Phosphorus deficiency in cattle may cause symptoms related to reduced appetite, including retarded growth rate of young cattle, low milk yield and impaired fertility. Skeletal abnormalities associated with osteomalacia may appear as stiffness, reluctance to move, shifting lameness, cracking sounds in joints when walking, an arched back and in severe cases, spontaneous fractures. Recently calved cows may become recumbent and display post parturient haemoglobinuria. Pica is commonly observed (though not specific to phosphorous deficiency), with animals craving bones, sticks, rocks and polyethylene pipe. Botulism may be encountered in phosphorus-deficient cattle from chewing bones.
RATIONALE FOR A SURVEY OF PHOSPHOROUS LEVELS IN GRAZING CATTLE
Assuming suckling calf growth rate is indicative of milk production, all of the symptoms of phosphorous deficiency listed above, with the exception of botulism, have been observed in a 450-cow beef breeding enterprise 40km south of Goulburn. The cattle had been grazing introduced and native pastures that had not been fertilised for two decades. Low serum Pi (inorganic phosphorus) levels, and dramatic response to supplementation (Property 12 in Table 1) confirmed phosphorus deficiency.
Phosphorus deficiency was diagnosed as the cause of lameness and poor growth rates in two further herds eleven and fifteen km south of Goulburn. No phosphorus fertiliser had been applied to the former property for at least 15 years, while the latter property (Property 13 in Table 1) received sporadic phosphate applications during the past decade.
Soils of much of the southern and central tablelands of NSW are naturally deficient in phosphorus. (Anon 2001). Plant-available soil phosphorus improves plant growth and vigour, especially of pasture legumes. Application of phosphate fertiliser together with distribution of subterranean clover seed (widely referred to as 'sub-and-super') was recommended to 'improve' native pastures in the district from the 1920's (Webster 1998).
Regular application of phosphate fertiliser on tablelands pastures is promoted to graziers to improve or maintain stocking rates and profitability (Mokany 2009). Despite this advice, fertiliser application to pasture has declined sharply over the past decade. The 250,000 tonnes of phosphate fertiliser applied to agricultural land in Australia in 2010 was half the level of 1998 (source: Fertilizer Industry Association of Australia). Fertiliser merchants and spreading contractors in the study area believe the percentage reduction in phosphate fertiliser applied to grazing land in the same period to be even greater.
Some graziers have reduced their use of fertiliser by more strategic application to the most productive paddocks, but a larger number of graziers have ceased to apply phosphate fertiliser (John Ryan, Director of Highland Fertilisers, pers com).
Our pilot survey sought to determine the phosphorus status of cattle on properties that were no longer applying phosphate fertiliser.
SIMPLIFIED PHOSPHORUS CYCLE
Application of phosphorus to soils not only increases plant growth and persistence, but leads to increased uptake of phosphorus by plants. This increased plant phosphorus becomes available to grazing animals.
Rumen microbes help make plant phosphorus available, aided by phosphorus secreted in saliva. Phosphorus is absorbed mainly from the small intestine. Efficiency of absorption is affected by age (reduced by about half in the first year of life), dry matter and phosphorus intake (reduced as DMI and P intake are increased) and calcium/phosphorus ratio in the ration (reduced by very high Ca:P). The source of phosphorus (type of forage or supplement), presence of intestinal worms, genetics and physiological state (increased in lactation) also affect absorption efficiency (NRC 1984, Poppi et al 1985). Excess phosphorus is excreted mainly in faeces.
Phosphorus has a number of important roles. Most is found in bone. Phosphorus is found also in red blood cells (up to eight times the plasma P concentration), brain, muscle, liver, spleen and kidneys. As a component of phospholipids, phosphorus is involved in cell membrane permeability and myelin sheaths. It is also involved in cellular energy transfer, blood-buffering mechanisms, phosphorylation of several B-vitamins, and is a part of RNA and DNA.
ESTIMATING PHOSPHORUS STATUS OF CATTLE
Analyses of blood, faeces and bone have been used to determine phosphorus status in animals. There is some correlation between plasma inorganic phosphorus and phosphorus intake (Cohen 1974). However, although it reflects low to normal dietary phosphorus, there is less correlation when phosphorus intakes is high (Ternouth 1990).
Plasma inorganic phosphorus was regarded as a reliable indicator of phosphorus status in 90-100% of cases in northern Australia, if sampled at the appropriate time. Sampling cattle at the end of the growing period proved most useful (Wadsworth et al 1990).
Plasma inorganic phosphorus generally parallels serum inorganic phosphorus, although the values are slightly lower than for serum (Williams et al, 1991). Blood phosphorus is significantly higher than serum inorganic phosphorus, reflecting the concentration of phosphorus within erythrocytes.
Faecal phosphorus provides a measure of recent dietary intake. Several factors affect faecal phosphorus concentration in single point samples, including recent grazing pattern (Ternouth 1990). Blood inorganic phosphorus is a better predictor of response to supplementation than faecal phosphorus (Coates 1994).
Cortical thickness of the twelfth rib varies with phosphorus intake, but poorly reflects a likely response to phosphorus supplementation (Coates 1994).
Blood samples were collected from up to ten lactating first calf heifers on selected farms on the central and southern tablelands. Sample collection was timed for the late spring pasture growth period and to correspond with high animal phosphorus requirements for lactation and growth.
Ten millilitre blood samples were collected into plain evacuated blood tubes from the coccygeal vessels and dispatched chilled on the clot to arrive at the laboratory within 24 hours of collection. Regional Laboratory Services, Benalla, determined the serum phosphorus level in the sample.
A composite sample comprising up to 60 cores was collected from the top 100mm of soil from the paddock in which the cows had been grazing. This sample was submitted to Industry and Investment Diagnostic and Analytical Services Environmental Laboratory, Wollongbar, and tested for pH (CaCl2) and phosphorus (Colwell test).
Serum and soil phosphorus levels are shown in Table 1 below;
|Property number||Locality||Animal Average P mmol/L||Range P mmol/L||Comment on serum P||Soil P mg/kg (Colwell)||Comment on soil P|
|1||Currawang||1.65||1.33-1.94||No P >10 yrs|
|2||Currawang||2.12||1.73-2.57||No P >10yrs|
|3||Parkesbourne||2.31||1.99-2.54||No P >10 yrs|
|4||Bannister||2.63||2.36-2.91||No P recent memory|
|5||Peelwood||2.03||1.85-2.91||15||No history P|
|7||Spring Hill||2.03||1.3-2.37||24||No P 10 yrs|
|8||Peel||1.29||0.56-2.54||1/10 samples low||4.3||No P<20yrs|
|11||Taralga||1.99||1.55-2.34||No P >10 yrs|
|Samples for Diagnosis:|
|12||Currawang||0.51||0.4-0.76||Stiffness/ill thrift/pyrexia affecting 3/5 cows (5/5 low Pi)||No P >mid 80s|
|12||Revisit property||0.89||0.58-1.2||Spontaneous vertebral fracture (0.58), and downer (1.2)|
|13||Gundary||1.7||0.74-2.4||2nd calf cows, ill thrift, shifting lameness, & 3xcohorts. 1/7 samples low||Irregular P|
|14,15,16||Samples not submitted|
There is disagreement about what indicates a phosphorus deficiency in cattle. One reference cites normal serum Pi as 1.3-1.7mmol/L, with clinical signs occurring at levels between 0.5 and 1.2mmol/L. The same reference expects a weight gain response to supplementation with levels less than 1.3mmol/L (Radostits et al, 2008). Researchers in Queensland expect to see a response to phosphorus supplementation with plasma Pi levels below 1.6mmol/L (Coates 1994). Regional Laboratory Services Benalla regards normal serum concentration of phosphorus is in the range 0.8 to 2.8 mmol/L, and these values have been used above to highlight results indicative of deficiency.
Only one of the 104 samples collected from the survey herds showed low serum phosphorus below 0.8mmol/L. This first calf heifer, with a serum Pi of 0.56mmol/L, was running on light shale soils that had not received applications of phosphate fertiliser for at least 20 years. At 4.3mg/kg, the soil sample from this property had the lowest Colwell P recorded in the survey, yet the heifer's cohorts recorded serum Pi values up to 2.54mmol/L.
Based on these survey results, one may conclude that phosphorus deficiency in cattle is not a common problem in the area. However, even where clinical symptoms of phosphorus deficiency exist (property 13), it is difficult to confirm from serum values.
There is no specific homeostatic mechanism for regulating blood phosphorus. Blood phosphorus is dependent upon dietary intake and phosphorus mobilised from bones. Bone phosphorus is usually mobilised in response to calcium homeostatic mechanisms. However, reabsorption of P from bones often masks P deficiency, and confounds attempts to diagnose the condition.
For example, rangeland pastures are commonly not calcium deficient, although they may be severely phosphorus deficient. The adequate calcium level provides no stimulus to reabsorb bone, resulting in a measurable reduction in blood phosphorus. As the quality and quantity of those same pastures declines, the animal loses weight from the negative energy balance. In response, bone is reabsorbed, and blood phosphorus levels return to the normal range.
Further complicating the diagnosis of phosphorus deficiency, serum inorganic phosphorus increases post collection, due to release of phosphate esters from erythrocytes. We attempted to avoid sample haemolysis during collection, handling and transport and the laboratory assay minimised the effects of haemolysis. However, the samples were consigned first to EMAI at Menangle, then forwarded to RLS Benalla, which increased the interval between collection and testing to about 48 hours.
Breakdown of phosphate esters in erythrocytes starts within a few hours of collection, and increases with time, independent of haemolysis (Zhang et al 1998). Working with human blood incubated at 320C, these researchers found the inorganic phosphorus level more than doubled within 24 hours when serum was left in contact with the clot. It is speculated the Pi levels in our samples could double in the 48 hours between collection and testing, despite chilling during transit (David Paynter, RLS Benalla, pers com).
Separating serum from the clot prior to consignment to the laboratory is advised (Anon 2005). However, waiting for the clot to form and contract takes considerably longer than 'a few hours', and achieves inconsistent results. Centrifugation and removal from the clot within three hours of collection is recommended (Zhang et al 1998). If blood samples are collected into lithium heparin tubes, recovery of plasma could occur immediately (David Paynter, RLS Benalla, pers com). As with serum, this also requires access to a high-speed centrifuge.
SOIL PHOSPHORUS LEVEL
Similarly, there is disagreement about not only what level of phosphorus in soil represents a deficiency, but even what test should be used to assess soil phosphorus. The Colwell test was chosen largely because it was inexpensive and convenient. However, other soil phosphorus tests may have been more appropriate for use with the acidic soils sampled.
Precise interpretation of the Colwell P test requires adjustment for soil type, or more specifically, the Phosphorus Buffering Index (Anon 2008). As a rough guide, soil with Colwell P of 5 mg/kg is very low in phosphorus, while 15mg/kg is moderate and 40mg/kg represents a generally satisfactory level of soil P.
Total soil phosphorus declines in the absence of fertiliser application. Phosphorus is removed from a cattle grazing property when livestock are sold. Estimates of the rate of removal of P from a typical tablelands grazing system are 1.5kg/ha/yr for a breeding operation and 1.7kg/ha/yr for a steer fattening enterprise, at 10DSE/ha (Leech 2009).
In a nine year trial, liveweight gains in response to initial fertiliser application declined significantly when fertiliser application ceased, compared with animals on pastures that were continually fertilised (Coates 1994).
In our survey, only one soil sample was demonstrably phosphorus deficient, despite most soils not receiving phosphate fertiliser in recent years.
With limited resources available for this pilot survey, some herds were specificallyinvited to participate based on a history of poor animal performance over a number of years. Owners of three such herds agreed to participate, but despite repeated requests, still have not managed to present the cattle for testing. Arrangements to test the cows at calf marking on one of these selected herds remain on hold; the late winter-born calves still have not been marked (now seven months of age). Is it possible there is a correlation?
We consider that some cattle grazing on tablelands pastures that have not had superphosphate applied recently are phosphorus deficient. However, the diagnosis of this problem is confounded by a number of factors.