Abstract

The fertile hen collects eggs in a nest to form her clutch. The egg’s asymmetrical ellipsoid shape encourages placement blunt end up. Chalaza formation centralizes ovum in the egg while its high lipid favors upward positioning as early rotations interface germ with outer thin and access its glucose. Repetitive heating during successive ovipositions together with glucose recovery sustain blastodisc viability. Further turning of eggs upon formal incubation distributes the chorio-allantois over the blunt end while consolidating albumen in its sac at the sharp end. Rupture of the sero-amnionic connection mixes albumen with amnion which the embryo consumes over the next several days. During consumption certain of the proteins directly enter the vascular system while most pass through the jejunum to enter the yolk sac and foster embryonic nutrition. Mineralization of the skeleton, pipping muscle enlargement, multiple fortifications of glycogen, and deposition of subcutaneous fat subsequently occur as liver cholesterol becomes exaggerated. Minimal oxygen during transition from chorio-allantois to pulmonary respiration necessitates umbilical closure together with the heart’s intra-auricle septum as inner to outer shell pipping proceeds. Abdominal pressures during yolk sac retraction force a portion of yolk contents back into the jejunum while bile and pancreatic enzymes initiate its digestion to enhance early mucosal maturation. Concurrently, glycogen is sourced for energy in support of emergence. A narrow hatch window exists for the clutch because of egg uniformity while intermittent pre-incubation heating enabled similar germ development. Hen confinement of emergents to the nest provides insulation and heat sharing to extend body reserves through completion of hatch. Confinement also exposes hatchlings to a mature microbial population from hen excreta that colonize the gastrointestinal tract (GIT). Microbe composition in concert with the hen’s environment advantages digestion of hatchling feedstuffs outside the nest while concurrent mucosal failures generate permanent immunoglobins to commensals as passive ones dissipate. Inherent delays to feed with commercial chicks and absence of a favorable microflora impair early intestinal maturation prior to initial feed access. A pre-starting feed providing high protein that assures amino acids favoring mucin is thought to resist lumen microbes while aiding recovery of delayed development. Concurrent dietary enzyme supplementation and a source of nucleic acids are believed to partially substitute for digestive and nutritional complementation expected from commensals.

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