Phosphorus Deficiency: Causes, Symptoms, and Management

PHOSPHORUS DEFICIENCY By Dr. Hussein AlNaji

ETIOLOGY 2 1- Phosphorus (P) deficiency occurs predominantly in arid regions of the world with low P content in soil. 2- Phosphorus deficiency is encountered whenever the daily dietary P intake is insufficient to cover the requirements for maintenance and production and the organism has to recur to the mobilization of bone P. 3- In dairy cattle, a rather acute and transient period of P deficiency is thought to occur in the first days to weeks of lactation and has been associated with recumbency and acute intravascular hemolysis in early lactating cows.

4- Rations with marginal P content in combination with low feed intake around calving are 3 thought to result in inadequate P intake to cover for the suddenly increasing P requirements for milk production at the onset of lactation. 5- The assumption that the commonly observed periparturient hypophosphatemia is an indicator for P depletion. 6- Pronounced hypophosphatemia is also seen around parturition in mastectomized cattle, which don t produce any milk. 7- Secondary Phosphorus Deficiency Secondary P deficiency is the result of hyperparathyroidism or vitamin D deficiency. This is of minor importance compared with the primary P deficiency.

PATHOGENESIS 1- Of the body P, 80% to 85% is located in the skeleton, where it is deposited in a metabolically inert form together with calcium as hydroxyapatite. 2- Hydroxyapatite is the compound that provides bone with its characteristic structural rigidity and stability. 3- Bone P also functions as an important P reservoir that can be mobilized when body requirements temporarily exceed dietary intake. The remainder of the body P is available as dissolved P that is either encountered as inorganic phosphate (Pi) or forming part of organic molecules such as phospholipids, phosphocreatine, different adenosine molecules, or various carbohydrate metabolites.

4- Phosphorus is a predominantly intracellular mineral, of which only small amounts are located in the extracellular space. 5- Phosphorus bound in phospholipid molecules is essential for the structural stability of cell membranes that are composed of these phospholipids. 6- Phosphorus furthermore functions as a buffer in rumen fluid, urine, and the intracellular space. Rumen microbes that are of critical importance for ruminant nutrition are inherently dependent of adequate P supply, which is not only provided by feed but also by the salivary glands, which produce large amounts of saliva rich in P.

7- Inadequate dietary P supply will result in the mobilization of hydroxyapatite, from which will release P together with calcium. Prolonged P deficiency is therefore associated with abnormal development of bone tissue, known as osteodystrophy. 8- The mechanism is a deficiency of Pi that may result in decreased concentration of phosphorylated molecules such as phosphocreatine and adenosine triphosphate (ATP) that are essential for energy storage on a cellular level lead to a- It has been proposed that it is through a depletion of these energy-storing molecules that P deficiency may result in muscle weakness and recumbency in periparturient cattle. b- A decline of the intracellular ATP con centration, this time of red blood cells, is the presumed mechanism behind intravas cular hemolysis observed in fresh cows with postparturient hemoglobinuria. Red blood cells (RBCs) require ATP to maintain their osmotic stability

CLINICAL FINDINGS 1. A plethora of clinical signs and conditions, such as unthriftiness, anorexia. 2. Pica, impaired growth and fertility. 3. Muscle weak ness, lameness, recumbency. 4. Intravascular hemolysis. postparturient hemoglobinuria. 5. Osteomalacia, and many more, have been associated with P deficiency in ruminants and other species 6. The animals have a leggy appearance with a narrow chest and small girth, the pelvis is small, and the bones are fine and break easily. 7. The chest is slab-sided as a result of weakness of the ribs, and the hair coat is rough and lacking in pigment.

Clinical pathology : 1- Serum inorganic phosphorus. 2- Phosphorus content of diet. Necropsy findings : 1-Rickets and osteomalacia; 2- lack of mineralization of bones. Diagnostic confirmation 1- Radiography of long bones. 2- Histology of bone lesions. 3- Bone ash analyses. Differential diagnosis 1- Those diseases resembling rickets and osteomalacia. 2- Milk fever and downer cow syndrome in periparturient recumbent cattle. 3- Other disorders associated with intravascular hemolysis in cases of periparturient hemoglobinuria.

Treatment Cattle: 1. Monosodium dihydrogen phosphate (36 g NaH2PO4 dihydrate in 300 mL distilled water IV as single dose) (R-2). 2. Disodium monohydrogen phosphate (90 g Na2HPO4 12 H20 in 500 distilled water IV as single dose) (R-2). 3. Monosodium dihydrogen phosphate (300 g NaH2PO4 PO q12h for 1 to 3 days) (R- 1) 4. Monopotassium dihydrogen phosphate (250 gKH2PO4 PO q12h for 1 to 3 days) (R2) 5. Monocalcium dihydrogen phosphate (250 g Ca [HPO4]2 PO q12h for 1 to 3 days) (R-2)

6- Dicalcium monohydrogen phosphate (300 g CaHPO4 2H20 PO q12h for 1 to 3 days) (R-3) 7- Monosodium dihydrogen phosphate IM or SC (R-3) 8- Disodium monohydrogen phosphate IM or SC (R-3) 9- Butafosfan (butylamino-methylethyl phosphoric acid) (R-3). 10- Toldimfos (dimethylamino-methylphenyl phosphinate) (R-3) Control Bone meal, calcium-phosphate salts, sodium-phosphate salts, and sodium pyrophosphate may be provided in supplementary feed or by allowing free access to their mixtures with salt. Fertilization of P-deficient pastures with phosphate

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