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Phosphorus deficiency in the Riverina, NSW

Courtney Simkin, District Veterinarian, Riverina Local Land Services, Hay and Alexandra Carleton DVM Graduate 2020, University of Sydney

Posted Flock & Herd August 2021


Four properties surrounding Hay and Hillston, Riverina LLS in southwestern NSW, suffered morbidities and mortalities of stock (both cattle and sheep) during autumn and spring 2019. These events occurred over a large area where grazing practices on native rangeland pastures are used and, in most cases, without supplementation or superphosphate application. Western NSW has usually low phosphate soils and had suffered an extended period of drought prior to the autumn/spring of 2019 which further reduced the amount of phosphorus-rich pasture available.

Phosphorus is the second-most plentiful mineral in cattle, present in biochemical reactions and structural components (Ternouth 1990). Usually 80-85% of body phosphorus is stored in the bones, up to 30% removed when amounts in the systemic circulation are deficient (ibid). Inorganic phosphorus, over half secreted and absorbed in saliva in cattle, acts as a pH buffer and provides phosphorus for rumeno-reticular microbes (ibid). As phosphorus intake declines, food intake also declines (ibid), thus there is a relationship to negative energy balance and periods of increased energy use. As animals lose weight with the decline in pasture quality and quantity, seasonally or in periods of drought, bone is reabsorbed to compensate for loss of blood phosphorus (Johnson & Watt, 2011). Where lameness, spontaneous fractures and sudden death occurs, particular during times of nutritional deficiency, phosphorus deficiency should be considered.

Clinical presentation, paired with as immediate and accurate observation as possible, is the first step in identifying conditions associated with hypophosphataemia and may be considered where hypocalcaemia is also suspected during times of high energy use or during drought. Bone ash was used on one property to confirm hypophosphataemia.


Four properties make up this case series where the diagnosis was phosphorus deficiency. It was not suspected initially at the first property in autumn 2019. In spring 2019 three further properties (two beef, one sheep) presented, with two suspected of phosphorus deficiency from the outset. Recumbency, fractured bones, and lameness were the most common presenting complaints of morbidity and coincided with incidences of sudden death. Fractured bones are commonly associated with osteodystrophy resulting in lameness or recumbency and are a sequelae of phosphorus deficiency.

At property one a total of eight cattle were found dead, and two down, of fifty three multiparous and mixed aged cattle (18.9%) over four weeks in April 2019. Hypocalcaemia and malnutrition were initially suspected. The cattle had been on the property for two years and been in a long joining process with a Wagyu bull. The cattle had no superphosphate supplementation and were malnourished, feeding on rangelands pasture of lignum, salt bush, annual grasses and dillon bush. Hypocalcaemia was highly suspected, though sudden death from anthrax, or toxin ingestion were also considered, as the property was within the anthrax belt. However, not all the cows had succumbed to sudden death. The two down cows were sternally recumbent with significant limb weakness and various stages of non weight-bearing lameness, forelimbs most affected. Even when hip clamps were used front legs would continue to splay out. Blood samples were collected and cows were treated with 4-in-1 intravenously and subcutaneously. One cow initially responded well to the treatment but became recumbent again after walking and was euthanised. The second cow was euthanised two days later for Transmissible Spongiform Encephalopathy (TSE) submission to rule out this differential diagnosis.

Blood chemistry found moderate hypophosphataemia (0.67mmol/L (1.39-2.55)) and mild hypocalcaemia (1.88mmol/L (1.95-2.62)) with a mild hyperglobulinaemia (49g/L (27-38). Post-mortem from the second visit found mildly jaundiced subcutaneous fat, absent omental fat with a 6-7 month gestation foetus, mesenteric lymphadenitis, liver adherence to diaphragm, hepatic fibrosis and mild cholangitis. Liver pathology may have been due to the ingestion of toxic grasses.

Image of cow with splayed legs
Image 1: Cow 2 at first visit. Even when hip clamps were used front legs would continue to splay out.

At property two 720 head of multiparous and mixed aged Angus cattle in three mobs, from same-producer properties, joined after weaning (10-14 days prior), were moving on the traveling stock route (TSR) in October 2019. The cattle had been drought lotted for the previous two years, fed on hay and cotton seed. Prior to moving onto the TSR the cattle had been paddock fed with sufficient feed for maintenance. During the first four days of movement on the TSR, ten were found dead (1.4%) with mid-shaft fractures of the humerus. Those with broken bones were the better conditioned animals. A number of other cattle had hunched backs and mild lameness and demonstrated pica for bones. It was unknown whether superphosphate supplement had been added to the native pastures or other crops. Hypophosphataemia was highly suspected, though primary hypocalcaemia/osteomalacia or osteodystrophy were also considered. Bone ash testing was conducted on samples taken from a humerus and rib during post-mortem where fat-free bone percentage (FFB %) was measured (Table 1). Salt blocks were introduced however the cattle did not consume these.

Table 1: Results of bone ash testing on property 2
Sample ID Ca (FFB %) P (FFB %) Bone Ash %
Cow 1 (humerus) 24 9.9 71
Cow 2 (rib) 19 8.1 56
Mean * 25.1 11.4 63.7
* Means taken from normal phosphorus content in the soil of SW NSW, from Holst et al, 2002. Using the formula derived from Holst et al 2002, the laboratory determined that this equated to 46% of the average phosphorus levels and 56% of the average calcium levels of a normal cow. These bone ash results indicate hypophosphataemia and hypocalcaemia.

Liver histopathology found centrilobular to mid-zonal, moderate, acute to sub-acute hepatocellular vacuolation, reported to be non-specific, possibly multifactorial and as a result of metabolic derangement. Levels of 1,25 dihydroxy-cholecalciferol were later tested (175 (>50 normal)).

At property three, in October 2019 eight cows of a mob 350 (2%) were found to have bone fractures (scapula, fetlock and hindlimb) over six weeks (six cows and two weaners) where two had died (0.6%). The whole mob of 700 cattle, which were heifers and adults, were rotationally grazing in two groups on native rangeland grasses and bushes. There was no superphosphate supplementation.​ Cattle were seen to have pica (chewing on bones of kangaroo carcasses). Hypophosphataemia was highly suspected and a trial treatment was instigated as bringing the cattle into holding yards risked further broken bones. Calcium deficiency was also considered, leading to osteomalacia or other forms of osteodystrophy. Phosphorus supplementation was given by lick-blocks (8% P lick-blocks) and an in-water treatment of white-sap liquid P supplement (Beachport Liquid Mineral). The blocks were consumed rapidly within a few months and the in-water treatment lasted six weeks. Over time the pica reduced significantly and the lick blocks were no longer consumed. Based on the response to the trial empirical diagnosis for this property was hypophosphataemia.

At property four, ten sudden deaths in a mob of 3000 (0.3%) 4-5 year-old merino ewes occurred at the edge of the Western division in Hillston in October 2019. Anthrax was initially suspected as the property was within the anthrax belt but was ruled out using ICT test kits and laboratory testing. The mob had been moved from an unfertilised wheat crop to a holding paddock in the previous ten days for shearing. They were unvaccinated and undrenched in the last twelve months and had been grazing in the holding pen on dry grasses (which the owner reported contained barley grass, rye grass and dry clover, but on site inspection none of these forages remained) without superphosphate supplementation. Prior to entering the holding pen they had been fed on a self-sown wheat crop also without superphosphate supplementation.

Juvenile Paterson’s curse was the only plant seen in the holding pen at time of site visit. Sheep at this time were malnourished. Blood samples were collected from two ewes from the mob with the sudden deaths to diagnose whether hepatopathy was present (Table 2). Samples revealed hypocalcaemia, hypomagnesaemia and hypophosphataemia. The presenting malnourishment indicated the need for immediate supplementation with lime/salt loose lick while at pasture and the need for feed supplement in the holding paddock.

Table 2: Biochemistry results for 2 ewes from property 4
Ewe One Ewe Two Reference interval
Calcium (Uncorr.) 2.49 mmol/L 2.64 mmol/L 2.88 - 3.20
Phosphate 1.37 mmol/L 1.48 mmol/L 1.62 - 2.36
Magnesium 0.77 mmol/L 0.88 mmol/L 0.90 - 1.26
Potassium 5.9 mmol/L 3.9 - 5.4
Chloride 113 mmol/L 95 - 108


Phosphorus deficiency in cattle can be linked to reduced appetite, poor performance, recumbency and skeletal abnormalities resulting in shifting lameness, hunched back or spontaneous fractures (Johnson & Watt, 2011). It is a common mineral deficiency linked to economic loss (Teixeira et al., 2015). Hypophosphataemia was initially suspected at properties two and three. The recumbency of the cows, incidents of broken bones and presence of pica on these two properties were strong indicators of hypophosphataemia. At properties one and four the finding of hypophosphataemia was found incidentally upon examination as it was not being targeted.

Indications of lameness across all properties may have been a first sign of phosphate deficiency. Hypophosphataemia is the primary reason for the development of rickets or osteomalacia in cattle and sheep (Uhl 2018). It presents as, and may lead to, osteophagia (pica), lameness and spontaneous fractures (ibid). When presented with broken bones on potential nutritionally deficient soils, metabolic bone diseases such as rickets/osteomalacia must be considered (distinguished by age, where rickets occurs in juveniles) , where "demineralization [sic] of the bones results in the animals suffering from 'spontaneous' fractures, having a reluctance to move, stiffness in the joints and reluctance to stand" (Ternouth, 1990). Rickets is more a developmental defect and produces effects on the growth plates of long bones and osteomalacia in adults affects remodelled bone (Uhl, 2018). Rickets may have been involved with the weaners at property three and cannot be definitively ruled out. Osteomalacia may have been also present. Where the trial treatment of phosphorus was used and received a good response, phosphorus deficiency was ruled in. At this property (three) there were no further fractures after the phosphorus supplementation.

Rickets/osteomalacia can be seen in the living animal with evidence of malformed or bowed limbs (ibid) and are reduced by correct nutrition where commercial diets are used (ibid). Fibrous osteodystrophy may be another metabolic deficiency. This is more associated with hypocalcaemia and may concurrently occur (ibid). Hypocalcaemia was seen in the three properties, where blood samples and bone ash samples were taken. Histopathological examination of the bones may have aided in identifying definitively which parts of the bone were affected: enlargement of the costochondral junctions and curvature of the long bones may be evidence of hypophosphataemic bone deficiency leading to osteomalacia (Uhl 2018). To rule out fibrous osteodystrophy examination of the teeth and jaw would have been useful as "bone loss around teeth and swelling in the mandible/maxilla" (ibid).

In sheep, phosphorus deficiency comes from poor nutrition. In particular, rye grass contains high levels of carotene which is an antagonist to the action of Vitamin D in the bone and intestine (Uhl 2018). The sheep on property four were consuming rye grass so this may have lead to a deficiency. The result is lameness, stiff gait and limb deformation (ibid).

Low phosphorus diets will decrease feed intake​ up to 50% in sheep (Ternouth 1990). High calcium diets (>4g/kg DM) also suppress phosphorus and calcium resorption from bone leading to rapid reduction in feed intake and further phosphorus deficiency (Ternouth 1990)​. Rangeland pastures are known for being phosphorus deficient but have sufficient calcium. Maintaining levels of calcium in ingesta does not trigger the necessary mechanisms to maintain homeostasis of phosphorus and bone reabsorption (Johnson & Watt 2011), resulting in normal calcium levels but hypophosphataemia. Evidence of hypophosphataemia in the blood samples of ewes on property four indicate chronicity as blood can regulate phosphorus levels, taking from the bones when deficient.

Calcium deficient nutrition, on the other hand, such as on property four with a self-sown wheat crop would lead eventually, if chronically deficient, to hypocalcaemia and hypophosphataemia. The concurrent hypocalcaemia and hypomagnesaemia at property four may indicate chronicity of condition or, alternatively, malnutrition.

In addition, none of the properties in this case series had superphosphate supplementation, which is normal practice for treating native pastures in this region of NSW. Phosphorus supplementation regimes have been trialled across several part of Northern Australia (Partridge 2012), regimes which may be utilised in the western part of NSW.

Sampling for determination of phosphorus deficiency is difficult in the live animal. Blood phosphorus depends on dietary intake and mobilisation from bone (Johnson & Watt, 2011) and phosphorus does not absorb across gastric mucosa (Ternouth 1990). Low phosphorus levels can be masked by bone resorption in response to calcium homeostasis (Johnson & Watt, 2011). Phosphorus can also be temporarily lowered with vigorous physical activity (decrease phosphorus for >1hr) or after administration of dextrose (decrease phosphorus by up to 30% for 4-6 hours).

Rib sampling by biopsy, whilst invasive (Ternouth 1990), can be used to determine FFB % phosphorus, FFB % calcium, and percentage ash (Holst et al., 2002). In the case of property two the bone samples were collected from the rib and humerus during post-mortem.

In those cases where hypophosphataemia was initially suspected bone ash was the preferred diagnostic tool. Bone ash is the gold standard for diagnosing phosphorus deficiency. As identified by Holst et al. 2002 "[i]dentification of osteodystrophy in...cattle was most readily diagnosed from ash density data and not from % P, % Ca, or Ca". Bone ash was only used for property two. Property three, where hypophosphataemia was initially suspected, underwent a treatment trial of phosphorus supplementation, which was successful. When blood samples from properties one and four were found to be hypophosphataemic, a result of chronic phosphorus deficiency, a diagnosis could be made and supplementation was advised.

It is common practice to use the rib for bone ash phosphorus measurement (ribs and vertebrae lose their calcium and phosphorus concentrations more readily as cancellous bone, Ternouth 1990), so this method has been used with property two to determine reference levels, taken from Beighle (1994) and Holst (2002). Ribs 9, 10, 11, and 12 may be used in serial sampling from bovines to measure phosphorus (Beighle et al. 1993). It has been suggested that phosphorus less than 5% in the ribs is indicative of deficiency (Ternouth 1990). Given the differences in phosphorus levels in soils in Australia (Rossel 2016) bone ash reference levels may shift depending on the region. Phosphorus availability varies depending on forage maturity (Ternouth 1990). Thus adding phosphorus to roughage may not make it more available (ibid).

Faecal phosphorus analysis may be used to assess phosphorus intake and secretion. Endogenous faecal excretion is the most significant form of loss of phosphorus from ruminants (Ternouth 1990). Whilst this was not used in these cases, it may be a cost effective alternative to liver biopsy. Faecal analysis is commonly used in northern Australia as a reference for supplementation (by way of urea) as northern soils are phosphorus deficient at least for part of every year (Partridge 2012). Normal results do not rule out phosphorus deficiency but strategic testing may be beneficial.

More recently, grazing experiments in Australia have revealed that tail bone mineral density (BMD) measured using single photon absorptiometry (SPA) can be used to assess phosphorus deficiency both in steers and first-calf pregnant and lactating cows from net demineralisation of bone (Coates et al., 2016) though whether this method is feasible for on-farm work is a separate question. In mature breeder cows cortical bone thickness of the rib was more affected than BMD measured at the tail (ibid).

Hepatic vacuolation was found in a post-mortem from property two and may have resulted from toxic insult. The liver produces 1,25 dihydroxy-cholecalciferol, which is secreted from the liver when there is low phosphorus and its release increases absorption of phosphorus from gastric mucosa and reabsorption from bone (Ternouth 1990). However, the levels tested do not appear abnormal. Phosphorus deficiency only indirectly affects the liver in association with negative energy balance (Grünberg et al., 2019).

Treatment and prevention are by way of phosphorus supplementation. Young cows in particular with poor BCS and lower body fat, "were at risk and should have responded to phosphorus supplementation with rain and better pasture conditions" (Holst et al., 2002). This may be the reason for the hepatic fibrosis and diaphragmatic adherence seen in one instance, particularly if the cow was dehydrated. It also indicates the early intervention by phosphorus supplementation, as used on one property. Phosphorus supplementation with either triple superphosphate (19.6% phosphorus) or monodicalcium phosphate (20.5% phosphorus) are good grain additions (Teixeira et al., 2015). On phosphorus-deficient soil monocalcium phosphate or dicalcium phosphate mixed with molasses at 1–2% by weight can also be used (McKiernan 2006).

Clinical presentation and acute and accurate observation is the first step in identifying conditions associated with hypophosphataemia and may be considered where hypocalcaemia is also suspected during times of high energy use or during drought. Where lameness, spontaneous fractures and sudden death occurs, particular during times of nutritional deficiency, phosphorus deficiency should be considered.

Where phosphate deficiency is suspected on clinical presentation, rib biopsy for bone ash testing should be considered early to save time in diagnosis. However, as it can take a month to receive results, phosphorus trial supplementation could be used as an immediate treatment. A finding of hypophosphataemia indicates a chronic condition though phosphorus levels in blood are unreliable and may be caused by other factors such as rigorous activity.


We thank Dr Des McCrae who was the veterinarian for reporting his findings and working with the LLS for property two. We also thank the team at Elizabeth Macarthur Agricultural Institute (EMAI) who gave their expertise in investigating these cases.


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