The owner of a small, semi-intensive piggery near Narrabri, north-western NSW, became concerned when a large proportion of his herd became afflicted with unusual clinical signs, including hindlimb paralysis and loud squealing when disturbed. The enterprise was based on free range Large White sows and Duroc boars, with piglets weaned into conventional shed pens at eight weeks and with sale at five to six months of age.
The first case was observed by the owner seven days prior to the initial property visit. Four days after the index case, a significant number of pigs began to show similar signs.
A similar enterprise run by the same owner on a nearby holding was not affected.
On visiting the piggery, 22 of the 47 shedded pigs were affected, with a further six having already been euthansed by the owner. All age groups were affected.
Ten years prior to this investigation, this herd was diagnosed as having clinical hypovitaminosis A in the shedded pigs. The main presenting sign at that incident was hind limb paralysis. Since then Vitamin A injections had been administered at weaning, and occasionally repeated at three months of age.
This herd also experienced neurological cases as a result of a water deprivation / salt poisoning incident two years prior to this investigation.
Clinical examination found varying degrees of hindlimb paralysis, with negligible withdrawal reflex in the hindlimbs, and normal forelimb reflexes. Some animals were completely recumbent, while others were ‘dog-sitting’ on their hind limbs.
Some could be lifted into a standing position, but vocalised profusely when moved. This appeared to be a response to pain and was the most striking of the clinical signs. The general noise in the piggery was characterised by these frequent loud squeals, as affected pigs attempted to move or were disturbed by other pigs.
The demeanour of the pigs was bright and responsive and all other clinical parameters including growth rates were normal.
Following the initial clinical examination, a presumptive diagnosis of hypovitaminosis A was made. Advice was given to administer Vitamin A. Concerned that this diagnosis was incorrect, on the basis of the unusual squealing, the owner asked for a second opinion from a private practitioner. The practitioner concurred with the initial diagnosis.
At the time of the investigation the shedded pigs were being fed a home-mixed diet of grain and mung beans at approximately 20:6. No other supplementation was included in the diet.
This diet had been fed for eight weeks. Prior to this the ration had been grain and meat meal at approximately 20:3, with the occasional addition of mung beans.
The meat meal was removed due to market pressures from processors supplying Asian markets. These markets are reluctant to accept meat meal fed pigs because of perceived beef taint from the practice.
Blood was collected from three affected pigs, initially to determine Vitamin A levels. On advice from Paul Gill, Veterinary Pathologist, NSW DPI Wollongbar Regional Veterinary Laboratory, that osteomalacia was a possible differential diagnosis, testing for calcium levels was also performed.
The animals sampled were marginally to moderately hypocalcaemic and had mild hypovitaminosis A. Both of these were most probably due to dietary insufficiency.
In one of the samples, the serum Vitamin A was at a level low enough to be causing clinical disease. This result is interesting given that this piggery supplements Vitamin A by injection at weaning into the sheds. However, the owner was in the habit of buying Vitamin A in large 500 ml clear plastic containers. As a result some product may have been damaged by age and exposure to light and heat. Alternatively, it suggests that injections of Vitamin A may need to be repeated at 2-3 month intervals.
The piggery was re-visited seven days after the initial visit and a 14 week old pig that had severe hindlimb paralysis was autopsied.
Grossly, there were no external abnormalities. Viscera and muscle appeared normal. Bones were extremely soft and the pelvis could be cut through with a knife. Transverse incision of the femur revealed an extremely thin cortical layer (Figure 1). Costochondral junctions were grossly enlarged in a classical rachitic rosary (Figure 2). The spinal vertebrae were removed and boiled down to facilitate removal of surrounding soft tissues. A transverse fracture of the T5 vertebra could then be visualised (Figure 4), along with unusual ridging on the ventral aspect of L3 and L5 (Figure 5). The bones were brittle, especially when compared with normal pig vertebrae (purchased bacon bones – Figure 3).
Osteomalacia due to inadequate mineral levels in the diet was confirmed by biochemistry results and post-mortem observations. There was also evidence that Hypovitaminosis A may have been contributing to the syndrome.
Calcium (Ca) and phosphorous (P) were added to the diet at a rate advised by a specialist pig products re-seller. The rates were in line with those recommended in the standard veterinary literature, that is from 0.9% Ca and 0.7% P at 3-5kg body weight to 0.45% Ca and 0.4% P for 80-120kg body weight. The ratio between calcium and phosphorous should not exceed 2:1 and should not be less than 1:1. Vitamin A injections were also given by the owner.
The herd was revisited five days after calcium, phosphorus and Vitamin A supplementation began. This revealed a dramatic improvement in affected pigs. Those that had been recumbent were sitting, and those that had been sitting were able to stand, although some showed stiffness. Pigs could be moved without eliciting the painful vocalisations of the previous visit.
This dramatic improvement was an unexpected finding. It had been assumed that if the clinical signs in these pigs were solely due to osteomalacia and associated fractures, then recovery would be expected to take weeks.
On the reported clinical signs, only Aujesky’s Disease was considered as a possible differential diagnosis of national or state significance. The initial clinical examination quickly excluded this and any other regulatory condition.
Osteomalacia is a condition caused by a relative or absolute deficiency of calcium, phosphorus and/or Vitamin D, that results in increased bone resorption without remodelling. The resultant reduction in cortical bone causes reduced bone strength and predisposes to pathological fractures. It is generally seen in pregnant or lactating sows due to increased calcium demands during these periods.
In this herd, the removal of bone meal from the diet of the pigs was the precipitating event. Following the removal of this source of calcium and phosphorous, there were insufficient levels of these minerals in the diet to maintain bone condition and strength.
Hindlimb paralysis and recumbency are common clinical manifestations of osteomalacia; however marked painful vocalisation is not.
These loud vocalisations made by the affected pigs when moved or disturbed, were the most characteristic clinical sign in this outbreak. This symptom had not been present in this piggery during a previous Hypovitaminosis A outbreak and had led the owner to correctly doubt the initial presumptive diagnosis of hypovitaminosis A. This clinical sign was also the one to disappear quickest and most completely following treatment.
The exact cause of the vocalisation and sudden recovery could not be identified during research for this paper. A possible explanation is that the vocalisation pain was due to periosteal tearing, and that this responded quickly to calcium and phosphorous supplementation. Alternatively, the pain vocalisation was related to a lesion at least mediated by hypovitaminosis A.
The equivalent condition to osteomalacia in growing animals, rickets, is characterised by ill thrift, anorexia and deformities of the limb bones. Even though rickets does affect animals in this age group, the affected animals had an osteomalacia presentation, with continued good growth rates. The sudden move from adequate dietary calcium and phosphorous to grossly deficient, may have been a factor in this presentation.
The other similar enterprise had shown no signs of hindlimb paralysis at the time of this outbreak. This was most probably because meat meal had been removed from the diet more recently in that piggery (three weeks as opposed to eight in the affected piggery), and thus deficiencies had not reached the critical point required for clinical manifestation. Calcium and phosphorus were supplemented on this property as a preventative measure.
The role of Vitamin A in this outbreak is unclear. Vitamin A has many functions within the body, including roles in normal bone growth, maintenance of night vision and normal epithelial tissues. Most notably for this case, progressive paralysis is a common clinical sign in hypovitaminosis A of Pigs.
Given the market pressure to remove meat meal from the diet of pigs, and the possible failure of producers to use replacements for both the protein and minerals that meat meal provides, there is the potential for further cases of osteomalacia to occur.