Rotational (Torsional) and Angular (Valgus/Varus) Deformity
These deformities often are seen as distinct flock problems. Bones all exhibit some degree or combination of lateral, medial, anterior, or posterior bend. They also show some torsion (rotation) about their long axis. The most common abnormalities are seen in the distal limb and involve lateral or medial deviation and/or external rotation. Deformity may be a consequence of rickets at a younger age (see below). Poor mineralization of the bone, as in rickets, increases the ease of deformation of the bone and therefore the incidence and severity of deformities. Rickets may be associated with nutritional deficiencies, enteric disease, or malabsorption. In breeds that are predisposed to deformities, the incidence may be reduced by slowing growth rate via feed restriction or lighting programs. Bone deformities also be due to chondrodystrophy due to B vitamin or trace mineral deficiencies. Rotated tibia has been a major problem in turkeys and a minor problem in Leghorns and guinea fowl.
Vertebral deformities and/or displacements (spondylopathies) are common in thoracic vertabrae, particularly the fifth or free thoracic vertabrae. Spondylolisthesis is the most common deformity, but incidence is low in most flocks of broiler chickens. It causes posterior paralysis due to spinal cord compression.
Dyschondroplastic lesions are masses of avascular cartilage extending from the growth plate into the metaphysis and are attributed to the failure of chondrocytes to differentiate. This results in a focal thickening of the growth plate in the proximal tibiotarsus (tibial dyschondroplasia) or sometimes the proximal tarsometatarsus. The lesion in the proximal tibiotarsus is often associated with anterior bowing of the tibiotarsus and sometimes fractures below the plug of cartilage. Factors shown to influence the incidence and severity of dyschondroplasia include genetic selection, calcium:phosphorus ratios in feed, metabolic acidosis through excess chloride in feed, acid/base balance, and mycotoxins. In a flock of modern broilers, the cause may be marginal inadequacies in dietary calcium or a calcium:phosphorus imbalance.
Rickets develops in growing birds due to deficiency of calcium or phosphorus (see Nutrition and Management: Poultry: Calcium and Phosphorus Imbalances) or insufficient vitamin D (see Nutrition and Management: Poultry: Vitamin D3 Deficiency). Malabsorption can also cause a mineral deficiency. In rickets, a failure of bone mineralization leads to flexibility of long bones. Subclinical rickets with only marginal thickening of the growth plates is fairly common and often associated with poor performance of broiler chickens. Bone ashing and estimates of calcium and phosphorus content combined with bone pathology are useful diagnostic tools. Bacterial infections are common in bones with rickets.
Ulceration of the metatarsal and digital footpads is a common cause of lameness in meat-type poultry. Wet or poor quality litter is a contributing factor, although a biotin deficiency will cause plantar pododermatitis even when litter quality is good. Ulcerated footpads may become secondarily infected and caked with litter.
Last full review/revision March 2012 by Barry H. Thorp, BVMS, PhD, MRCVS