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ENVIRONMENT, WELL-BEING, AND BEHAVIOR |
* Department of Animal and Poultry Science, and Department of Biomedical Sciences, University of Guelph, Ontario, Canada N1G 2W1
1 Corresponding author: tsmith{at}uoguelph.ca
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Key Words: Fusarium mycotoxin • broiler breeder • eggshell thickness • hatchability • embryonic mortality
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Trichothecenes are the most studied group of Fusarium mycotoxins and have been implicated in many cases of mycotoxicoses in animals and humans (Placinta et al., 1999). Trichothecenes are of great importance, because they may occur in toxicologically relevant concentrations in grains, which can affect the health and productivity of farm animals (Doll and Danicke, 2004). Although acute mycotoxicoses are rare in poultry production, chronic exposure to low levels of mycotoxins is responsible for reduced productivity and increased susceptibility to infectious diseases (Hussein and Brasel, 2001).
The trichothecenes include over 150 secondary fungal metabolites (Rocha et al., 2005), which are now recognized as having multiple inhibitory effects on eukaryotic cells, including inhibition of protein, DNA, and RNA synthesis; inhibition of mitosis; interference with cell-membrane integrity; and induction of apoptosis (Bennett and Klich, 2003; Rocha et al., 2005). The rapidly proliferating cells and tissues with high rates of protein turnover, including the immune system, liver, and small intestine, are primarily affected by these mycotoxins (Feinberg and McLaughlin, 1989).
There are many published studies on the effects of feeding Fusarium mycotoxins on the health and performance of broilers and laying hens (Danicke et al., 2002, 2003; Swamy et al., 2002, 2004; Chowdhury and Smith, 2004). It is known that dietary inclusion of a polymeric glucomannan mycotoxin adsorbent (GMA), extracted from the cell wall of yeast, has some beneficial effects in preventing adverse effects of Fusarium mycotoxins in broilers (Swamy et al., 2002, 2004), laying hens (Chowdhury and Smith, 2004), and ducklings (Chowdhury et al., 2005).
There is a dearth of literature regarding the effects of trichothecene mycotoxins on broiler breeders (Brake et al., 2000). The objectives of the current study were, therefore, to investigate the effects of feeding grains naturally contaminated with Fusarium mycotoxins on the performance and metabolism of broiler breeders and to determine the efficacy of GMA in preventing these effects.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Hens and roosters were fed corn-, wheat-, and soybean meal-based standard breeder diets, which included the following: (1) control, (2) contaminated grains, and (3) contaminated grains + 0.2% GMA (MTB-100, Alltech Inc., Nicholasville, KY) for 12 wk. Nutrient concentrations in the control diet met or exceeded minimum requirements according to the NRC (1994). The mycotoxin-contaminated diets were formulated to the nutrient specifications of the control diet, with control corn and wheat replaced by contaminated grains. All birds received the control diet for 2 wk to become environmentally acclimated and then were fed experimental diets.
The project was approved by the University of Guelph Animal Care Committee, and it met the guidelines of the Canadian Council on Animal Care.
Determination of Dietary Mycotoxin Concentrations
Dietary concentrations of 19 mycotoxins, including deoxynivalenol (DON), 3-acetyl-DON, 15-acetyl-DON, nivalenol, T-2 toxin, iso-T-2 toxin, acetyl-T-2 toxin, HT-2 toxin, T-2 triol, T-2 tetraol, fusarenone-X, diacetoxyscirpenol, scirpentriol, 15-acetoxyscirpentriol, neosolaniol, zearalenone, zearalenol, aflatoxin, and fumonisin, were analyzed by gas chromatography and mass spectrometry at the Veterinary Diagnostic Laboratory, North Dakota State University, Fargo (Raymond et al., 2003). The detection limits were 0.2 mg/kg, with the exception of aflatoxin and fumonisin, which were detected at 0.02 and 2 mg/ kg, respectively.
Experimental Parameters Measured
Feed Consumption and Changes in BW.
Hens were weighed individually at the beginning and end of the experiment. Feed consumption was measured with trays set under each feeder, enabling feed spills to be weighed weekly during the experiment.
Egg Production and Egg Parameters.
Daily egg production was recorded throughout the experiment. Eggs were collected from birds on the last day of the first, second, and third months of the experiment. Egg weight, shell deformity, albumen height, yolk weight, shell weight, and shell thickness were determined. Eggshell deformity was expressed as a mean value of 2 measurements on the equator of the egg using a shell-deformity measuring instrument (Summers et al., 1976). Eggs were kept at 7°C overnight and then broken to determine albumen height and yolk weight. Yolk weight was determined after rolling the yolk on surgical gauze to remove adhering albumen. Albumen height was determined using a micrometer (Ames S-5428, B.C. Ames Co., Melrose, MA). After removing any residue of albumen from the eggshell, the shell with membranes was weighed to determine shell weight. Shell thickness was determined as a mean of measurement at 3 locations on the egg (air cell, equator, and sharp end) using a shell-thickness measuring gauge (Ames 25M-5, B.C. Ames Co.).
Hatchability and Embryonic Mortality.
Hens were individually inseminated (3 times) during the week before egg collection with 50 µL of fresh, pooled semen from roosters fed corresponding diets. All eggs laid in wk 4, 8, and 12 were collected and stored for 1 wk in an egg cooler maintained at 16°C and 80% RH. The eggs were set in a conventional forced-air incubator (RI 14, Natureform Hatchery Systems, Jacksonville, FL). All eggs were weighed before setting. The incubator was maintained at 37.5°C and 50% RH. All eggs were then transferred to a hatcher (H5W, Natureform Hatchery Systems) at 19 d of incubation maintained at 36°C and 85% RH until d21 of incubation, when trays were removed. Hatchability was expressed as the percentage of chicks hatched from the total number of fertile eggs set. All remaining unhatched eggs were opened at 21 d of incubation and examined macroscopically to determine embryonic developmental stages (Leeson and Summers, 2000). These eggs were classified as infertile, early dead (1 to 7 d), middead (8 to 14 d), or late dead (15 to 21 d). Eggs showing no macroscopic signs of development were considered infertile.
Progeny Performance.
All chicks hatched were individually weighed, wing-banded, vaccinated against infectious bronchitis (Massachusetts live virus, Intervet Canada Ltd.) and Marek’s disease (MD-VAC CFL, Fort Dodge Animal Health, Madison, NJ), and distributed into floor pens. The removal of chicks from hatching trays was done as quickly as possible to prevent possible weight loss, which might affect subsequent performance during the starter period. Chicks were initially maintained at 31°C, and the temperature was gradually lowered by 2°C/wk to reach 25°C by the end of wk 3. All chicks were fed a corn- and soybean meal-based standard broiler starter diet for 3 wk. The diet was formulated to meet or exceed minimum requirements according to the NRC (1994) and primary breeder recommendations for broiler chicks. Mortality was recorded daily throughout the experiment. Individual BW and feed consumption per pen were measured weekly. Cumulative weight gain and feed consumption were determined, whereas cumulative gain:feed ratios were calculated.
Rooster Fertility.
Roosters were kept in individual cages during the experiment. At the end of wk 4, 8, and 12, semen was collected from roosters individually in graduated tubes to assess semen quality and sperm characteristics. In addition to actual milking for artificial insemination and laboratory assessments, roosters were being teased weekly throughout the experiment to prevent any possible negative effect on reproductive efficiency, which might have resulted from the absence of natural floor mating. Semen volume was measured visually. Sperm concentration was determined by a calibrated spectrophotometer (Spectronic 20D, Milton Roy, Ivyland, PA), using 5 µL of semen diluted in 5,000 µL of 2.9% sodium citrate. Motility was estimated by computer-assisted sperm analysis (Hamilton-Thorne Biosciences Inc., Beverly, MA). Five microliters of semen was diluted in 1 mL of sodium citrate-egg yolk buffer. A 10 µL drop of diluted semen was put on a microscopic slide, covered with a cover slip, and at least 200 sperm, in a minimum of 3 fields, were analyzed. The motility was expressed as a percentage of motile sperm. Five microliters of semen, diluted in 500 µL of 2.9% sodium citrate, was put in an Eppendorf tube for viability analysis. In the dark, 5 µL of SYBR-14 (LIVE/DEAD Sperm Viability Kit, Molecular Probes, Invitrogen Corp., Carlsbad, CA) and 3 µL of propidium iodide (LIVE/DEAD Sperm Viability Kit, Molecular Probes, Invitrogen Corp.) were added. Propidium iodide stains nonviable sperm red, and SYBR-14 stains viable sperm green. The preparation was incubated for 30 min to 1 h at room temperature. One hundred sperm were counted in each of 2 fields, using a fluorescence microscope (Leitz Laborlux S, Leica Microsystems Inc., Buffalo, NY) equipped with a blue filter. Viability was calculated as green sperm as a percentage of total sperm (Bongalhardo, 2002).
Organ Weights.
At the end of the experiment, all birds were weighed and killed by instantaneous cervical dislocation. The liver, spleen, kidney, and testes were excised and weighed. Organ weights were expressed on a relative BW basis.
Blood Biochemistry.
At the end of wk 4, 8, and 12, 4 blood samples per treatment were collected from the wing vein in tubes containing sodium heparin to determine biochemical parameters. Plasma concentrations of Ca, P, glucose, cholesterol, total bilirubin, uric acid, total protein, albumin, globulin, and activities of serum enzymes, including 
-glutamyltransferase, aspartate aminotransferase, creatine kinase, lactate dehydrogenase, glutamate dehydrogenase, amylase, and lipase, were determined (Laboratory Service Division, University of Guelph).
Hematology.
Four blood samples per treatment were collected for hematological evaluation. Hemoglobin and hematocrit were measured, and mean corpuscular hemoglobin concentration was calculated. Total white blood cell and differential leukocyte count (heterophils, lymphoctes, monocytes, and basophils) were also determined (Laboratory Service Division, University of Guelph, Guelph).
Serum Antibody Titers.
Sera were separated from blood samples and frozen until analyzed by Elisa test kit (flock check, IDEXX Laboratories Inc., Westbrook, ME) for detecting serum antibody titers against Newcastle disease virus (NDV) and infectious bronchitis virus (IBV).
Statistical Analysis
Data were analyzed by ANOVA using the GLM procedure of SAS as a completely randomized block design (Kuehl, 2000; SAS Institute, 2000). Multiple comparisons were made using Dunnett’s test to determine the nature of the response exhibited by different parameters in birds fed control and contaminated diets. Hatching BW was used as a covariate for chick BW at the end of wk 3 for analyzing data related to progeny performance. Hens and rooster BW were used as covariate for organ weight analysis. Statements of statistical significance were based on P 
0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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. In the control diet for hens and roosters, DON levels were 0.2 and 0.9 mg/kg, respectively, but other mycotoxins were not detected. The DON concentrations in the contaminated hen diet and contaminated hen diet + GMA were 12.6 and 13.8 mg/kg. In the diets of roosters, the corresponding levels were 6.4 and 9.2 mg/kg. Zearalenone and 15-acetyl-DON were detected in lesser quantities.
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Egg Production and Egg Parameters
There were no significant effects of diet (P > 0.05) on monthly or overall egg production. Egg production was significantly reduced in the sixth week, however, with the feeding of contaminated grains (data not shown). The feeding of contaminated grains decreased (P < 0.05) eggshell thickness after 4 wk of feeding, and GMA supplementation prevented this effect (Table 2). There was no effect of diet on other egg parameters, including weight, yolk weight, albumen height, eggshell deformity, or eggshell weight (data not shown).
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). There was a significant increase (P < 0.05) in early (1 to 7 d) embryonic mortality at wk 4 in eggs from birds fed contaminated grains compared with controls; this was prevented by the feeding of GMA (Table 2). Mid (8 to 14 d) and late (15 to 21 d) mortalities were not affected by diet.
Progeny Performance
There was no effect of previous dietary treatment of the dam on weight or viability of newly hatched chicks (P > 0.05). The ratio of chick weight to egg weight was not affected (P > 0.05) by diets. There were no differences in weight gains of chicks at 7, 14, and 21 d of age, and there were also no differences in weekly or cumulative feed efficiency (data not shown).
Rooster Fertility
Semen volume and sperm concentration, viability, and motility were not significantly affected by diet (data not shown).
Organ Weights
The relative weights of liver, spleen, kidney, and testes (BW as a covariate) were not significantly affected by diet (data not shown).
Blood Biochemistry and Hematology
Plasma P concentrations were higher (P < 0.05) in the GMA-supplemented group compared with controls at the end of wk 12 (Table 3). Other blood biochemical parameters, including enzyme activities and hematological parameters, were not, however, significantly affected by diet (data not shown).
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). There was no effect of diet on serum antibody titers against NDV.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Feed Consumption, BW Changes, and Feed Efficiency
In the current experiment, broiler breeder hens and roosters were subject to a restricted feeding program and housed in individual cages. Feed restriction might have played a role in reducing the exposure level of the birds to Fusarium mycotoxins, and this may have contributed to the lack of effect of diet on feed consumption, BW changes, and feed efficiency.
Hamilton et al. (1985) demonstrated that the feeding of naturally contaminated grains containing 4.9 mg of DON/kg of diet to White Leghorn hens for 24 wk had no effects on feed intake, BW, or feed efficiency. In another study, laying hens tolerated the feeding of naturally contaminated grains containing 82.8 mg of DON/kg of diet for 27 d without any effects on feed consumption or BW (Lun et al., 1986). No effect was observed due to the feeding of naturally contaminated grains containing 18 mg of DON/kg of feed on BW of laying hens fed from 1 d of age until the beginning of egg production and six 28-d production periods (Kubena et al., 1987a). Moran et al. (1987) demonstrated that inclusion of high levels of DON (38 mg/kg of feed) for 4 wk had no effects on BW or feed consumption of laying hens, and Kubena et al. (1987b) reported that BW and the efficiency of feed use of laying hens were not affected by the feeding of naturally contaminated grains containing 18 mg of DON/kg of diet for 112 d.
Numerous other researchers have reported, however, that poultry are sensitive to the feeding of grains naturally contaminated with Fusarium mycotoxins with respect to feed intake, BW, and feed efficiency. Kubena and Harvey (1988) reported that the feeding of naturally contaminated grains containing 18 mg of DON/kg of feed to White Leghorn chicks for 12 wk decreased BW at wk of 4 and 8, but this effect was not observed at wk 12. It was shown that the feeding of laying hens with naturally contaminated grains containing 12.3 mg of DON/kg of feed for 16 wk resulted in a reduction in feed intake and BW (Danicke et al. 2003). Chowdhury and Smith (2004) observed that the feeding of grains naturally contaminated with Fusarium mycotoxins to laying hens for 12 wk reduced feed consumption.
The reason for this discrepancy might be attributed to differences in the source of contamination (natural and purified), using a single source of contaminated grain compared with a blend of contaminated grains, and the level and duration of exposure. These studies have also been conducted under different experimental conditions, which may influence the effect of feeding contaminated grains on performance.
Egg Parameters
Brake et al. (2002) reported that broiler breeders have high energy reserves that can protect them against mycotoxicoses. In the present study, feed intake was not affected by diet, and this may explain, in part, why there was no overall effect of diet on egg production in broiler breeder hens.
In the current study, it was observed that the feeding of contaminated grains reduced eggshell thickness after 4 wk of feeding. This finding is in contrast with studies of laying hens (Hamilton et al., 1985; Kubena et al., 1985; Moran et al., 1987; Keshavarz, 1993; Chowdhury and Smith, 2004).
The observation that egg weight, eggshell deformity, albumen height, yolk weight, and shell weight were not altered by diet is in agreement with studies of laying hens (Hamilton et al., 1985; Kubena et al., 1985; Lun et al., 1986; Moran et al., 1987; Keshavarz, 1993; Chowdhury and Smith, 2004; Sypecka et al., 2004).
Hatchability
There was no obvious explanation as to why hatchability increased with the feeding of contaminated diets for 4 wk. The findings of the current study were in agreement with Brake et al. (1999), who also observed an increase in the hatchability of eggs from broiler breeders fed diets containing up to 5 mg of diacetoxyscirpenol/kg of feed for 3 wk. Previous reports with White Leghorn breeder hens indicate no effects of feeding on hatchability (Hamilton et al., 1985; Kubena et al., 1985, 1987a, Kubena et al., b; Moran et al., 1987; Bergsjo et al., 1993; Keshavarz, 1993).
Embryonic Mortality
The frequency of early embryonic mortality arising from the feeding of contaminated grains to broiler breeders has not been previously described. No such effect has been reported in studies of laying hens (Moran et al., 1987; Bergsjo et al., 1993). The absence of effect on mid and late embryonic mortalities in the current experiment with broiler breeders is in accordance with studies of laying hens (Moran et al., 1987; Bergsjo et al., 1993). The reason for significant difference in early embryonic mortality rates in the present study is not clear, but it might be related to differences in eggshell thickness. Eggshell thickness can affect moisture loss during incubation, and hatchability can be reduced as shell quality deteriorates, resulting in early embryonic mortality (Leeson and Summers, 2000).
It is not known if the feeding of contaminated grains caused any changes in the composition and availability of nutrients in the setting eggs, which might have subsequently affected embryonic development and survival. There are many reports concerning the embryotoxicity of Fusarium mycotoxins in mammalians (Khera et al., 1982, 1984, 1986), but this effect is not fully understood in poultry, although Bergsjo et al. (1993) reported chick developmental anomalies when laying hens were fed diets containing 4.9 mg of DON/kg of feed for 10 wk. It has been shown, however, that only trace amounts of Fusarium mycotoxins are transferred into the eggs of laying hens, which are unlikely to be of significance with respect to embryonic mortality (El-Banna et al., 1983; Prelusky et al., 1987; Sypecka et al., 2004).
Progeny Performance
The performance of chicks hatched from eggs of broiler breeder hens fed contaminated grains has not been previously reported, but the results were in agreement with studies of laying hens (Kubena et al., 1985, 1987a,Kubena et al., b; Moran et al., 1987; Bergsjo et al., 1993). This is probably a reflection of lack of effect of diet on setting egg weight and a positive correlation among egg weight, chick weight, and subsequent growth rate.
Rooster Fertility
There are no literature reports of the effects of feeding grains naturally contaminated with Fusarium mycotoxins on the reproductive performance of broiler breeder males. In the present experiment, roosters were subjected to a restricted feeding program in individual cages. This might have minimized exposure to Fusarium mycotoxins, and it may have contributed to the lack of effect of diet on rooster fertility.
Brake et al. (1999) demonstrated that feeding diets contaminated with 10 and 20 mg of diacetoxyscirpenol per kg of feed decreased fertility in broiler breeder males, although no difference was observed in the volume of semen produced. It was found that many males had small, translucent, fluid-filled cysts (2 to 5 mm in diameter) on the testes.
Organ Weights
There are many reports with contradictory results concerning the effects of feeding Fusarium mycotoxins on poultry organ weights. In the current experiment with broiler breeder hens, no effect of diet was found on relative weights of the liver, spleen, or kidney, which is in agreement with studies of laying hens and broilers (Moran et al., 1982; Hamilton et al., 1985; Kubena and Harvey, 1988; Keshavarz, 1993; Danicke et al., 2002; Swamy et al., 2004). Chowdhury and Smith (2004) reported, however, an increase in relative weights of the kidney, perhaps caused by elevation in blood uric acid concentrations in laying hens fed with diets containing a combination of Fusarium mycotoxins for 12 wk. In the present study, no significant difference in the relative weights of the testes was also observed, which is in agreement with Brake et al. (1999).
Blood Biochemistry and Hematology
Blood biochemical parameters were measured at 3 times during the experiment to detect any changes in metabolism. There was no effect of diet on blood chemistry except for an increase in plasma P concentrations. It is not clear if this effect is associated with increased P absorption from the gastrointestinal tract, although plasma Ca concentrations were unaffected. In the present study, activities of serum enzymes reflecting liver damage were not affected by diets. It can be concluded that the feeding of the diets containing Fusarium mycotoxins to broiler breeders did not result in hepatotoxicity in contrast to observations with horses (Raymond et al., 2003). This finding is supported by the fact that there were no changes in the concentrations of blood total protein, globulin, albumin, and relative weights of livers of broiler breeder hens. Studies with laying hens support these findings (Danicke et al., 2002, 2003), although the feeding of combinations of Fusarium mycotoxins has been reported to reduce hepatic protein synthesis rates in laying hens (Chowdhury and Smith, 2005).
The absence of effect of diet on hematological parameters measured in the current study with broiler breeder hens indicates that feeding a combination of Fusarium mycotoxins did not result in hematotoxicity. Kubena et al. (1987a) reported that the feeding of naturally contaminated diets containing 18 mg of DON/kg of feed had no effects on hematological parameters in laying hens. The feeding of broiler chicks with naturally contaminated diets containing 16 and 50 mg of DON/kg of feed for 3 wk did not change hematological values significantly (Harvey et al., 1991, 1997). Kubena and Harvey (1988) fed growing White Leghorn chicks naturally contaminated diets containing 18 mg of DON/kg of diet for 12 wk and demonstrated a significant decrease in hemoglobin concentration at 4 wk of age, but this was no longer present at 8 or 12 wk of age. No effect on hematocrit was observed. Harvey et al. (1991) also found significant differences in hematologic values when White Leghorn chicks were fed 18 mg of DON/kg of feed for 9 wk.
Serum Antibody Titers
The effects of trichothecene mycotoxins on the immune system have been previously reviewed (Rotter et al., 1996). The rapidly proliferating cells of the immune system are primarily affected by these mycotoxins due to the principal mode of action of trichothecene mycotoxins, which includes inhibition of protein synthesis (Feinberg and McLaughlin, 1989). Determination of serum antibody titers to NDV and IBV after regular vaccination can be used to evaluate the effects of feeding Fusarium mycotoxin-contaminated diets on immune system competence (Danicke et al., 2003). In the present study, the feeding of contaminated grains decreased antibody titers against IBV at the end of wk 12. There are no reports of the effect of feeding contaminated grains on IBV serum titers in broiler breeder hens, but Swamy et al. (2002) found no effect of feedborne Fusarium mycotoxins on IBV antibody levels in broilers after 6 wk of feeding.
There was no effect of diet on antibody titers against NDV. This finding is in accordance with Harvey et al. (1991), who observed no effect on NDV antibody titers in White Leghorn chicks fed 18 mg of DON/kg of feed for 9 wk. In a subsequent experiment with White Leghorn chicks, when the same concentration of DON was fed for 18 wk, however, a decrease in serum antibody titers to NDV was reported. Danicke et al. (2002) found decreased antibody titers against NDV in laying hens fed with 12.3 mg of DON/kg of feed for 16 wk. Feeding 14 mg of DON/kg of feed to broiler chicks for 5 wk resulted in a significant decrease in serum NDV antibody titers (Danicke et al., 2003).
Preventive Effects of GMA
The use of dietary adsorbents to prevent mycotoxicoses has been reviewed (Doll and Danicke, 2004). Mycotoxin adsorbents prevent mycotoxicoses by adsorbing mycotoxins in the intestinal lumen and preventing transfer through the blood to target tissues (Ramos et al., 1996). It has been shown that GMA is efficacious in preventing some adverse effects of Fusarium mycotoxins in broilers (Swamy et al., 2002), layers (Chowdhury and Smith, 2004), and ducklings (Chowdhury et al., 2005). In the current study, dietary GMA supplementation prevented many of the few adverse effects of feedborne Fusarium mycotoxins in broiler breeders.
It was concluded that blends of feed ingredients contaminated with Fusarium mycotoxins should be fed to broiler breeder hens with caution because of the possible adverse effects on performance and immune status.
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ACKNOWLEDGMENTS |
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Received for publication February 20, 2006. Accepted for publication April 11, 2006.
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