Rickets is a complex mineral deficiency disease of young, growing animals. It is characterized by defective mineralization of growing bones, persistence of hypertrophic cartilage and enlargement of the epiphyses of long bones and ‘rachitic rosary’.
Aetiology: The most common causes of rickets are absolute dietary deficiencies of phosphorous or vitamin D alone or in combination in young animals. Calcium deficiency can also cause rickets. Rapid growth rate, indoor housing of calves for long period and insufficient solar radiation are important predisposing factors for rickets in cattle. Lambs thriving on green cereals and lush green grass show high incidence of r ic ke ts. He r e d ita r y fo r m o f r ic ke ts ha s b e e n r e p o r te d in p igs, whic h wa s indistinguishable from deficiency rickets. Pups and kittens, which are fed all-meat diets, commonly suffer from rickets. Rickets and other bone pathologies have been reported in piglets housed indoors and fed processed feed.
Clinical findings: Typical cases of rickets are characterized by bone pain, stiffness in gait, enlargement of costochondral junction and limb joints, especially the knee joints, abnormal curvature of different degrees of long bones (bowed limbs) and pathological fracture. The curvatures depend on the level of deficiencies. The bending at carpus is usually outward and forward in claves and lambs. Prominently, long bones of forelimbs including humerus, metacarpals and carpals show curvature. However, long bones of hind limbs are also affected and cause incoordination of movement.
Eruption of teeth is usually delayed and defective due to poor calcification. Teeth show pitting, grooving, pigmentation, defective alignment, and rapid and excessive wear. Severely affected lambs and calves are unable to close their mouth due to thickness and softness of jaw bones and defective dentition. Severe chest deformity may be associated with dyspnoea and ruminal tympani. Terminal signs include hypersensitivity, tetany, recumbency and death.Predominant signs in kittens and pups include reluctance to move, posterior lameness and ataxia. The kittens often stand with characteristic deviation of paw and progressively assume sitting position or sternal recumbency with hind limbs abducted. Pups show slight limping or inability to walk.
Diagnosis: Characteristic clinical sings involving long bones and stiffness of gait in rapidly growing young animals, supported by history of vitamin D deficiency and radiological examination of long bones are used for diagnosis. The serum alkaline phosphatase activities are commonly elevated and serum phosphorous values are usually < 3mg/dl. Vitamin D concentration in serum may be as low as 0.4 mg/ml. Final diagnosis is made by histopathological examination of the epiphysis. Ratio of ash to organic matter in the bones (1:2 – 1:3 in rachitic bones) is an important diagnostic aid.
Treatment and prevention: Primary treatment of rickets is correction of diet. Housed animals should be provided adequate exposure to sunlight. Specific therapy includes oral administration of dicalcium phosphate @ 3-5 g, three to four times daily for the 6 days, together with single intramuscular injection of vitamin D3 @ 10000 IU/kg body weight in calves. Lambs can effectively be treated by using vitamin A, vitamin D3 and calcium borogluconate solution containing phosphorus and magnesium.
Prevention: Feeding of properly balanced diet during pregnancy significantly reduces rickets in new born animals. Supplementing diet with bone meal and protein is highly effective in treatment and control of rickets.