Rickets and osteomalacia (Table 1) are disease names associated with metabolic bone disease in growing and adult animals, respectively. The causes of metabolic bone diseases are usually related to deficiencies or imbalances in phosphorus, calcium and/or vitamin D deficiency.
Calcium and phosphorus are essential nutrients that are tightly regulated in the blood because of thecritical metabolic roles they play. Both are needed for normal mineralization of bone matrix which provides for normal bone density and strength. Bone is the reservoir for calcium and phosphorus, and acts as a buffer to assure calcium and phosphorus are adequate in blood.
Nutritional causes of noninfectious bone diseases were identified and generally controlled in swine during the 20th century. Cases of “metabolic bone disease” were rarely submitted to the Iowa State University Veterinary Diagnostic Laboratory (ISU-VDL) during the 1990s and early 2000s. Metabolic bone disease cases during this period usually were attributable to mixing errors in feed.
However, Figure 1 illustrates a recent increase in the number of cases of bone disorders diagnosed by ISU-VDL. This figure does not include cases of primary joint diseases (i.e. osteochondrosis), which have also increased in recent years.
Clinical signs depend on the age of pigs, the specific mechanisms involved and the magnitude and the duration of the cause, which is usually related to the diet. Growing pigs with rickets will have weak bones that bend before they break and enlarged growth plates that give the appearance of swollen joints. Conformation may be abnormal because of bending or bowing of bones.
Lameness due to metabolic bone disease may be confused with infectious causes of joint disease at this point. Osteomalacia is usually seen in late finishing or adult swine since this is a condition of increased absorption of previously formed bone. Fractures of femurs, vertebrae or ribs during movements or at slaughter occur with increased frequency with osteomalacia. Lactational osteoporosis has similar features but occurs in lactating or newly weaned sows.
It is noteworthy that metabolic bone diseases may have abrupt onset of clinical signs from acute hypocalcemia, including tremors, tetany, seizure-like muscle fasciculations, weakness, lameness, painful gait, weakness, reluctance to move and bone fractures (macroscopic and/or microscopic). Often, the first clinical sign observed in these situations are pigs simply found dead or savaged by penmates. In a large population of pigs, several clinical presentations may be present simultaneously.
Tools that are useful for implicating a diagnosis of metabolic bone disease include:
1. Gross examination of bones is the most useful tool for implicating rickets or osteomalacia. Thoroughly necropsy and examine ribs, long bone cortex, joints, skull and turbinates. In pigs more than 5 weeks of age, isolate a rib and test strength by breaking it. If it bends before breaking, be suspicious. If it does not “snap,” be very suspicious.
2. Histopathology of bones (especially growth plates and articular cartilage) can confirm suspicions of disease.
3. Analysis of bone for calcium, phosphorus, ash and density can be useful if the age of pig, bone selected, bone section tested and laboratory methods used are considered in the interpretation of results.
4. Serum chemistry to determine calcium and phosphorus levels in acutely affected pigs that may be weak, down or have tremors can confirm hypocalcemia quite inexpensively.
5. Serum vitamin D3 levels that are extremely and consistently low can implicate vitamin D deficiency as contributor for weak bones.
6. Analysis of feed for calcium and phosphorus can be helpful. Often, the feed being fed at the time of clinical signs may not be the feed that started the problem. Retaining feed samples from each batch can be useful to identify problems in mixing or formulation.
Laboratory submission in suspect cases should include:
1. Several intact ribs, intact swollen/affected joints, turbinates (histopathology, ash, density, calcium, phosphorus, culture of joint).
2. Serum from acutely affected pigs (vitamin D3, calcium, phosphorus).
3. Feed samples (retained pending outcome of other diagnostic tests).
Metabolic bone disease, similar to many other diseases, is often clinically apparent in only a small subset of pigs within a population (Figure 2). Mechanisms of calcium homeostasis are sufficiently robust such that disease does not occur unless there are prolonged dietary inadequacies or high batch variation in feed preparation and/or feed consumption. Diagnosis requires that individually affected pigs be carefully examined.
The nutritional contributors to bone and joint disease revolve around absorption and homeostasis of calcium, phosphorus and vitamin D. Until 2005, a simple corn-soy-supplement diet predominated in swine production in North America. The last decades have also seen changes (introducing more variation) in facility design, swine genetics, sow prolificacy, weaning age, pig growth rates, nutrient values of various feedstuffs, dietary formulations and use of phytase. Diets now vary considerably in source of energy (corn, wheat, fats, distiller’s by-products), protein (soy, synthetic, distiller’s by-products), and the formulation assumptions (the sources, availability, quantities and ratios of calcium and phosphorus; phytase).
It seems likely that the innumerable permutations of risk factors, coupled with inevitable variation in execution of details, will increase the risk that some portion of the pig population will be clinically impacted.
Steve Ensley, Darin Madson, DVM and Kent Schwartz, DVM
Iowa State University Veterinary Diagnostic Laboratory