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Rickets in grower pigs

Kate Atkinson, District Veterinarian, Coonabarabran

Posted Flock & Herd December 2021


Rickets occurring in swine poses both production and welfare issues. Pigs are particularly susceptible to rickets due to their rapid growth rate.1 This report describes a case of rickets in grower pigs due to chronic nutritional imbalances.


An investigation was undertaken into lame grower pigs in the Coolah district in February 2021. The piggery had 14 sows and 50 grower pigs. The owner had initially noticed approximately 50% or more of the grower pigs (3-4 months old) were stiff, sore and reluctant to move. A treatment trial had been undertaken by a private veterinarian for polyarthritis with amoxicillin and meloxicam several weeks earlier, but they had not responded to treatment.

During a swill feeding inspection by myself (District Veterinarian) and a biosecurity officer, it was noticed that the grower pigs were still exhibiting these signs. Additionally, there were now three pigs paralysed in the hind limbs. The affected pigs were otherwise bright, responsive, eating and drinking, and in good body condition. The breeding sows and boars did not appear to be affected.

Their diet was formulated by the owner and was a mixture of hammer-milled barley, soya bean meal and salt of unknown quantities. They were semi-housed pigs and fed from raised feeders made from old chemical shuttles. No tail docking was performed in this enterprise.


Three grower pigs were paralysed in the hind limbs with varying degrees of neurological deficits (Figure 1). Some retained withdrawal reflexes and pain perception in the hind limbs while another had complete loss of withdrawal reflexes and pain perception. A large proportion of the grower pigs (>50%) were showing signs of lameness, stiffness and reluctance to move. There was also varying degrees of kyphosis (humpback) in many pigs (Figure 2). One animal with kyphosis was noticeably constipated / obstipated. The joints did not feel hot and there was no evidence of a joint effusion. The rectal temperature taken of several affected pigs was within normal limits.

Image of weaner pig with hindlimb paralysis
Figure 1. Grower pig with hind limb paralysis
Images of weaner pigs with hunched backs
Figure 2. Grower pigs displaying varying degrees of humpback (kyphosis). Note constipation in the top pig.


Two of the paralysed grower pigs were selected for post-mortem examination and humanely euthanised with a captive bolt.

Post-mortem of a paralysed female grower revealed a lumbar vertebral fracture. The pig had significant kyphosis formation of the spine. There were also enlarged costochondral junctions (rachitic rosary) on the ribs and sporadic calluses on the ribs that were indicative of previous fractures (Figure 3). The bones were soft and could be cut with a knife (Figure 4).

The gastrointestinal tract was full of sand / dirt, also causing impaction and constipation.

The female pig also had a urinary tract infection and cystitis.

Images of pig post-mortem showing rib fractures
Figure 3. Enlarged costochondral junctions (rachitic rosary) on ribs and sporadic mid-diaphyseal calluses
Image of pig post-mortem showing cut pelvic bones
Figure 4. Knife cut though part of the pelvis


(Regional Laboratory Services, Benalla; PathWest Laboratory Medicine WA)
Test Reference range Pig 1 Pig 2 Pig 3 Pig 4 Pig 5
Phosphorus 1.7-2.8 mmol/L 5.65 7.41 7.9 5.38 5.72
Calcium 2.4-2.9 mmol/L 2.17 2.36 2.28 1.93 2.36
Vitamin D3 >50nmol/L 75 75 79 101 107

Histopathology of rib: Failure of endochondral ossification.

‘The growth plate cartilage is diffusely irregular and thickened, with disorganisation of chondrocyte columns in the proliferative and hypertrophy zones. There are clusters of hypertrophic chondrocytes within areas of primary spongiosa. In the areas of the primary spongiosa there are numerous spicules of cartilage with no discernible osteoid production, lined by numerous osteoblasts and large number of osteoclasts. There is marked reduction in bone marrow precursors, with replacement by abundant fibromyxomatous tissue. Within the central diaphysis, there is absence of trabecular bone and bone marrow, with replacement by abundant fibroblasts, connective tissue, numerous osteoblasts and haemorrhage. There is marked enlargement of the cortical bone and periosteum, with abundant deposits of fibrillar eosinophilic material (fibrin), disorganised proliferated chondroblasts, numerous osteoblasts, deposits of connective tissue and fibroblasts, and large numbers of osteoclasts in the Howship lacunae.’ (Interpretation by Pedro Pinczowski, Pathologist, Elizabeth Macarther Agricultural Institute, Menangle)

Diagnosis: Rickets.

Rickets was diagnosed from both the blood pathology and histopathology. It was a result of calcium deficiency and a dietary calcium and phosphorus imbalance (Table 1).


Treatment involved correcting the dietary calcium levels and the calcium to phosphorus ratio in the diet. The pigs primarily lacked calcium due to the low calcium diet.

With pig nutritionist advice it was recommended that the pigs’ diet should be supplemented with premix additive supplements or switched to a pre-formulated pellet designed for growers to correct the dietary calcium and phosphorus imbalance. The energy content of barley was also likely to be inadequate for grower pigs due to its fibrous husk and wheat / triticale was recommended as the energy source for this class of pig.

Humane euthanasia of a further two paralysed pigs was carried out during the visit when the post-mortem examination was performed. This recommendation was made due to suspected spinal fractures and a guarded prognosis for recovery.

The landholder obtained a form of pig ration supplement from a rural store and said he was seeing resolution of lameness and stiffness after four weeks.


Rickets is a disease of young, rapidly growing animals and primarily occurs due to a deficiency of calcium, phosphorus and / or vitamin D. Less commonly, genetic, hormonal or toxic disturbances can also result in rickets.1 The basic abnormality is failure of mineralisation of osteoid and cartilaginous matrix, especially in the growth plates, otherwise known as failure of endochondral ossification.

Signs of rickets include poor growth, short stature, lameness, enlargement of the ends of the long bones and deformation of the long, weight bearing bones. On post-mortem examination the common signs are a number of recent or healing fractures, particularly in the ribs.2 Clinical signs in this case were consistent with rickets and were only seen in the growers due to their rapid growth and high calcium demand. Pica (dirt eating) and the resulting constipation in the pigs was seen behaviourally in response to the calcium deficiency.

Low serum calcium and high phosphorus levels (Table 1) in all pigs tested suggest the cause of rickets in this case was inadequate dietary calcium resulting in a dietary calcium and phosphorus imbalance. A primary lack of dietary calcium causes a secondary nutritional hyperparathyroidism where parathyroid hormone is secreted and stimulates resorption of calcium from bone.1 The histopathology results including the high level of osteoclast activity in the rib suggest calcium resorption was occurring in the affected pigs.

Rickets occurring due to inadequate dietary calcium is also often accompanied by osteoporosis.1 Signs of osteoporosis are lameness, recumbency, fractures, and paraplegia. Fractures are particularly common of the lumbar vertebrae, humerus and femur.2 The development of vertebral fractures in these pigs suggests osteoporosis was also present in this case.

The kyphosis / lordosis deformities seen can also develop secondary to osteoporosis or rickets.1 Other causes of this deformity include osteomyelitis, spinal fractures, neoplasms and metabolic disease.3

High-level cereal grain diets contain excessive phosphate and low calcium and vitamin D levels.4 Hyperphosphataemia may have been the result of excessive dietary phosphate but also can occur if there is excessive bone breakdown.1 The increased osteoclast activity seen on histopathology suggests that excessive bone breakdown may have been contributing to the hyperphosphataemia seen in this case.

Serum vitamin D levels were adequate. Madson et al., 20121 suggests pigs can develop rickets if Vitamin D3 is less than 37.5 nmol/L. Deficiency of vitamin D was not implicated as a cause of rickets in these animals likely due to their ready access to sunlight.

The urinary tract infection was likely an ascending infection secondary to the spinal injury. Neurological deficits of the urethral sphincter and the hind limb paralysis resulted in the vulva being dragged in dirt, both contributing to development of the urinary tract infection and cystitis.

Differential diagnoses included spinal abscess and polyarthritis. These were excluded at the time of post-mortem examination as none of the gross findings were consistent with these diagnoses.

Treatment for rickets involves correcting nutritional deficiencies and imbalances of the calcium to phosphorus ratio in feed, which should be approximately 1.2:1.1 Animals with fractures should be humanely euthanised for welfare reasons.


Thanks to Luke Milsom for his assistance with the post-mortem examinations and Linda Scott for her nutritional advice.


  1. Madson, D, Ensley, S, Gauger, P, Schwartz, K, Stevenson, G, Cooper, V, Janke, B, Burrough, E, Goff, J, Horst, R (2012). Rickets: case series and diagnostic review of hypovitaminosis D in swine, Journal of Veterinary Diagnostic Investigation 24(6) 1137-1144
  2. Neumann, E, Ramirez, A, Schwartz, K (2009). Swine Disease Manual, American Association of Swine Veterinarians, p108
  3. Nielsen, L, Hogedal, P, Arnbjerg, J, Jensen, H (2005). Juvenile Kyphosis in Pigs, Journal of Pathology, Microbiology and Immunology 113(10) 702-707
  4. Radostits, O, Gay, C, Hinchcliff, K, Constable, P (2007). Veterinary Medicine – A Textbook of the disease of cattle, horses, sheep, pigs and goats, Elsevier, p1767


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