Unlock Optimal Growth and Health with a High Phosphorus Diet for Turkeys!

Phosphorus is a vital mineral for turkeys, playing a crucial role in bone development, overall health, and various metabolic functions. However, maintaining the right balance of phosphorus in a turkey's diet is essential. Both deficiency and excess can lead to health problems. This article explores the complexities of high-phosphorus diets for turkeys, examining their impact on growth, bone health, and potential risks.

Understanding Phosphorus in Turkey Nutrition

Phosphorus, alongside calcium, is a key component of bone tissue. It also participates in energy metabolism and various enzymatic processes. In poultry diets, phosphorus is often present in two forms: organic phosphorus, found naturally in feed ingredients like grains and protein sources, and inorganic phosphorus, added as a supplement to ensure adequate levels.

Cereal grains contain phytate-bound phosphorus, which is digestible by ruminant animals but not by single-stomached animals like pigs and chickens. Since phytate-bound phosphorous is unavailable to them, phosphorus from other sources is supplemented to meet their needs.

Calcium and Phosphorus Requirements

The calcium and total phosphorus requirements for optimum growth were estimated to be 12.5 and 10.0 g/kg diet respectively. Bone ash was adequate at these levels of Ca and total P, but maximum bone ash was not achieved until much higher levels of Ca and total P were employed. At the required levels of Ca and total P for growth the incidences of Ca- and P-deficiency rickets were very low.

Experimentation with Phosphorus and Calcium Levels

Researchers have conducted experiments to determine the optimal levels of calcium (Ca) and phosphorus (P) in turkey diets.

Read also: High-Fiber Diet for Better Health

Experiment 1

The first experiment was a central composite rotatable design with calculated calcium levels of 6.2, 7.0, 9.0, 11.0, and 11.8 g/kg diet and total phosphorus levels of 5.2, 6.0, 8.0, 10.0, and 10.8 g/kg diet (2.8 g phytin-P/kg by analysis). This design involved three replicates for each rotatable point and fifteen replicates of the central point.

Experiment 2

The second experiment was a 4 × 4 factorial design with calculated Ca levels of 8.0, 10.0, 12.0, and 14.0 g/kg diet and calculated total P levels of 7.0, 9.0, 11.0, and 13.0 g/kg diet (2.5 g phytin-P/kg by analysis). There were four replicates for each treatment.

In both 16 d experiments maize-soya-bean diets were used and each replicate consisted of one pen containing 10-d-old broad-breasted, white tom turkeys.

Key Findings

Bone Ash: Adequate bone ash was observed at the estimated requirements of calcium and total phosphorus for growth (12.5 and 10.0 g/kg diet, respectively). However, maximum bone ash was achieved only at much higher levels of both minerals.
Rickets: The incidence of calcium and phosphorus deficiency rickets was very low when calcium and phosphorus levels met the requirements for growth. There were no treatment effects on feed efficiency.
Calcium Deficiency: Increasing dietary calcium decreased the incidence of calcium-deficiency lesions.
Phosphorus Deficiency: There was a quadratic response due to dietary total phosphorus on both phosphorus-deficiency rickets and plasma dialyzable P. Intermediate levels of dietary phosphorus resulted in a low incidence of phosphorus-deficiency lesions and high levels of plasma dialyzable P. A strong negative correlation was found between the incidence of phosphorus-deficiency rickets and plasma dialyzable P.
Phosphorus Retention: Percentage retention was very low at high levels of dietary P and low levels of Ca which corresponded with slightly higher P-deficiency rickets and low plasma dialysable P. No such obvious relationships existed between Ca retention, incidence of Ca-deficiency rickets, and plasma Ca.
Tibial Dyschondroplasia: The incidence of tibial dyschondroplasia was very low in the present study.
Phytin-P Retention: There were pronounced dietary treatment effects on phytin-P retention; at 14 d percentage phytin-P retention treatment means ranged from 18 to 46 in Experiment 1 and from 0 to 40 in Experiment 2 with the highest retention of phytin-P at low levels at both Ca and total P.

Potential Problems with High Phosphorus Levels

While phosphorus is essential, excessive levels can lead to several problems:

Phosphorus-Induced Rickets

An excess of calcium (which induces a phosphorus deficiency) may require analysis of blood phosphorus levels and investigation of parathyroid activity.

Mineral Imbalances

Overfeeding calcium can limit the availability of phosphorus.

Environmental Concerns

Phosphorus is required in the diet of animals, but if overfed or wasted, can contaminate the environment and water supplies.

Strategies for Optimizing Phosphorus Utilization

Several strategies can be employed to improve phosphorus utilization in turkey diets and minimize the risk of deficiencies or excesses:

Phytase Supplementation

An enzyme called phytase can be included with the diet. Phytase will break down phytate and release digestible phosphorus. In addition, trace minerals bound by phytic acid also are released and made available.

Careful Diet Formulation

Ingredients notoriously variable in their content of these minerals, such as animal proteins, should be used with extra caution. Diets must also provide a correct balance of calcium to available phosphorus.

Monitoring and Adjustment

Regularly monitor the flock's health and adjust the diet as needed based on growth, bone development, and overall well-being.

Other Nutritional Considerations in Turkey Diets

Calcium and Phosphorus Imbalances

A deficiency of either calcium or phosphorus in the diet of young growing birds results in abnormal bone development, even when the diet contains adequate vitamin D3. A deficiency of either calcium or phosphorus results in lack of normal skeletal calcification. Rickets is seen mainly in growing birds, whereas calcium deficiency in laying hens results in reduced shell quality and subsequently osteoporosis. This depletion of bone structure causes a disorder commonly referred to as cage layer fatigue since it was first seen with the introduction of cage housing systems some 60 years ago. The condition is rarely seen in noncage systems, although this situation is confounded with lower egg production. Over time, excessive mobilization of bone calcium to overcome a dietary deficiency causes structural bone to erode, and it is then unable to support the weight of the hen.

Rickets

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 ribs become 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.

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.

Cage Layer Fatigue

High-producing laying hens maintained in cages sometimes show paralysis during and just after the period of peak egg production due to a fracture of the vertebrae that subsequently affects the spinal cord. The fracture is caused by an impaired calcium flux related to the high output of calcium in the eggshell. Layers are capable of early egg production exceeding 95% for at least 6 months, which places even more pressure on maintenance of adequate calcium flux between the diet, the skeleton, and the oviduct. As the hen ages, medullary bone is replaced on a daily basis as the demands for calcium diminish greatly immediately after oviposition and before the start of shell calcification of the next egg. However, structural (cortical and trabecular) bone is not replaced while the hen is in production. Over time, the medullary bone, which initially forms a protective layer over the structural bone, becomes more diffuse in the medullary cavity. This exposes more structural bone surface area to the activity of osteoclasts, and over time, osteoporosis can develop.

Manganese Deficiency

A dietary manganese deficiency in immature chickens and turkeys is one of the potential causes of perosis and chondrodystrophy and also the production of thin-shelled eggs and poor hatchability in mature birds (also see Calcium and Phosphorus Imbalances). The most dramatic classic effect of manganese deficiency syndrome is perosis, characterized by enlargement and malformation of the tibiometatarsal joint, twisting and bending of the distal end of the tibia and the proximal end of the tarsometatarsus, thickening and shortening of the leg bones, and if severe, slippage of the gastrocnemius tendon from its condyles. Increased intakes of calcium and/or phosphorus will aggravate the condition because of reduced absorption of manganese via the action of precipitated calcium phosphate in the intestinal tract.

Iron and Copper Deficiencies

A deficiency of either iron or copper in poultry can lead to anemia. Iron deficiency causes a severe anemia, with a reduction in PCV. In color-feathered strains, there is also loss of pigmentation in the feathers. The birds’ requirements for synthesis of red blood cells takes precedence over metabolism of feather pigments, although if a fortified diet is introduced, all subsequent feather growth is normal and lines of demarcation on the feathers are part of diagnosis. Copper deficiency in birds, and especially in turkeys, can lead to rupture of the aorta.

Iodine Deficiency

Iodine deficiency results in a decreased output of thyroxine from the thyroid gland, which in turn stimulates the anterior pituitary to produce and release increased amounts of thyroid stimulating hormone (TSH). This increased production of TSH results in subsequent enlargement of the thyroid gland, usually termed goiter.

Magnesium Deficiency

Natural feed ingredients are rich in magnesium; thus, deficiency is rare and magnesium is never specifically used as a supplement to poultry diets.

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