Phosphorus deficiency causing rickets in a group of nursery pigs

Rebecca Egan

Animal Health Laboratory, University of Guelph, Guelph, ON.

AHL Newsletter 2022;26(3):14.

Approximately 4 days following arrival from the nursery, one 28 kg gilt was submitted to the AHL for necropsy to investigate suspected metabolic bone disease in a group of grower pigs.  Several animals were exhibiting lameness and reluctance to move with minimal response to treatment with antibiotic and anti-inflammatory medications.  Two on-farm necropsies revealed abnormal thoracic cages with ribs that were rubbery and bent prior to breaking.  Necropsy at the AHL revealed similar rib changes including pliable rib bones and discrete nodular thickenings at costochondral junctions (rachitic lesions), and vertebral bodies and long bones that were either slightly pliable or brittle.  On cut section, growth plates had an irregular or widened appearance typical of rickets.  Most prominent in the humerii, there was obvious thinning and malalignment of the diaphyseal cortex which was brittle and easily broken with slight pressure.  In addition, transverse sectioning of both scapulae revealed bilaterally symmetric step-like irregularities in the cortex with no mobility, consistent with chronic fractures.  Dissection also revealed areas of hemorrhage in the muscles of the RH hip and femur and surrounding the RF elbow and shoulder.  Histology confirmed failure of endochondral ossification which was most prominent in humeri and ribs, accompanied by fibrous osteodystrophy with osteopenia, medullary and periosteal fibrosis (Fig. 1A).  In addition, a section of humeral growth plate displayed focally extensive tongues of retained hypertrophic cartilage (Figs. 1B, 1C).  It was also evident that these changes led to instability and fractures in the scapulae and humeri, with resulting deposition of granulation tissue and periosteal new bone formation identified microscopically, along with adjacent areas of localized myonecrosis and hemorrhage.

Bone ash profiles of the second rib from two affected pigs revealed low bone ash (50% and 51%; normal reference range 58-62%), and reduced bone density (1.28 g/ml and 1.22 g/ml; normal reference range 1.4-1.5 g/ml), consistent with osteopenia.  Bone ash levels of calcium and phosphorus were within the normal range, but this can occur in cases of metabolic bone disease where calcium and phosphorus deposits are present in relatively normal quantities within structurally abnormal bone.  Overall, the constellation of clinical, gross and microscopic findings was highly characteristic of rickets, which is typically the result of inappropriate dietary levels of calcium, phosphorus, and/or vitamin D.

Further investigation uncovered a high likelihood of inappropriate phytase levels in the ration, thus phosphorus deficiency was presumed to be the inciting cause of metabolic bone disease in this group.  Phytase supplementation of low-phosphorus (e.g., corn-soybean) rations is done to improve phosphorus digestibility and bone mineralization in growing pigs.  In feedstuff derived from plants, phosphorus is primarily stored bound to phytate, and this form is mostly unavailable to pigs, with an overall digestibility of approximately 20 to 30%, therefore, the phytase enzyme acts to release phosphorus in a bioavailable form.  Phytate can also form complexes with proteins and minerals leading to reduced nutrient absorption, so strategic application of phytase in swine diets is required to improve phosphorus digestibility, while also reducing the antinutritional effects.  Use of phytase to improve utilization of phosphorus in feedstuffs is advantageous, in that it also decreases the environmental impact of phosphorus excretion in swine waste and minimizes the use of expensive inorganic phosphorus.   AHL

Figure 1. A. Microscopic section of humerus capturing growth plate and thin irregular trabecular (>) and cortical bone with failure of endochondral ossification and deposition of fibrous tissue (^) typical of fibrous osteodystrophy.  B, C. Microscopic sections of humeral growth plate with focally extensive tongues of retained hypertrophic cartilage arranged in poorly organized columns that extend from the physis into the metaphysis (*). H&E stain.

Figure 1. A. Microscopic section of humerus capturing growth plate and thin irregular trabecular (>) and cortical bone with failure of endochondral ossification and deposition of fibrous tissue (^) typical of fibrous osteodystrophy.  B, C. Microscopic sections of humeral growth plate with focally extensive tongues of retained hypertrophic cartilage arranged in poorly organized columns that extend from the physis into the metaphysis (*). H&E stain.

 

References

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