By Peter R. Ferket PhD
In ovo feeding shows promise
By Peter R. Ferket PhD
The growth performance and meat yield of commercial turkeys has
improved linearly each year with greater input efficiency.1,2 This
trend will likely continue in the future as new technologies in
genetics, biotechnology, and developmental biology are introduced and
adopted by the poultry industry. As the time it takes meat birds to
achieve market size decreases, the period of embryonic development
becomes a greater proportion of a bird’s life.
The growth performance and meat yield of commercial turkeys has improved linearly each year with greater input efficiency.1,2 This trend will likely continue in the future as new technologies in genetics, biotechnology, and developmental biology are introduced and adopted by the poultry industry. As the time it takes meat birds to achieve market size decreases, the period of embryonic development becomes a greater proportion of a bird’s life.
|The degree of response to in ovo feeding may depend upon genetics, breeder hen age, egg size and incubation conditions.|
Commercial turkeys are more susceptible to aberrations in early growth and development than their ancestors were because their metabolic demands for growth are much greater. Indeed, these birds are becoming more altricial (birds like pigeons and songbirds that require parental feeding after hatch) and less precocial (birds like chickens and ducks that require little parental nutritional support).
A major difference between precocial and altricial birds is how they manage the constraints on growth, including the availability of nutrient resources, the capacity to utilize the available nutrient resources, and the compromise between somatic growth and tissue maturation and function.3,4 In contrast to altricial birds, precocial birds quickly adapt to carbohydrate metabolism and seek food on their own to satisfy their nutrient requirements. Precocial birds have the capacity to digest and utilize complex dietary nutrients at hatch, whereas altricial birds need a much more simple diet that does not require many body resources to digest and absorb, leaving more resources for somatic growth. Finally, precocial birds grow more slowly than altricial birds because they partition more energy towards tissue maturation and maintenance than somatic growth. Although altricial birds may hatch with a less mature digestive tract, they have the advantage over precocial chicks in growth rate.
So the turkey industry has a dilemma: they are selecting birds to be more altricial to take advantage of rapid growth rate and shorter days to market, but they want to manage these birds as if they are self-sufficient, precocial animals. Consequently, early survival problems will increase as the poultry industry moves toward more fast-growing strains. Just as the altricial hatchling is much more dependent upon its parents for adequate nutrition than the precocial hatchling, modern turkey poults are becoming more dependent upon the quality of their nutrition during the perinatal period. The perinatal period begins when the turkey embyo first begins to consume the amnion fluid (about 22 days of incubation) until about 10 days of age.
Incubation conditions and digestive capacity
The few days before and after hatch are critical for the development and survival of commercial turkeys. During this period these birds make the metabolic and physiological transition from egg nutrients to exogenous feed. When oxygen availability to the late-term embryo is limited by low egg conductance or poor incubator ventilation, the embryos and hatchlings may suffer a low glycogen status and impaired enteric development.5-7 Much of the glycogen reserve in the late-term chicken embryo is utilized for hatching. Subsequently, the chick must rebuild that glycogen reserve by gluconeogenesis from body protein (mostly from the breast muscle) to support post-hatch thermoregulation and survival until the poults are able to consume and utilize dietary nutrients.
Excessive temperature during the plateau stage of oxygen consumption of the late-term embryo will impair intestinal and cardiac development in poults.8,9 Immediately post-hatch, the poult draws from its limited body reserves and undergoes rapid physical and functional development of the gastrointestinal tract in order to digest feed and assimilate nutrients. Because the intestine is the primary nutrient supply organ, the sooner it achieves this functional capacity, the sooner the young bird can utilize dietary nutrients, efficiently grow at its genetic potential and resist infectious and metabolic disease.10
Commercial turkeys are more susceptible to aberrations in early growth and development than their ancestors were because their metabolic demands for growth are much greater.
Early nutrition and post-hatch development
Although the digestive capacity begins to develop after the embryo consumes the amnionic fluid, most of the development occurs post-hatch when the neonatal chick begins consuming feed. During the post-hatch period, the small intestine weight increases at a faster rate than the body mass because of rapid enterocyte proliferation and differentiation.11-13 Feeding immediately post-hatch accelerates the morphological development of the small intestine, while delayed access to external feed arrests the development of the small intestine mucosal layer.14-16 Furthermore, birds denied access to first feed for 24 to 48 hours post-hatch have decreased villi length, decreased crypt size and crypts per villi, and decreased enterocytes migration rate.17,18 In addition, delayed access to feed for 48 hours post-hatch resulted in changes in mucin dynamics, which affects the absorptive and protective functions of the small intestine.19
Dietary factors and feeding behaviour during the first few days after hatch can have marked effects on how residual yolk is used to support growth and development. Different sources of protein and energy have varying levels of impact on poults, showing a need for more digestible nutrients.20 Researchers have found that offering nutrients to poults in solid, semi-solid, or liquid form immediately post-hatch improved body weight and breast meat percentage of body weight at market age.14 Without access to feed and water, however, the development of the neonatal poult is dependent on residual nutrients found in the yolk sac that have been depleted during the hatching process.10
Delayed access to feed and water will result in a mortality rate of about five per cent, poor growth, decreased disease resistance, and impaired levels of muscle development.10 It is often thought that the residual yolk found in the poult or chick is sufficient to maintain the bird until feed is offered. However, the initiation of growth may be more dependent on feed consumption than the nutrients found in the yolk post-hatch.21 When feed consumption starts soon after hatch, the nutrients provided by the feed are complementary to the yolk nutrients.
Initiation of feed consumption soon after hatch is necessary to support early muscle development, which may ultimately affect meat yield. In contrast, early muscle development is seriously compromised when feed is withheld during the first few days after hatch. It is has been observed that fasted chicks exhibit lower protein synthesis in the Pectoralis thoracicus, and others have observed increased levels of apoptosis.22,23 Satellite cell mitotic activity, the major source of myofibre growth via myonuclear accretion, is highest early post-hatch and decreases with age as birds mature.24
Muscle satellite activity in turkeys begins as early as 25 days of incubation, peaking shortly after hatch, and decreases significantly by seven days post-hatch.25 Poults that experience delayed access to feed immediately post-hatch exhibit lower satellite cell mitotic activity when compared to their fed counterparts.23,26 Researchers observed that a 72 hour post-hatch fast significantly compromises beast muscle development as measured by myofibre cross-sectional area for at least 10 days post-hatch.25 Although satellite activity remained depressed for one day after the period of fasting, it subsequently rebounded to a level above the fed birds even though it was not enough to compensate for earlier losses in muscle growth.
In ovo feeding a ‘jump-start’
Since access to feed soon after hatch is critical for the development of digestive capacity and muscle, we hypothesized that “feeding” the embryo when it consumes the amniotic fluid can accelerate enteric development and its capacity to digest nutrients. By injecting an isotonic in ovo feeding (IOF) solution into the embryonic amnion, the embryo can naturally consume supplemental nutrients orally before hatching. In ovo feeding may “jump-start” or stimulate development to begin earlier than would otherwise occur after the birds hatch. Improving the nutritional status of the neonate by in ovo feeding may yield several advantages: greater efficiency of feed nutrient utilization; reduced post-hatch mortality and morbidity; improved immune response to enteric antigens; reduced incidence of developmental skeletal disorders; increased muscle development; and increased breast meat yield. These benefits will ultimately reduce the production cost of poultry meat by alleviating the growth constraints of “altricial” broilers selected for rapid growth rate.
The benefits of in ovo feeding for early growth and development on turkeys have been demonstrated by several experiments in our laboratory.10 In each experiment, in ovo feeding turkeys has increased hatchling weights by three per cent to seven per cent (P<.05) over controls, and this advantage has been observed to sustain at least until 14 days. The degree of response to in ovo feeding may depend upon genetics, breeder hen age, egg size and incubation conditions.
Above all, IOF solution formulation has the most profound effect on the neonate. Positive effects have been observed with IOF solutions containing NaCl, sucrose, maltose, and Dextrin, beta-hydroxy beta-methylbutyrate (HMB), egg white protein, and carbohydrate, arginine, and zinc-methionine.10, 27-31 In addition to the increased body weights typically observed at hatch, the positive effects of in ovo feeding may include increased hatchability; advanced morphometic development of the intestinal tract and mucin barrier; enhanced expression of genes for brush boarder enzymes (sucrase-isomaltase, leucine aminopeptidase) and their biological activity, along with enhanced expression of nutrient transporters, SGLT-1, PEPT-1, and NaK ATPase; increased liver glycogen status; enhanced feed intake initiation behaviour; and increased breast muscle size at hatch.27-32 In ovo feeding clearly advances the digestive capacity, energy status, and development of critical tissues of the neonate by about two days at the time of hatch.
Enhanced gut development
This is the goal of in ovo feeding: the sooner the neonate develops the functional capacity to digest and absorb nutrients, the more likely it is able to grow according to its genetic potential. Digestive capacity is a function of both the gut mucosa surface area and the brush boarder enzyme activity per unit of tissue mass. Development of the mucosal surface area and brush boarder enzyme activity is determined by the rate of enterocyte proliferation and differentiation.
In ovo feeding has been demonstrated to significantly increase the absorptive surface area in several segments of the gut of newly hatched poults by increasing villus height and villus apical and basal width, and this was associated with increased early growth rate.33
Researchers have also demonstrated that in ovo feeding enhanced enteric brush boarder enzyme activity of turkeys.30 In an experiment, turkeys were in ovo fed at 23 days of incubation with 1.5mL of a) 0.1% HMB + 0.7% Arginine in 0.4% saline (HMB + ARG); b)18% Egg white protein + 0.1% HMB + 0.7% Arginine in 0.4% saline (EWP + HMB + ARG); or c) a non-injected control. In ovo feeding of ARG + HMB significantly enhanced sucrase, maltase and LAP brush border activity within 48 hours of nutrient administration. Additionally, in ovo fed poults of the ARG + HMB treatment group had increased sucrase, maltase and LAP activity at 14-day post-hatch. These results imply that in ovo feeding HMB and ARG may positively affect intestinal brush border enzymes for up to two weeks.
As with the broiler experiments, the increased brush board enzyme activity corresponded with improvements in post-hatch growth. In addition to providing nutrients to fuel the development of the late-term embryo, in ovo feeding effects the expression of genes that control the development of digestive capacity. In turkeys, it’s been observed that the increase in brush boarder enzyme activity and nutrient transporters by in ovo feeding was preceded by a corresponding increase in the expression of related genes (mRNA).30 In ovo feeding may also enhance the protective function of enteric mucosa.
Hatchlings are very susceptible to the colonization of enteric pathogens due to minimal competitive exclusion by symbiotic microflora that populate the mucin layer of the gut mucosa. The mucus gel layer of the intestinal epithelium is the first barrier to enteric infection. It’s been observed the proportion of goblet cells containing acidic mucin increased 50 per cent over controls at 36 h after in ovo feeding, which corresponded to enhanced expression of the mucin mRNA.34 Using scanning electron microscopy, it’s been observed that in ovo feeding significantly increased functional maturity and mucus secretion of goblet cells of villi of ileum and ceca of turkey poults.33 Associated with these goblet cells was the colonization of lactobacilli. Therefore, in ovo feeding may help improve the colonization resistance of enteric pathogens of neonatal chicks and poults.
In ovo feeding improves glycogen status. Glycogen reserves in the avian embryo provide the critical energy needed for hatching. In turkeys, extensive embryonic mortality occurs toward the end of the incubation period when hatching-related events occur, such as pipping of the egg membrane and shell, beginning of pulmonary respiration, and the actual egg emergence.5 Glycogen reserves in the embryo are significantly depleted during the peri-hatch period in order to meet the high energy demand during the process of emergence.35-37 Hepatic and muscle glycogen reserves are depleted due to carbohydrate utilization for muscular activity during the hatching process and for post-hatch growth, activity and maintenance.38-41
It has been demonstrated that turkey poults in ovo fed HMB had approximately a 40 per cent increase in hepatic glycogen over the injected and non-injected controls.10 Moreover, hatchability rates were positively correlated with liver glycogen content of turkey embryos before hatch. Focused gene array technology has confirmed that in ovo feeding up-regulates the expression of critical enzymes associated with glycogen deposition prior to pipping and its utilization during pipping and hatching.32
In ovo feeding clearly enhances glycogen status as indicated by hepatic gluconeogenic activity and hepatic glycogen reserves, which provide the fuel needed to support the hatching process, thermal regulation, and rapid growth during the critical post-hatch period until sufficient energy resources are consumed upon feed intake initiation.
In conclusion, in ovo feeding offers promise of sustaining the progress in production efficiency and welfare of commercial poultry. Although selection for fast growth rate and meat yield may favour the modern broiler to become more altricial, proper early nutrition and in ovo feeding may help these birds adapt to a carbohydrate-based diet and metabolism typical of a precocial bird at hatch. Our research on in ovo feeding has established a new science of neonatal nutrition, and we are gaining greater understanding of the developmental transition from embryo to chick. However, much more work must be done before in ovo feeding can be adopted for commercial practice.
Presented at the Midwest Poultry Federation Convention. Full references are available at www.canadianpoultrymag.com.