| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
ENVIRONMENT, WELL-BEING, AND BEHAVIOR |
Adaptation Physiology Group, Wageningen Institute of Animal Sciences, Wageningen University, P.O. Box 338, 6700 AH Wageningen, the Netherlands
1 Corresponding author: henk.parmentier{at}wur.nl
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Key Words: body weight • feed intake • heat stress • hen-day egg production • lipopolysaccharide
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Two environmental stressors that might act synergistically are heat stress and microbial challenges. Understanding of the interactions between these 2 stressors is of interest, first, because both stressors are common in poultry farming and can occur together, and second, because these 2 stressors represent 2 physiological drives that utilize common effectors but induce opposite responses (Blatteis, 2000). During heat exposure a rise in body temperature is prevented by panting and vasodilatation of the skin, whereas an infection [induced by lipopolysaccharide (LPS)] is associated with a rise in body temperature (fever), which is achieved by increased metabolic heat production and vasoconstriction of the skin.
Effects of single heat stress in poultry has been frequently studied. Hens raised under moderate climatic circumstances and placed in hot climatic circumstances at the start of lay showed reduced feed intake, BW gain, egg production, egg weight (Njoya and Picard, 1994; Mashaly et al., 2004), and egg shell thickness (Usayran et al., 2001; Lin et al., 2004) compared with hens kept under moderate circumstances during lay. High environmental temperatures affect not only these performance parameters, but require also various physiological (Koelkebeck and Odom, 1995; Maak et al., 2003) and immunological (Thaxton et al., 1968; Mashaly et al., 2004; Mahmoud and Yaseen, 2005) adaptations of birds.
Lipopolysaccharide, derived from intestinal gram-negative microbiota, is often used as a model antigen to study the animal’s susceptibility to (nonspecific components of microbiological) pathogens and capability to adapt to immune stressors. Administration of LPS causes sickness symptoms including changes in body temperature (fever), reduced BW gain, and changes in behavior (Adler and DaMassa, 1978; Macari et al., 1993; Xie et al., 2000; Cheng et al., 2004). Effects of microbial challenges, mimicked by LPS, on performance (feed intake, egg production, egg quality) and other physiological responses of adult laying hens are less studied. Besides, effects of combined challenge of heat stress and LPS administration on performance parameters have, to our knowledge, never been studied in adult laying hens.
In a previous study (Star et al., 2007) differences in natural humoral immunity were investigated in 12 pure-bred layer lines. For the present experiment, 4 of the 12 lines were selected, based on high or low natural immune competence and a high or low survival rate. These lines were exposed to the following environmental stressors: heat (climatic stress), LPS (hygienic stress), or combined exposure to heat and LPS. According to Blatteis (2000), we hypothesized that chickens are able to cope with single environmental stressors, but that problems in coping ability occur when chickens are exposed to combined environmental stressors. To evaluate coping ability of different layer lines, effects of climatic and hygienic stress on performance (e.g., feed intake, BW, hen-day egg production, egg weight, and egg shell thickness) and physiological responses were investigated. The current paper will focus on the effect of different stressors on performance of 4 different layer lines. First, we investigated responses, as expressed in performance parameters, by single exposure to high temperature or LPS administration, or combined exposure to both stressors. Second, we investigated if different chicken lines had different responses in performance parameters when exposed to climatic or hygienic stress, and whether one line was better able to withstand stress than another line. In an accompanying paper (Star et al., 2008), effects of exposure to climatic and hygienic stress on physiological responses in these layer lines is reported.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
At 22 wk of age, 80 hens per line (320 in total) were transported from a housing facility at Hendrix Genetics to 2 identical climate respiration chambers at Wageningen University. In each climate chamber, 40 hens per line were individually housed in battery cages (45 cm height x 40 cm depth x 24 cm width). Lines were randomly divided over cages. Hens were fed a standard commercial phase 1 diet (15.9% crude protein, 3.9% crude fiber, and 11.8 MJ of ME/kg). At 22 wk of age, hens were kept under a 13L:11D light scheme. In each of the following 2 wk, the light period was increased with 1 h. At the start of the experimental period (at 24 wk of age), hens were kept under a 15L:9D light scheme until the end of the experimental period (27 wk of age). Hens received routine vaccinations to Marek’s disease (d 1), Newcastle disease (wk 2, 6, 12, 15), infectious bronchitis (d 1, wk 2, 10, 12, 15), infectious bursal disease (wk 3, 15), fowl pox (wk 15), and avian encephalomyelitis (wk 15). Beak trimming was not performed.
Experimental Design
After an adaptation period of 12 d (temperature maintained at 21°C), hens in the first climate chamber were exposed to acute heat stress. Within approximately 1 h, the temperature in this chamber was increased from 21 to 32°C, and was maintained at 32°C for the following 23 d. In the second chamber, the (control) temperature was maintained at 21°C. At d 1 after the start of the heat stress period, half of the hens in the heat treatment and half of the control hens were i.v. injected with 1 mg/kg of BW of Escherichia coli LPS (serotype O55:B5, Sigma Chemical Co., St. Louis, MO). The remaining hens received a placebo treatment of PBS. An overview of the experimental design is given in Table 1
. The Institutional Animal Care and Use Committee of Wageningen University approved the experimental protocol.
|
Statistical Analysis
Differences in feed intake, hen-day egg production, and egg shell thickness were analyzed by a 3-way ANOVA for the effect of line, temperature, LPS administration, and their interactions. Daily measured feed intake and hen-day egg production were, after primary analyses of the daily measurements, divided in 3 periods; P1 is the adaptation period (d –11 to 0), P2 is the experimental period where temperature and LPS administration were of influence (d 1 to 7), and P3 is the experimental period where only temperature was of influence (d 8 to 22). Statistical analyses were done for each period, and no statistical analyses were done between periods. Differences in BW and egg weight were analyzed by a 4-way ANOVA for the effect of line, temperature, LPS administration, time, and their interactions by a repeated measurement procedure using a "hen nested within line, temperature, and LPS administration" option.
Mean differences among lines and treatments were tested with Bonferroni’s test. All analyses were carried out using SAS (SAS Institute, 2004). Effects were considered significant at P < 0.05.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Feed Intake
Main effects of exposure to heat, LPS administration, or combined exposure to heat and LPS are shown in Figure 1 and will be described first, whereas more detailed results per line are given in Table 2 and will be described after the main effects.
|
|
shows that exposure to heat reduced feed intake during the whole experimental period (P2 and P3; P < 0.0001), whereas the effect of LPS was only noticeable during the first week after administration (P2; P < 0.0001). During P2, the control group had an average feed intake of 106.5 g, whereas hens injected with LPS had an average feed intake of 90.2 g. Hens exposed to heat stress or to combined heat and LPS had an average feed intake of 70.9 and 64.7 g, respectively. There was a significant heat x LPS interaction during P2 (P < 0.01), indicating that combined exposure had less effect on feed intake than the sum of the individual effects.
Heat stress significantly reduced feed intake during P3, with a difference of 27.1 g feed intake between hens exposed to 21 or 32°C.
Feed intake was affected by line during P1, P2, and P3 (P < 0.0001, P < 0.05, and P < 0.01, respectively). Significant line x heat interaction was found during P2 and P3 (P < 0.05 and P < 0.0001, respectively). Decreases in feed intake between heat-stressed group (32°C + PBS) and control group (21°C + PBS) were 42.9, 41.1, 28.5, and 29.7 g for line B1, WA, WB, and WF, respectively, during P2. Decreases in feed intake between heat-stressed group (32°C + PBS and 32°C + LPS) and control group (21°C + PBS and 21°C + LPS) were 36.9, 24.6, 23.8, and 23.1 g for line B1, WA, WB, and WF, respectively, during P3. Although each line had a reduced feed intake during heat exposure, the feed intake of the Rhode Island Red line B1 seemed to be more influenced by heat stress than the feed intake of the White Leghorn lines.
Body Weight
Main effects of exposure to heat, LPS administration, or combined exposure to heat and LPS will be described first, whereas more detailed results per line will be described after the main effects.
Figure 2 shows that exposure to heat decreased BW during the whole experimental period (heat x time interaction; P < 0.0001), whereas the effect of LPS administration was only noticeable at d 2 after start of the heat stress period (LPS x time interaction; P < 0.0001). At d 8 after the start of heat stress (i.e., d 7 after LPS administration) hens were recovered from the LPS administration. They gained weight and had a comparable BW as their counterparts housed at 21 or 32°C (heat x LPS x time interaction; P < 0.05).
|
) and a line x LPS x time interaction (P < 0.05). On the one hand, lines B1 and WA gained lesser weight in the control chamber (BW gain of 57 and 37 g, respectively) compared with lines WB and WF (BW gain of 84 and 106 g, respectively). On the other hand, lines B1 and WA lost most weight in the heat stress chamber (BW loss of 163 and 121 g, respectively) compared with lines WB and WF (BW loss of 60 and 48 g, respectively).
|
and will be described first, whereas more detailed results per line are given in Table 3 and will be described after the main effects.
|
|
). Exposure to heat reduced hen-day egg production during the complete experimental period [P2 (P < 0.01) and P3 (P < 0.0001)]. Hens exposed to heat had a hen-day egg production of 83.8 and 83.6% compared with a hen-day egg production of 93.2 and 93.0% in the control group during P2 and P3, respectively. Administration of LPS decreased hen-day egg production during P2 (P < 0.0001) and increased hen-day egg production during P3 (P < 0.05). Single LPS administration or combined with heat stress gave comparable reductions in hen-day egg production during P2 (hen-day egg production of 55.0 and 51.4%, respectively). After LPS administration, hen-day egg production was 43.7, 51.5, 54.6, and 62.9% for line B1, WA, WB, and WF during P2, respectively, which was a significant lower hen-day egg production then their PBS treated counterparts (line x LPS interaction; P < 0.01). Decrease in hen-day egg production caused by heat stress was less than 10% and was not significant in each of the White Leghorn lines. Rhode Island Red line B1 had a hen-day egg production of 96.4 and 73.6% when housed by 21 and 32°C, respectively (line x heat interaction; P < 0.01).
Decreases in hen-day egg production between heat-stressed and control group during P3 were 24.0, 4.3, 0.0, and 1.1% for line B1, WA, WB, and WF, respectively. Line B1 was the only line in which heat-stressed hens differed in hen-day egg production from non-heat stressed hens (line x heat interaction; P < 0.0001). Interestingly, this is mainly caused by heat-stressed hens that did not receive LPS.
Egg Weight
Average egg weight per line per treatment is given in Table 4. Each of the main effects had an interaction with time [heat x time (P < 0.0001), LPS x time (P < 0.0001), line x time (P < 0.05)]. Heat stress reduced egg weight at d 4, 11, and 18 after the start of heat stress. Administration of LPS reduced egg weight at d 4 after the start of heat stress. The line x time interaction suggests that the lines had a different response pattern (data not shown). At the end of the experiment, hens housed in the heat chamber laid eggs with, on average, a 5.2 g lower weight compared with hens housed in the control chamber. Line B1 and WB had the largest difference in egg weight; 5.8 g (10.8%) and 5.5 g (10.3%), respectively. The difference in line WB is mainly caused by an increase in egg weight in the control chamber (+4.5 g), whereas the difference in line B1 is caused by a lower increase in egg weight in the control chamber (+3.4 g) and a stronger decrease in egg weight in the heat chamber (–2.4 g). Line WA and WF had an increase in egg weight in the control chamber of 4.1 and 4.2 g, respectively, and a decrease in egg weight in the heat chamber of 1.0 and 0.5 g, respectively, with a total difference of 8.8 and 8.6%, respectively.
|
). Line WF had the thickest egg shell in both control and heat chamber, 385 and 357 µm, respectively, whereas line WB had the thinnest egg shell in both control and heat chamber, 322 and 296 µm, respectively. Difference in egg shell thickness between control and heat chamber was comparable among lines. Line B1, WA, WB, and WF had a difference in shell thickness of 9.7, 9.3, 8.1, and 7.0%, respectively, between control and heat chamber. |
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
In the present study, heat stress reduced feed intake, BW, hen-day egg production, egg weight, and egg shell thickness. Hens did not completely adapt to heat stress because hens were still losing weight and had a lower feed intake and lower hen-day egg production after 23 d of continuous exposure to heat stress. Although there was no replication of the heat stress environment (possible confounded results), these findings confirm earlier studies (Njoya and Picard, 1994; Usayran et al., 2001; Lin et al., 2004; Mashaly et al., 2004). Maak et al. (2003), however, did not find differences in BW and hen-day egg production when birds were exposed to permanent heat stress (from chick to 68 wk of age). In the present study, reduction in feed intake during heat stress may cause a decrease in BW, hen-day egg production, and egg weight, indicating a negative nutrient balance of heat-stressed laying hens (Mashaly et al., 2004). Decrease in egg shell thickness at high temperature might be due to disturbance of shell formation (Lin et al., 2004).
Administration of LPS causes sickness behavior. Sickness behavior includes nonspecific symptoms of infection [e.g., weakness, malaise, listlessness, and fever (Dantzer, 2001)]. During the first 24 h after LPS administration chickens were very inactive, illustrated by an increase in sitting behavior and a decrease of standing, feeding, drinking, and moving behavior (Cheng et al., 2004). In the present study, sickness was not studied. Sickness was, however, indirectly measured by feed intake and hen-day egg production. Feed intake was significantly reduced by LPS administration, and it took at least 5 d to recover from this challenge. Sickness was well illustrated by hen-day egg production. Within hours after LPS administration almost all challenged hens laid a shell-less egg. Thereafter it took also 5 d to recover hen-day egg production. Sickness and reduction in feed intake caused a decrease in BW 1 d after LPS administration, which confirms earlier findings of Cheng et al. (2004) and Parmentier et al. (1998). One week after LPS administration, hens were recovered, illustrated by a comparable feed intake, BW, and hen-day egg production to their PBS-treated counterparts, suggesting an acute but short-term effect of LPS administration.
Hens exposed to combined heat and LPS administration had a lower feed intake during the first week after the start of the heat stress period than hens exposed to heat or LPS. The strong reduction in feed intake after LPS administration combined with heat stress resulted in the lowest BW for this treatment group at d 2 after the start of the heat stress period. At d 8, 15, and 22, however, the effect of combined heat exposure and LPS administration was less negative on BW than single exposure to heat. This indicates that the combined treatment has a stronger, although not additive, effect in the first week. Hereafter, the hens were recovered from LPS administration and were able to maintain a constant feed intake comparable with feed intake of hens exposed to single heat stress. Feed intake was, however, too low to maintain BW under high temperature treatment.
In the present study, 4 purebred layer lines were used. Lines were characterized by natural humoral immune competence and survival rate as described in a previous study (Star et al., 2007). Neither natural humoral immune competence nor survival rate was indicative for the physiological and reproductive responses of the 4 lines to the different environmental stressors. Although the lines showed similar response patterns, they differed in response levels. Rhode Island Red line B1 had the strongest reduction in feed intake, BW, and hen-day egg production during heat stress compared with the White Leghorn lines. Marsden et al. (1987) found a stronger reduction in feed intake and BW in a Brown layer type compared with a White layer type when exposed to a temperature of 30°C, but they did not find a difference in egg production between the lines. In the present study, differences in performance were also found between the White Leghorn lines, although these differences were smaller than between the Rhode Island Red type and White Leghorn types. Line WA had a stronger decrease in BW and a lower hen-day egg production during heat stress than line WB and WF. Hester et al. (1996b) used 3 White Leghorn lines: a line selected for high group productivity and survivability, a random bred control line, and a commercial line. Compared with hens of the control line and commercial line, hens of the high selection line had an improved adaptability to high temperature conditions. Hester et al. (1996a,b,c) concluded from their studies that, from criteria used to evaluate stress (e.g., physiological and immunological parameters), egg production and mortality provided the best evidence for adaptability to stress. Our data, from the previous and current study, also suggest that some lines are better able to cope with environmental stressors than other lines based on egg production and mortality. Line B1 had a high mortality rate under commercial circumstances (previous study) and showed a decline in hen-day egg production by exposure to high temperatures. Line WA had a decline in production at the end of the laying period (60 to 69 wk of age) under commercial circumstances (previous study; unpublished data) and had more problems with keeping up production under heat stress than the other White Leghorn lines. Line WB and WF were able to maintain a high hen-day egg production under heat stress. However, line WF was a better survivor under commercial circumstances than line WB (previous study), which makes line WF a more robust line.
Under the given circumstances (temperature of 21 or 32°C with or without injection of 1 mg/kg of BW of LPS), the results of this study indicate that heat exposure and LPS administration were independent stressors. Hens were able to recover from LPS administration, but did not completely adapt to heat stress, since hens were still losing weight, had a lower feed intake and hen-day egg production after 23 d of continuous exposure to heat stress. The 4 purebred layer lines had similar response patterns, but differed in response levels (especially for hen-day egg production and feed intake), suggesting that some lines were better able to adapt to stressors than other lines. Neither natural humoral immune competence nor survival rate, on which bases the lines were characterized, was indicative for the stress response to different stressors.
Finally, studies in broiler chickens indicated that neonatal heat exposure at 5 d of age reduced mortality (Arjona et al., 1990; Yahav and Hurwitz, 1996) and improved performance and thermo tolerance later in life (Yahav and Plavnik, 1999) by elevation of the thermoregulatory set point (Tzschentke, 2004). In the present study, adult laying hens were exposed to acute, long-term heat stress. Early-age thermal conditioning of layer chicks might improve thermo tolerance and might prevent strong reductions in feed intake, BW, and hen-day egg production during thermal challenge later in life.
|
ACKNOWLEDGMENTS |
|---|
Received for publication April 3, 2007. Accepted for publication February 21, 2008.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Arjona, A. A., D. M. Denbow, and W. D. Weaver Jr. 1990. Neonatally-induced thermotolerance: Physiological responses. Comp. Biochem. Physiol. 95:393–399.[CrossRef][Medline]
Bijlsma, R., and V. Loeschcke. 2005. Environmental stress, adaptation and evolution: An overview. J. Evol. Biol. 18:744–749.[CrossRef][Web of Science][Medline]
Blatteis, C. M. 2000. Thermoregulation in complex situations: Combined heat exposure, infectious fever and water deprivation. Int. J. Biometeorol. 44:31–43.[CrossRef][Web of Science][Medline]
Cheng, H. W., R. Freire, and E. A. Pajor. 2004. Endotoxin stress responses in chickens from different genetic lines. 1. Sickness, behavioral, and physical responses. Poult. Sci. 83:707–715.
Dantzer, R. 2001. Cytokine-induced sickness behaviour: Mechanisms and implications. Ann. N. Y. Acad. Sci. 933:222–234.[Web of Science][Medline]
Hester, P. Y., W. M. Muir, and J. V. Craig. 1996a. Group selection for adaptation to multiple-hen cages: Humoral immune response. Poult. Sci. 75:1315–1320.[Web of Science][Medline]
Hester, P. Y., W. M. Muir, J. V. Craig, and J. L. Albright. 1996b. Group selection for adaptation to multiple-hen cages: Production traits during heat and cold exposures. Poult. Sci. 75:1308–1314.[Web of Science][Medline]
Hester, P. Y., W. M. Muir, J. V. Craig, and J. L. Albright. 1996c. Group selection for adaptation to multiple-hen cages: Hematology and adrenal function. Poult. Sci. 75:1295–1307.[Web of Science][Medline]
Kamerman, P. R., R. Brooksbank, N. Pitts, and H. P. Laburn. 2001. Heat stress increases the rate of tolerance development to lipopolysaccharide in rats. J. Therm. Biol. 26:589–594.[CrossRef][Web of Science]
Kluger, M. J., K. Rudolph, D. Soszynski, C. A. Conn, L. R. Leon, W. Kozak, E. S. Wallen, and P. L. Moseley. 1997. Effect of heat stress on LPS-induced fever and tumor necrosis factor. Am. J. Physiol. Regul. Integr. Comp. Physiol. 273:R858–R863.
Koelkebeck, K. W., and T. W. Odom. 1995. Laying hen responses to acute heat stress and carbon dioxide supplementation: II. Changes in plasma enzymes, metabolites and electrolytes. Comp. Biochem. Physiol. 112:119–122.
Lin, H., K. Mertens, B. Kemps, T. Govaerts, B. de Ketelaere, J. de Baerdemaeker, E. Decuypere, and J. Buyse. 2004. New approach of testing the effect of heat stress on eggshell quality: Mechanical and material properties of eggshell and membrane. Br. Poult. Sci. 45:476–482.[CrossRef][Web of Science][Medline]
Maak, S., A. Melesse, R. Schmidt, F. Schneider, and G. von Lengerken. 2003. Effect of long-term heat exposure on peripheral concentrations of heat shock protein 70 (Hsp70) and hormones in laying hens with different genotypes. Br. Poult. Sci. 44:133–138.[CrossRef][Web of Science][Medline]
Macari, M., R. L. Furlan, F. P. Gregorut, E. R. Secato, and J. R. Guerreiro. 1993. Effects of endotoxin, interleukin-1β and prostaglandin injections on fever response in broilers. Br. Poult. Sci. 34:1035–1042.[Web of Science][Medline]
Mahmoud, K. Z., and A. M. Yaseen. 2005. Effect of feed withdrawal and heat acclimatization on stress responses of male broiler and layer-type chickens (Gallus gallus domesticus). Asian-australas. J. Anim. Sci. 18:1445–1450.
Marsden, A., T. R. Morris, and A. S. Cromarty. 1987. Effects of constant environmental temperatures on the performance of laying pullets. Br. Poult. Sci. 28:361–380.[CrossRef][Web of Science][Medline]
Mashaly, M. M., G. L. Hendricks, M. A. Kalama, A. E. Gehad, A. O. Abbas, and P. H. Patterson. 2004. Effect of heat stress on production parameters and immune responses of commercial laying hens. Poult. Sci. 83:889–894.
Mumma, J. O., J. P. Thaxton, Y. Vizzier-Thaxton, and W. L. Dodson. 2006. Physiological stress in laying hens. Poult. Sci. 85:761–769.
Njoya, J., and M. Picard. 1994. Climatic adaptation of laying hens. Trop. Anim. Health Prod. 26:180–186.[CrossRef][Web of Science][Medline]
Parmentier, H. K., M. Walraven, and M. G. B. Nieuwland. 1998. Antibody responses and body weights of chicken lines selected for high and low humoral responsiveness to sheep red blood cells. 1. Effect of Escherichia coli lipopolysaccharide. Poult. Sci. 77:248–255.
SAS Institute. 2004. SAS User’s Guide: Statistics. Release 9.1. SAS Institute Inc., Cary, NC.
Star, L., E. Decuypere, H. K. Parmentier, and B. Kemp. 2008. Effect of single or combined climatic and hygienic stress in four layer lines: 2. Endocrine and oxidative stress responses. Poult. Sci. 87:1031–1038.
Star, L., K. Frankena, B. Kemp, M. G. B. Nieuwland, and H. K. Parmentier. 2007. Natural humoral immune competence and survival in layers. Poult. Sci. 86:1090–1099.
Thaxton, P., C. R. Sadler, and B. Glick. 1968. Immune response of chickens following heat exposure or injection with ACTH. Poult. Sci. 47:264–266.[Web of Science][Medline]
Tzschentke, B. 2004. Importance of thermoregulatory behaviour in poultry during the first days after hatching: interactions between temperature preference and thermoregulatory heat production. Avian Poult. Biol. Rev. 15:253–254.
Usayran, N., M. T. Farran, H. H. O. Awadallah, I. R. Al-Hawi, R. J. Asmar, and V. M. Ashkarian. 2001. Effects of added dietary fat and phosphorus on the performance and egg quality of laying hens subjected to a constant high environmental temperature. Poult. Sci. 80:1695–1701.
Xie, H., N. C. Rath, G. R. Huff, W. E. Huff, and J. M. Balog. 2000. Effects of Salmonella typhimurium lipopolysaccharide on broiler chickens. Poult. Sci. 79:33–40.
Yahav, S., and S. Hurwitz. 1996. Induction of thermotolerance in male broiler chickens by temperature conditioning at an early age. Poult. Sci. 75:402–406.[Web of Science][Medline]
Yahav, S., and I. Plavnik. 1999. Effect of early-age thermal conditioning and food restriction on performance and thermotolerance of male broiler chickens. Br. Poult. Sci. 40:120–126.[CrossRef][Web of Science][Medline]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
