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Hypocalcemia, Sudden Death, Osteoporosis, or Cage Layer Fatigue (in Poultry)

By

Rodrigo A. Espinosa

, DVM, MAM, DACPV, Aviagen, Inc

Last full review/revision Aug 2019 | Content last modified Sep 2019
Topic Resources

Pullets or hens with insufficient dietary calcium, phosphorus, or vitamin D3 may die suddenly or be found paralyzed from hypocalcemia while shelling an egg. This may be associated with high production and withdrawal of calcium from bones for egg shell production, in which case the main lesion may be osteoporosis. At necropsy, there is an egg in the shell gland and the ova are active and fully developed. There are no other lesions, although medullary bone may be lacking. Paralyzed hens respond to calcium IV, and this response may be useful in diagnosis.

Osteoporosis is a major cause of death in high-production flocks. Hens with osteoporosis may show similar signs at necropsy, or the ova may be regressing with no egg in the oviduct. The femur is always fragile, and medullary bone is always absent in osteoporosis. These hens may also respond to calcium IV if there are no fractures of the legs or vertebrae. The use of large particle size calcium (limestone, oyster shell) in the diet may be beneficial. High rates of mortality due to fractures are common in birds affected with osteoporosis. This situation is more common in broiler breeder hens in slatted houses due to the trauma caused by jumping on and off the slats. Ruptured egg follicles indicating trauma can be found during necropsy examination of these birds.

A condition known as hypocalcemia, or calcium tetany (paralysis), has been seen in modern or high-yielding broiler breeder hens. This syndrome is characterized by an acute and sudden onset, usually in flocks with good hen/day production. Signs such as panting, spread wings, and prostration may be seen in the early morning hours preceding paralysis and death by asphyxia. Hens may be down in the scratch, unable to rise. They become paralyzed and are the object of male aggression (often misdiagnosed as male kills).

Careful postmortem examination reveals a fully active ovary (8–9 large, yellow follicles), the presence of a partially or fully formed egg in the shell gland, and signs of asphyxia such as a cyanotic comb, congested lungs, and dark musculature. This indicates that the hen used all available calcium from the bloodstream in an effort to complete the egg shell. The condition is common in flocks with poor body weight uniformity that are fed high-calcium diets (Ca levels >1.2%) in the weeks before the onset of lay and brought into production by drastic increases in day length and feed allocation. Less common causes of hypocalcemia are low calcium levels in breeder feed, too-small limestone particle size, and exaggerated separation of heavy minerals in mash feed. This condition seems to be more common during the hot weather months, and it can be exacerbated by inadequate cooling and ventilation.

Hypocalcemia can be prevented by management practices that promote body weight uniformity and avoid excessive/premature allocation of high-calcium diets and light stimulation. Mortality can be reduced by the administration (“topping of the feed”) of 5 g of oyster shell per hen for 3 consecutive days, and addition of vitamin D3 to the drinking water. This treatment should be suspended for 3 days and then repeated. Severe cases will require continual treatment for 2–3 weeks (3 days of treatment followed by 3 days without). Overtreatment can be harmful. Feeding of recommended levels of calcium, using large-particle-size calcium, and providing adequate ventilation and cooling are helpful to prevent or reduce the incidence of this condition.

Mortality and the presence of an egg in the shell gland also can be caused by a condition referred to as sudden death syndrome, first reported in Australia. Sudden death syndrome has been associated with refeeding syndrome, named for prisoners of war who developed heart and nervous problems when they were re-fed after starvation. Immature and undersized pullets that have been fed too much too fast could develop sudden death if the feeding program provides higher nutrients than their requirements. Typically, birds will present with bulked pectoral muscles, juvenile ovarian development, generalized internal congestion, hydropericardium, enlargement of the left side of the heart, and a dilated right side. Often, this syndrome is confused with calcium tetany. Some trigger factors are feed rations low in phosphorus, potassium, protein, and energy levels while rich in calcium levels, resulting in cardiomyopathy.

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