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Feed Gorging and Extended Water Restriction Do Not Produce Knockdown in Male Turkeys Fed Monensin
RESEARCH NOTES Feed Gorging and Extended Water Restriction Do Not Produce Knockdown in Male Turkeys Fed Monensin K. L. WATKINS and M. N. NOVILLA Lilly Research Laboratories, Greenfield, Indiana 46140
1994 Poultry Science 73:587-590
INTRODUCTION
Since 1987, monensin has been used in the United States for the control of coccidiosis in turkeys at a dosage range of 60 to 100 ppm. Recently, monensin has been implicated as a causative factor in a syndrome known as turkey knockdown (Cardona et al., 1992). Turkey knockdown has been defined as any condition affecting the neuromuscular system to the extent that a bird is unable to stand or walk (Wages, 1993). Although the clinical signs of ionophore toxicosis can resemble these manifestations, ionophores are only one of many factors that may be involved in this syndrome (Wages, 1993).
Received for publication September 30, 1993. Accepted for publication December 10, 1993.
Field observations suggest that feed gorging and inadequate water intake may result in adverse effects in young turkeys fed monensin (Wages and Ficken, 1988; Cardona et al, 1992). Cardona et al. (1993) reported that 5- to 6-wk-old turkeys gavaged for several days with monensin developed ataxia. Stuart (1978), however, showed that feeding diets containing more than 200 ppm monensin had no adverse effects on turkeys less than 11 wk old, and Czarnecki (1990) demonstrated that monensin could be fed safely to 1- to 5-wk-old turkeys at dosages up to 150 ppm. A previous investigation failed to demonstrate any connection between feed gorging and growth performance, health status, or livability of torn turkeys fed monensin (Watkins et al., 1993). However, it has been suggested that this study was
587
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
ABSTRACT A study was conducted to determine the effects of feed restriction with subsequent gorging during extended water restriction on 27- to 57-d-old toms fed excess monensin. Four treatments were factorially arranged with two levels of dietary monensin (0 and 140 ppm) and two feeding-watering regimens (ad libitum and restricted). Ad libitum birds had full access to feed and water but restricted birds only had access to feed from 0800 to 1200 h daily. A 24-h water restriction regimen was imposed biweekly from 28 to 42 d and a 36-h water restriction regimen was imposed biweekly from 43 to 57 d. The restricted feeding and watering regimen decreased (P < .01) feed intake, weight gain, and feed efficiency. Excess monensin had no effect (P > .10) on feed intake regardless of feeding and watering regimen. Monensin had no effect on the weight gain and feed efficiency of ad libitum birds, but monensin exacerbated the decrease on gain (monensin by regimen, P < .01) and feed efficiency (monensin by regimen, P < .09) induced by feed and water restriction. No treatment-related abnormalities were observed during either interim or terminal necropsies. Neither clinical signs of ionophore toxicity nor pathologic findings attributed to monensin treatment were observed during the study. Based on these observations, feed gorging and water restriction will not adversely affect the health status of, or increase the mortality rate of, 4- to 8-wk-old male turkeys fed monensin. (Key words: turkey, monensin, feed restriction, water restriction, weight gain)
588
WATKINS AND NOVILLA
not rigorous enough to induce knockdown (Elanco Animal Health, 1992). Concerns included the duration of water restriction, the number of replicates, and the brooding of birds on monensin-treated feed. Therefore, a second study was conducted to address these concerns. In the current study the water restriction regimen was extended from 4 to 24 or 36 h, the number of replicates was increased from four to eight, and poults were brooded on monensin-free feed. MATERIALS AND METHODS
^anssen Hatcheries, Zeeland, MI 49464.
RESULTS Restricted birds consumed approximately 70% (ranged from 20 to over 90%) of the feed as their ad libitum counterparts. Feed and water restriction decreased (P < .01) feed intake and gain and increased (P < .01) feed:gain ratio (Table 1). Excess monensin had no effect on ad libitum birds but decreased gain and increased feed: gain ratio in restricted birds (monensin by regimen interaction; P < .03 and P < .09, respectively). Monensin had no effect (P > .10) on feed intake. Although restricted birds had a 70% lower mortality rate than ad libitum birds, neither monensin level nor feed and water regimen affected (P > .10) rate of mortality (Table 1). Two birds were culled during the study due to swollen infraorbital sinuses, and nine birds died from congestive heart failure
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
A floor pen trial was conducted to evaluate the effect of feed gorging and water restriction on turkeys fed excess monensin. Four treatments were factorially arranged in a completely randomized design with two levels of dietary monensin (0 and 140 ppm) and two feedingwatering regimens (ad libitum and restricted). Each treatment group was replicated eight times with 24 birds per replicate. Male Nicholas poults were obtained from a commercial hatchery 1 and group brooded in a thermostatically controlled raised wire floored brooding unit. Poults were fed a monensin-free prestarter ration from hatch to 19 d, a starter ration from 20 to 34 d, and a grower ration from 35 to 57 d. All diets were formulated to simulate standard industry practices (Watkins et al., 1993). On Day 14, poults were moved into a floor pen facility. Each pen was fitted with a bell waterer and a stainless steel trough feeder. Birds were grouped by weight and randomly allotted to pen and treatment. The 24 toms in each pen provided a stocking density of .17 m 2 per bird. From 20 to 26 d, restricted birds were trained to gorge on monensin-free feed, and ad libitum birds had free access to the same feed. During the pretrial period all birds received free access to water. The experimental period began on Day 27 when the dietary treatments and feeding regimens were initiated. Ad libitum birds had free access to feed and water throughout the study but restricted birds only had
access to feed from 0800 to 1200 h daily. Water restriction was imposed twice a week (Mondays and Thursdays) starting at 0700 h. A 24-h water restriction was i m p o s e d from 28 to 42 d a n d a 36-h water restriction was imposed from 43 to 57 d. Feeders were weighed daily and overall gain was determined from initial and final birds weights. Birds that died during the study were necropsied and tissue samples were taken for histopathological evaluations. At trial termination, three preidentified birds from each pen (24 birds per treatment group) were necropsied and sampled for histopathology. Terminal examinations included heart, abdominal, superficial Pectoralis, Quadriceps, and Gastrocnemius muscles, and all tissues associated with gross pathology. Gain, feed intake, feed:gain ratios, and mortality data were analyzed using analysis of variance procedures appropriate for a completely randomized factorially arranged design (Steel and Torrie, 1980). Orthogonal single degree of freedom comparisons were used to test monensin and feed and water regimen main effects and interactions. Individual mean separation was accomplished using the least squares means test. Mortality data were transformed (^X + .5) prior to analysis (SAS Institute, 1985).
589
RESEARCH NOTE TABLE 1. Effect of dietary monensin level and feeding regimen on growth performance and mortality
Monensin (ppm) 0 140 0 140 SEM
Feeding regimen
Feed: gain
2.75* 2.73* IT/* 1.64< .03
4.74" 4.76a 3.16b 3.04b .04
(kg:kg) 1.728a 1.742* 1.792b 1.855c .014
3.13 2.08 .52 1.04
2.26 2.19
3.95 3.90
1.760 1.799
1.83 1.56
2.74 1.71
4.75 3.10
1.735 1.824
2.61 .78
(kg) Ad libitum Ad libitum Restricted Restricted
Source of variatic>n Monensin level Feed and water regimen Monensin by regimen
.009 .001 .030
.240 .001 .122
.010 .001 .089
Mortality
(%)
1.11
.816 .112 .487
Means in columns with no common superscript differ significantly (P < .05).
exhibiting alterations consistent with spontaneous cardiomyopathy. Knockdown did not occur during the study, and no treatment-related gross or microscopic abnormalities were observed in either birds dying during the study or examined at trial termination. DISCUSSION This study provides further evidence that neither feed gorging nor water restriction can precipitate knockdown in turkeys fed up to 140 ppm monensin. The results of the current study were similar to those previously reported by Watkins et al. (1993). Recently, Cardona et al. (1993) reported that gavaging turkeys with crystalline monensin at dosages of 4.7, 8.8, or 17.6 mg/kg body weight in a vegetable oil suspension resulted in clinical signs of ataxia and rear limb paresis paralysis. Histological lesions of necrotizing myopathy of rear limb skeletal muscles, intrafiber edema, and vacuolation of heart muscle fibers were also reported. The single oral dosages corresponded to birds consuming 1 d worth of feed containing approximately 75, 150, and 300 ppm monensin.
Even birds receiving the lowest dosage (4.7 mg/kg body weight) were ataxic after 3 d of dosing, whereas birds receiving the highest dosage (17.6 mg/kg body weight) were ataxic 3 h after the first dose. During the current study, the restricted birds consumed on average 7.7 mg monensin/kg of body weight with a range of 1.4 to 14.2 mg monensin/kg of body weight in less than 2 h. This rate of monensin consumption was similar to that achieved in a previous experiment; however, no clinical or pathological evidence of knockdown was observed in either the current experiment or that previously conducted in our laboratory (Watkins et al, 1993). Except for the method of drug administration, we are unable to explain the discrepancy between the results obtained in our laboratory and those reported by Cardona et al. (1993). It is possible that the monensin extraction method or the vegetable oil carrier used by Cardona et al. (1993) may have increased monensin bioavailability. It is known that drug exposure from a gavage dose does not simulate drug ingestion under normal feeding conditions (Buck and Osweiler,
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
Monensin level, ppm 0 140 Feeding regimen Ad libitum Restricted
a_c
Feed intake
Gain
590
WATKINS AND NOVILLA
REFERENCES Buck, W. B., and G. D. Osweiler, 1976. Clinical and Diagnostic Veterinary Toxicology. 2nd ed. G. A. Van Gelder, ed. Kendal/Hunt Publishing Co., Dubuque, LA. Cardona, C. J., F. D. Galey, and A. A. Bickford, 1992. Turkey knockdown syndrome. Lab Notes 5:5. Cardona, C. J., F. D. Galey, A. A. Bickford, B. R. Charlton, and G. L. Cooper, 1993. Skeletal myopathy produced with experimental dosing
of turkeys with monensin. Avian Dis. 37: 107-117. Czarnecki, C. M, 1990. Effect of including lasalocid or monensin singly or in combination with furazolidone on the growth and feed consumption of turkey poults. Res. Vet. Sci. 49:256-260. Elanco Animal Health, 1992. A Report of Presentations and Discussions at the Third Elanco Turkey Technical Seminar, May 8-10. Nashville, TN. Leek, R. G., R. Fayer, and D. K. McLoughlin, 1976. Effect of monensin on experimental infections of Eimeria ninakohlyakimovae in lambs. Am. J. Vet. Res. 37:339-341. Novilla, M. N., 1992. The veterinary importance of the toxic syndrome induced by ionophores. Vet. Human Toxicol. 34:66-70. Salyi, G., 1985. Monensin poisoning in turkeys. Magy. Allatorv. Lapja 40:225-228. SAS Institute, 1985. SAS® User's Manual. Version 5 Edition. SAS Institute, Inc., Cary, NC. Steel, R.G.D., and J. H. Torrie, 1980. Principles and Procedures of Statistics: A Biometrical Approach. McGraw-Hill Book Co., Inc. New York, NY. Stuart, J. C, 1978. An outbreak of monensin poisoning in adult turkeys. Vet. Rec. 102:303-304. Van Vleet, J. F., V. J. Ferrans, and E. Herman, 1991. Cardiovascular and skeletal muscle system. Pages 539-624 in: Handbook of Toxicologic Pathology. W. M. Haschek and C. G. Rousseaux, ed. Academic Press Inc., San Diego, CA. Wages, D. P., 1993. Turkey knockdown is a multifaceted puzzle. Turkey World 69:24-25. Wages, D. P., and M. D. Ficken, 1988. Skeletal muscle lesions in turkeys associated with the feeding of monensin. Avian Dis. 32:583-586. Watkins, K. L., M. N. Novilla, and T. W. Campi, 1993. Effects of feed restriction and subsequent gorging with limited access to water on male turkeys fed graded level of monensin. Poultry Sci. 72: 677-683.
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
1976), and Leek et al. (1976) identified possible difference between gavage and in feed dosing of monensin in lambs. Turkey knockdown syndrome poses a diagnostic challenge because its association with monensin is primarily due to alterations in skeletal muscles similar to those induced by toxic levels of ionophores. Unfortunately, striated muscles have limited responses to injury (Van Vleet et al, 1991), and ionophore-induced skeletal and cardiac lesions are not pathognomonic (Novilla, 1992). Monensin has been fed to turkeys at levels between 100 and 300 ppm without observing knockdown (Stuart, 1978; Salyi, 1985; Czarnecki, 1990; Watkins et al, 1993). This syndrome is clearly a multifactorial problem involving a variety of nutritional, environmental, infectious, and toxic factors. This study confirms previous observations that feed gorging and water restriction alone will not result in knockdown in turkeys fed recommended or excess levels of monensin.
1994 Poultry Science 73:587-590
INTRODUCTION
Since 1987, monensin has been used in the United States for the control of coccidiosis in turkeys at a dosage range of 60 to 100 ppm. Recently, monensin has been implicated as a causative factor in a syndrome known as turkey knockdown (Cardona et al., 1992). Turkey knockdown has been defined as any condition affecting the neuromuscular system to the extent that a bird is unable to stand or walk (Wages, 1993). Although the clinical signs of ionophore toxicosis can resemble these manifestations, ionophores are only one of many factors that may be involved in this syndrome (Wages, 1993).
Received for publication September 30, 1993. Accepted for publication December 10, 1993.
Field observations suggest that feed gorging and inadequate water intake may result in adverse effects in young turkeys fed monensin (Wages and Ficken, 1988; Cardona et al, 1992). Cardona et al. (1993) reported that 5- to 6-wk-old turkeys gavaged for several days with monensin developed ataxia. Stuart (1978), however, showed that feeding diets containing more than 200 ppm monensin had no adverse effects on turkeys less than 11 wk old, and Czarnecki (1990) demonstrated that monensin could be fed safely to 1- to 5-wk-old turkeys at dosages up to 150 ppm. A previous investigation failed to demonstrate any connection between feed gorging and growth performance, health status, or livability of torn turkeys fed monensin (Watkins et al., 1993). However, it has been suggested that this study was
587
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
ABSTRACT A study was conducted to determine the effects of feed restriction with subsequent gorging during extended water restriction on 27- to 57-d-old toms fed excess monensin. Four treatments were factorially arranged with two levels of dietary monensin (0 and 140 ppm) and two feeding-watering regimens (ad libitum and restricted). Ad libitum birds had full access to feed and water but restricted birds only had access to feed from 0800 to 1200 h daily. A 24-h water restriction regimen was imposed biweekly from 28 to 42 d and a 36-h water restriction regimen was imposed biweekly from 43 to 57 d. The restricted feeding and watering regimen decreased (P < .01) feed intake, weight gain, and feed efficiency. Excess monensin had no effect (P > .10) on feed intake regardless of feeding and watering regimen. Monensin had no effect on the weight gain and feed efficiency of ad libitum birds, but monensin exacerbated the decrease on gain (monensin by regimen, P < .01) and feed efficiency (monensin by regimen, P < .09) induced by feed and water restriction. No treatment-related abnormalities were observed during either interim or terminal necropsies. Neither clinical signs of ionophore toxicity nor pathologic findings attributed to monensin treatment were observed during the study. Based on these observations, feed gorging and water restriction will not adversely affect the health status of, or increase the mortality rate of, 4- to 8-wk-old male turkeys fed monensin. (Key words: turkey, monensin, feed restriction, water restriction, weight gain)
588
WATKINS AND NOVILLA
not rigorous enough to induce knockdown (Elanco Animal Health, 1992). Concerns included the duration of water restriction, the number of replicates, and the brooding of birds on monensin-treated feed. Therefore, a second study was conducted to address these concerns. In the current study the water restriction regimen was extended from 4 to 24 or 36 h, the number of replicates was increased from four to eight, and poults were brooded on monensin-free feed. MATERIALS AND METHODS
^anssen Hatcheries, Zeeland, MI 49464.
RESULTS Restricted birds consumed approximately 70% (ranged from 20 to over 90%) of the feed as their ad libitum counterparts. Feed and water restriction decreased (P < .01) feed intake and gain and increased (P < .01) feed:gain ratio (Table 1). Excess monensin had no effect on ad libitum birds but decreased gain and increased feed: gain ratio in restricted birds (monensin by regimen interaction; P < .03 and P < .09, respectively). Monensin had no effect (P > .10) on feed intake. Although restricted birds had a 70% lower mortality rate than ad libitum birds, neither monensin level nor feed and water regimen affected (P > .10) rate of mortality (Table 1). Two birds were culled during the study due to swollen infraorbital sinuses, and nine birds died from congestive heart failure
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
A floor pen trial was conducted to evaluate the effect of feed gorging and water restriction on turkeys fed excess monensin. Four treatments were factorially arranged in a completely randomized design with two levels of dietary monensin (0 and 140 ppm) and two feedingwatering regimens (ad libitum and restricted). Each treatment group was replicated eight times with 24 birds per replicate. Male Nicholas poults were obtained from a commercial hatchery 1 and group brooded in a thermostatically controlled raised wire floored brooding unit. Poults were fed a monensin-free prestarter ration from hatch to 19 d, a starter ration from 20 to 34 d, and a grower ration from 35 to 57 d. All diets were formulated to simulate standard industry practices (Watkins et al., 1993). On Day 14, poults were moved into a floor pen facility. Each pen was fitted with a bell waterer and a stainless steel trough feeder. Birds were grouped by weight and randomly allotted to pen and treatment. The 24 toms in each pen provided a stocking density of .17 m 2 per bird. From 20 to 26 d, restricted birds were trained to gorge on monensin-free feed, and ad libitum birds had free access to the same feed. During the pretrial period all birds received free access to water. The experimental period began on Day 27 when the dietary treatments and feeding regimens were initiated. Ad libitum birds had free access to feed and water throughout the study but restricted birds only had
access to feed from 0800 to 1200 h daily. Water restriction was imposed twice a week (Mondays and Thursdays) starting at 0700 h. A 24-h water restriction was i m p o s e d from 28 to 42 d a n d a 36-h water restriction was imposed from 43 to 57 d. Feeders were weighed daily and overall gain was determined from initial and final birds weights. Birds that died during the study were necropsied and tissue samples were taken for histopathological evaluations. At trial termination, three preidentified birds from each pen (24 birds per treatment group) were necropsied and sampled for histopathology. Terminal examinations included heart, abdominal, superficial Pectoralis, Quadriceps, and Gastrocnemius muscles, and all tissues associated with gross pathology. Gain, feed intake, feed:gain ratios, and mortality data were analyzed using analysis of variance procedures appropriate for a completely randomized factorially arranged design (Steel and Torrie, 1980). Orthogonal single degree of freedom comparisons were used to test monensin and feed and water regimen main effects and interactions. Individual mean separation was accomplished using the least squares means test. Mortality data were transformed (^X + .5) prior to analysis (SAS Institute, 1985).
589
RESEARCH NOTE TABLE 1. Effect of dietary monensin level and feeding regimen on growth performance and mortality
Monensin (ppm) 0 140 0 140 SEM
Feeding regimen
Feed: gain
2.75* 2.73* IT/* 1.64< .03
4.74" 4.76a 3.16b 3.04b .04
(kg:kg) 1.728a 1.742* 1.792b 1.855c .014
3.13 2.08 .52 1.04
2.26 2.19
3.95 3.90
1.760 1.799
1.83 1.56
2.74 1.71
4.75 3.10
1.735 1.824
2.61 .78
(kg) Ad libitum Ad libitum Restricted Restricted
Source of variatic>n Monensin level Feed and water regimen Monensin by regimen
.009 .001 .030
.240 .001 .122
.010 .001 .089
Mortality
(%)
1.11
.816 .112 .487
Means in columns with no common superscript differ significantly (P < .05).
exhibiting alterations consistent with spontaneous cardiomyopathy. Knockdown did not occur during the study, and no treatment-related gross or microscopic abnormalities were observed in either birds dying during the study or examined at trial termination. DISCUSSION This study provides further evidence that neither feed gorging nor water restriction can precipitate knockdown in turkeys fed up to 140 ppm monensin. The results of the current study were similar to those previously reported by Watkins et al. (1993). Recently, Cardona et al. (1993) reported that gavaging turkeys with crystalline monensin at dosages of 4.7, 8.8, or 17.6 mg/kg body weight in a vegetable oil suspension resulted in clinical signs of ataxia and rear limb paresis paralysis. Histological lesions of necrotizing myopathy of rear limb skeletal muscles, intrafiber edema, and vacuolation of heart muscle fibers were also reported. The single oral dosages corresponded to birds consuming 1 d worth of feed containing approximately 75, 150, and 300 ppm monensin.
Even birds receiving the lowest dosage (4.7 mg/kg body weight) were ataxic after 3 d of dosing, whereas birds receiving the highest dosage (17.6 mg/kg body weight) were ataxic 3 h after the first dose. During the current study, the restricted birds consumed on average 7.7 mg monensin/kg of body weight with a range of 1.4 to 14.2 mg monensin/kg of body weight in less than 2 h. This rate of monensin consumption was similar to that achieved in a previous experiment; however, no clinical or pathological evidence of knockdown was observed in either the current experiment or that previously conducted in our laboratory (Watkins et al, 1993). Except for the method of drug administration, we are unable to explain the discrepancy between the results obtained in our laboratory and those reported by Cardona et al. (1993). It is possible that the monensin extraction method or the vegetable oil carrier used by Cardona et al. (1993) may have increased monensin bioavailability. It is known that drug exposure from a gavage dose does not simulate drug ingestion under normal feeding conditions (Buck and Osweiler,
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
Monensin level, ppm 0 140 Feeding regimen Ad libitum Restricted
a_c
Feed intake
Gain
590
WATKINS AND NOVILLA
REFERENCES Buck, W. B., and G. D. Osweiler, 1976. Clinical and Diagnostic Veterinary Toxicology. 2nd ed. G. A. Van Gelder, ed. Kendal/Hunt Publishing Co., Dubuque, LA. Cardona, C. J., F. D. Galey, and A. A. Bickford, 1992. Turkey knockdown syndrome. Lab Notes 5:5. Cardona, C. J., F. D. Galey, A. A. Bickford, B. R. Charlton, and G. L. Cooper, 1993. Skeletal myopathy produced with experimental dosing
of turkeys with monensin. Avian Dis. 37: 107-117. Czarnecki, C. M, 1990. Effect of including lasalocid or monensin singly or in combination with furazolidone on the growth and feed consumption of turkey poults. Res. Vet. Sci. 49:256-260. Elanco Animal Health, 1992. A Report of Presentations and Discussions at the Third Elanco Turkey Technical Seminar, May 8-10. Nashville, TN. Leek, R. G., R. Fayer, and D. K. McLoughlin, 1976. Effect of monensin on experimental infections of Eimeria ninakohlyakimovae in lambs. Am. J. Vet. Res. 37:339-341. Novilla, M. N., 1992. The veterinary importance of the toxic syndrome induced by ionophores. Vet. Human Toxicol. 34:66-70. Salyi, G., 1985. Monensin poisoning in turkeys. Magy. Allatorv. Lapja 40:225-228. SAS Institute, 1985. SAS® User's Manual. Version 5 Edition. SAS Institute, Inc., Cary, NC. Steel, R.G.D., and J. H. Torrie, 1980. Principles and Procedures of Statistics: A Biometrical Approach. McGraw-Hill Book Co., Inc. New York, NY. Stuart, J. C, 1978. An outbreak of monensin poisoning in adult turkeys. Vet. Rec. 102:303-304. Van Vleet, J. F., V. J. Ferrans, and E. Herman, 1991. Cardiovascular and skeletal muscle system. Pages 539-624 in: Handbook of Toxicologic Pathology. W. M. Haschek and C. G. Rousseaux, ed. Academic Press Inc., San Diego, CA. Wages, D. P., 1993. Turkey knockdown is a multifaceted puzzle. Turkey World 69:24-25. Wages, D. P., and M. D. Ficken, 1988. Skeletal muscle lesions in turkeys associated with the feeding of monensin. Avian Dis. 32:583-586. Watkins, K. L., M. N. Novilla, and T. W. Campi, 1993. Effects of feed restriction and subsequent gorging with limited access to water on male turkeys fed graded level of monensin. Poultry Sci. 72: 677-683.
Downloaded from http://ps.oxfordjournals.org/ by guest on May 28, 2015
1976), and Leek et al. (1976) identified possible difference between gavage and in feed dosing of monensin in lambs. Turkey knockdown syndrome poses a diagnostic challenge because its association with monensin is primarily due to alterations in skeletal muscles similar to those induced by toxic levels of ionophores. Unfortunately, striated muscles have limited responses to injury (Van Vleet et al, 1991), and ionophore-induced skeletal and cardiac lesions are not pathognomonic (Novilla, 1992). Monensin has been fed to turkeys at levels between 100 and 300 ppm without observing knockdown (Stuart, 1978; Salyi, 1985; Czarnecki, 1990; Watkins et al, 1993). This syndrome is clearly a multifactorial problem involving a variety of nutritional, environmental, infectious, and toxic factors. This study confirms previous observations that feed gorging and water restriction alone will not result in knockdown in turkeys fed recommended or excess levels of monensin.