Mineral Deficiencies in Poultry
Calcium and Phosphorus Imbalances
Rickets occurs most commonly in young meat birds; the main characteristic is inadequate bone mineralization. Calcium deficiency at the cellular level is the main cause, although feeding a diet deficient or imbalanced in calcium, phosphorus, or vitamin D3 can also induce this problem. Young broilers and turkey poults can exhibit lameness at ~10–14 days of age. Their bones are rubbery, and the rib cage is flattened and beaded at the attachment of the vertebrae. Rachitic birds exhibit a disorganized cartilage matrix, with an irregular vascular penetration. There is an indication of impaired metabolism of collagen precursors such as hyaluronic acid and desmosine. Rickets is not caused by a failure in the initiation of bone mineralization but rather by impairment of the early maturation of this process. There is often an enlargement of the ends of the long bones, with a widening of the epiphyseal plate. A determination of whether rickets is due to deficiencies of calcium, phosphorus, or vitamin D3, or to an excess of calcium (which induces a phosphorus deficiency) may require analysis of blood phosphorus levels and investigation of parathyroid activity.
In most field cases of rickets, a deficiency of vitamin D3 is suspected. This can be due to simple dietary deficiency, inadequate potency of the D3 supplement, or other factors that reduce the absorption of vitamin D3. Rickets can best be prevented by providing adequate levels and potency of vitamin D3supplements, and by ensuring that the diet is formulated to ensure optimal utilization of all fat-soluble compounds. Young birds have limited ability to digest saturated fats, and these undigested compounds can complex with calcium to form insoluble soaps, leading to an induced deficiency of calcium. Again, this situation cannot be diagnosed through diet assay for calcium but rather through excreta assay of this mineral. Diets must also provide a correct balance of calcium to available phosphorus. For this reason, ingredients notoriously variable in their content of these minerals, such as animal proteins, should be used with extra caution. In recent years, the use of 25(OH)D3 has become very popular as a partial replacement for vitamin D3, with reports of greatly reduced incidence of rickets, especially in poults. This metabolite is similar to that naturally produced in the liver of birds in the first step of conversion of vitamin D3 to 1,25(OH)2D3, the active form of the vitamin. The commercial form of 25(OH)D3 is therefore especially useful if normal liver metabolism is compromised in any way, such as occurs with mycotoxins or other “natural” toxins in the feed that potentially impair liver metabolism.
Tibial Dyschondroplasia (Osteochondrosis):
Tibial dyschondroplasia is characterized by an abnormal cartilage mass in the proximal head of the tibiotarsus. It has been seen in all fast-growing types of meat birds but is most common in broiler chickens. Regardless of diet or environmental conditions, fast versus slow growth rate seems to at least double the incidence of tibial dyschondroplasia. Signs can occur early but more usually are not initially seen until 14–25 days of age. Birds are reluctant to move, and when forced to walk, do so with a swaying motion or stiff gait. Tibial dyschondroplasia results from disruption of the normal metaphyseal blood supply in the proximal tibiotarsal growth plate, where the disruption in nutrient supply means the normal process of ossification does not occur. The abnormal cartilage is composed of severely degenerated cells, with cytoplasm and nuclei appearing shrunken. Affected cartilage contains less protein and less DNA.
The exact cause of tibial dyschondroplasia is unknown. Incidence can quickly be altered through genetic selection and is likely affected by a major sex-linked recessive gene. Imbalance of dietary electrolyte, and particularly high levels of chloride relative to other dietary cations, seem to be a major contributor in many field outbreaks. More tibial dyschondroplasia is also seen when the level of dietary calcium is low relative to that of available phosphorus, or more commonly when diet phosphorus is high relative to calcium. Treatment involves dietary adjustment of the calcium:phosphorus ratio and by achieving a dietary electrolyte balance of ~250 mEq/kg. Dietary changes rarely result in complete recovery. Tibial dyschondroplasia can be prevented by tempering growth rate; however, programs of light or feed restriction must be considered in relation to economic consequences of reduced growth rate. There is evidence that replacement of some of the dietary vitamin D3 with metabolites such as 1,25(OH)D3 improves chondrocyte differentiation and hence limits occurrence of this skeletal disorder.