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Calcium and phosphorus

Problems that may arise with calcium, phosphorus, vitamin A and D

(625) With modern dietary formulations actual deficiencies arising due to defective diet would be unusual. Problems however occur due to faulty storage, the incorrect application of the feed or interactions that reduce the availability to the pig. The latter can result from intestinal disease, metabolic failures or adverse interactions between nutrition, the pig, management and the environment.

Calcium contributes to wide variety of functions in the body including blood clotting, muscle and nervous activity, hormone production and milk production to name but a few. Its major role however, together with phosphorus is involved in the formation of bone where on a dry matter basis it forms approximately 38% of the structure and phosphorus 20%.

Bone is a very strong and dynamic structure with minerals constantly being removed and replaced. The intestines control the rates of absorption both into the body and skeleton and these are necessary to maintain an equilibrium between demand and excretion. The ratio of calcium to phosphorus in the diet is also an important factor in this equation and this should not rise above 2:1, when it does the absorption of calcium may be impaired, likewise if the ratio drops below 1:1. The ideal is approximately 1.25:1 to 1.50:1. Vitamin D3 is also required in calcium metabolism together with controlling hormones produced by the parathyroid gland.


This is a general term to describe specific diseases that arise whenever there is a failure of bone structure and metabolism due to faulty nutrition. Such diseases include osteoporosis, rickets and osteomalacia, periostitis describing disease of the periosteum and osteomyelitis, disease of the centre or medullary cavity of the bone.

Osteoporosis (OP) and Osteomalacia (OM)

Both these conditions are becoming more common in modern pig producing systems particularly in the first litter gilt where the skeleton is still growing and there are heavy demands on calcium for milk production.

Bones affected with OP are quite normal in their structure but they become thinner particularly in the dense parts and shafts of the long bones. As a result they become more prone to fracture. OP can arise due to a shortage of calcium in the diet and imbalance of calcium and phosphorus, poor or inadequate absorption from the diet, heavy losses during lactation and where there is a lack of exercise. Osteomalacia is the adult form of rickets and is associated with a phosphorus or vitamin D3 deficiency. There is a failure of the mineral to be deposited in the bones, which become soft and they either bend or fracture.

Clinical signs

These are most common in the first litter female and occasionally after the second litter.

The onset may be gradual with the pig having difficulty rising and showing pain or sudden lameness associated with complete fracture of the long bones. Spinal fractures occur in some animals and they often remain in a dog sitting position. Most pigs are affected in late lactation or shortly after weaning associated with the onset of oestrus and the trauma that results from other animals, or the weight of the boar at service.


This is based on clinical signs, a history in lactating and newly weaned sows and evidence of fractures of the long bones. If the herd has a problem it is necessary to examine the bones of an affected animal by x-ray to differentiate between OP and OM.

Similar diseases

These include:

  • Leg weakness or osteochondrosis.
  • Spinal fractures.
  • Torn muscles at their insertions into the bones.
  • Mycoplasma hyosynoviae infection
  • In cases of bone fracture the sow is best destroyed on humane grounds.
Management control and prevention
  • Outbreaks are often more apparent in new gilt herds. Selection of animals for good conformation is essential.
  • Investigate the growth rates and nutrition and feeding in the gilt.
  • Increase exercise during pregnancy if possible.
  • Check the levels of calcium and phosphorus in the diet. They should be 10-12g/kg of calcium and 8-10g/kg of phosphorus.
  • Only mate gilts from 220 days onwards and if the disease is a persistent problem in a particular genotype change the source.
  • Check that floor surfaces are not slippery.
  • The problem is less common in outdoor herds.
  • Feed a good lactation diet during suckling and consider top dressing the diet daily with 20g of di calcium bone phosphate.
  • Inject pregnant animals with 50,000iu vitamin D3 three weeks prior to farrowing. Repeat again in the second week after farrowing.
  • Maximise feed intake to appetite during lactation.
  • Check the ratio of calcium : phosphorus in bone ash. The normal ratio is approximately 2:1 or less. In problem sows this is often 3:1 or more.

This arises in a similar way to OM except it occurs in young growing animals, again as a failure of mineralisation of bone and growth plate cartilage. Phosphorus and vitamin D deficiencies are the common cause but the condition today is rare.

Where it occurs young animals are often housed in dark surroundings and fed starch feed waste with no mineral vitamin supplements. It usually takes 6 to 8 weeks before symptoms become evident, by which time the disease has progressed to become irreversible.

The symptoms are similar to OM but because the growth plate and cartilage does not develop to bone the joints swell with stiffness and pain is evident. Bone fractures are also common. In the few cases treated the response to injections of vitamin D3 has been very poor with pigs being totally uneconomical.

Vitamin A

The classical descriptions of vitamin A deficiency are described in Fig.14-4 but in the authors experience in the field such diseases would be rare. Most if not all rations are well fortified with the vitamin, indeed in many cases to excess and gross intake leading to disease is more likely to be experienced, but not well recognised.

Two problems arise in the field. The first is where high levels of vitamin A up to 15,000 to 18,000 iu/kg are fed. This has been shown to lower the vitamin E status of the pig and therefore make it potentially more susceptible to mulberry heart disease. This depression of vitamin E may also reduce antibody production and thereby increase susceptibility to disease. This scenario has coincided with out breaks of respiratory disease in the field and lowering the vitamin A levels to around 8,000iu/kg and raising the vitamin E by 50-100iu/kg had been undertaken with improvements.

Piglets born from sows fed high levels of vitamin A may produce piglets with a low vitamin E status and this can be a fruitful line of investigation where iron dextran problems persist in sucking pigs.

The second problem arises when excessively high levels of vitamin A - 25,000 to 30,000iu/kg are fed. At these levels the growth plates of the foetus become affected with classical signs of leg weakness and grossly shortened and bent bones in pigs as young as three weeks of age.

Further evidence for the effects of vitamin A on growth plates was also illustrated in a severe outbreak of leg weakness in weaners and growers fed rations containing high lysine 1.5% and high vitamin A levels of 18,000iu/kg. The pigs were housed on very smooth slats the surfaces of which sloped to the edges. This resulted in the claws remaining in the gaps for long periods and by the time the pigs were 16 weeks of age the claws were completely crossed over due to a combination of pressure and weakened growth plates. When levels were reduced to 10,000iu and the lysine levels dropped to 1.1% and the slat surfaces roughened, the problem gradually disappeared.

Leg Weakness or Osteochondrosis

See also chapter 7.
Degenerative changes in the joints and cartilage are generally described under the term leg weakness or osteochondrosis. These changes involve erosion of the articular cartilage and alterations to the normal patterns of growth at the growth plates at the ends of the long bones.

The use of both vitamins and minerals in cases of disease problems to try and prevent the conditions have been singularly disappointing and it is doubtful if specific nutrient factors are involved.

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