The failure of a high proportion of fertile eggs to hatch still remains a major cause of financial loss to the poultry industry. Payne (1919) pointed out the consistent manner in which embryonic mortality manifested peak periods at the fourth day and the nineteenth day of incubation, and he drew attention to the fact that the latter period of susoeptibility showed an increased level of mortality with artificial incubation compared with natural methods. Romanoff (1949) summarized the explanations put forward to account for these two peaks of embryonic mortality. Riddle (1930) suggested that the first period was caused by respiratory maladjustments, and he, and others, considered that the failure of the developing embryo to make the fine adjustments at this time and to deal effectively with the excretion of various toxic substances may be a major cause of death. The second peak period of mortality occurs at the transition from allantoic to pulmonary respiration. Failure to achieve this change, with the consequent death of the chick in the last stages of development, may be greatly influenced by the cumulative effect of all the unfavourable conditions to which the hatching egg has been subjected. Not the least of these will be environmental conditions in the incubator and the incubator house adversely affecting the oxygen supply and the relative humidity.
Reference is made to the depression in hatching rates occasionally recorded when fishmeal is fed to breeding hens. In a previous communication this depression was tentatively ascribed to the presence of aerobic sporing bacteria, support for this theory being given by the high early death-rate from yolksac infection in the chicks hatched from the affected pens. In this experiment samples of white fishmeal from widely separated points of origin were employed. With one group of birds extreme hatching depression was recorded; in one other group a moderate depression was found. Bacterial assays showed that only one sample contained aerobic sporing bacteria capable of coagulating yolk and the count was not high. But the birds fed this sample were those manifesting the mild depression in the hatching rate and this was the only group to show an appreciably above normal early death-rate in the chicks. The major cause of death was yolk-sac infection, and it is concluded that in this group the presence of aerobic sporing bacteria was partially responsible for the depression in hatching, but that the degree of contamination was not as high as that which probably occurred in the previous year.The hatching rate in all groups was inversely related to the depth of coloration in the fishmeal samples. The theory is advanced that, as a result of overheating during manufacture, degradation of the proteins occurred giving rise to toxic products which in turn led to a high embryonic death-rate during the last 4 days of incubation. The highest embryonic death-rate in total, and during this period, was found with those birds fed the fishmeal with the darkest colour. The egg production in all groups of birds was high and it therefore seemed improbable that overheating had proceeded to the stage of materially damaging the essential aminoacid contents of the meal, for it seems widely accepted that if the amino-acid level is sufficient for egg production it is sufficient for good hatchability.
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