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ENVIRONMENT, WELL-BEING, AND BEHAVIOR |
* Department of Poultry Science, Texas A&M University, College Station 77843-2472; and USDA-Agricultural Research Service, Southern Plains Agricultural Research Center, Food and Feed Safety Research Unit, College Station, TX 77845
4 Corresponding author: jackson.mcreynolds{at}ars.usda.gov
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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0.05) in hens fed FOS-containing diets compared with hens subjected to feed withdrawal. Significant decreases in ce-cal Salmonella Enteritidis counts were also observed in 2 of the 4 trials. In 3 of the 4 trials, the same diets did not affect (P > 0.05) the production of cecal total volatile fatty acids when compared with hens undergoing feed withdrawal. However, in all 3 alfalfa molt diets, the concentrations of lactic acid were greater (P 0.05) than hens with feed withdrawal, but no differences (P > 0.05) were observed among hens fed alfalfa combined with FOS and hens fed alfalfa/layer ration without FOS. Overall, given the similarities between hens fed 0.750% FOS (H) and 0.375% FOS (L), molt diets combined with the lower level of FOS should be sufficient.
Key Words: Salmonella Enteritidis • molting • laying hen • alfalfa • fructooligosaccharide
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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The addition of prebiotics to diets has been shown to increase fermentation both in vitro (Rycroft et al., 2001) and in vivo (Xu et al., 2003). A common prebiotic compound used both in human as well as in animal diets is fructooligosaccharide (FOS; Gibson and Roberfroid, 1995; Bomba et al., 2002). Due to the β-linkages possessed by FOS, it is able to resist enzymatic degradation and absorption in the upper gastrointestinal tract to reach the cecum, where the majority of fermentation occurs in chickens (Gibson and Roberfroid, 1995; Xu et al., 2003; Ju
kiewicz et al., 2004). Fermentation of prebiotics produces end products including short-chain fatty acids, which have been shown to modify the bacterial ecosystem in the ceca and inhibit the growth of enteric bacteria such as Salmonella, Escherichia coli, and Clostridium perfringens (Cummings et al., 2001; Cummings and Macfarlane, 2002). In addition to inhibiting the growth of enteric bacteria, FOS has been proven to serve as a fermentable substrate to promote the growth of beneficial microflora such as lactic acid bacteria and Bifidobacterium sp. (Allen et al., 1997; Cummings and Macfarlane, 2002; Jukiewicz et al., 2004). The objective of this research was to examine the effects of the FOS combined with alfalfa molt diets on Salmonella Enteritidis colonization on internal organs, crop pH, volatile fatty acids (VFA) and lactic acid production.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
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On d 4 of each study, all hens in each treatment group were challenged by crop gavage with 1 mL of inoculum containing approximately 105 cfu of a poultry isolate of Salmonella enterica serovar Enteritidis (phage type 13A, National Veterinary Services Laboratory, Ames, IA), which was selected for resistance to novobiocin and nalidixic acid at the USDA-Agricultural Research Service facility (College Station, TX). The challenge dosage approximated the 5.6 x 106 cfu dose reported to be the mean infectious dosage for Salmonella Enteritidis in nonmolted hens (Holt et al., 1993). On d 9 of the study, 6 hens from each treatment group were euthanized, and the crop, ceca, liver, spleen, and ovary were aseptically excised. The crop, ceca, liver, spleen, and ovary of each hen were then cultured for Salmonella Enteritidis. After the molting period, the remaining 6 hens from each treatment group were placed on a maintenance diet and monitored for intestinal shedding of Salmonella Enteritidis.
Crop Lactic Acid Concentrations and pH
Crop lactic acid concentration and pH were determined as described by Durant et al. (1999). Crop pH was determined by insertion of a sterile glass pH electrode through an incision in the crop wall ensuring the electrode remained in contact with the crop mucosal surface. Each crop was aseptically excised, cut open, and blended with 10 mL of sterile Butterfield’s Buffer (Difco Laboratories, Sparks, MD) for 1 min in a Stomacher 80 blender (Seward Medical, London, UK). Samples of blended crop were collected and analyzed for lactic acid concentrations (Hohorst, 1974; Moore et al., 2004).
Cecal VFA and Lactic Acid Concentrations
Cecal content concentrations of VFA (acetic, propionic, butyric, isobutryic, valeric, and isovaleric acids) were determined by gas-liquid chromatography as described by Corrier et al. (1990). The analysis was conducted with a gas chromatograph equipped with a flame ionization detector and peak profiles integration-quantification integrator (model 110 gas chromatograph, SR1 Instruments, Torrence, CA). Each sample peak profile was integrated and quantified relative to an internal standard of methylbutyric acid placed in the same sample. Lactic acid concentrations were determined by an enzymatic method (Hohorst, 1974).
Crop, Cecal, and Organ Colonization by Salmonella Enteritidis
One milliliter of blended crop sample was transferred into 10 mL of Rappaport-Vassiliadis (RV) broth (EM Science, Gibbstown, NJ) and incubated for 24 h at 42° C. One cecum from each hen was cut into several pieces, placed in 30 mL of RV broth, shaken vigorously, and incubated for 24 h at 42° C. Liver, spleen, and ovary specimens were minced with scissors and cultured for 24 h at 42° C in RV broth. After incubation, the respective broths were streaked onto BGA plates containing novobiocin (25 µg/mL) and nalidixic acid (20 µg/mL), incubated for an additional 24 h at 37° C, and examined for the presence of Salmonella Enteritidis colonies. Suspect colonies were serologically identified as Salmonella Enteritidis using Salmonella O antiserum group D, factors 1, 9, and 12.
Salmonella Enteritidis Colony-Forming Units per Gram of Crop and Cecal Contents
The contents of the crop and 1 cecum from each hen were serially diluted and spread-plated on novobiocin and nalidixic acid-BGA plates at dilutions 101 through 108. The plates were incubated for 24 h at 37° C, after which the number of colony-forming units of Salmonella Enteritidis per gram of crop or cecal content was determined, and Salmonella Enteritidis colonies were serologically confirmed as described in the previous section.
Intestinal Shedding of Salmonella Enteritidis
Hens were monitored for intestinal shedding of Salmonella Enteritidis on d 4, 10, 17, and 24 post-Salmonella Enteritidis challenge for 6 hens per treatment group (equivalent to d 8, 14, 21, and 28 after molt induction). The birds were sampled using a modification of a procedure described by Seo et al. (2001). Aluminum foil sheets were placed under each hen for approximately 1 h, and the secretions were collected. Approximately 0.5 mL of the samples was weighed and added to dilution tubes containing 4.5 mL of sterile Butterfield’s Buffer. The aliquots were subsequently serially diluted at 101 through 108 dilutions and plated on novobiocin and nalidixic acid-BGA plates. The plates were incubated for 24 h at 37° C, after which the number of colony-forming units of Salmonella Enteritidis per gram of intestinal shedding was determined, and Salmonella Enteritidis colonies were confirmed by using Salmonella O antiserum group D, factors 1, 9, and 12. The remaining samples were added to 25 mL of RV broth for selective enrichment and incubated for 24 h at 42° C, at which time they were plated on novobiocin and nalidixic acid-BGA plates and incubated at 37° C for another 24 h. The plates were subsequently examined for the presence of suspect Salmonella Enteritidis colonies. Suspect colonies were identified as Salmonella Enteritidis serologically using Salmonella O antiserum group D, factors 1, 9, and 12.
Statistical Analysis
Chi-squared analysis was used to determine significant differences among treatment groups for Salmonella Enteritidis incidences of crop, cecal, liver, spleen, and ovary (Luginbuke and Schlotzhauer, 1987). Differences in VFA and lactic acid concentrations were determined by ANOVA using the GLM procedures. Significant differences were further separated using Duncan’s multiple range test and commercial statistical analysis software (SAS Institute, Cary, NC). All data were analyzed by an individual trial, and statistical analyses were considered significant at P 0.05.
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RESULTS AND DISCUSSION |
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0.05) in full fed (FF) non-molted hens (Table 1
). No differences (P > 0.05) were observed between any molting treatments in either trial. The decrease in feed intake of alfalfa molt diets could be attributed to low energy levels of alfalfa and reduced palatability (NRC, 1994; Biggs et al., 2004) or anorexia that hens voluntarily undergo at a natural molt (Mrosovsky and Sherry, 1980). Body weights also decreased markedly as a result of the decreased feed intake (Table 1). In trial 1 and trial 2, FF nonmolted hens exhibited lower (P 0.05) body weight losses compared with all molted treatments, which were not different (P > 0.05) from each other. Trial 3 and 4 hens exhibited a similar pattern, but the body weight losses of hens fed alfalfa were intermediate compared with FW- and FF-treated hens. In all trials, FF-treated hens exhibited greater (P 0.05) ovary weights typical of nonmolted hens, whereas all molted hens showed no significant differences among treatments (Table 1). We have previously observed a 5- to 6-fold decrease in ovary weights with alfalfa meal and pellets (Landers et al., 2005a; Woodward et al., 2005). Ovary regression is an important factor that influences both postmolt egg production and egg quality (Biggs et al., 2004). Overall, the addition of FOS at either level (H or L) to alfalfa diet did not significantly influence either feed intake or body and ovarian weights of the hens.
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. Lactobacillus spp. are the primary bacteria in the crop that produce lactic acid as their main fermentation product (Fuller, 1977; Rubio et al., 1998). No differences (P > 0.05) in lactic acid concentrations among any of the treatments were seen in trial 1 and 2. Alfalfa diet, however, supplemented with a higher level FOS (H) resulted in lactic acid production similar to that in FF hens in trial 3 and 4 and was significantly higher than hens with FW. In all 4 trials, H and L diets did not have any effect on the crop pH of hens when compared with hens fed A90. As expected, hens fed FF yielded lower (P 0.05) crop pH levels compared with hens with FW in trial 1, 3, and 4. The data agree with Durant et al. (1999), who established that FW reduce lactobacilli populations thus increasing crop pH.
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). When percentage of Salmonella Enteritidis colonization in the crop of hens fed H and L were compared with A90 and FF treatments, no significant differences (P > 0.05) were observed in trial 2, 3, and 4. Upon the examination of colony-forming units per gram counts, FW hens yielded higher counts than FF hens, and all other molted treatments (A90, H, L) were not found significantly different from each other in 3 of the 4 trials. Salmonella Enteritidis colonization of the ceca is shown in Table 4. Greater Salmonella Enteritidis colonization (%; P 0.05) occurred in FW-treated hens compared with hens from all other treatments, which were not different (P > 0.05) from each other in trial 1. The results from trials 2, 3, and 4 showed similar patterns with FW-treated hens having higher percentage of Salmonella Enteritidis (P 0.05) cecal colonization than FF birds but not with birds in the other molted treatments. In general, FF hens exhibited less (P 0.05) Salmonella Enteritidis per gram, whereas FW hens yielded greater (P 0.05) colony-forming units per gram and all other molted treatments appeared to be intermediate. Similar results were seen by Woodward et al. (2005) and Moore et al. (2004) with FW molted hens resulting in greater Salmonella Enteritidis colony-forming units per gram counts than nonmolted hens.
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). The increase in organ invasion of FW hens could be due to a decrease of peristalsis muscle contractions and mucin production (Sturkie, 1965), which can facilitate the bacterial colonization by pathogens (Holt and Porter, 1992; Holt et al., 1993). The lack of feed in the gastrointestinal tract also alters the normal intestinal microflora and pH, which can create a microenvironment favoring pathogen development (Ricke, 2003). In our study, FOS-containing diets reduced (P 0.05) ovary and liver colonization by Salmonella Enteritidis in 3 and 2 of the 4 trials, respectively, when compared with hens subjected to FW. The Salmonella Enteritidis colonization of liver, spleen, and ovary of hens fed FOS diets, however, was not found to be different from that of hens fed A90. Seo et al. (2001) reported that by providing some form of bulk in the gastrointestinal tract, hens can clear an infection more readily than if the gut was empty. By providing alfalfa in the diet, the Salmonella Enteritidis was unable to fully colonize and was therefore possibly cleared from the tract. In our study, FOS addition to alfalfa-containing diets did not further prevent invasion by Salmonella Enteritidis in the organs of hens.
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and 7. Significant differences in Salmonella Enteritidis log counts (P 0.05) were observed only on d 8 in trial 1, 2, and 3 when FW hens shed more Salmonella Enteritidis than FF- or L-treated hens. Seo et al. (2001) concluded that although the conditions were static and aseptic techniques were used, the birds could still be reinfected, because Salmonella can easily be transmitted from bird to bird being housed in confined spaces. They also observed that FW hens shed more Salmonella Enteritidis than FF hens.
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and Figure 2. In half of the trials, FF hens yielded greater (P 0.05) acetic acid concentrations in the ceca than hens undergoing FW. Likewise, Woodward et al. (2005) reported higher acetic acid production in FF hens than in FW- and alfalfa-fed hens. The A90, H, and L diets did not differ from each other by acetate production in contrast to the study of Kass et al. (1980), in which cecum and colon production of acetate in growing swine were stimulated by the addition of 40% alfalfa to swine diets. There were no significant (P 0.05) differences in propionic acid concentrations (Figure 1b) in the ceca of alfalfa-molted hens in any of the 4 trials as well. Concentrations of isobutyric acid (Figure 1c) were significantly higher in H- and L-treated hens when compared with FW hens in trial 1. Compared with alfalfa-molted birds, isobutyric acid concentrations in trial 4 were higher (P 0.05) in L-fed hens than in A90 birds but not different (P > 0.05) from any other treatment. Although no differences in the concentrations of isobutyric acid in FF and FW hens were observed by Moore et al. (2004), Woodward et al. (2005) reported high variability in isobutyric concentrations in the different treatments among different trials. Butyric acid concentrations (Figure 1d) were lower (P 0.05) in FW hens when compared with all other treatments in trial 1. Although relatively inconsistent, our butyric acid results followed the trend observed by Woodward et al. (2005), in which non-molted birds in half of the trials were characterized with higher production of cecal butyric acid when compared with molted and alfalfa-fed chickens. The H-treated hens in our study yielded greater (P 0.05) butyric acid concentrations in the ceca compared with FW- and FF-treated hens in 1 of the trials but were not significantly different from any other alfalfa-molted hens.
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). Similarly, there were no differences (P > 0.05) in isovaleric acid concentrations between any treatments in trial 1, 3, or 4 (Figure 2a). Concentrations of valeric acid (Figure 2b) were lower (P 0.05) in the ceca of FW-treated hens than in the ceca of all alfalfa molt-treated hens in trial 1. However, in trial 2, valeric acid concentrations in the ceca of FF hens were greater (P 0.05) than valeric acid concentrations in the ceca of FW hens. Alfalfa-molted hens did not exhibit differences (P > 0.05) in valeric acid concentration when compared with either FW- or FF-treated hens. No differences (P > 0.05) in valeric acid concentrations were seen between any treatments in trial 3 or 4.
Total VFA concentrations (Figure 2c) were lower (P 0.05) in the ceca of FW hens than in all alfalfa molt treatments but not FF-treated hens in trial 1. Hens from trials 2 and 4 were opposite of each other when total VFA concentrations were estimated. The total VFA concentrations in the ceca of FF hens were greater (P 0.05) than all molt treatments in trial 2 and greater (P 0.05) than all other treatments except H in trial 4. Similar to individual VFA concentrations in trial 3, there were no differences (P > 0.05) among treatments when total VFA were quantified. The results from trial 1 were similar to the results seen by Moore et al. (2004), in which no differences were found in total VFA in molted and nonmolted treated hens, whereas the results of trial 2 and 4 corresponded to the observations of Woodward et al. (2005) that FF hens produced greater total VFA concentrations than hens molted by alfalfa or FW hens.
Concentrations of lactic acid (Figure 2d) were significantly greater in birds fed all 3 alfalfa molt diets compared with FF or FW hens in trials 1 and 3. In trial 2 only FW-treated hens exhibited lower (P 0.05) lactic acid concentrations than the hens fed the 3 alfalfa molt diets. This trend was consistent with the findings of Woodward et al. (2005), who observed an approximately 2-fold increase of lactic acid concentration in alfalfa molt diets when compared with FW treatments. The alfalfa results are not surprising, because lactate is considered a predominant end product of a successful fermentation of alfalfa silage (Owens et al., 2002). In contrast to our study, Moore et al. (2004) observed 3-fold higher concentrations of lactic acid in FF hens compared with FW birds.
In summary, in half of the trials in our study, FOS-containing diets significantly reduced Salmonella Enteritidis in ovaries and livers compared with hens subjected to feed withdrawal. A similar trend was monitored in cecal Salmonella Enteritidis counts. However, no differences (P > 0.05) were observed among these hens and the hens fed alfalfa/layer ration not containing FOS. These results could have been affected by feed intake by alfalfa-treated hens. Feed intake in alfalfa-treated hens may have been affected by saponins, which are undesirable compounds found in alfalfa that have been shown to decrease feed intake (Sen et al., 1998). The addition of layer ration in the A90 diets has been shown to increase feed intake (Donalson et al., 2005); however, the correlation between amount of layer ration included in a diet and Salmonella Enteritidis colonization has not been quantified. Limited responses to FOS may also be a result of either minimal microflora capable of direct utilization or similar substrates being more readily available in the highly fermentable alfalfa. Another potential reason for the low effect of FOS might be the low consumption of the prebiotic. The FOS was homogenously mixed with alfalfa/layer ratios; however, homogenous intake of all ingredients of the feeding mixture cannot be ensured. Chickens could selectively avoid certain compounds in mash diets for a variety of reasons. In future studies, FOS may need to be introduced to chickens as a part of a stabilized feed matrix where it is more closely associated physicochemically with the primary dietary components to ensure a consistent intake (Huang et al., 2006). Overall, given the minimal differences between hens fed 0.750% FOS (H) and 0.375% FOS (L), molt diets combined with the lower concentration of FOS would appear to be sufficient to retain effectiveness as a prebiotic in alfalfa-molted hens.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Current address: Department of Cardiology, David Geffen School of Medicine, Los Angeles, CA 90095.
3 Current address: Center for Food Safety and Microbiology, IFSE, and Department of Food Science, University of Arkansas, Fayetteville, AR 72704.
Received for publication April 23, 2007. Accepted for publication February 8, 2008.
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REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONREFERENCES |
|---|
Andrews, W. H., G. A. June, P. S. Sherrod, T. S. Hammack, and R. M. Amaguana. 1992. Bacteriological Analytical Manual. 8th ed. AOAC Int., Arlington, VA.
Biggs, P. E., M. E. Persia, K. W. Koelkebeck, and C. M. Parsons. 2004. Further evaluation of nonfeed removal methods for molting programs. Poult. Sci. 83:745–752.
Bomba, A., R. Nemcová, S. Gancar
ikov, R. Herich, P. Guba, and D. Mudro
ová. 2002. Improvement of the probiotic effect of micro-organisms by their combination with maltodextrins, fructo-oligosaccharides and polyunsaturated fatty acids. Br. J. Nutr. 88:S95–S99.[CrossRef][Web of Science][Medline]
Corrier, D. E., A. J. Hinton, R. L. Ziprin, R. C. Beier, and J. R. DeLoach. 1990. Effect of dietary lactose on cecal pH, bacteriostatic volatile fatty acids, and Salmonella Typhimurium colonization of broiler chicks. Avian Dis. 34:617–625.[CrossRef][Web of Science][Medline]
Cummings, J. H., and G. T. Macfarlane. 2002. Gastrointestinal effects of prebiotics. Br. J. Nutr. 87:S145–S151.[Web of Science][Medline]
Cummings, J. H., G. T. Macfarlane, and H. N. Englyst. 2001. Prebiotic digestion and fermentation. Am. J. Clin. Nutr. 73:S415–S420.
Donalson, L. M., W. Kim, V. I. Chalova, P. Herrera, C. L. Woodward, J. L. McReynolds, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2007a. In vitro anaerobic incubation of Salmonella enterica serotype Typhimurium and laying hen cecal bacteria in poultry feed substrates and a fructooligosaccharide prebiotic. Anaerobe. doi:10.1016/j.anaerobe.2007.05.001.
Donalson, L. M., W. Kim, V. I. Chalova, P. Herrera, V. G. Gotcheva, D. Vidanovi
, C. L. Woodward, J. L. McReynolds, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2007b. In vitro fermentation response of laying hen cecal bacteria to combinations of fructooligosaccharide (FOS) prebiotic with alfalfa or layer ration. Poult. Sci. 87:1263–1275.
Donalson, L. M., W. K. Kim, C. L. Woodward, P. Herrera, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2005. Utilizing different ratios of alfalfa and layer ration for molt induction and performance in commercial laying hens. Poult. Sci. 84:362–369.
Dunkley, K. D., C. S. Dunkley, N. L. Njongmeta, T. R. Callaway, M. E. Hume, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2007a. Comparison of in vitro fermentation and molecular microbial profiles of high fiber-feed substrates incubated with chicken cecal inocula. Poult. Sci. 86:801–810.
Dunkley, K. D., J. L. McReynolds, M. E. Hume, C. S. Dunkley, T. R. Callaway, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2007b. Molting in Salmonella Enteritidis-challenged laying hens fed alfalfa crumbles. I. Salmonella Enteritidis colonization and virulence gene hilA response. Poult. Sci. 86:1633–1639.
Dunkley, K. D., J. L. McReynolds, M. E. Hume, C. S. Dunkley, T. R. Callaway, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2007c. Molting in Salmonella Enteritidis-challenged laying hens fed alfalfa crumbles. II. Fermentation and microbial ecology response. Poult. Sci. 86:2101–2109.
Durant, J. A., D. E. Corrier, J. A. Byrd, L. H. Stanker, and S. C. Ricke. 1999. Feed deprivation affects crop environment and modulates Salmonella Enteritidis colonization and invasion of Leghorn hens. Appl. Environ. Microbiol. 65:1919–1923.
Frenzen, P. D., T. L. Riggs, J. C. Buzby, T. Breuer, T. Roberts, D. Voetsch, and S. Reddy, and the FoodNet Working Group, 1999. Salmonella cost estimate update using Food Net data. Food Rev. 22:10–15.[Medline]
Fuller, R. 1977. The importance of lactobacilli in maintaining normal microbial balance in the crop. Br. Poult. Sci. 18:85–94.[Web of Science][Medline]
Gibson, G. R., and M. B. Roberfroid. 1995. Dietary modulation of the human colonic microbiota: Introducing the concept of prebiotics. J. Nutr. 125:1401–1412.
Guard-Petter, J. 2001. The chicken, the egg, and Salmonella Enteritidis. Environ. Microbiol. 3:421–430.[CrossRef][Medline]
Hedberg, C. W., M. J. David, K. E. White, K. L. MacDonald, and M. T. Osterholm. 1993. Role of egg consumption in sporadic Salmonella Enteritidis and Salmonella Typhimurium infections in Minnesota. J. Infect. Dis. 167:107–111.[Web of Science][Medline]
Hohorst, J. J. 1974. Lactate. Pages 266–270 in Methods of Enzymatic Analysis. H. U. Bergmeyer, ed. Acad. Press Inc., New York, NY.
Holt, P. S. 2003. Molting and Salmonella enterica serovar Enteritidis infection: The problem and some solutions. Poult. Sci. 82:1008–1010.
Holt, P. S., N. P. Macri, and R. E. Porter Jr. 1993. Microbiological analysis of the early Salmonella Enteritidis infection in molted and unmolted hens. Avian Dis. 39:55–63.[CrossRef]
Holt, P. S., and R. E. Porter Jr. 1992. Microbiological and histopathological effects of an induced-molt fasting procedure on a Salmonella Enteritidis infection in chickens. Avian Dis. 36:610–618.[CrossRef][Web of Science][Medline]
Huang, D. S., D. F. Li, J. J. Xing, Y. X. Ma, Z. J. Li, and S. Q. Lv. 2006. Effects of feed particle size and feed form on survival of Salmonella typhimurium in the alimentary tract and cecal S. typhimurium reduction in growing broilers. Poult. Sci. 85:831–836.
Humphrey, T. J. 1994. Contamination of egg shell and contents with Salmonella Enteritidis: A review. Int. J. Food Microbiol. 21:31–40.[CrossRef][Web of Science][Medline]
Jukiewicz, J., Z. Zdu
czyk, and J. Jankowski. 2004. Selected parameters of gastrointestinal tract metabolism of turkeys fed diets with flavomycin and different inulin content. World’s Poult. Sci. J. 60:177–185.[CrossRef][Web of Science]
Kass, M. L., P. J. Van Soest, and W. G. Pond. 1980. Utilization of dietary fiber from alfalfa by growing swine. II. Volatile fatty acid concentrations in and disappearance from the gastrointestinal tract. J. Anim. Sci. 50:192–197.
Landers, K. L., Z. R. Howard, C. L. Woodward, S. G. Birkhold, and S. C. Ricke. 2005a. Potential of alfalfa as an alternative molt induction diet for laying hens: Egg quality and consumer acceptability. Bioresour. Technol. 96:907–911.[CrossRef][Web of Science][Medline]
Landers, K. L., R. W. Moore, C. S. Dunkley, P. Herrera, W. K. Kim, D. A. Landers, Z. R. Howard, J. L. McReynolds, J. A. Byrd, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2007. Immunological cell and serum metabolite response of 60-week-old commercial laying hens to an alfalfa meal molt diet. Bioresour. Technol. doi:10.1016/j.biortech.2006.12.036.[CrossRef][Web of Science][Medline]
Landers, K. L., C. L. Woodward, X. Li, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2005b. Alfalfa as a single dietary source for molt induction in laying hens. Bioresour. Technol. 96:565–570.[CrossRef][Web of Science][Medline]
Luginbuke, R., and S. D. Schlotzhauer. 1987. SAS/SAT Guide for Personal Computers. 6th ed. SAS Inst. Inc., Cary, NC.
McReynolds, J., L. Kubena, J. Byrd, R. Anderson, S. Ricke, and D. Nisbet. 2005. Evaluation of Salmonella Enteritidis in molting hens after administration of an experimental chlorate product (for nine days) in the drinking water and feeding an alfalfa molt diet. Poult. Sci. 84:1186–1190.
McReynolds, J. L., R. W. Moore, L. F. Kubena, J. A. Byrd, C. L. Woodward, D. J. Nisbet, and S. C. Ricke. 2006. Effect of various combinations of alfalfa and standard layer diet on susceptibility of laying hens to Salmonella Enteritidis during forced molt. Poult. Sci. 85:1123–1128.
Mohle-Boetani, J. C., S. B. Werner, S. Abbott, N. Bendana, R. Bryant, M. Fenstersheib, M. Ginsberg, L. Gresham, J. Koehler, and L. Mascola. 1998. Salmonella Enteritidis infections from shell eggs: Outbreaks in California. West. J. Med. 169:299–303.[Web of Science][Medline]
Moore, R. W., S. Y. Park, L. F. Kubena, J. A. Byrd, J. L. McReynolds, M. R. Burnham, M. E. Hume, S. G. Birkhold, D. J. Nisbet, and S. C. Ricke. 2004. Comparison of zinc acetate and propionate addition on gastrointestinal tract fermentation and susceptibility of laying hens to Salmonella Enteritidis during forced molt. Poult. Sci. 83:1276–1286.
Mrosovsky, N., and D. F. Sherry. 1980. Animal anorexias. Science 207:837–842.
NRC. 1994. Nutrient Requirements of Poultry. 9th ed. Natl. Acad. Press, Washington, DC.
Owens, V. N., K. A. Albrecht, and R. E. Muck. 2002. Protein degradation and fermentation characteristics of unwilted red clover and alfalfa silage harvested at various times during the day. Grass Forage Sci. 57:329–341.[CrossRef]
Park, S. Y., S. G. Birkhold, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2004a. Effects of high zinc diets using zinc propionate on molt induction, organs, and postmolt egg production and quality in laying hens. Poult. Sci. 83:24–33.
Park, S. Y., S. G. Birkhold, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2004b. Review on the role of dietary zinc in poultry nutrition, immunity, and reproduction. Biol. Trace Elem. Res. 101:147–163.[CrossRef][Web of Science][Medline]
Park, S. Y., W. K. Kim, S. G. Birkhold, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2004c. Induced moulting issues and alternative dietary strategies for the egg industry in the United States. World’s Poult. Sci. J. 60:196–209.[Web of Science]
Park, S. Y., W. K. Kim, S. G. Birkhold, L. F. Kubena, D. J. Nisbet, and S. C. Ricke. 2004d. Using a feed-grade zinc propionate to achieve molt induction in laying hens and retain postmolt egg production and quality. Biol. Trace Elem. Res. 101:165–179.[CrossRef][Web of Science][Medline]
Poppe, C. 1999. Epidemiology of Salmonella enterica serovar Enteritidis. Pages 3–18 in Salmonella enterica serovar Enteritidis in humans and animals–epidemiology, pathogenesis, and control. A. M. Saeed, R. K. Gast, M. E. Potter, and P. G. Wall, ed. Iowa State Univ. Press, Ames, IA.
Ramirez, G. A., L. L. Sarlin, D. J. Caldwell, C. R. Yezak Jr., M. E. Hume, D. E. Corrier, J. R. DeLoach, and B. M. Hargis. 1997. Effect of feed withdrawal on the incidence of Salmonella in the crops and ceca of market age broiler chickens. Poult. Sci. 76:654–656.
Ricke, S. C. 2003. The gastrointestinal tract ecology of Salmonella Enteritidis colonization in molting hens. Poult. Sci. 82:1003–1007.
Ricke, S. C., S. Y. Park, R. W. Moore, Y. M. Kwon, C. L. Woodward, J. A. Byrd, D. J. Nisbet, and L. F. Kubena. 2004. Feeding low calcium and zinc molt diets sustains gastrointestinal fermentation and limits Salmonella enterica serovar Enteritidis colonization in laying hens. J. Food Safety 24:291–308.[CrossRef]
Rubio, L. A., A. Brenes, I. Setién, G. de la Asunción, N. Durán, and M. T. Cutuli. 1998. Lactobacilli counts in crop, ileum and caecum of growing broiler chickens fed on practical diets containing whole or dehulled sweet lupin (Lupinus angustifolius) seed meal. Br. Poult. Sci. 39:354–359.[CrossRef][Web of Science][Medline]
Rycroft, C. E., M. R. Jones, G. R. Gibson, and R. A. Rastall. 2001. A comparative in vitro evaluation of the fermentation properties of prebiotic oligosaccharides. J. Appl. Microbiol. 91:878–887.[CrossRef][Medline]
Sen, S., H. P. S. Makkar, and K. Becker. 1998. Alfalfa saponins and their implication in animal nutrition. J. Agric. Food Chem. 46:131–140.[CrossRef][Web of Science][Medline]
Seo, K., P. S. Holt, and R. K. Gast. 2001. Comparison of Salmonella Enteritidis infection in hens molted via long-term feed withdrawal versus full-fed wheat middling J. Food Prot. 64:1917–1921.
Sturkie, P. D. 1965. Avian Physiology. 2nd ed. Comstock Publ. Assoc., Ithaca, NY.
Woodward, C. L., Y. M. Kwon, L. F. Kubena, J. A. Byrd, R. W. Moore, D. J. Nisbet, and S. C. Ricke. 2005. Reduction of Salmonella enterica serovar Enteritidis colonization and invasion by an alfalfa diet during molt in Leghorn hens. Poult. Sci. 84:185–193.
Xu, Z. R., C. H. Hu, M. S. Xia, X. A. Zhan, and M. Q. Wang. 2003. Effects of dietary fructooligosaccharide on digestive enzyme activities, intestinal microflora and morphology of male broilers. Poult. Sci. 82:1030–1036.
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