This spike in mortality is associated with hypophospha-temia (Frank Edens, 1996, personal communication, North
Carolina State University, Raleigh, NC). While the birds are off feed, their phosphate reserves deplete, but when they
begin to consume feed again, the high demand to phosphorylate the influx of glucose for ATP production in the liver
and muscle tissue, drains blood phosphate reserves to fatally low levels. This response is especially evident during
stressful conditions, which require a cascade of ATP phosphorylation. In addition, it is common for animals to develop
respiratory alkalosis and metabolic acidosis during periods of starvation, and this will also cause a shifting of
phosphorus into cells (Mostellar et al., 1964). This phenomenon is thought to be created by the phosphate trap
resulting from glucose-6-phosphatase deficiency leading to type I glycogen storage disorder. Therefore, it is important
that a grower take every measure possible to keep the afflicted poults eating to maintain blood phosphorus and other
critical nutrients. In realimentation after starvation, hypophosphatemia can be induced by inadequate dietary
phosphorus. Therefore, top dressing the feed with a highly available source of phosphate or supplementation of
drinking water with a soluble source of phosphorus when the poults show the first signs of feed refusal may help
prevent the birds from becoming hypophosphatemic and dying upon realimentation.