| Mortality suffered by most turkey flocks is usually most extensive through the first two weeks of life. Reasons for these deaths are overwhelmingly due to "starve-outs" and yolk sac infections (Table 1). Although each type loss is different they are interrelated. In order to best manage poults at placement and minimize mortality, an overview of the events preceding, during, and following emergence is necessary. Based on these events, one can rationalize a workable strategy for relief.
The egg comprises shell, white and yolk, each of which supports embryo development and early poult survival. Calcium is supplied by the calcium reserve assembly that connects to the outer shell membrane. White in addition to providing protein directly for growth and carbohydrate indirectly via gluconeogenesis also is the source of IgA for protection of mucosal surfaces at hatch until immunocompetence becomes established.
The yolk contains about one-third aqueous compounds and two-thirds lipid. IgG is an important part of the aqueous proteins that represent passive immunity to systemic infections. The very low density lipoproteins have a high proportion of triglyceride which dominate the lipid portion. The essential fatty acids are favored for use in membrane assembly; whereas, the most saturated ones are combusted for energy. Vitellogenin is another major lipoprotein synthesized in the liver and transported to the yolk. During transfer this macromolecule is cleaved into lipovitellin and phosvitin, and their composite rearranges to form the yolk granules that play a role in calcium and phosphorus nutrition, especially during emergence and several days thereafter.
Embryonic development through hatching can simplistically be divided into three phases. The first third of incubation establishes the germ followed by the second third with organ growth and development. The last one-third essentially involves changes and preparations by the embryo for emergence. These alterations are particularly important to subsequent survival.
Initiation of preparations for hatching occurs with rupture of the sac holding the remaining albumen, and its flow into the amniotic cavity with the embryo. Over the next several days, the albumen is consumed, and a large portion is absorbed by the intestine with the remainder passing through the yolk stalk into the yolk sac. The IgA consumed provides passive protection at mucosal surfaces and in the yolk sac.
The intestinal surface in place with the embryo is specialized to absorb macromolecules such as immunoglobins, but it is incompetent at digestion and active transport. Cells on the intestinal are substantially replaced with competent ones by hatch; however, a mosaic of both types exists and complete replacement does not occur for another two weeks.
An immature absorptive surface enables increased concentrations of nutrients to exist within the intestinal lumen. Consumed microflora that reach the small intestine are kept "in check" under these enriched circumstances by the IgA consumed earlier until the bird's own immune system becomes established. The yolk stalk remains open to the intestine several days after hatching, and microflora are kept from being established by resident IgA and IgG. Ability of the poult to ward off intestinal and yolk sac infections relates to the consumed microbial load together with "experience" of breeder hen in the pattern and extent of passive resistance.
Failure to control consumed microbes leads to infections that are more opportunistic in nature than true pathogens. E. coli, B. cereus, S. aureus, Enterococci, Pseudomonas, Clostridia, and Proteus are all common to the environment and intestine. The hen would ordinarily protect the hatchlings at her nest by the full array of immunoglobins from a continuing experience; however, experience of hen may not fully resemble exposure of poults at hatch and placement.
Reducing extent of microbial exposure for the first week until the poult's immune system fully responds to challenges seems to be the best approach to minimizing infections. Two phases of infection losses are indicated in Table 1. The first peak is likely due to hatchery conditions with the second occurring from exposure after placement. Inclusion of antibiotics and other feed additives in the starting feed is only as good as the "sensitivity" of acute microbes at that specific instance.
Starve-outs die from a failure in transition from yolk-sac nutrition to external food. The GIT is totally devoid of contents, and absence of intake also negates microbial infections as a militating factor. Reason for occurrence is not obvious, but indirect evidence suggests that nutrition provided during emergence is inadequate for the transition.
Nutrition of the embryo that is specific for eventual emergence and subsequent survival is largely determined with "consumption" of albumen. This albumen is the primary precursor of glycogen. In addition, one or more components appear to alter yolk granules for sequestering calcium. Stored glycogen by the embryo and sequestered calcium in the yolk sac play separate but important roles in emergence.
Glycogen stores accrue in the embryo as albumen and VLDL protein are removed from the yolk sac. This glycogen is in particularly high concentration in the liver and muscles that actively participate in hatching. Once the air cell is pierced, and choriantois as a source of oxygen diminishes, then utilization of lipid as a source of energy becomes limited until the lungs are fully functional. Alternatively, glycogen is mobilized to support muscle activity in emergence through anaerobic means.
Lipid oxidation can fully resume after hatching to meet energy needs, but small quantities of glucose are still needed to facilitate its complete combustion to carbon dioxide and water. Otherwise, ketone bodies progressively escalate as glucose decreases. Presumably, ketosis leads to a certain amount of listlessness and confusion that reduces the likelihood of initiating feed intake. Glycogen reserve after hatch is a function of egg size, and poults from small eggs of young breeds are marginal in this respect.
Depletion of glycogen and increased ketosis are completely avoided if food is realized. A single intubation of any source nutrient immediately after hatch provides a substantial advantage to initiating voluntary food intake and improved live performance (Table 2). Although such intubation is impractical on commercial basis, including glucose or gluconeogenic source with injection provides a commercially feasible alternative. Unfortunately, this advantage is limited because only small doses are possible in conjunction with vitamins, electrolytes, etc.
Calcium is not mobilized from the shell for use by the embryo until after the albumen is consumed. The skeleton is in place as cartilage at this time, and long bones must become calcified to provide integrity enabling leverage for meaningful muscular activity during hatching. This skeletal stabilization must continue after interruption of chorioallantois and access to shell calcium. A continuation of calcium with emergences is derived from the yolk sac.
Yolk sac membrane has the capacity to remove calcium from embryonic circulation. This calcium is transferred to the yolk granules where extensive phosphorus from phosvitin exists. Yolk calcium phosphate-protein-lipid spherules are held in the yolk sac until interruption of chorioallantois, then these are removed by the membrane to provide continued skeletal development until feed intake is established.
Lipid released with spherule catabolism exceeds the birds oxidative needs, and body depots expand as yolk sac contents deplete. Transitory subcutaneous depots are developed to provide a back-up energy reserve; whereas, massive amounts of cholesterol esters are held in the liver to support rapid membrane expansion. Both of these reserves progressively disappear as feed intake becomes established, and de novo synthesis is commensurate with demands for growth.
Poult survival is inextricably related to passive immunity, together with reserves of glycogen, lipid, and calcium-phosphorus at emergence. This adequacy depends to a large extent on age of the breeder and egg weight. Young breeders are expected to have minimal "experience" that is conveyed as passive immunity. The advantage of such diversity becomes important when breeders are reared in one set of conditions and lay in another subsequently, eggs are hatched in another environment, and poult placement is again remote. Given the wide possibilities in microbial array and shifts in their accentuation, then encounters and likelihood of infections escalate.
Minimizing infections by reducing microbial exposure is a primary approach. Hatchery sanitation is expected to be of greatest benefit to reducing early losses; whereas, house sanitation likely lowers yolk sac infections appearing after the first week. Undoubtedly, broad spectrum antibiotic inclusion in the starter would alleviate late deaths, but its use can be expected to confound establishing a normal population and reduce its effectiveness in pathogen control.
Young breeders also have small eggs and reduced albumen and yolk to nutritionally support the post emergent poult. Reducing time to feed access is crucial as is presentation of nutrients central to need. Carbohydrate appears to be of particular importance in order to support complete lipid combustion that avoids ketosis and provides metabolic water. Increasing level of dietary carbohydrate must be at the expense of protein, and such a trade-off appears to have no repercussion on early performance as long as yolk sac complementation is high (Table 3).
High calcium and phosphorus in this feed at placement may be of similar advantage to support a likely decrease in yolk calcified granules from low weight eggs. "Flips" have poorly stabilized long bones, and this condition can be rationalized as an inadequacy to continue bone stabilization during emergence.
Propionic acid at high levels in the feed at placement may relieve microbial threats as well as provide glucose. Although pH of feed is seldom sufficiently low to enable propionic acid to be in the non-dissociated form and incapacitate many microbes, these levels are attained with passage through the proventriculus-gizzard. Non-dissociated propionic acid may also pass through the walls of these organs and readily be converted to glucose. High propionate in feed through the first seven days with broilers reduced deaths, particularly using young breeders as egg source. Loss in body weight concurrent with improved feed conversion suggest a reduction in body fat. (Table 4).
In summary, early poult management is primarily concerned with deaths due to yolk sac infections and starve-outs. In large part, infections arise because common microbes overwhelm an immature system because passive immunity is lacking. Starve-outs fail to initiate feed consumption which appears to occur because of a ketotic "lethargy" at placement. Presumably, insufficient carbohydrate at emergence leads to incomplete lipid combustion. Both problems are greatest with eggs from young breeders where immunological experience is minimal as are yolk sac reserves after emergence. Relief from infections relates to sanitation in the hatchery and at placement; whereas, early access to feed high in carbohydrate can reduce the likelihood of starve-outs.
Table 1. Proportions of starve-outs and yolk sac infections with poults in commercial flocks two weeks after placement 1
Table 2. Performance of poults intubated with nutrients immediate to hatching, g 1
Age (days) | g, Body Weight 2 |
 | Glucose | Starch | Oil | Nil |
0 | 72 | 73 | 73 | 72 |
1 | 65 | 63 | 65 | 64 |
7 | 141a | 140a | 144a | 126b |
14 | 284a | 289a | 287a | 263b |
21 | 490a | 471a | 470ab | 444b |
| g, Feed Consumption |
0-7 | 179 | 178 | 179 | 160 |
1 From Noy and Pinchsov (1993).
2 0.5 ml intubations of 50:100 wt:vol (.2 ml oil). |
Table 3. Effect of dietary carbohydrate level in the starting feed for turkey poults 24 hours after access 1
Available CHO | Diet Protein | Blood glucose | Liver Glycogen |
% | % | mg/dL | Conc. (mg/g) | Total (mg) |
50 | 20 | 274 | 275 | 634 |
33 | 28 | 257 | 129 | 290 |
15 | 35 | 269 | 70 | 159 |
| 1 From Donaldson et al. (1992). |
Table 4. Effect of propionic acid in feed for first 5 days on performance and mortality of broilers from extremes in breeder flock age 1
Age of
Breeder Flock | Dietary
Propionate 2 | BW
(3 wks) | F:G
(0-3 wks) 3 | Deaths |
(wks) | (%) | (g) | (g) | 0-1 wk
(%) | 0-3 wk
(%) |
62 | 0 | 776a | 1.48a | 3.5 | 5.1 |
3 | 754b | 1.45b | 4.3 | 6.3 |
27 | 0 | 697c | 1.48a | 5.9 | 10.6 |
3 | 670d | 1.42b | 4.3 | 6.6 |
1 Moran (unpublished). Each value represents 8 replicate pens of 50 birds/pen (4 male, 4 female) on used litter.
2 Ammonium proprionate: feed, wt:wt.
3 Corrected for mortality. |
References
Donaldson, W. E., C. E. Brewer, P. R. Ferket, and V. L. Christensen, 1992. Posthatch carbohydrate feeding and subsequent performance of turkey poults. Poultry Sci., 71:128-132.
Mayes, F. J., 1987. A survey of early poult mortality in turkey flocks. Irish Vet. J., 41:367-370.
Noy, Y., and Y. Pinchasov, 1993. Effect of a single posthatch intubation of nutrients on subsequent early performance of broiler chicks. Poultry Sci., 72:1861-1866.
Edwin T. Moran, Jr.
Poultry Science Department, Alabama Agricultural Experiment Station, Auburn University, AL 36849 USA |