Rotational and Angular Leg Deformities in Poultry
Rotational and angular leg deformities in poultry are often interpreted as distinct flock problems. The most common abnormalities occur in the distal limb and involve lateral or medial deviation and/or external rotation. Valgus deformation (see valgus deformation image) is more common than varus deformation.
Courtesy of Dr. H. J. Barnes.
One or both legs can be affected by rotational or angular deformation. 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.
Tibiotarsal rotation is more common in turkeys than in chickens. It occurs in other birds as well, such as guinea fowl and ratites. Tibiotarsal rotation occurs in the shaft with no or minimal varus or valgus deformation. One or both legs can be affected. Affected legs extend laterally, and the foot is rotated.
The pathogenesis of leg deformation is not well defined. Deformity can be a consequence of rickets at a younger age. Poor mineralization of the bone, as in rickets, increases the potential for deformation and therefore the incidence and severity of deformities. Bone deformities can also be due to chondrodystrophy secondary to nutritional deficiencies (eg, insufficient choline, biotin, pyridoxine, folic acid); see Nutritional Requirements of Poultry.
In breeds predisposed to deformities, the incidence of leg deformation can be decreased by slowing the growth rate via feed restriction or modification of 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 flocks. 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 conditions, and feed management to avoid an overly rapid growth rate.
Spondylopathies in Poultry
Spondylolisthesis (Kinky Back) in Poultry
Spondylolisthesis (“kinky back”) is a developmental disorder resulting in rotation of the free thoracic vertebra (T4) with ventral displacement of the cranial end and overriding of the caudal end, causing spinal cord compression and posterior paresis or paralysis (see spondylolisthesis image).
Courtesy of Dr. H. J. Barnes.
Spondylolisthesis is the most common vertebral column deformity, but the incidence is low. The disease is most common in broilers; it also occurs occasionally in turkeys and other fowl. Females are more often affected than males. Genetic background and growth rate influence this developmental disorder.
Clinical signs of spondylolisthesis usually arise in 2- to 8-week-old broilers. Affected chickens sit on their hocks or tail with the legs extended outward or lie on their side, unable to stand. Spondylolisthesis must be differentiated from scoliosis, which usually 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 based on evaluation of a sagittal section of the vertebral column at necropsy. Culling of affected birds is recommended because they are nonambulatory, cannot access food and water, and will die of starvation or dehydration.
Other Spondylopathies in Poultry
Vertebral deformities and/or displacements (spondylopathies) such as lordosis, scoliosis (see scoliosis image), and kyphosis are common vertebral column developmental malformations, particularly in the notarium and at the level of the free thoracic vertebra. Broilers are the most commonly affected. Genetics, growth rate, and nutrition influence these developmental disorders.
Courtesy of Dr. H. J. Barnes.
Dyschondroplasia in Poultry
Dyschondroplastic lesions are masses of avascular cartilage extending from the growth plate into the metaphysis. They are attributed to failure of adequate chondrocyte hypertrophy, lack of vascular penetration into the physeal cartilage, and failure of endochondral ossification. The result is focal thickening of the growth plate and occurs most commonly in the proximal tibiotarsus (tibial dyschondroplasia; see tibial dyschondroplasia image). Dyschondroplasia can develop in other bones as well, such as the proximal and distal femur and tarsometatarsus.
Courtesy of Dr. H. J. Barnes.
Most birds do not show clinical signs of dyschondroplasia. Severe lesions in the proximal tibiotarsus can be associated with reluctance to move, enlargement of the stifle joint, anterior bowing of the tibiotarsus, and, rarely, fractures distal to the plug of cartilage. The etiology of tibial dyschondroplasia is still poorly understood. Dyschondroplasia affects broiler chickens, turkeys, and ducks.
Factors that influence the incidence and severity of dyschondroplasia include the following:
genetic selection
rapid growth
nutritional calcium:phosphorus ratio imbalance
metabolic acidosis due to excess chloride in feed
acid/base imbalance
copper deficiency
contamination of feed by Fusarium spp mycotoxins
amount of dietary cysteine and homocysteine amino acids
exposure to dithiocarbamate fungicides and certain antimicrobials (eg, salinomycin)
Prevention focuses on adequate feed quality and feed management to avoid an overly rapid growth rate. Vitamin D supplementation decreases the incidence of dyschondroplasia.
Rickets in Poultry
Rickets develops in growing birds that have a deficiency of vitamin D, calcium, or phosphorus or a calcium:phosphorus imbalance. Imbalances or deficiencies can result 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 or valgus deformation), and fractures. Lesions are most prominent at sites of rapid growth (eg, long bones, ribs; see normal ribs and tibial growth plate image).
Courtesy of Dr. David E. Swayne.
Pearls & Pitfalls
|
Birds with rickets can show delayed growth, unsteadiness in walking, frequent lying down, inability to stand, and fractures. Pliable long bones and thick, pliable ribs and/or knobs at the costochondral junction (rachitic rosary) due to thickened and flared metaphyses are typical gross lesions (see rickets image). Sectioning the long bones reveals growth plates with increased length and width. Beaks and digits can be soft and pliable. The parathyroid glands show hypertrophy and hyperplasia.
Courtesy of Dr. David E. Swayne.
Subclinical rickets with only marginal thickening of the growth plates is fairly common and often associated with poor performance of broiler chickens. Diagnosis is usually based on gross and microscopic lesions. Bone ash analysis to estimate calcium and phosphorus content, measurement of hepatic vitamin D concentration, and feed analysis (eg, vitamin D, calcium, and phosphorus content and ratio) are useful diagnostic tools.
Treatment of rickets consists of correcting nutritional imbalances or deficiencies in the diet. Prevention focuses on adequate feed quality that provides amounts of vitamin D, calcium, and phosphorus, as well as a calcium:phosphorus ratio, adapted to the growth and production stage of the bird.
Degenerative Joint Disease in Poultry
Degenerative joint disease occurs mainly in the coxofemoral, femorotibiotarsal, and intertarsal joints of broilers and male turkeys near market weight. It can also occur in aged backyard chickens. Clinical signs include reluctance to move, leg abduction, and lameness.
The pathogenesis of degenerative joint disease is not well defined; however, osteochondrosis or cartilage lesions, genetic factors, and heavy body weight could be involved.
Osteoporosis in Poultry
Osteopenia is a decrease in bone mineral density; osteoporosis is clinically evident disease with increased fragility and susceptibility to bone fractures. Osteopenia/osteoporosis affects laying hens raised in cages toward the end of the laying cycle and has been termed cage layer fatigue (see cage layer fatigue image). Commercial laying hens housed in noncage systems can also be affected.
Courtesy of Dr. D. Frame.
Slow chronic loss of calcium stored in the skeleton occurs during the laying period, leading to osteopenia. Disease develops when the bone mass becomes inadequate to support the bird's body weight.
Clinical signs of osteoporosis are variable and include leg weakness, vertebral and leg fractures, posterior paralysis, and sudden death. The sternum is often deformed (see osteoporosis image), with the ribs folded inward at the costochondral junction. Fractures occur in the long bones, vertebrae, and keel. Bone cortices are thin and brittle. Parathyroid glands are hypertrophic and hyperplastic.
Courtesy of Dr. D. Frame.
Birds with osteoporosis that die suddenly often have a partially shelled egg in the oviduct, and death is presumed to be due to hypocalcemia.
Osteopenia is due in part to a lack of mechanical stress on the bone in hens confined to cages (because of a lack of exercise) and to selection for high egg production. Suboptimal nutrition, with inadequate calcium, phosphorus, and/or vitamin D, contributes to the condition.
Excessive dietary calcium during the growing period can predispose hens to the development of osteoporosis during laying.
Although attempts at preventing osteopenia/osteoporosis in laying hens through nutritional management only alleviate osteoporosis, sources of calcium that enable the slow release of mineral, such as oyster shell and limestone granules, appear the most effective at minimizing the development of osteopenia and improving eggshell quality.
In addition to being a problem during egg production, osteopenia/osteoporosis can lead to fractures during transport and processing, at the end of flock production life, that are important animal welfare and economic issues.
Keel Bone Fractures in Poultry
Keel bone fractures are an important problem in commercial laying hens and have a detrimental impact on egg production and animal welfare. The factors involved in the development of keel bone fractures are not fully understood; however, suboptimal nutrition, particular housing systems (eg, noncaged housing), and genetic determinants (eg, early laying onset) are likely key contributing factors.
Fractures occur most commonly at > 25 weeks of age and are often located in the caudal third of the keel, which is the last part of the keel to ossify. External impact could be a contributing factor for fractures occurring in the cranial third of the keel. Internal forces might be a more important factor for fractures in the caudal third of the keel.
A comprehensive management strategy that includes adequate nutrition, genetic selection, and environmental modifications is essential to mitigate the development of keel bone fractures.
Articular Gout in Poultry
Key Points
Noninfectious diseases of the skeleton in poultry result mainly from inadequacies in nutrition and/or husbandry, as influenced by genetic background and excessive growth rate or high egg production.
Prevention focuses on adequate feed quality and feed management to avoid an excessive growth rate.
For More Information
Klasing KC, Korver DR. Nutritional diseases. In: Swayne DE, ed. Boulianne M, Logue CM, McDougald LR, Nair V, Suarez DL, associate eds. Diseases of Poultry. 14th ed. Wiley Blackwell; 2020:1255-1285.
Crespo R. Developmental, metabolic, and other noninfectious disorders. In: Swayne DE, ed. Boulianne M, Logue CM, McDougald LR, Nair V, Suarez DL, associate eds. Diseases of Poultry. 14th ed. Wiley Blackwell; 2020:1286-1329.
