Rotational (Torsional) and Angular (Valgus/Varus) Leg Deformities
These leg deformities are often seen as distinct flock problems. The most common abnormalities are seen in the distal limb and involve lateral or medial deviation and/or external rotation. Valgus deformation is more common than varus. One or both legs can be affected. Valgus or varus deviation of the intertarsal joint is the most common deformation in broiler chickens and predisposes to slippage of the gastrocnemius tendon. Males are more commonly affected. Varus/valgus deformation is less common in turkeys than in chickens. Birds with severe deformation, especially if both legs are affected, die from starvation and dehydration because they cannot reach the feeders.
Rotation of the tibiotarsus is more often seen in turkeys than in chickens. It occurs in other birds as well, such as guinea fowl and ratites. Rotation of the tibiotarsus occurs in the shafts without or with minimal varus or valgus deformation. One or both legs can be affected. Affected legs extend laterally, and the foot is rotated.
The pathogenesis of the leg deformation is not well defined. Deformity may be a consequence of rickets at a younger age (see below). Poor mineralization of the bone, as in rickets, increases the potential for deformation and therefore the incidence and severity of deformities. Bone deformities may also be due to chondrodystrophy secondary to nutritional deficiencies (eg, choline, biotin, pyridoxine, folic acid). In breeds predisposed to deformities, the incidence may be reduced by slowing the growth rate via feed restriction or lighting programs. Excessive external tibiotarsal rotation occurs during development, but the pathogenesis is not well understood. Genetic, nutritional, and management factors are thought to be involved.
Culling of birds that cannot ambulate adequately to access food and water is recommended in commercial fowl. Bandaging, when the disease is detected early, and surgery can be performed in pet or other valued birds. Prevention focuses on genetic selection, adequate housing condition, and feed management to avoid an overly rapid growth rate.
Spondylolisthesis (Kinky Back)
Spondylolisthesis (“kinky back”) is a developmental disorder resulting in rotation of the free thoracic vertebra (T4) with ventral displacement of the cranial end and over-riding of the caudal end, causing spinal cord compression and posterior paresis or paralysis. Spondylolisthesis is the most common vertebral column deformity, but the incidence is low. The disease is most common in broilers but occurs occasionally in turkeys and other fowl. Females are more often affected than males. Genetic background and growth rate influence this developmental disorder.
Clinical manifestation usually occurs in 2- to 8-week-old broilers. Affected chickens sit on their hocks or tail with the legs extended outward or lay on their side unable to stand. Spondylolisthesis must be differentiated from scoliosis, which in most cases does not cause clinical signs, and from vertebral osteomyelitis, which produces similar clinical signs. Deformation of the vertebral column can be palpated at necropsy. Diagnosis is best performed by evaluating a sagittal section of the vertebral column at necropsy. Culling of the birds is recommended because they are not ambulatory, unable to access food and water, and will die of starvation or dehydration.
Vertebral deformities and/or displacements (spondylopathies) such as lordosis, scoliosis, and kyphosis are common vertebral column developmental malformations, particularly in the notarium and at the level of the free thoracic vertebra. Broilers are more commonly affected. Genetics, growth rate, and nutrition influence these developmental disorders.
Dyschondroplastic lesions are masses of avascular cartilage extending from the growth plate into the metaphysis and are attributed to failure of adequate chondrocyte hypertrophy, lack of vascular penetration into the physeal cartilage, and failure of endochondral ossification. This results in focal thickening of the growth plate and is most commonly seen in the proximal tibiotarsus (tibial dyschondroplasia). Dyschondroplasia can develop in other bones, such as the proximal and distal femur and tarsometatarsus.
Most birds do not show clinical signs. Severe lesions in the proximal tibiotarsus can be associated with reluctance to move, enlargement of the knee joint, anterior bowing of the tibiotarsus, and rarely, fractures distal to the plug of cartilage. The etiology of tibial dyschondroplasia is still poorly understood. The disease is seen in broiler chickens, turkeys, and ducks.
Factors shown to influence the incidence and severity of dyschondroplasia include:
nutritional calcium:phosphorus ratio imbalance
metabolic acidosis due to excess chloride in feed
contamination of the feed by Fusarium spp mycotoxins
amount of dietary cysteine and homocysteine amino acids
exposure to dithiocarbamate fungicides and certain antibiotics such as salinomycin
Rickets develops in growing birds due to deficiency of vitamin D Vitamin D3 Deficiency Vitamin deficiencies are most commonly due to inadvertent omission of a complete vitamin premix from the birds’ diet. Multiple signs are therefore seen, although in general, signs of B vitamin... read more , calcium Calcium and Phosphorus Imbalances A deficiency of either calcium or phosphorus in the diet of young growing birds results in abnormal bone development, even when the diet contains adequate vitamin D3 ( see Vitamin D3 Deficiency)... read more , or phosphorus Calcium and Phosphorus Imbalances A deficiency of either calcium or phosphorus in the diet of young growing birds results in abnormal bone development, even when the diet contains adequate vitamin D3 ( see Vitamin D3 Deficiency)... read more ) or calcium:phosphorus imbalance Calcium and Phosphorus Imbalances A deficiency of either calcium or phosphorus in the diet of young growing birds results in abnormal bone development, even when the diet contains adequate vitamin D3 ( see Vitamin D3 Deficiency)... read more . Imbalances or deficiencies can results from inadequate nutrition or intestinal disease with malabsorption. In rickets, abnormal endochondral ossification with failure of mineralization leads to defective bone formation, flexible long bones with subsequent bone deformities (eg, varus, valgus), and fractures. Lesions are most prominent at sites of rapid growth (eg, long bones, ribs).
Retarded growth, unsteadiness walking, laying down frequently, inability to stand, and fractures can be observed in affected birds. Pliable long bones and thick and pliable ribs and/or knobs at the costochondral junction (rachitic rosary) due to thickened and flared metaphyses are classic gross lesions. Sectioning of the long bones reveals growth plates with increased length and width. Beaks and digits can be soft and pliable. Hypertrophy and hyperplasia of the parathyroid glands are present. Subclinical rickets with only marginal thickening of the growth plates is fairly common and often associated with poor performance of broiler chickens. Gross and microscopic lesions are used most often to reach a diagnosis. Bone ash analysis to estimate calcium and phosphorus content, liver vitamin D concentration, and feed analysis (eg, vitamin D, calcium, and phosphorus content and ratio) are useful diagnostic tools. Treatment consists of correcting the nutritional imbalance or deficiencies in the diet.
Degenerative Joint Disease
Degenerative joint disease is seen mainly in the coxofemoral, femorotibiotarsal, and intertarsal joints of broilers and male turkeys near market weight. Degenerative joint disease can also be observed in aged backyard chickens. Clinical signs include reluctance to move, abducted legs, and lameness. The pathogenesis is not well defined, but osteochondrosis or cartilage lesions, genetic factors, and heavy body weight may be involved.