Phosphorus is the second most abundant mineral in the animal body and about 80% is found in the bones and teeth. As with calcium, the formation and maintenance of bone are quantitatively the most important function, and the changes in bone structure and composition that result from phosphorus deprivation are in most respects the same as those described for calcium deprivation in Chapter 4. Phosphorus, however, is required for the formation of the organic bone matrix as well as the mineralization of that matrix. The 20% of phosphorus not present in the skeletal tissues is widely distributed in the fluids and soft tissues of the body, where it serves a range of essential functions. Phosphorus is a component of deoxy- and ribonucleic acids, which are essential in cell growth and differentiation; as phospholipid, it contributes to cell-membrane fluidity and integrity; as phosphate, it helps to maintain osmotic and acid–base balance; and it plays a vital role in a host of metabolic functions, including energy utilization and transfer via AMP, ADP and ATP, with implications for glucogenesis, fatty acid transport, amino acid and protein synthesis and the activity of the sodium/potassium (Na+/K+) pump.
Disturbances of glycolytic metabolism have been noted in the erythrocytes from phosphorus-deficient cattle (Wang et al., 1985). In ruminants, the requirements of the rumen and caecocolonic microflora are also important, and microbial protein synthesis may be impaired on low-phosphorus diets (Petri et al., 1989; Ternouth and Sevilla, 1990b). Phosphorus is further involved in the control of appetite, in a manner not yet fully understood, and in the efficiency of feed utilization (Ternouth, 1990). Phosphorus is arguably the most potent of all the mineral elements.
The clinical sequelae of phosphorus deprivation are accompanied or preceded by biochemical changes in the blood and tissues.
The chemical changes in the bones that precede or accompany the structural changes associated with phosphorus dysfunction are apparent from two early experiments with pigs and sheep. Growing pigs fed for 6 weeks on a synthetic milk diet containing 2.0 g P kg21 had bones which were less well mineralized than those of comparable animals receiving phosphorus- supplemented diets (Table 5.1). In a longer experiment (14–18 months) with growing sheep fed on a moderately phosphorus-deficient diet, the ash concentration of the ribs and vertebrae was some 20% lower and that of the long bones over 8% lower than that of similar bones from sheep supple- mented with phosphate (Stewart, 1934/35). Reductions occur in both the ash and organic-matter content of the bone in phosphorus-deprived pigs (Koch and Mahan, 1985) and lambs (Field et al., 1975), so that ash percentage
underestimates the degree of deprivation. Long bones tend to be depleted more rapidly than metacarpals or metatarsals. In young calves depleted of phosphorus, the ends of the long bones showed greater reductions than the shaft, while the rib showed no change after short-term (6 week) depletion (Fig. 5.4). However, phosphorus (or calcium) is removed more extensively from the rib than from axial and limb bones after prolonged depletion (Little, 1984), a fact confirmed histologically (Field et al., 1975). Careful histological comparisons of the rachitic long bones from phosphorus- and calcium- deprived chicks showed that the former could be distinguished by elongated metaphyseal vessels within the physis and by hypertrophic chondrocytes (Lacey and Huffer, 1982). Histologically diagnosed, hypophosphataemic rickets in broilers was associated with low bone ash (49.6 vs. 55.6%), low calcium + phosphorus content of ash (40.5 vs. 50.2%) and a low P : Ca ratio in the long bones (Thorp and Waddington, 1997). Histological abnormalities of the growth plate were the most sensitive index of phosphorus status in turkey poults (Fig. 1.3; Qian et al., 1996). Demineralization is also accom- panied by changes in physical properties indicating the strength of bone, and shear strength is now regarded as one of the more dependable and sensitive tests in the pig (Combs et al., 1991c).
Early responses to a diet low in phosphorus are a fall in serum or plasma Pi (Fig. 5.5), a rise in serum alkaline phosphatase (Table 5.1) and a small rise in serum calcium (see Fig. 4.5). After a few weeks or months, serum values fall to 1.0 mmol Pi l21 or below but by then the first clinical sign, severe loss of appetite, may have appeared. The onset and severity of hypophosphataemia is not simply a reflection of dietary phosphorus supply. In young lambs given Table 5.1. Effects of dietary phosphorus concentrations on selected performance, skeletal and blood indices of phosphorus status in the baby pig given a synthetic milk diet from 0 to 6 weeks of age (Trial 1; Miller et al., 1964).
Dietary P (g kg21DM)
Criterion 2 4 6
Live-weight gain (g day21) 130 290 290 Performance
Dry-matter intake (g) 240 380 370
Feed/gain (g g21) 1.85 1.31 1.28
Serum inorganic P (mmol l21) 1.03 2.71 3.03 Blood
Serum Ca (mmol l21) 3.20 3.05 2.58
Serum alkaline phosphatase (BL units) 20.5 8.3 4.5
Humerus ash (%) 33.4 44.1 47.5 Bone
Femur s.g. 1.11 1.15 1.17
Eighth rib weight (g) 3.30 4.49 4.67
Femur breaking load (kg) 24 61 81
s.g., specific gravity.
Changes in the blood
Fig. 5.4. Effects of sample site on the degree of bone demineralization recorded after short-term phosphorus depletion in calves (Miller et al., 1987).
Fig. 5.5. Effects of diets low in phosphorus and/or calcium on plasma inorganic phosphorus (Pi) in lambs: note that feeding a diet low in both minerals (∆) delays the fall in Picompared with a diet low only in phosphorus (n), while feeding one low in calcium but adequate in phosphorus (l) raises Piwhen compared with a diet adequate in both minerals (X) (from Field et al., 1975).
diets equally low in phosphorus (1.2 g P kg21DM), the decline in plasma Pi occurred 5 weeks later, when the diet was also low in calcium (0.66 vs. 4.3 g Ca kg21 DM) (Fig. 5.5; Field et al., 1975). Supplementary calcium does not invariably decrease phosphorus absorption from such diets (Field et al., 1983, 1985), and the lowering of serum Pi may be partly due to an increase in phosphorus retention by the skeleton, a common response to calcium supplementation (Braithwaite, 1984a; Field et al., 1985; Rajaratne et al., 1994).
Such dietary interactions do not invalidate the use of serum Pifor diagnostic purposes.
Like levels in blood, rumen phosphorus concentrations are also influenced by factors other than dietary phosphorus intake. With a diet marginal in phosphorus (1.9 g P kg21 DM), rumen Pi levels in lambs were 66% lower when the diet contained 6.8 rather than 3.5 g Ca kg21 DM and accompanied by a major reduction in plasma Pi, from over 2.0 to around 1.3 mmol l21 (Wan Zahari et al., 1990). Rumen phosphorus had fallen towards levels asso- ciated with impaired rumen microbial activity (3 mmol l21) and were linked to a 20% reduction in growth rate on the high-calcium diet. Reductions in rumen microbial activity are usually accompanied by reductions in food intake.
Phosphorus concentrations in saliva can reflect the concentrations in plasma in some circumstances (Challa et al., 1989), but they are unreliable indices of dietary phosphorus supply. Levels in saliva are about three to eight times those in plasma, but they are influenced by both salivary flow rate and phosphorus intake. At low flow rates, salivary phosphorus concentrations are much the same in both replete and phosphorus-deficient sheep, but, at high flow rates, concentrations are much lower in the phosphorus-deficient animal (Wright et al., 1984). This variability makes spot saliva samples unreliable as an indicator of phosphorus status.
The majority of sheep and cattle fed roughage diets excrete very little phosphorus in their urine, even at plasma Pi levels that are well above 1 mmol l21, and this situation continues despite an increase in phosphorus intake sufficient to increase plasma Pilevels to over 2 mmol l21. If they are switched to diets that promote low salivary flow (e.g. pelleted concentrates), a similar increase in phosphorus intake is matched by a proportional increase in urinary phosphorus excretion. This seems to involve a change in renal reabsorptive efficiency (proportion of filtered phosphorus which is reabsorbed), rather than a change in renal threshold. Similar renal adaptation to physiological demand (pregnancy, lactation or low phosphorus intake) has been reported in other species and is not under any known hormonal control. A low urinary phosphorus level is therefore not a good indicator of Changes in rumen phosphorus
Changes in saliva
Changes in urine
phosphorus status in the grazing situation, where deficiencies are mostly likely to arise.
Although faecal phosphorus levels reflect endogenous loss as well as intake of phosphorus, they are being used to monitor the response of grazing cattle to phosphorus supplementation on pastures deficient in both nitrogen and phosphorus (Holechek et al., 1985; Grant et al., 1996; Karn, 1997). Faecal phosphorus levels below 2 g kg21 faecal DM, together with plasma Pi levels less than 1 mmol l21, indicate low phosphorus status.
A dietary deficiency of phosphorus, if sufficiently severe or prolonged, leads to abnormalities of the bones and teeth, subnormal growth, milk yield and egg production, depressed appetite, poor efficiency of feed use and the development of pica or depraved appetite; fertility may be impaired.
The abnormalities associated with phosphorus deprivation are almost identical to those described in Chapter 4 for calcium deficiency, since bone and tooth mineral cannot be produced if either mineral is lacking. This was illustrated by parallel studies of phosphorus and calcium requirements in baby pigs (Miller et al., 1964; Tables 5.1 and 4.2), which revealed similar rachitic lesions whichever element was lacking.
Loss of appetite and subnormal growth in young animals and weight loss in mature animals are characteristic of phosphorus deprivation in all species and are illustrated by data for yearling cattle in Table 5.2 (Little, 1968) and for young pigs in Table 5.1. In newly weaned pigs deprived of phosphorus, growth can be retarded before appetite is impaired (Fig. 5.2; Reinhart and Mahan, 1986), but the primary effect in ruminants is on food intake. The anorexia may be immediate (Fig. 4.5; Field et al., 1975) but usually takes several weeks or months to develop in lambs (Wan Zahari et al., 1990), beef cattle (Call et al., 1978, 1986; Gartner et al., 1982) and dairy cows (Call et al., 1986), depending perhaps on the adequacy of phosphorus supply for rumen microbes. Early reductions in appetite have been confined to situations in which semipurified diets very low in phosphorus have been fed (Field et al., 1975; Miller et al., 1987; Ternouth and Sevilla, 1990a); these diets stimulate little or no rumination, depriving the rumen microflora of salivary as well as dietary phosphorus. It is noteworthy that a more severe anorexia eventually develops in such circumstances (Fig. 4.5). Dry-matter intake can be closely related to serum Pi and governed by systemic as well as gut-based mechanisms (Ternouth and Sevilla, 1990a, b). In beef cattle, improvements in
Changes in faeces