on d i e t a r y treatment and reared i n Petersime b a t t e r y brooder cages to 4 weeks of age. The c h i c k s were wing-banded and randomly a l l o t t e d to 128 pens. A s t o c k i n g rate of 10 b r o i l e r s per pen was used, g i v i n g a t o t a l of 1280 c h i c k s . The pens were 68 x 99 cm i n s i z e , g i v i n g a space allotment of .07 2 2 m / b r o i l e r or 14.9 b r o i l e r s / m . A 4x4 f a c t o r i a l design was used and there were 4 blocks with 2 r e p l i c a t i o n s per b l o c k . The b r o i l e r s were fed i s o n i t r o g e n o u s d i e t s c o n t a i n i n g corn s t a r c h , corn o i l , soybean meal and h e r r i n g meal. D i e t a r y calcium l a c t a t e l e v e l s v a r i e d from 0 to 7.5% and c e r e l o s e (glucose) l e v e l s from 0 to 45%, both at the expense of corn s t a r c h . Limestone content was adjusted to maintain d i e t a r y calcium c o n c e n t r a t i o n s of 1.35%. The d i e t compositions are shown in t a b l e 4.1. A l l d i e t s were fed i n mash form and each d i e t was fed to 8 pens (2 pens randomly s e l e c t e d in each of the 4 b l o c k s ) . 4.3.2 Management: The b r o i l e r s r e c e i v e d 23 hours of l i g h t per day. Water and feed were a v a i l a b l e ad l i b i turn. Mean body weights and feed consumption were measured on a pen bas i s at 2 and 4 weeks of age. I n i t i a l brooder temperature was set at 35 °C and reduced by 2.5°C weekly. At 3 weeks of age the brooder heaters were turned o f f . Pens were checked twice d a i l y f o r m o r t a l i t y and a l l dead b r o i l e r s were n e c r o p s i e d . Death was a t t r i b u t e d to SDS i f there was no evidence of other disease and the b r o i l e r s were i n good body c o n d i t i o n with a f u l l d i g e s t i v e t r a c t , an empty or small g a l l bladder and c o n t r a c t e d v e n t r i c l e s . 4.3.3 S t a t i s t i c a l a n a l y s i s : Performance and m o r t a l i t y data were s t a t i s t i c a l l y analyzed using three-way a n a l y s i s of variance procedures of the S t a t i s t i c a l A n a l y s i s System (SAS I n s t i t u t e Inc., 1982). Any s i g n i f i c a n t d i f f e r e n c e s were f u r t h e r analyzed using the Ryan-Einot-Gabrie1-We 1sch m u l t i p l e range t e s t (SAS Table 4.1. Co m p o s i t i o n and c a l c u l a t e d a n a l y s i s of d i e t s used in Experiment 1 D i e t s I n g r e d i e n t s 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 1 6 H e r r i n g meal 10.7 10.7 10. 7 10.7 10.7 10. 7 10.7 X -10.7 10.7 10 . 7 10 . 7 10 . 7 10 . 7 10 . 7 10 . 7 10.7 Soybean meal* 30 . 4 30 . 4 30.4 30.4 30.4 30.4 30 .4 30 . 4 30 . 4 30 . 4 30 . 4 30 . 4 3 0 . 4 30 . 4 30 . 4 30.4 Corn o i l 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 3 . 7 Corn s t a r c h 49 . 8 34 . 8 19.8 4 . 8 48 . 2 33.2 18.2 3 . 2 46.6 31 . 6 1 6 . 6 1 . 6 45 . 0 30 . 0 1 5 . 0 0 . 0 C e r e l o s e 0 . 0 15.0 30.0 45.0 0 . 0 15.0 30.0 4 5 . 0 0 . 0 1 5 . 0 30 . 0 45 . 0 0 . 0 1 5 . 0 30 . 0 45.0 Ca l c ium l a c t a t e 0 . 0 0 . 0 0 . 0 0 . 0 2 . 5 2 . 5 2 . 5 2 . 5 5 . 0 5 . 0 5 . 0 5 . 0 7 . 5 7 . 5 7 . 5 7 . 5 Limes tone 2 . 7 2 . 7 2 . 7 2 . 7 1 . 8 1 . 8 1 . 8 1 . 8 0 . 9 0 . 9 0 . 9 0 . 9 0 . 0 0 . 0 0 . 0 0 . 0 Sodium phosphate 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 1 . 5 (monobas i c ) # Premix 1 .0 1.0 1.0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 D , L-Me t h i o n ine 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 0 . 2 TOTAL 100 100 100 100 100 100 100 100 100 100 100 100 100 100 100 100 C a l c u l a t e d a n a l y s i s : M e t a b o l i z a b l e energy (ME), k c a l / k g 3226 3223 3220 3217 3168 3165 3162 3 159 3 110 3107 3104 3101 3051 3048 3045 3042 Crude P r o t e i n , X 22.5 22.5 22.5 22.5 22.5 22 . 5 22.5 22.5 22.5 22 . 5 22 . 5 22 . 5 22 . 5 22 . 5 22 . 5 22.5 L i n o l e i c Ac i d , X 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 1 . 54 Meth. & Cys. ( X ) 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 0 . 94 L y s i n e , X 1 . 58 1 . 58 1 . 58 1 . 58 1 . 58 1 . 58 1 . 56 1 . 58 1.58 1 . 58 1 . 58 1 . 58 1 . 58 1 . 58 1 . 58 1 . 58 Ca, X 1.35 1.35 1 .35 1.35 1.36 1.36 1 .36 1.36 1.36 1 . 36 1 . 36 1 . 36 1 . 36 1 . 36 1 . 36 1.36 P, a v a i l a b l e , X 0 . 54 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 0 . 64 Premix p r o v i d e d the f o l l o w i n g per kg d i e t : 9,000 IU v i t a m i n A; 1,500 IU v i t a m i n D3 ; 10 IU v i t a m i n E; 0.5 mg v i t a m i n K; 0.007 mg v i t a m i n B12; 0.4 mg t h i a m i n ; 6 mg r i b o f l a v i n ; 1 mg f o l i c a c i d ; 0.15 mg b i o t i n ; 12 mg p a n t o t h e n i c a c i d ; 35 mg n i a c i n ; 4 mg p y r i d o x i n e ; 1000 mg c h o l i n e ; 1,184 mg m e t h i o n i n e ; 0.125 mg eth o x y q u i n ; 2 g s a l t ; 60 mg manganese; 5 mg copper; 50 mg z i n c ; 0.1 mg seleni u m ; 0.35 mg i o d i n e . * 47X crude p r o t e i n # 26X P and 20X Na 32 I n s t i t u t e Inc., 1982). An a r c s i n t r a n s f o r m a t i o n was used before a n a l y z i n g the m o r t a l i t y data, but f o r i n t e r p r e t a t i o n purposes the r e s u l t s are presented as percentages. 4.4 RESULTS: S i m i l a r r e s u l t s were obtained at 2 and 4 weeks of age so only the 4 week data are presented. T o t a l m o r t a l i t y ( t a b l e 4.2) was 6.64% of which 32.9% was a t t r i b u t e d to SDS. Twenty-seven percent of the t o t a l m o r t a l i t y occurred during the f i r s t week and was a t t r i b u t e d p r i n c i p a l l y to o m p h a l i t i s and s t a r v e - o u t s . There were no s t a t i s t i c a l l y s i g n i f i c a n t d i f f e r e n c e s between treatments f o r the incidence of SDS expressed as a percent of b r o i l e r s housed ( t a b l e 4.3) or as a percent of t o t a l m o r t a l i t y ( t a b l e 4.4). Feed consumption, mean body weight and feed conversion at 4 weeks of age are shown in t a b l e s 4.5 to 4.7. Feed consumption was s i g n i f i c a n t l y (p<.05) a f f e c t e d by both d i e t a r y l a c t a t e and glucose c o n c e n t r a t i o n s . As l a c t a t e c o n c e n t r a t i o n s increased above 2.5%, feed consumption d e c l i n e d . C o n v e r s e l y , feed consumption increased as glucose content i n c r e a s e d . There was a s i g n i f i c a n t (p<.05) l a c t a t e x glucose i n t e r a c t i o n a f f e c t i n g f i n a l body weight. This i s d e p i c t e d i n f i g u r e s 4.1 and 4.2. The e f f e c t of d i e t a r y l a c t a t e supplementation was dependent on the l e v e l of d i e t a r y g l u c o s e , but, in g e n e r a l , i n c l u s i o n of d i e t a r y l a c t a t e decreased, while d i e t a r y glucose i n c r e a s e d , mean body weight. The depressing e f f e c t of d i e t a r y l a c t a t e was most dramatic when there was no glucose i n the d i e t . Feed conversion (g feed/g body weight gain) was s i g n i f i c a n t l y (p<.05) reduced by Table 4.2 E f f e c t of d i e t a r y l a c t a t e and glucose (Experiment 1): Results at 4 weeks of age on t o t a l m o r t a l i t y LACTATE (% of d i e t ) No . GLUCOSE (% of d i e t ) 1 5 No 30 No 45 No TOTAL No 0 . 0 2 . 5 5 . 0 7 . 5 9 11.25 4 5.00 5 6.25 3 3.75 TOTAL 21 6.56 9 11.25 5 6.25 5 6.25 2 2.50 4 5 5 5 5.00 6.25 6.25 6.25 5 6.25 6 7.50 8 10.00 5 6.25 27 8.44 2 0 6.2 5 2 3 7.19 15 4.69 2 1 6.56 19 5 . 94 24 7.50 | 85 6.64 1 Percent of b r o i l e r s housed (80 per d i e t a r y treatment) Note: No s i g n i f i c a n t d i f f e r e n c e s between d i e t a r y treatments Table 4.3 E f f e c t of d i e t a r y l a c t a t e and glucose on SDS m o r t a l i t y as a percent of b r o i l e r s housed (Experiment 1): Resu l t s at 4 weeks of age LACTATE (% of d i e t ) No % GLUCOSE (% of d i e t ) 15 No , 30 No 45 No . %' TOTAL No . % 0 . 0 2 . 5 5 . 0 7 . 5 TOTAL 3 3.75 2 2.50 1 1.25 0 0.00 1 . 88 1 1.25 3 3.75 2 2.50 0 0.00 0 0.00 1 1.25 2 2.50 2 2.50 2 2.50 1 1.25 6 7.50 2 2.50 6 1.88 7 2.19 11 3.44 4 1.25 1 . 88 1.56 11 3.44 | 28 2.19 1 Percent of b r o i l e r s housed (80 per d i e t a r y treatment) Note: No s i g n i f i c a n t d i f f e r e n c e s between d i e t a r y treatments Table 4.4 E f f e c t of d i e t a r y l a c t a t e and glucose on SDS m o r t a l i t y as percent of t o t a l m o r t a l i t y (Experiment 1): Results at 4 weeks of age LACTATE (% of d i e t ) 0 GLUCOSE (% of d i e t ) 15 30 45 TOTAL 0 . 0 2 . 5 5 . 0 7 . 5 33.3 50 . 0 20.0 0 . 0 11.1 60 . 0 40 . 0 0 . 0 0 . 0 20.0 40 . 0 40 . 0 40 . 0 16.7 75.0 40 . 0 22.2 35.0 47.8 26.7 TOTAL 28.6 28.6 26.3 45.8 32.9 Note: No s i g n i f i c a n t d i f f e r e n c e s between d i e t a r y treatments Table 4.5 E f f e c t of d i e t a r y l a c t a t e and glucose on mean t o t a l feed consumption ( g / b r o i l e r ) (Experiment 1): Results at 4 weeks of age LACTATE GLUCOSE (% of d i e t ) AVE : d i e t ) 0 1 5 30 45 0 . 0 1173 + 25 1294 + 27 1357 + 3 2 1426 + 32 1312 +_ 223 2 . 5 1065 32 1290 + 25 1334 39 1443 + 14 1283 + 28a 5 . 0 944 + 16 1187 + 41 1305 + 3 1 1347 + 45 1 196 33b 7 . 5 883 36 1031 + 38 1236 _+ 36 1257 + 18 1102 3 2° AVE: 1016 + 24a 1201 25b 1308 18C 1368 + 1223 + 1 6 Data shown as mean +_ SEM a,b,c,d Means w i t h i n a row are s i g n i f i c a n t l y o r (P< column with d i f f e r e n t 05) d i f f e r e n t s u p e r s c r i p t s Table 4.6 E f f e c t of d i e t a r y l a c t a t e and glucose on mean body weight ( g / b r o i l e r ) at 4 weeks of age (Experiment 1) LACTATE (% of d i e t ) GLUCOSE (% of d i e t ) 1 5 30 45 TOTAL 878 + 2 0b° 922 + 18a b 948 + 2 6a b 981 + 2 4a b 0 . 0 2 . 5 5 . 0 7 . 5 793 + 2 7 °d 941 + 19a b 954 + 2 9a b 998 + 19a 734 + 12d e 878 + 27b c 929 + 24a b 962 + l la b 665 + 226 786 + 2 3c d 886 + 20b c 903 + 1 8a b 932 + 13 922 jf 1 8 8 76 +. 1 8 810 + 20 TOTAL 768 + 17 882 + 15 930 + 13 961 + 11 885 + 10 Data shown as mean +_ SEM S i g n i f i c a n t glucose x l a c t a t e i n t e r a c t i o n (p<.05) a,b,c,d,e Means with d i f f e r e n t s u p e r s c r i p t s are s i g n i f i c a n t l y (p<.05) d i f f e r e n t Table 4.7 E f f e c t of d i e t a r y l a c t a t e and glucose on mean feed conversion (g feed/g body weight gain) from 0 to 4 weeks of age (Experiment 1) LACTATE (% of d i e t ) GLUCOSE (% of d i e t ) 1 5 30 45 TOTAL 0.0 1.425+ .016 2.5 1.420 + .013 5.0 1.368+ .012 7.5 1.420 +.011 1.471 + .012 1.436 + .014 1.421 + .013 1.385 + .016 1.501 + .022 1.466 + .023 1.473 + .016 1.465 + .016 1.521 + .007 1.513 + .021 1.468 + .044 1.465 + .019 1.480 + .010 1.459 + .011 ab 1.432 + .014 1 .434 + .010 1.408 + .0083 1.428 + .009* 1.476 + .010b 1.492 + .0 1 3b j 1.451 + .006 Data shown as mean _+ SEM a,b Means within a row or column with d i f f e r e n t s u p e r s c r i p t s are s i g n i f i c a n t l y d i f f e r e n t (p<.05) Figure 4.1 Effect* of dietary lactate, at different levels of dietary glucose, on mean body weight at 4 weeks of age (Experiment 1) 11001 1 CD 6 0 0 i 1 1 . 0 2.6 6.0 7.6 Dietary calcium lactate (%) Dietary glucose (%) 0 16 30 46 Figure 4.1 Effects of dietary lactate, at different levels of dietary glucose on mean body weight at 4 weeks of age (Experiment 1) 1100i 1 600' ' 1 1 0 2.6 6.0 7.6 Dietary calcium lactate (%) Dietary glucose (%) 0 — a — 1 6 - e - 30 - A - 45 Figure 4.2 Effect of dietary glucoae, at different levels of dietary lactate, on mean body weight at 4 weeks of age (Experiment 1) 1100 £ 700 600 16 30 Dietary glucose (%) 46 O Figure 4.2 Effect of dietary glucose, at different levels of dietary lactate, on mean body weight at 4 weeks of age (Experiment 1) CO ••-» sz cp T J O c 0> 1100 1000 -900 800 700 -600 16 30 Dietary glucose (%) 46 Dietary lactate (%) •*~0 - ^ 2 . 6 -^-6.0 -^-7.6 41 i n c l u s i o n of 5 or 7.5% l a c t a t e . I n c l u s i o n of 30 or 45% glucose s i g n i f i c a n t l y (p<.05) increased feed c o n v e r s i o n . 4.5 DISCUSSION: Summers et a l . (1987) induced an SDS-like death by i n j e c t i n g a 20% l a c t i c a c i d s o l u t i o n i n t o the wing v e i n of male b r o i l e r c h i c k e n s . P i p e t t i n g 5 ml of the same l a c t i c a c i d s o l u t i o n i n t o the crop produced v a r i a b l e r e s u l t s depending on the previous d i e t of the b r o i l e r . Those reared on glucose based d i e t s " f l i p p e d " w i t h i n 30 minutes of dosing while those on corn s t a r c h based d i e t s took over an hour and a h a l f to d i e . It was t h e r e f o r e hypothesized that l a c t i c a c i d was i n v o l v e d in the e t i o l o g y of SDS. The r e s u l t s of t h i s experiment, however, do not support t h i s h y p o t h e s i s . Supplementation with calcium l a c t a t e to 7.5% of the d i e t of male b r o i l e r chickens had no e f f e c t on t o t a l m o r t a l i t y or m o r t a l i t y due to SDS. The l e v e l of d i e t a r y glucose had no e f f e c t on the incidence of SDS and did not modify the e f f e c t s of calcium l a c t a t e supplementation. The l e v e l of l a c t i c a c i d used by Summers et a l . (1987) to produce the SDS-like death i s probably in excess of what would normally occur i n the crop of b r o i l e r s . It i s t h e r e f o r e u n l i k e l y that l a c t i c a c i d i s i n v o l v e d i n the e t i o l o g y of SDS. Growth rate was s i g n i f i c a n t l y depressed by l a c t i c a c i d supplementation with no e f f e c t on SDS m o r t a l i t y . Thus the r e s u l t s of t h i s experiment do not support the hypothesis of Bowes et a l . (1988) that there i s a r e l a t i o n s h i p between growth rate and the i n c i d ence of SDS. 42 5.0 EFFECT OF DIETARY PROTEIN SOURCE AND CEREAL TYPE ON THE INCIDENCE OF SDS IN MALE BROILER CHICKENS 5.1 ABSTRACT: Three experiments were conducted to compare the incidence of SDS, growth rate and feed conversion f o r male b r o i l e r chickens fed i s o c a l o r i c and is o n i t r o g e n o u s d i e t s with e i t h e r corn or wheat as the g r a i n type and meat meal or soybean meal as the main p r o t e i n source. In the f i r s t two experiments the b r o i l e r s were r a i s e d i n f l o o r pens to 6 weeks of age while in the t h i r d experiment the b r o i l e r s were r a i s e d in b a t t e r y brooder cages to 4 weeks of age. A l l b r o i l e r s were Peterson x Arbor Acre. The e f f e c t of c e r e a l type on m o r t a l i t y , mean body weight and feed c o n v e r s i o n was i n c o n s i s t e n t over the three s t u d i e s . In both f l o o r pen s t u d i e s t o t a l m o r t a l i t y and the in c i d e n c e of SDS were s i g n i f i c a n t l y higher f o r wheat-fed b r o i l e r s while SDS as a percent of b r o i l e r s housed was not a f f e c t e d by c e r e a l type. In the brooder study n e i t h e r t o t a l m o r t a l i t y nor SDS m o r t a l i t y was s i g n i f i c a n t l y a f f e c t e d by c e r e a l type. F i n a l mean body weights were s i g n i f i c a n t l y higher f o r the wheat-fed b r o i l e r s i n the f i r s t f l o o r pen study (p<.01) and i n the brooder study (p<.01). In the second f l o o r pen study, however, c e r e a l type d id not have a s i g n i f i c a n t e f f e c t on mean body weight. There was a s i g n i f i c a n t (p<.05) c e r e a l x p r o t e i n i n t e r a c t i o n a f f e c t i n g feed c o n v e r s i o n i n the two f l o o r pen s t u d i e s , but i n the brooder study feed conversion was not a f f e c t e d by e i t h e r c e r e a l type or p r o t e i n source. The e f f e c t of p r o t e i n source on m o r t a l i t y , mean body weight and feed c o n v e r s i o n was also i n c o n s i s t e n t across the three 43 s t u d i e s . In the f l o o r pen s t u d i e s the incidence of SDS, as a percent of b r o i l e r s housed, was reduced by the i n c l u s i o n of meat meal in the d i e t . In the f i r s t f l o o r pen study t o t a l m o r t a l i t y was u n a f f e c t e d by p r o t e i n source while SDS as a percent of t o t a l m o r t a l i t y was reduced. The reverse occurred in the second f l o o r pen study in that t o t a l m o r t a l i t y was reduced by the i n c l u s i o n of meat meal in the d i e t while SDS as a percent of t o t a l m o r t a l i t y was u n a f f e c t e d . In the brooder study t o t a l m o r t a l i t y and the i n c i d e n c e of SDS were not a f f e c t e d by p r o t e i n source, but SDS as a percent of t o t a l m o r t a l i t y was reduced with the i n c l u s i o n of meat meal in the d i e t . In the f i r s t f l o o r pen study f i n a l mean body weight was s i g n i f i c a n t l y higher f o r the b r o i l e r s r e c e i v i n g meat meal in the d i e t , but there was no e f f e c t of p r o t e i n source on f i n a l mean body weight in the other two s t u d i e s . 5.2 INTRODUCTION: Sudden Death Syndrome (SDS) i s a c o n d i t i o n i n which apparently healthy f a s t growing b r o i l e r c h i c k s die suddenly from no apparent cause. There i s u s u a l l y a s h o r t , wing-beating c o n v u l s i o n p r i o r to death so that the m a j o r i t y of a f f e c t e d b r o i l e r s are found dead l y i n g on t h e i r backs. As a r e s u l t , the c o n d i t i o n has o f t e n been r e f e r r e d to as " F l i p - O v e r " d i s e a s e . SDS has a l s o been r e f e r r e d to as "Acute Death Syndrome", "heart a t t a c k " , "lung edema", "died i n good c o n d i t i o n " and " f a t a l syncope" (Merck, 1986). SDS i s a major cause of m o r t a l i t y i n Canadian b r o i l e r f l o c k s with i n d i v i d u a l i n c i d e n c e s ranging from .71 to 4.07% of b r o i l e r s housed ( R i d d e l l and S p r i n g e r , 1985). B r o i l e r s of a l l ages are a f f e c t e d s t a r t i n g as e a r l y as two days of age and c o n t i n u i n g through to market age with peak m o r t a l i t y u s u a l l y o c c u r r i n g between three and four weeks of age (Brigden and R i d d e l l , 1975; Ononiwu et a l . , 1979b; Gardiner et a l . , 1988b). The c o n d i t i o n appears to be i n f l u e n c e d by the sex of the chicken since more than 70% of SDS a f f e c t e d b r o i l e r s are male (Hemsley, 1965; Brigden and R i d d e l l , 1975; Steele and Edgar, 1982; R i d d e l l and S p r i n g e r , 1985). The e t i o l o g y of SDS i s unknown, but i t i s g e n e r a l l y b e l i e v e d to be a metabolic d i s o r d e r ( J u l i a n and Bowes, 1987). Various d i e t a r y (Hulan et a l . , 1980; Hunt and G a r d i n e r , 1982; Proudfoot et a l . , 1982; Steele et a l . , 1982; M o l l i s o n et a l . , 1984 and Wu and Nakaue, 1987) and management (Ononiwu et a l . , 1979b; Newberry et a l . , 1985 and Newberry et a l . , 1986) p r a c t i c e s and a v a r i e t y of chemicals (Proudfoot and Hul an, 1983 and Gardiner and Hunt, 1984) have been s t u d i e d to t r y and a l t e r the occurrence of SDS. The r e s u l t s have been i n c o n s i s t e n t from study to study. The involvement of d i e t a r y c e r e a l type on the e t i o l o g y of SDS i s u n c l e a r . Hunt and Gardiner (1982) reported no d i f f e r e n c e s in t o t a l or SDS m o r t a l i t y between f l o c k s fed corn- or wheat-soy based d i e t s . M o l l i s o n (1983), however, noted that a higher i n c i d e n c e of SDS was a s s o c i a t e d with wheat-soy based d i e t s than with corn-soy based d i e t s . In a l a t e r study, however, M o l l i s o n et a l . (1984) showed that corn-fed b r o i l e r s had s i g n i f i c a n t l y b e t t e r weight gain and feed to gain r a t i o s than wheat-fed groups but t o t a l and SDS m o r t a l i t y were not s i g n i f i c a n t l y a f f e c t e d by c e r e a l t y p e . R i d d e l l and Springer (1985), in a survey of 51 b r o i l e r f l o c k s i n A l b e r t a and Saskatchewan, reported a r e l a t i o n -ship between d i e t a r y c e r e a l type and the incidence of SDS. The incidence of SDS was higher in f l o c k s s u p p l i e d by a feed company which used l e s s c o r n , and more wheat, than the feed companies supplying the other b r o i l e r f l o c k s surveyed. Proudfoot et a l . (1982) observed a higher i n c i d e n c e of SDS a s s o c i a t e d with p e l l e t i n g of f e e d . When the d i e t a r y p r o t e i n supplements by-passed the p e l l e t i n g process the i n c i d e n c e of SDS was reduced (Proudfoot et a l . , 1984). They hypothesized that a t o x i c f a c t o r ( s ) was produced when p r o t e i n supplements are subjected to p e l l e t i n g , which may be i n v o l v e d in causing SDS. There was no comparison done on which type of p r o t e i n supplement, animal or p l a n t , was most a f f e c t e d by p e l l e t i n g . The purpose of the three experiments conducted was to compare the e f f e c t of c e r e a l type (wheat versus corn) and p r o t e i n source (soybean meal versus meat meal) on the incidence of SDS i n male b r o i l e r c h i c k e n s . 5.3 MATERIALS AND METHODS: A l l three experiments used day-old commercial male b r o i l e r c h i c k s (Peterson X Arbor Acre) v a c c i n a t e d against Marek's d i s e a s e . 5.3.1 Experiments 2 and 3 - Design and treatments: In Experiment 2, s i x thousand ch i c k s were randomly d i s t r i b u t e d among 16 f l o o r pens (4.95 x 8.59 m each) at a s t o c k i n g d e n s i t y 2 2 of 8.8 b r o i l e r s / m or .11 m / b r o i l e r (375 b r o i 1 e r s / p e n ) . In Experiment 3, nine thousand and s i x hundred c h i c k s were randomly d i s t r i b u t e d among the same 16 f l o o r pens at a s t o c k i n g d e n s i t y 2 2 of 14.1 b r o i l e r s / m or .07 m / b r o i l e r (600 b r o i 1 e r s / p e n ) . Wood shavings were used as l i t t e r . Both experiments used a 2x2 f a c t o r i a l design with 4 blocks and 1 r e p l i c a t i o n per b l o c k . The b r o i l e r s were fed e i t h e r a corn or wheat based d i e t . D i e t a r y p r o t e i n was s u p p l i e d as soybean meal with or without supplemental meat meal. A s t a r t e r s e r i e s of d i e t s (22.5% CP) medicated with monensin sodium as the c o c c i d i o s t a t were fed from day-old to 21 days of age. A grower s e r i e s of d i e t s (21% CP) medicated with sa l i n o m y c i n as the c o c c i d i o s t a t were fed from 21 to 40 days of age. The compositions of the d i e t s are shown in t a b l e 5.1. The s t a r t e r d i e t s were fed as crumbles and the grower d i e t s as p e l l e t s (10 mm long x 5 mm in d i a m e t e r ) . A l l d i e t s were p e l l e t e d and crumbled using a steam-pressure-die p r o c e s s . Each d i e t was fed to four pens (1 pen per b l o c k ) . 5.3.2 Experiments 2 and 3 - Management: Feed and water were s u p p l i e d ad l i b i turn. At 21 and 40 days of age days pen feed consumption and body weights were record e d . A sample of approximately 75 b r o i l e r s per pen was taken and the b r o i l e r s weighed i n d i v i d u a l l y to c a l c u l a t e average pen body weight. For the f i r s t week the chi c k s of each pen were kept w i t h i n a 12 foot diameter confinement r i n g . Each pen was equipped with 1 gas brooder, 2 water f o u n t s , 2 feed t r a y s and 6 tube f e e d e r s . At one week of age the confinement r i n g s were removed. For the remainder of the experiment the b r o i l e r s were provided with f i f t e e n tube feeders and four 2.4 m automatic water troughs in each pen. I n i t i a l brooder temperature was set at 35°C and was reduced Table 5.1. Composition and c a l c u l a t e d a n a l y s i s of d i e t s used in Experiments 2, 3 and 4 S t a r t e r d i e t s F i n i s h e r d i e t s Ingredients A B C D A B C D Corn 58 . 8 53 . 0 0 . 0 0 - % . 0 62 . 9 57 . 9 0 . 0 0 . 0 Wheat 0 . 0 0 . 0 57 . 4 52 . 8 0 . 0 0 . 0 62 . 1 57 . 3 Meat me a1 8 . 8 0 . 0 7 . 2 0 . 0 7 . 5 0 . 0 7 . 2 0 . 0 Soybean meal* 26 . 0 36 . 4 26 . 4 34 . 9 2 3 . 6 3 2 . 5 22 . 3 30 . 9 Corn o i l 3 . 6 5 . 0 5 . 9 6 . 8 3 . 0 4 . 2 5 . 4 6 . 3 Salt 0 . 1 0 . 3 0 . 1 0 . 3 0 . 1 0 . 3 0 . 1 0 . 3 Limes tone 1 . 0 1 . 9 1 . 3 2 . 1 1 . 3 1 . 9 1 . 3 1 . 9 D i c a l . phosphate# 0 . 0 1 . 7 0 . 0 1 . 4 0 . 0 1 . 7 0 . 0 1 . 7 D,L-Methionine 0 . 22 0 . 22 0 . 23 0 . 23 0 . 05 0 . 05 0 . 07 0 . 07 Premix 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 1 . 0 Hardener 0 . 5 0 . 5 0 . 5 0 . 5 0 . 5 0 . 5 0 . 5 0 . 5 TOTAL 100 . 0 100 . 0 100 . 0 100 . 0 100 . 0 100 . 0 100 . 0 100 . 0 Cal c u l a t e d a n a l y s i s : Metabo1izab1e energy (ME), kc a 1/kg 3100 3100 3100 3100 3 100 3 100 3 100 3 1.0 0 Crude P r o t e i n , % 22.5 22.5 22.5 22.5 2 1.0 2 1.0 2 1.0 21.0 L i n o l e i c A c i d , % 3 . 54 4.18 3.57 4.09 3.25 3.85 3.62 3 .80 Methionine, % 0 . 59 0.59 0 . 56 0.56 0 . 40 0 . 40 0.38 0.38 Ly s i n e , % 1.23 1.29 1.23 1.23 1.13 1.17 1.16 1.16 Ca, % 1 . 2 1 . 2 1 . 2 1 . 2 1 . 2 1 . 2 1 . 2 1 . 2 P, a v a i l a b l e , % 0 . 60 0 . 54 0 . 60 0 . 54 0 . 54 0 . 54 0 . 60 0 . 60 Premix provided the f o l l o w i n g per kg d i e t : 9,000 IU v i t a m i n A; 1,500 IU vitamin D3; 10 IU vitamin E; 0.5 mg v i t a m i n K; 0.007 mg vitamin B12; 0.4 mg thiamin; 6 mg r i b o f l a v i n ; 1 mg f o l i c a c i d ; 0.15 mg b i o t i n ; 12 mg pantothenic a c i d ; 35 mg n i a c i n ; 4 mg pyr i d o x i n e 1,000 mg c h o l i n e ; 0.125 mg ethoxyquin; 60 mg manganese; 5 mg copper; 50 mg z i n c ; 0.1 mg selenium; 0.35 mg i o d i n e . The s t a r t e r premix also provided 99 mg/kg d i e t of monensin sodium as the c o c c i d i o s t a t while the f i n i s h e r premix provided 60 mg/kg d i e t of salinomycin as the c o c c i d i o s t a t . * 47% Crude p r o t e i n # 16% Ca; 20% P by 2.5°C weekly. At 5 weeks of age the brooder heaters were turned o f f . Barn temperature was maintained at around 18.5°C ( d a i l y average of 18.9 _+ .1 f o r blocks 1 and 2 and 18.1 _+ .1 for block 3 and 4 ) . The b r o i l e r s r e c e i v e d 23 hours of l i g h t per day. L i g h t i n t e n s i t y , measured 5 inches above the l e v e l of the shavings, was 7.5 lux from 1-4 days, 5 lux from 5-9 days, 3 lux from 10-14 days and 1 lux t h e r e a f t e r . L i g h t s were brightened while checking f o r m o r t a l i t y and f o r f e e d i n g . The b r o i l e r s were checked twice d a i l y f o r m o r t a l i t y and a l l dead b r o i l e r s were n e c r o p s i e d . Death was a t t r i b u t e d to SDS i f there was no evidence of other disease and the b r o i l e r s were in good body c o n d i t i o n with a f u l l d i g e s t i v e t r a c t , a small or empty g a l l bladder and c o n t r a c t e d v e n t r i c l e s . Experiment 2 s t a r t e d i n September of 1987 while Experiment 3 s t a r t e d i n May of 1988. 5.3.3 Experiment 4 - Design and treatments: In Experiment 4, s t a r t e d i n J u l y of 1987, the same s t a r t e r s e r i e s of d i e t s used in the f l o o r pen s t u d i e s were fed to c h i c k s reared i n Petersime b a t t e r y brooder cages to four weeks of age. The design was a 2x2 f a c t o r i a l with 2 blocks and 8 r e p l i c a t i o n s per block. Six hundred and f o r t y day-old c h i c k s were randomly a l l o t t e d to 64 pens to give a d e n s i t y of 10 b r o i l e r s per pen. Each pen was 2 68 x 99 cm i n s i z e and t h e r e f o r e provided .07 m / b r o i l e r . Each d i e t was fed to s i x t e e n pens (8 pens per b l o c k ) . 5.3.4 Experiment 4 - Management: The b r o i l e r s r e c e i v e d 23 hours of l i g h t per day and were s u p p l i e d feed and water ad l i b i turn. Mean body weights and feed consumption were determined 49 at 2 and 4 weeks of age. I n i t i a l brooder temperature was set at 35°C and reduced by by 2.5°C weekly. At 3 weeks of age the brooder heaters were turned o f f . 5.3.5 S t a t i s t i c a l a n a l y s i s : The performance and m o r t a l i t y data f o r a l l three experiments were analyzed using the a n a l y s i s of v a r i a n c e procedures of the S t a t i s t i c a l A n a l y s i s System (SAS I n s t i t u t e Inc., 1982). Any s i g n i c a n t i n t e r a c t i o n s were f u r t h e r analyzed using the Ryan-Einot-Gabrie1-We 1sch m u l t i p l e range t e s t . M o r t a l i t y data were converted by an a r c s i n t r a n s f o r m a t i o n before a n a l y s i s but f o r i n t e r p r e t a t i o n purposes are presented as percentages. 5.4 RESULTS: 5.4.1 Experiment 2: The performance and m o r t a l i t y data of Experiment 2 at 21 and 40 days of age are shown i n t a b l e s 5.2 and 5.3, r e s p e c t i v e l y . At 21 days of age c e r e a l type d id not s i g n i f i c a n t l y a f f e c t t o t a l m o r t a l i t y , the in c i d e n c e of SDS, SDS as a percent of t o t a l m o r t a l i t y , or feed c o n v e r s i o n . Body weights, however, were s i g n i f i c a n t l y lower f o r the b r o i l e r s fed the wheat-based d i e t s . SDS m o r t a l i t y was s i g n i f i c a n t l y (p<.01) reduced by i n c l u s i o n of meat meal in the d i e t , but there was no e f f e c t of p r o t e i n source on t o t a l m o r t a l i t y , SDS as a percent of t o t a l m o r t a l i t y , body weight or feed c o n v e r s i o n . By 40 days of age g r a i n source s i g n i f i c a n t l y (p<.05) a f f e c t e d both t o t a l m o r t a l i t y and SDS m o r t a l i t y expressed as a percent of b r o i l e r s housed. A higher i n c i d e n c e of t o t a l and SDS m o r t a l i t y was a s s o c i a t e d with the wheat based d i e t s . Table 5.2 E f f e c t of d i e t on f i n a l body weight, feed conversion and m o r t a l i t y (Experiment 2): Results at 21 days of age F i n a l Feed To t a l M o r t a l i t y SDS M o r t a l i t y SDS M o r t a l i t y DIET body weight conversion ^ % of t o t a l ( g / b r o i l e r ) (g feed/g gain) No. % No. % m o r t a l i t y corn/meat meal 769 2 1 . .278 + .005 23 1 . 5 1 5 1 . 0 65.2 corn/SBM 744 + 5 1 . .289 + . 007 30 2 . 0 25 1 . 7 83.3 wheat/meat meal 715 + 9 1 , . 304 + .015 29 1 . 9 1 7 1 . 1 58.6 wheat/SBM 723 + 4 1 , .2 76 + . 005 30 2 . 0 20 1 . 3 66.7 ove r a i l : 737 +_ 6 1 , .287 + .005 1 1 2 1 . 9 7 7 1 . 3 68 . 8 Main e f f e c t s : corn 756 + 5 1 , ,284 + . 005 53 1 . 8 40 1 . 3 7 5.5 whe at 719 + 5 1 , .289 + .009 59 2 . 0 37 1 . 2 6-2 . 7 s i g n i f icance: * NS NS NS NS meat meal 742 + 11 1 . .291 + .009 52 1 . 7 32 1 . 1 6 1.5 SBM 734 +_ 5 1 . ,282 +. . 005 60 2 . 0 45 1 . 5 75.0 s i g n i f i c a n c e : NS NS NS ** NS Data shown as mean +_ SEM * p<.05 ** p<.01 1 Percent of b r o i l e r s housed (1500/dietary treatment) O Table 5.3 E f f e c t of d i e t on f i n a l body weight, feed conversion and m o r t a l i t y (Experiment 2): Results at 40 days of age DIET F i n a l body weight ( g / b r o i l e r ) (g Feed conve r s i o n feed/g gain) T o t a l No . M o r t a l i t y Z1 SDS No Mo r t a 1i t y %l SDS M o r t a l i t y % of t o t a l m o r t a l i t y corn/meat meal 2130 + 12 . 1 .682 + , .013 46 3 . 1 28 1 . 8 60 . 9 corn/SBM 2112 + 20 1 .673.+ , . 009 56 3 . 7 43 2 . 9 76.8 wheat/meat meal 2061 + 19 1 .606 + , .013 80 5 . 3 46 3 . 1 57.5 wheat/SBM 1978 + 14 1 .648 + . . 007 76 5 . 1 52 3 . 5 68 . 4 ove r a l 1 : 2070 + 1 7 1 .652 + . . 009 258 4 . 3 169 2 . 8 66.8 Main e f f e c t s : corn 2121 + 1 1 1 .677 ± . . 007 102 3 . 4 7 1 2 . 4 69.6 whe at 2020 + 19 1 .627 + . .011 156 5 . 2 98 3 . 3 62.8 s i g n i f i c a n c e : ** * i n t e r a c t ion * * NS meat meal 2096 + 17 1 . 644 + . 017 126 4 . 2 74 2 . 5 58 . 7 SBM 2 04 5 +• 28 1 .660 + . , 007 132 4 . 4 95 3 . 2 72.0 s i g n i f i c a n c e : * * i n t e r a c t i o n NS * * Data shown as mean + SEM * p<.05 ** p<.01 1 Percent of b r o i l e r s housed (1500/dietary treatment) Figure 6.1 Effect of dietary cereal type on feed conversion ^ (g feed/g body weight gain) at 40 days of age (Experiment 2) TJ o H — U) w c o '</) d) > c o o " D <D 0) LL corn wheat Dietary cereal Main dietary protein I 8BM I B meat meal c "eg CO § CO c o if) > c o o TJ 0 <D LL Figure 5.2 Effect of dietary protein source on feed conversion (g feed/g body weight gain) at 40 days of age (Experiment 2) meat meal SBM Main dietary protein source 00 There was no e f f e c t of c e r e a l type on SDS as a percent of t o t a l m o r t a l i t y . The incidence of SDS was s i g n i f i c a n t l y (p<.05) a f f e c t e d by d i e t a r y p r o t e i n source. SDS as a percent of t o t a l m o r t a l i t y and as a percent of b r o i l e r s housed was. increased when meat meal was excluded from the d i e t . There was no e f f e c t of d i e t a r y p r o t e i n source on t o t a l m o r t a l i t y . Body weights were s i g n i f i c a n t l y a f f e c t e d by both c e r e a l type (p<.01) and d i e t a r y p r o t e i n source (p<.05). B r o i l e r s r e c e i v i n g meat meal in the d i e t weighed more than those r e c e i v i n g only SBM as the d i e t a r y p r o t e i n source. Corn based d i e t s supported a higher f i n a l body weight than wheat based d i e t s . There was a s i g n i f i c a n t (p<.05) c e r e a l x p r o t e i n i n t e r a c t i o n a f f e c t i n g feed c o n v e r s i o n . This i s shown g r a p h i c a l l y i n f i g u r e s 5.1 and 5.2. B r o i l e r s fed wheat based d i e t s had lower feed conversion r a t i o s than those fed corn based d i e t s only when meat meal was incl u d e d in the d i e t . The i n c l u s i o n of meat meal in corn based d i e t s d i d not s i g n i f i c a n t l y a f f e c t feed c o n v e r s i on r a t i o s but i n c l u s i o n of meat meal did s i g n i f i c a n t l y (p<.05) reduce feed conversion r a t i o s of b r o i l e r s fed wheat based d i e t s . 5.4.2 Experiment 3: The performance and m o r t a l i t y data of Experiment 3 at 21 and 40 days of age are shown i n t a b l e s 5.4 and 5.5, r e s p e c t i v e l y . At 21 days of age the b r o i l e r s fed the wheat based d i e t s had s i g n i f i c a n t l y (p<.05) higher t o t a l m o r t a l i t y but the incidence of SDS was not s i g n i f i c a n t l y a f f e c t e d . There was no s i g n i f i c a n t e f f e c t of c e r e a l type on mean body weight or feed c o n v e r s i o n . P r o t e i n source did not s i g n i f i c a n t l y a f f e c t t o t a l m o r t a l i t y or m o r t a l i t y due to SDS, but the i n c l u s i o n of meat meal r e s u l t e d i n s i g n i f i c a n t l y (p<.05) Table 5.4 E f f e c t of d i e t on f i n a l body weight, feed conversion and m o r t a l i t y (Experiment 3): Result s at 21 days of age DIET F i n a l Feed To t a l M o r t a l i t y SDS M o r t a l i t y SDS M o r t a l i t y body weight conversion ^ % of t o t a l ( g / b r o i l e r ) (g feed/g gain) No. % No. % m o r t a l i t y c o rn/me at me a1 699 + 7 1 . .3 2 5 + .012 70 2 . 9 40 1 . 7 57.1 corn/SBM 744 _+ 7 1 . . 308 + . 007 74 3 . 1 4 5 1 . 9 60 . 8 wheat/meat meal 689 + 6 1 . , 344 + .013 93 3 . 9 47 2 . 0 50.5 wheat/SBM 721 +13 1 . .313 + .013 1 16 4 . 8 66 2 . 8 56.9 o v e r a l l : 713 + 7 1 . .3 2 3 + . 006 353 3 . 7 198 2 . 1 56.1 Main e f f e c t s : corn 721 + 10 1 . .317 + .007 144 3 . 0 95 2 . 0 66.0 wheat 705 + 9 1 . , 329 + .010 209 4 . 4 1 1 3 2 . 4 54 . 1 s i g n i f i c a n c e : NS NS * NS NS me at me a 1 694 + 5 1 . .3 3 5 + .009 163 3 . 4 87 1 . 8 53.4 SBM 7 3 2 + 8 1 . .311 + .007 190 4 . 0 1 1 1 2 . 3 58 . 4 s i g n i f icance: NS NS NS NS NS Data shown as mean +_ SEM * p<.05 ** p<.01 1 Percent of b r o i l e r s housed (2400/dietary treatment) L/l Table 5.5 E f f e c t of d i e t on f i n a l body weight, feed conversion and m o r t a l i t y (Experiment 3): Results at 40 days of age DIET F i n a l Feed To t a l M o r t a l i t y SDS M o r t a l i t y SDS M o r t a l i t y body weight conversion ^ % of t o t a l ( g / b r o i l e r ) (g feed/g gain) No. % No. % m o r t a l i t y corn/meat meal 1 892 + 25 1 .810 + .022 123 5 . 1 62 2 . 6 50 . 4 corri/SBM 1 974 + 16 1 . 790 + .005 148 6 . 2 94 3... 9 63.5 wheat/meat meal 1 978 + 5 1 .767 + .012 175 7 . 3 96 4... 0 54 . 9 wheat/SBM 1 976 + 33 1 .814 .018 227 9 . 5 131 5 . 5 57.7 o v e r a l l : 1955 + 14 1 .795 . 008 673 7 . 0 383 4 . 0 56.9 Main e f f e c t s : corn 1 933 + 21 1 .800 + .011 271 5 . 6 156 3 . 3 57.6 whe at 1 9 7 7 + 16 1 . 790 + .013 402 8 . 4 22 7 4 .7 56.5 s i g n i f i c a n c e : NS * int e ract ion ** ** NS meat meal 1 93 5 + 20 1 . 788 + .014 298 6 . 2 158 3 . 3 53.0 SBM 1 975 + 1 7 1 .802 .010 375 7 . 8 225 4 . 7 60 . 0 s i g n i f i c a n c e : NS * i n t eract ion * * NS Data shown as mean _+ SEM * p<.05 ** p<.01 1 Percent of b r o i l e r s housed (2400/dietary treatment) Figure 6.3 Effect of dietary cereal type on feed conversion (g feed/g body weight gain) at 40 days of age (Experiment 3) corn wheat Dietary cereal Main dietary protein meat meal HH SBM \ 1 Figure 6.4 Effect of dietary protein source on feed conversion (g feed/g body weight gain) at 40 days of age (Experiment 3) meat meal SBM Main dietary protein source ui 0 0 Table 5.6 E f f e c t of d i e t on f i n a l body weight, feed conversion and m o r t a l i t y (Experiment 4): Results at 28 days of age DIET F i n a l Feed Total M o r t a l i t y SDS M o r t a l i t y SDS M o r t a l i t y body weight conversion ^ ^ % of t o t a l ( g / b r o i l e r ) (g feed/g gain) No. % No. % m o r t a l i t y c o rn/me at me a 1 1123 + 18 1 .473 + .011 10 6 . 3 4 2 . 5 40 . 0 corn/SBM 1121 + 10 1 .514 + .012 7 4 . 4 6 3 . 8 85.7 wheat/meat meal 1071 +. 1 5 1 . 508 + .014 9 5 . 6 2 1 . 2 22.2 wheat/SBM 1062 + 14 1 .513 + .019 6 3 . 8 3 1 . 9 50 . 0 o v e r a l l : 1095 + 8 1 . 502 + . 007 32 5 . 0 1 5 2 . 3 46 . 9 Main e f f e c t s : corn 1122 + 10 1 .494 + . 009 1 7 5 . 3 10 3 . 1 58 . 8 whe at 1067 + 10 1 . 510 + .012 15 4 . 7 5 1.6 33.3 s i g n i f i c a n c e : ** NS NS NS NS meat meal 1 097 + 12 1 . 490 + . 009 19 5 . 9 6 1 . 9 3 1.6 SBM 1092 + 10 1 .513 + .011 13 4 . 1 9 2 . 8 69.2 s i g n i f i c a n c e : NS NS NS NS * Data shown as mean _+ SEM * p<.05 ** p<0.01 1 Percent of b r o i l e r s housed (160/dietary treatment) Ln lower mean body weight. By 40 days of age both g r a i n type and p r o t e i n source s i g n i f i c a n t l y a f f e c t e d t o t a l m o r t a l i t y and the in c i d e n c e of SDS, but not SDS as a percent of t o t a l m o r t a l i t y . The b r o i l e r s r e c e i v i n g the wheat based d i e t s had s i g n i f i c a n t l y (p<.01) higher o v e r a l l m o r t a l i t y and a higher incidence of SDS. B r o i l e r s fed d i e t s which did not con t a i n meat meal had s i g n i f i c a n t l y (p<.05) higher t o t a l m o r t a l i t y . There was no e f f e c t of c e r e a l type or p r o t e i n source on f i n a l body weights, but there was a s i g n i f i -cant c e r e a l x p r o t e i n i n t e r a c t i o n a f f e c t i n g feed c o n v e r s i o n . This i s shown g r a p h i c a l l y i n f i g u r e s 5.3 and 5.4. Adding meat meal to the d i e t decreased feed conversion r a t i o s of b r o i l e r s fed wheat based d i e t s but increased the feed c o n v e rsion r a t i o s f o r b r o i l e r s fed corn based d i e t s . 5.4.3 Experiment 4: Since the 2 and 4 week r e s u l t s of Experiment 4 were s i m i l a r , only the data from week 4 are presented ( t a b l e 5.6) There was no s i g n i f i c a n t e f f e c t of c e r e a l type or p r o t e i n source on t o t a l m o r t a l i t y or the incidence of SDS. SDS m o r t a l i t y as a percent of t o t a l m o r t a l i t y was s i g n i f i c a n t l y (p<.05) lower f o r the b r o i l e r s fed d i e t s which contained meat meal. F i n a l body weights were s i g n i f i c a n t l y (p<.01) lower f o r the b r o i l e r s fed the corn based d i e t s but there was no e f f e c t of d i e t a r y p r o t e i n source. There was no s i g n i f i c a n t e f f e c t of c e r e a l type or p r o t e i n source on feed c onve rs i on. 5.5 DISCUSSION: 5.5.1 E f f e c t of c e r e a l type: 5.5.1.1 M o r t a l i t y : In both f l o o r pen s t u d i e s (Experiments 2 and 3) t o t a l m o r t a l i t y and the i n c i d e n c e of SDS were higher at 40 days of age when wheat was s u b s t i t u t e d for corn in the d i e t of male b r o i l e r c h i c k e n s . If the increase in t o t a l • mortality was due s o l e l y , to the i n c r e a s e in SDS m o r t a l i t y , SDS as a percent of t o t a l m o r t a l i t y would also be expected to i n c r e a s e . This was not the case since in n e i t h e r f l o o r study was SDS as a percent of t o t a l m o r t a l i t y a f f e c t e d by c e r e a l type. There must have been, t h e r e f o r e , an increased i n c i d e n c e of death due to causes other than SDS a s s o c i a t e d with the wheat-based d i e t s . The i n c r e a s e in SDS m o r t a l i t y a s s o c i a t e d with the wheat based d i e t s i s i n agreement with the work of M o l l i s o n (1.9.8 3) who also found an increase i n SDS m o r t a l i t y when b r o i l e r s were fed wheat-soy versus corn-soy based d i e t s . In a subsequent study, however, M o l l i s o n et a l . (1984) found no e f f e c t of c e r e a l type on the i n c i d e n c e of SDS. In the brooder study (Experiment 4) there was no observed e f f e c t of c e r e a l type on t o t a l m o r t a l i t y or the incidence of SDS. This may have been due to the s h o r t e r time p e r i o d (4 versus 6 weeks) used in the study. 5.5.1.2 Mean body weight and feed c o n v e r s i o n : In Experiments 2 and 4 the b r o i l e r s fed the corn-based d i e t s had s i g n i f i c a n t l y (p<.01) higher f i n a l body weights than the b r o i l e r s fed the wheat based d i e t s . This was unexpected since the d i e t s were formulated to be i s o c a l o r i c and i s o n i t r o g e n o u s . M o l l i s o n et a l . (1984) a l s o obtained s u p e r i o r growth rates f o r corn-fed b r o i l e r s . S e l l et a l . (1976) found that the i n c l u s i o n 6 2 of f a t i n corn, oat and barley based d i e t s of White Leghorns increased apparent ME, as measured e x p e r i m e n t a l l y , above that a n t i c i p a t e d based on ME1s c a l c u l a t e d from r e f e r e n c e v a l u e s . This may e x p l a i n the improved growth rate found f o r the corn-fed b r o i l e r s . In Experiment 3, however, the same d i e t s had no e f f e c t on f i n a l body weight. Bowes et a l . (1988) reported that a 25% feed r e s t r i c t i o n reduced SDS m o r t a l i t y and hypothesized that there was a r e l a t i o n s h i p between growth rate and the i n c i d e n c e of SDS. In Experiment 2 the incidence of SDS was reduced by e i t h e r a corn-based d i e t or the i n c l u s i o n of meat meal. Both these f a c t o r s increased growth rate as r e f l e c t e d i n higher f i n a l body weights. Thus, the r e s u l t s of Experiment 2 do not support the hypothesis of Bowes et a l . ( 1988 ) . In Experiment 2 and 3 there was a s i g n i f i c a n t c e r e a l x p r o t e i n i n t e r a c t i o n a f f e c t i n g feed c o n v e r s i o n . Feed c o n v e r s i o n was the lowest with the wheat/meat meal d i e t s and highest with the corn/meat meal d i e t . Thus the e f f e c t of meat meal on feed to gain r a t i o s depends on the d i e t a r y c e r e a l used. In Experiment 4 there was no e f f e c t of c e r e a l type or p r o t e i n source on o v e r a l l feed c o n v e r s i o n . 5.5.2 E f f e c t of d i e t a r y p r o t e i n source: 5.5.2.1 M o r t a l i t y : In both f l o o r pen s t u d i e s (Experiments 2 and 3) the incidence of SDS was reduced when meat meal was i n c l u d e d i n the d i e t . In Experiment 3 there was also a decrease i n t o t a l m o r t a l i t y with no e f f e c t on SDS as a percent of t o t a l m o r t a l i t y , i n d i c a t i n g that death due to causes other than SDS was also reduced. In Experiment 2, however, SDS as a 63 percent of t o t a l m o r t a l i t y , but not t o t a l m o r t a l i t y , was decreased by i n c l u s i o n of d i e t a r y meat meal. This would i n d i c a t e that there was an increase i n m o r t a l i t y due to causes other than SDS when meat meal was included in the d i e t . Thus the e f f e c t of d i e t a r y meat meal on the i n c i d e n c e of SDS was c o n s i s t e n t i n both f l o o r pen s t u d i e s but the e f f e c t on m o r t a l i t y due to causes other than SDS was not. In the brooder study (Experiment 4) there was no e f f e c t of d i e t a r y meat meal on t o t a l m o r t a l i t y or on the i n c i d e n c e of SDS. SDS as a percent of t o t a l m o r t a l i t y , however, was s i g n i f i c a n t l y reduced. This e f f e c t was probably due to the n o n s i g n i f i c a n t decrease in SDS and the n o n s i g n i f i c a n t i n c r e a s e i n t o t a l m o r t a l i t y a s s o c i a t e d with the i n c l u s i o n of meat meal in the d i e t . A l l of the d i e t s used in t h i s study were p e l l e t e d and contained v a r y i n g q u a n t i t i e s of soybean meal. The s u b s t i t u t i o n of a p o r t i o n of the soybean meal with meat meal appeared to reduce the i n c i d e n c e of SDS. Proudfoot et a l . (1984) proposed that a t o x i c f a c t o r ( s ) was produced when p r o t e i n supplements were subjected to p e l l e t i n g which may be i n v o l v e d in causing SDS. If t h i s were the case, i t can be s p e c u l a t e d that the t o x i c f a c t o r ( s ) must be produced when soybean meal, and not meat meal, i s p e l l e t e d since r e d u c t i o n in the q u a n t i t y of soybean meal in the d i e t reduced the incidence of SDS. It i s more l i k e l y , however, that the i n c l u s i o n of meat meal s u p p l i e s a p r e v i o u s l y u n i d e n t i f i e d f a c t o r present in animal p r o t e i n which provides some p r o t e c t i o n against the occurrence of SDS. One p o s s i b i l i t y i s t a u r i n e . Taurine i s a n a t u r a l l y o c c u r r i n g amino acid found in a l l animal t i s s u e s but which i s almost nonexistent in plan t s (Jacobsen and Smith, 1968). Taurine has been shown to be a membrane s t a b i l i z e r (Kuriyama, 1980) and may be p r o v i d i n g p r o t e c t i o n to the c a r d i a c c e l l membranes and reducing the incidence of SDS. 5.5.2.2. Mean body weight and feed c o n v e r s i o n : In Experiment 1 the i n c l u s i o n of meat meal in the d i e t r e s u l t e d in s u p e r i o r growth rates as r e f l e c t e d in s i g n i f i c a n t l y higher f i n a l body weight. In Experiments 2 and 3, however, there was no e f f e c t of d i e t a r y p r o t e i n source on the i n c i d e n c e of SDS. 65 6.0 THE EFFECT OF A TAURINE TRANSPORT INHIBITOR ON THE INCIDENCE OF SUDDEN DEATH SYNDROME IN MALE BROILER CHICKENS 6.1 ABSTRACT: Guandinoethy1 s u l f o n a t e (GES), which has been found to i n h i b i t t a u r i n e t r a n s p o r t in r a t s , was added to the d i e t of male b r o i l e r chickens to study the e f f e c t on t i s s u e t a u r i n e content and the i n c i d e n c e of Sudden Death Syndrome (SDS). GES was inclu d e d in the d i e t at 0, .25 and .50% from one to two weeks of age. In the t h i r d week the l e v e l s were modified to 0, 1.50 and .50% r e s p e c t i v e l y , and maintained at these l e v e l s through to the end of the f o u r t h week. The b r o i l e r s r e c e i v i n g 1.50% GES supplementation during weeks 3 and 4 had s i g n i f i c a n t l y lower c a r d i a c c o n c e n t r a t i o n s at 4 weeks of age, but s i g n i f i c a n t l y higher b r a i n t a u r i n e c o n c e n t r a t i o n s than c o n t r o l s . At 4 weeks of age c a r d i a c t a u r i n e l e v e l s of the 1.50% GES supplemented b r o i l e r s were 85% of c o n t r o l s while b r a i n t a u r i n e l e v e l s were 129% of c o n t r o l s . It appeared that GES supplementation at 1.50% prevented the normal increase i n c a r d i a c t a u r i n e c o n c e n t r a t i o n and decrease in b r a i n t a u r i n e c o n c e n t r a t i o n that occurs during the development of the male b r o i l e r c h i c k e n . Although the 2 week b r a i n t a u r i n e c o n c e n t r a t i o n s of the .25% GES supplemented b r o i l e r s were s i g n i f i c a n t l y higher than c o n t r o l s there were no s i g n i f i c a n t d i f f e r e n c e s at 3 and 4 weeks of age. Of the 360 b r o i l e r s housed, only 4 of 8 deaths were a t t r i b u t e d to SDS. Nei t h e r t o t a l nor SDS m o r t a l i t y was s i g n i f i -c a n t l y a f f e c t e d by GES supplementation. 66 6.2 INTRODUCTION: Sudden Death Syndrome (SDS) r e f e r s to a c o n d i t i o n i n which apparently h e a l t h y , fast-growing b r o i l e r c h i c k s die suddenly from no apparent cause. Immediately preceding death there i s a s h o r t , wing-beating convulsions so that the m a j o r i t y of a f f e c t e d b r o i l e r s are found dead l y i n g on t h e i r backs (Newberry et a l . , 1985; Bowes and J u l i a n , 1986). As a r e s u l t , the c o n d i t i o n i s of t e n r e f e r r e d to as "F l i p - O v e r d i s e a s e " . SDS has a l s o been r e f e r r e d to as "Acute Death Syndrome", "heart a t t a c k " , "lung edema" and "died i n good c o n d i t i o n " (Merck, 1986). SDS i s the main cause of m o r t a l i t y i n Canadian b r o i l e r f l o c k s with i n c i d e n c e s in i n d i v i d u a l f l o c k s v a r y i n g from .71% to 4.01% of b r o i l e r s housed ( R i d d e l l and S p r i n g e r , 1985). B r o i l e r s of a l l ages are a f f e c t e d s t a r t i n g as e a r l y as two days of age and c o n t i n u i n g through to marketing age with peak m o r t a l i t y u s u a l l y o c c u r r i n g between 3 and 4 weeks of age. The c o n d i t i o n appears to be i n f l u e n c e d by the sex of the chicken since more than 70% of SDS a f f e c t e d b r o i l e r s are male (Hemsley, 1965; Brigden and R i d d e l l , 1975; Steele and Edgar, 1982; R i d d e l l and S p r i n g e r , 1985). The a c t u a l cause of death in SDS cases i s unknown. Some authors have found lung congestion and edema and have proposed that the lung congestion was a r e s u l t of heart f a i l u r e and that a f f e c t e d b r o i l e r s die of s u f f o c a t i o n (Brigden and R i d d e l l , 1975; Ononiwu et a l . , 1979b). Further s t u d i e s have shown that lung congestion i s not a c o n s i s t e n t feature and that f r e s h l y dead b r o i l e r s diagnosed as dying from SDS had no lung congestion (Riddel and O r r , 1980). This suggests that lung congestion i s a 67 postmortem change probably r e l a t e d to p o s i t i o n at death. SDS death appears to involve heart damage. M i c r o s c o p i c examination of c a r d i a c muscle from SDS a f f e c t e d b r o i l e r s showed degeneration of the f i b e r s , s e p a r a t i o n of the f i b e r s by edema, and i n f i l t r a t i o n of h e t e r o p h i l s (Ononiwu et a l . , 1979b). J u l i a n and Bowes (1987) have suggested that the death i s due to l e f t v e n t r i c u l a r f i b r i l l a t i o n , but there i s s t i l l no c o n c l u s i v e evidence as to the cause of t h i s f i b r i l l a t i o n . It has also been suggested that SDS i s a metabolic disease r e l a t e d to high carbohydrate intake and that a b u i l d up of in t e r m e d i a r y m e t a b o l i t e s causes c a r d i a c arrhythmias ( J u l i a n and Bowes 1987). An e a r l i e r study in t h i s l a b o r a t o r y showed that the inc i d e n c e of SDS was i n f l u e n c e d by the source of d i e t a r y p r o t e i n . The i n c l u s i o n of meat meal in the d i e t of male b r o i l e r chickens s i g n i f i c a n t l y reduced the incidence of SDS. One chemical d i f f e r e n c e between animal and p l a n t t i s s u e s i s the presence of t a u r i n e in animal t i s s u e s . T a u r i n e , or 2-amino-ethane s u l f o n i c a c i d , i s a n a t u r a l l y o c c u r r i n g amino a c i d found in a l l v e r t e b r a t e t i s s u e , but which i s almost n o n - e x i s t e n t i n p l a n t s (Jacobsen and Smith, 1964; Kataoka and O n h i s h i , 1986). I n t e r e s t in t a u r i n e increased when i t was d i s c o v e r e d to be e s s e n t i a l f o r c a t s . In t h i s s p e c i e s , a d e f i c i e n c y of t a u r i n e r e s u l t s i n r e t i n a l degeneration leading to b l i n d n e s s (Berson et al . , 1 9 7 6 ) . The c o n c e n t r a t i o n of t a u r i n e i n heart t i s s u e s , r e l a t i v e to other t i s s u e s , i s high i n a l l animal s p e c i e s s t u d i e d and may represent c l o s e to 50% of the t o t a l f r e e amino a c i d s present (Kocsis et a l . , 1976). The myocardial metabolism of ra t s has 6 8 been reported to be s i g n f i c a n t l y a l t e r e d by a d e p l e t i o n of c a r d i a c t a u r i n e ( M o z a f f a r i et a l . , 1986). Taurine d e f i c i e n t cats have been shown to s u f f e r from myocardial f a i l u r e (Pion et a l . , 1987). Reduced c a r d i a c t a u r i n e c o n c e n t r a t i o n s have been found to be a s s o c i a t e d with cardiomyopathies in turkeys ( S c h a f f e r et a l . , 1982). Furazolidone t r e a t e d turkey p o u l t s showed an i n c r e a s e in the incidence of cardiomyopathies and had s i g n i f i c a n t l y reduced c a r d i a c t a u r i n e c o n c e n t r a t i o n s . A d m i n i s t r a t i o n of exogenous t a u r i n e to turkeys t r e a t e d with f u r a z o l i d o n e r e s t o r e d myocardial t a u r i n e to normal l e v e l s but did not a l t e r the incidence of f u r a z o l i d o n e induced c a r d i o -myop a t h i e s . Cardiac t a u r i n e i s acquired e i t h e r from the d i e t or from b i o s y n t h e s i s . In r a t s , a marked decrease in t i s s u e t a u r i n e c o n c e n t r a t i o n has been achieved by supplementing with t a u r i n e t r a n s p o r t i n h i b i t o r s and thus preventing t i s s u e uptake of t a u r i n e (Huxtable et a l . , 1981). Guandinoethy1 s u l f o n a t e (GES) i s a s t r u c t u r a l analogue of t a u r i n e and in v i t r o i n h i b i t s t a u r i n e t r a n s p o r t ( A z a r i et a l . , 1 9 7 9 ) . Cardiac t a u r i n e c o n c e n t r a t i o n s of r a t s can be reduced i n  v i v o to 20-30% of normal while the c o n c e n t r a t i o n s of the other amino acids remain u n a f f e c t e d (Huxtable et a l . , 1981). The i r r e d u c i b l e p o r t i o n i s due to b i o s y n t h e s i s w i t h i n the h e a r t . The e f f e c t s of GES supplementation on t i s s u e t a u r i n e c o n c e n t r a t i o n s vary between species (Huxtable and L i p p i n c o t t , 1981). Mice are s i m i l a r to r a t s in that t a u r i n e c o n c e n t r a t i o n s are reduced by a 1% GES supplementation in the d r i n k i n g water. Cats are able to metabolize GES to t a u r i n e so that i t does not 69 have an i n h i b i t o r y e f f e c t . Guinea pigs are intermediate i n t h e i r a b i l i t y to metabolize GES. Since GES a d m i n i s t r a t i o n i s e f f e c t i v e in reducing t a u r i n e c o n c e n t r a t i o n s in the t i s s u e s of mice and r a t s , both omnivores, i t may be p o s s i b l e to use GES supplementation to reduce t a u r i n e c o n c e n t r a t i o n s i n the t i s s u e s of the omnivorous c h i c k e n . The purpose of t h i s experiment was two f o l d . F i r s t to study the e f f e c t of GES supplementation on the t i s s u e t a u r i n e content of male b r o i l e r c h i c k e n s , and, second, to see i f there was any e f f e c t on the incidence of SDS. 6.3 MATERIALS AND METHODS: 6.3.1 Design and Treatments: Three hundred and s i x t y day-old commercial male b r o i l e r chicks (Peterson X Arbor Acre) were reared i n Peterson b a t t e r y brooder cages to four weeks of age. The c h i c k s were wing-banded and randomly d i s t r i b u t e d among 36 pens at d e n s i t y of 10 c h i c k s / p e n . The brooders were 68 x 99 2 cm i n s i z e g i v i n g a space allotment of .07 m / b r o i l e r . Chicks from nine of the pens were reserved f o r the supply of organ samples f o r t a u r i n e a n a l y s i s while the ch i c k s of the remaining twenty-seven pens were used f o r a m o r t a l i t y study. The m o r t a l i t y study used a completely randomized design with 9 r e p l i c a t i o n s per t re atme n t . For the f i r s t week a l l the b r o i l e r s r e c e i v e d a t a u r i n e free basal d i e t ( t a b l e 6.1). From the second week to the end of the study, the b r o i l e r s were d i v i d e d i n t o three treatment groups. Treatment A was a c o n t r o l and these b r o i l e r s continued to r e c e i v e the basal d i e t throughout the experiment. During week 2 70 Table 6.1 Composition and c a l c u l a t e d a n a l y s i s of the basal d i e t used in Experiment 5 INGREDIENT % Wheat 2 7 . 9 Corn 2 7 . 9 Soybean meal (47% CP ) 35 . 8 Corn o i l 4 . 7 L ime stone 1 . 7 Dic a l c j u m phosphat e (16% Ca; 20% P) 1 . 5 Premix 0 . 4 D,L-Methionine 0 . 2 100 . 0 C a l c u l a t e d a n a l y s i s : Crude prote i n (%) 22 . 5 Me t a b o l i z a b l e energy (kcal/kg) 3 100 C a 1c i um (%) 1 . 00 Phosphorus, av a i l a b l e (%) 0 . 45 Methionine ( % ) 0 . 55 Lysine ( % ) 1 . 32 1 Premix provided the f o l l o w i n g per kg d i e t : 9000 IU v i t a m i n A; 1500 IU vit a m i n D3; 10 IU vi t a m i n K; 0.007 mg vit a m i n B12; 0.4 r i b o f l a v i n ; 1 mg f o l i c a c i d ; 0.15 mg pantothenic a c i d ; 35 mg n i a c i n ; 4 mg mg c h o l i n e ; 2 gm i o d i z e d s a l t ; 60 mg v i t am in E ; 0 . 5 mg mg thiamin; 6 mg b i o t i n ; 12 mg p y r i d o x i n e ; 1000 manganese; 5 mg copper; 50 mg zinc and 0.1 mg selenium, b r o i l e r s i n Treatment B r e c e i v e d the basal d i e t supplemented with .25% GES. This was increased the t h i r d week to 1.50% and remained at t h i s l e v e l to the end of the study. The b r o i l e r s of Treatment C r e c e i v e d the basal d i e t supplemented with.0.50% GES from week 2 to the end of the study. Each d i e t a r y treatment was fed to twelve pens - nine f o r the m o r t a l i t y study and three for the p r o v i s i o n of organ samples. 6.3.2 Management: The b r o i l e r s r e c e i v e d 23 hours of l i g h t per day and were provided feed and water ad l i b i turn. I n i t i a l brooder temperature was set at 35°C and was reduced by 2.5°C weekly. At three weeks of age the brooder heaters were turned o f f . The b r o i l e r s were checked twice d a i l y f o r m o r t a l i t y and a l l dead b r o i l e r s n e c r o p s i e d . Death was a t t r i b u t e d to SDS i f there was no evidence of other disease and the b r o i l e r s were in good body c o n d i t i o n with a f u l l d i g e s t i v e t r a c t , a small or empty g a l l bladder and c o n t r a c t e d v e n t r i c l e s . At 2, 3 and 4 weeks of age mean body weight and feed consumption were determined f o r a l l b r o i l e r s on a pen b a s i s (36 pens). For the nine pens reserved f o r the supply of organ samples, two b r o i l e r s per pen were randomly s e l e c t e d each week. They were weighed and k i l l e d by c e r v i c a l d i s l o c a t i o n and the hearts and b r a i n s removed. A l l samples were immediately frozen and stored at -20°C u n t i l analyzed f o r t a u r i n e c o n t e n t . Sakaguchi et a l . (1982) reported that the t a u r i n e c o n c e n t r a t i o n of f i s h muscle ( S e r i o l a q u i nqurediat a) was not s i g n i f i c a n t l y a l t e r e d by 40 days of ice s t o r a g e . It was t h e r e f o r e assumed that the t a u r i n e c o n c e n t r a t i o n s of the c h i c k heart and b r a i n samples would not be s i g n i f i c a n t l y a f f e c t e d by storage at -20°C. 6.3.3 Synthesis of GES: Guanidinoethy1 s u l f o n a t e was sy n t h e s i z e d according to the procedure of Huxtable et a l . (1979). S-methy1isothiourea (300 g) was mixed with t a u r i n e (180g) d i s s o l v e d in concentrated ammonium hydroxide (360 m l ) . The mixture was heated to 6 0°C and maintained at t h i s temperature u n t i l the e v o l u t i o n of gas ceased ( o v e r n i g h t ) . (WARNING: methane t h i o l , a t o x i c and f o u l s m e l l i n g gas, was evolved i n t h i s r e a c t i o n ) . The c r y s t a l s formed were f i l t e r e d and then r e c r y s t a l l i z e d three times from water. Taurine contamination was detected by use of the amino a c i d a n a l y z e r . Residual t a u r i n e contamination was found to be .27%. The S-methy1isothiourea and t a u r i n e were purchased from Sigma (Sigma Chemical Co., St. L o u i s , M i s s o u r i ) while the concentrated ammonium hydroxide was obtained from BDH (BDH Inc., Vanc ouve r , BC). 6.3.4 Taurine a n a l y s i s : P r i o r to a n a l y s i s , the heart and b r a i n samples were f r e e z e - d r i e d and ground i n a mortar and p e s t l e . Heart samples were prepared f o r t a u r i n e a n a l y s i s by an e x t r a c t i o n t e c h n i q u e . Approximately 75 mg of f r e e z e - d r i e d sample were homogenized in 2.5 ml of d e i o n i z e d water. Two ml of the homogenate were t r a n s f e r r e d to a c e n t r i f u g e tube c o n t a i n i n g 8 ml of 10% (w/v) s u l f o s a l i c y l i c a c i d , mixed w e l l and allowed to s i t f o r 30 minutes. The mixture was then c e n t r i f u g e d at lOOOOxg f o r 6 minutes and 5 ml of the supernatant t r a n s f e r r e d to a 10 ml vo l u m e t r i c f l a s k . The f l a s k was f i l l e d to volume with 0.2M sodium c i t r a t e b u f f e r (pH 2.2), mixed we l l and allowed to s i t overnight i n the r e f r i g e r a t o r before a n a l y s i s . B r a i n samples prepared using the above e x t r a c t i o n procedure contained a substance which e l u t e d c l o s e l y with t a u r i n e . It was t h e r e f o r e necessary to prepare the b r a i n samples f o r t a u r i n e a n a l y s i s using an ac i d h y d r o l y s i s procedure. The substance was destroyed and c l e a r s e p a r a t i o n of t a u r i n e was p o s s i b l e . Approximately 75mg of f r e e z e - d r i e d b r a i n sample was placed in a f l a t - b o t t o m b o i l i n g f l a s k . A f t e r the a d d i t i o n of approximately 20ml of 3N HCl the samples were autoclaved at 12 1 °C and 15 p s i f o r 17 hours. HCl was removed by ro t o e v a p o r a t i o n i n a water bath at 60°C. Each sample was r e d i s s o l v e d i n 0 . 2M sodium c i t r a t e b u f f e r (pH 2.2), f i l t e r e d through a medium p o r o s i t y gooch apparatus and t r a n s f e r r e d q u a n t i t a t i v e l y i n t o a 50 ml vo l u m e t r i c f l a s k c o n t a i n i n g 3 ml 0.IN NaOH. The f l a s k was f i l l e d to volume with the sodium c i t r a t e b u f f e r and stored overnight in the r e f r i g e r a t o r before a n a l y s i s . Taurine content was measured on a Beckman 6300 automatic amino a c i d a n a l y z e r . A sequence of two temperatures (50°C and 65°C), three b u f f e r s (Na-A, Na-B and Na-C in order of i n c r e a s i n g pH) and a c a t i o n exchange column were used. Sodium hydroxide was used to regenerate the column a f t e r each sample. A b u f f e r flow rate of 15 ml/h and a solvent flow rate of 8 ml/h was used. Recovery of t a u r i n e was cl o s e to 100%. 6.3.5 S t a t i s t i c a l a n a l y s i s : Performance and m o r t a l i t y d a t a , as w e l l as t a u r i n e content, were s t a t i s t i c a l l y analyzed as a completely random design using one-way a n a l y s i s of variance procedures of the S t a t i s t i c a l A n a l y s i s System (SAS I n s t i t u t e Inc . , 1 982 ) . Any s i g using the Ryan-Einot-a r c s i n t r a n s f o r m a t i o n d a t a . n i f i c a n t d i f f e r e n c e s we Gabrie1-We 1sch m u l t i p l e was used before analyz 74 re f u r t h e r analyzed range t e s t . An ing the m o r t a l i t y 6.4 RESULTS: F i n a l mean body weights, feed consumption and feed conversion data from Experiment 5 are shown in t a b l e 6.2. GES supplementation had no s i g n i f i c a n t e f f e c t on f i n a l body weight, but did s i g n i f i c a n t l y (p<.05) increase feed consumption. This i s r e f l e c t e d i n a s i g n i f i c a n t l y (p<.05) higher feed to gain r a t i o . Cardiac ( t a b l e 6.3 and f i g u r e 6.1) and b r a i n ( t a b l e 6.4 and f i g u r e 6.2) t a u r i n e c o n c e n t r a t i o n s were a f f e c t e d by GES supplementation. At 4 weeks of age the b r o i l e r s r e c e i v i n g 1.50% GES d i e t a r y supplementation had c a r d i a c t a u r i n e c o n c e n t r a t i o n s that were s i g n i f i c a n t l y (p<.05) lower than c o n t r o l s . At 3 and 4 weeks of age the b r o i l e r s r e c e i v i n g 1.50% GES supplementation had b r a i n t a u r i n e c o n c e n t r a t i o n s that were s i g n i f i c a n t l y (p<.05) higher than those of the c o n t r o l s . Cardiac t a u r i n e c o n c e n t r a t i o n s of the c o n t r o l b r o i l e r s and the b r o i l e r s r e c e i v i n g .50% GES supplementation increased over time so that at 4 weeks of age the c o n c e n t r a t i o n s were s i g n i f i c a n t l y higher than at 1 week of age. This was not the case f o r the b r o i l e r s of Treatment B. The b r o i l e r s in Treatment B r e c e i v e d .25% GES supplementation during week 2 and 1.50% GES t h e r e a f t e r . While on the .25% supplementation, c a r d i a c t a u r i n e c o n c e n t r a t i o n s increased so that the c o n c e n t r a t i o n at 2 weeks of Table 6.2 E f f e c t of feed consumption and 4 weeks of age GES supplementation on mean feed conversion (Experiment body we i g h t , 5): Results at FINAL FEED FEED DIET BODY WEIGHT CONSUMPTION CONVERSION ( g / b r o i l e r ) ( g / b r o i l e r ) (g feed/g gain) A 915 + l l3 1376 + 23a 1.580 + .031* B 907 +. 93 1430 + 16a 1.656 _+ .014?' C 927 + 123 1454 + 18 1.647 + .010 Data shown as mean +_ SEM 1 Diets a l l had 0% GES week 1. Week 2, d i e t A had 0%, di e t B 0.25% and d i e t C 0.50%. Weeks 3 and 4, d i e t A had 0.0%, d i e t B 1.50% and d i e t C 0.50% a,b Means wi t h i n a column with d i f f e r e n t s u p e r s c r i p t s are s i g n i f i c a n t l y d i f f e r e n t (p<.05) Table 6.3 E f f e c t of GES supplementation on ca r d i a c t a u r i n e content (umol/g wet weight) (Experiment 5) DIET1 WEEKS OF AGE A 23.81 + .473 X 28.34 + .68a y 27.60 + .58a y 3 1.64 +. 1.233 Z . B 22.66 + 1.463 X 28.14 + 1 . 2 1 a y 28.11 + .91a y 2 6 . 90 +. 1 . 4 1 b x y C 24.55+ .483 X 29.18+ . 8 7a y Z 25.23 + 2.163 X 7 30.37+ .673 Z Data shown as mean _+ SEM of 6 animals per point 1 Diets a l l had .0% GES week 1. Week 2, d i e t A had 0%, d i e t B .25%, and d i e t C .50%. Weeks 3 and 4, d i e t A had 0%, d i e t B 1.50% and d i e t C .50% a,b Means w i t h i n a column with d i f f e r e n t s u p e r s c r i p t s are s i g n i f i c a n t l y d i f f e r e n t (p<.05) x,y,z Means w i t h i n a row with d i f f e r e n t s u p e r s c r i p t s are s i g n i f i c a n t l y d i f f e r e n t (p<.05) Figure 6.1 Effect of GES supplementation on cardiac taurine concentration (Experiment 6) week 1 week 2 week 3 Age In weeks week 4 GES (% diet) CONTROL 0/.26/1.50- 0/.60/.5O • QE8 levle at wk1/wk2/wfc3,4 a,b means within a week with different letters are significantly different Table 6.4 E f f e c t of GES supplementation on b r a i n t a u r i n e content (umol/g wet weight) (Experiment 5) WEEKS OF AGE DIET 1 2 3 4 A 5.88+ . 3 03 X 5.30 + .103 X 5.12 + . 2 ?a x 4.12 + .17a y B 5.69+ .16a X y 5.57 + .26a b y 6.35 + . 1 7b X 5 . 3 2 ± -20b y C 5.88+ .103 X y 6.07 + .17b X 5.20+ . 3 3a y 4.40. + .163 Z Data shown as mean +_ SEM of 6 animals per point 1 Diets a l l had 0% GES week 1. Week 2, d i e t A had 0%, d i e t B . .25% and d i e t C .50%. Weeks 3 and 4, d i e t A had 0%, d i e t B 1.50% and d i e t C . 50% a,b Means wi t h i n a column, with d i f f e r e n t supe rsc r i p t s are s i g n i f i c a n t l y d i f f e r e n t (p<.05) x,y,z Means wi t h i n a row, with d i f f e r e n t s u p e r s c r i p t s are s i g n i f i c a n t l y d i f f e r e n t (p<.05) Figure 6.2 Effect of QES supplementation on brain taurine concentration (Experiment 6) week 1 week 2 week 3 week 4 Age In weeks QES (% diet) H i CONTROL H I 0/.26/1.60* I I 0/.50/.60* • QE8 Uv«l» at wkl/wk2/wka.4 a,b means within a week with different letters are significantly different 80 age was s i g n i f i c a n t l y higher than at 1 week of age. By 4 weeks of age, however, the c a r d i a c t a u r i n e c o n c e n t r a t i o n s were no longer s i g n i f i c a n t l y d i f f e r e n t from those at 1 week of age. Bra i n t a u r i n e c o n c e n t r a t i o n of the b r o i l e r s i n the c o n t r o l group and the b r o i l e r s r e c e i v i n g .50% GES supplementation decreased over time so that at 4 weeks of age t a u r i n e concen-t r a t i o n s were s i g n i f i c a n t l y lower than at 1 week of age. This was not the case f o r the b r o i l e r s of Treatment B which r e c e i v e d .25% GES supplementation during week 2 and 1.50% GES t h e r e a f t e r . B r a i n t a u r i n e c o n c e n t r a t i o n s were maintained so that the c o n c e n t r a t i o n at 4 weeks of age was not s i g n i f i c a n t l y d i f f e r e n t from the c o n c e n t r a t i o n at week 1. In the m o r t a l i t y study p o r t i o n of the experiment only s i x b r o i l e r s d i e d . Treatments A, B and C had 1, 2 and 3 b r o i l e r s die r e s p e c t i v e l y . Each treatment had only 1 b r o i l e r die of SDS. 6.5 DISCUSSION: From t h i s study i t was concluded that GES supplementation a f f e c t s t i s s u e t a u r i n e content in male b r o i l e r chickens quite d i f f e r e n t l y from that of r a t s (Huxtable et a l . , 1981). In ra t s t a u r i n e c o n c e n t r a t i o n s were reduced i n a l l t i s s u e s examined, by a 1% supplementation of GES i n the d r i n k i n g water. In t h i s experiment, supplementation with 1.50% GES i n the feed r e s u l t e d in 4 week c a r d i a c t a u r i n e l e v e l s that were 85% of c o n t r o l s , but b r a i n t a u r i n e l e v e l s that were 129% of c o n t r o l s . The c a r d i a c t a u r i n e c o n c e n t r a t i o n s of the c o n t r o l b r o i l e r s i n c r e a s e d over time. It would appear that GES supplementation prevented t h i s increase r a t h e r than causing a r e d u c t i o n i n 81 t a u r i n e c o n c e n t r a t i o n s to occur. The b r a i n t a u r i n e concentra-t i o n s of the c o n t r o l b r o i l e r s decreased over time. GES supplementation appeared to prevent t h i s decrease. B r a i n t a u r i n e c o n c e n t r a t i o n s vary between species,- but in most, t a u r i n e c o n c e n t r a t i o n i s highest at b i r t h (Sturman et a l . , 1977). While the c o n c e n t r a t i o n of most of the amino acids in the b r a i n e i t h e r i ncrease or remain constant over time, the c o n c e n t r a t i o n of t a u r i n e decreases with age. It would appear that t a u r i n e c o n c e n t r a t i o n s i n the b r a i n of male b r o i l e r chickens f o l l o w s t h i s p a t t e r n of decreasing with age. Although an animal's b r a i n t a u r i n e c o n c e n t r a t i o n s are highest at b i r t h , t h e i r b i o s y n t h e t i c c a p a c i t y i s at i t s lowest at t h i s time. It has been suggested that the b r a i n has an e f f i c i e n t and h i g h l y s e l e c t i v e t r a n s p o r t system f o r a t t a i n i n g and m a i n t a i n i n g t a u r i n e c o n c e n t r a t i o n s (Sturman et a l . , 1977). It i s p o s s i b l e that the b r a i n was able to compensate f o r the e f f e c t of GES i n h i b i t i o n by i n c r e a s i n g the h a l f - l i f e of the endogenous t a u r i n e . This would e x p l a i n the apparently higher l e v e l s of b r a i n t a u r i n e i n the 1.50% GES supplemented b r o i l e r s . C a rdiac t a u r i n e l e v e l s also change during development but the d i r e c t i o n of change v a r i e s between species (Sturman et a l . , 1977). In some s p e c i e s , such as the rat and r a b b i t , the c o n c e n t r a t i o n s f l u c t u a t e during development but there i s l i t t l e d i f f e r e n c e between c o n c e n t r a t i o n s at b i r t h and at m a t u r i t y . In other s p e c i e s , such as the cat and monkey, there i s no apparent change in c a r d i a c t a u r i n e c o n c e n t r a t i o n during development. Cardiac t a u r i n e l e v e l s of the male b r o i l e r chicken appear to i n c r e a s e during development. 82 GES supplementation did not a f f e c t t o t a l m o r t a l i t y or the i n c i d e n c e of SDS. Since c a r d i a c t a u r i n e l e v e l s were only reduced to 85% of c o n t r o l s i t i s premature to r u l e out a r o l e f o r t a u r i n e i n the p r e v e n t i o n of SDS in b r o i l e r s . 83 7.0 CONCLUSIONS: Four f a c t o r s were stu d i e d f o r p o s s i b l e involvement i n the e t i o l o g y of SDS in male b r o i l e r chickens - l a c t i c a c i d , c e r e a l type, p r o t e i n source and t a u r i n e . It appears u n l i k e l y that l a c t i c a c i d i s inv o l v e d i n SDS since supplementation with c a l c i u m l a c t a t e to 7.5% of the d i e t had no e f f e c t on the inc i d e n c e of SDS. Feeding glucose based d i e t s d i d not modify the e f f e c t of l a c t i c a c i d supplementation. Cereal type was shown to a f f e c t the in c i d e n c e of SDS. Male b r o i l e r chickens r a i s e d on wheat-based d i e t s had a higher incidence of SDS than those r a i s e d on corn-based d i e t s . This increase i n SDS m o r t a l i t y could not be explained on the basi s of growth rate since the e f f e c t of c e r e a l type on mean body weight was i n c o n s i s t e n t across the three s t u d i e s . P r o t e i n source was also shown to e f f e c t the incidence of SDS. The i n c l u s i o n of meat meal in the d i e t s of male b r o i l e r chickens reduced the incidence of SDS. It was suggested that t a u r i n e present i n meat meal, but absent i n soybean meal, was in v o l v e d i n p r o t e c t i n g the b r o i l e r from SDS. This hypothesis was t e s t e d by reducing c a r d i a c t a u r i n e l e v e l s with the aid of a t a u r i n e t r a n s p o r t i n h i b i t o r , guanidinoethy1 s u l f o n a t e (GES). At 4 weeks of age, the b r o i l e r s r e c e i v i n g 1.5% GES supplementation in the feed had c a r d i a c t a u r i n e c o n c e n t r a t i o n s that were 85% of c o n t r o l s and there was no e f f e c t on the incidence of SDS. It i s p o s s i b l e that a g r e a t e r d e p l e t i o n of t a u r i n e i s r e q u i r e d before an e f f e c t can be seen, but i t seems u n l i k e l y that the presence of t a u r i n e i n meat meal i s the reason f o r the increased p r o t e c t i o n against SDS. The e f f e c t of GES supplementation on b r o i l e r t i s s u e t a u r i n e c o n c e n t r a t i o n merits f u r t h e r i n v e s t i g a t i o n . While the 4 week c a r d i a c t a u r i n e c o n c e n t r a t i o n s of the 1.5% GES t r e a t e d b r o i l e r s were 85% of c o n t r o l s , the b r a i n l e v e l s were 129%. It appeared that GES was preventing the normal increase in c a r d i a c t a u r i n e c o n c e n t r a t i o n s and decrease in b r a i n t a u r i n e c o n c e n t r a t i o n s that occur in the developing male b r o i l e r . Bowes et a l . (1988) reported that a 25% feed r e s t r i c t i o n reduced SDS m o r t a l i t y and hypothesized that there was a r e l a t i o n s h i p between growth rate and the inc i d e n c e of SDS. In Experiment 2 the incidence of SDS was higher when the b r o i l e r s were fed a wheat-based r a t h e r than a corn-based d i e t or when meat meal was excluded in the d i e t . Both these f a c t o r s reduced growth rate as r e f l e c t e d in s i g n i f i c a n t l y lower f i n a l body weights. The l e v e l of r e d u c t i o n i n e i t h e r case was l e s s than the 41% r e d u c t i o n in body weight obtained by Bowes et a l . (1988). In Experiment 2, s u b s t i t u t i n g wheat f o r corn r e s u l t in only a 5% r e d u c t i o n i n 40 day mean body weight. Excluding meat meal from the d i e t r e s u l t e d in only a 2% r e d u c t i o n i n 40 day mean body weight. M o l l i s o n et a l . (1984) reported that a 15% r e d u c t i o n obtained by using 13% feed r e s t r i c t i o n d i d not s i g n i f i c a n t l y a f f e c t the incidence of SDS. A g r e a t e r r e d u c t i o n in growth rate may have been necessary to see an e f f e c t . It i s , t h e r e f o r e , not p o s s i b l e to r u l e out the r o l e of growth rate in the e t i o l o g y of SDS on the basis of the r e s u l t s of Experiment 2 . In Experiment 1 growth rate was al s o reduced by d i e t a r y treatment without an e f f e c t on the incidence of SDS. There was a 33% d i f f e r e n c e between the highest and lowest 4 week mean body weights o b t a i n e d , but the incidence of SDS was not s i g n i f i c a n t l y a f f e c t e d . On the basi s of the r e s u l t s of Experiment 1, i t appears u n l i k e l y that there i s a r e l a t i o n s h i p between growth rate and the incidence of SDS. 86 8.0 LITERATURE CITED: A i r a k s i n e n , E.M. and J . Partanen. 1985. Muscle t a u r i n e i n chicken and diseased human muscle. Prog. C l i n . B i o l . Res. 179:407-412. A l l e n , J.A. and M.R. G a r r e t t . 1971. Taurine in marine i n v e r t e b r a t e s . Adv. Mar. B i o l . 9:205-253. Anonymous. 1988. Taurine supplementation i n c y s t i c f i b r o s i s . Nutr. Rev. 46:257-258. Awapara, J . , A.J. Landua and R. F u e r s t . 1950. 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