Submitted to: Feedinfo.com
Publication Type: Popular publication
Publication Acceptance Date: 9/4/2003
Publication Date: 9/4/2003
Citation: RATH, N.C. TIBIAL DYSCHONDROPLASIA, A POULTRY LEG PROBLEM. FEEDINFO.COM. 2003. Interpretive Summary: Leg problems which include lameness, bone breakage, and infection are major production related health and welfare problems in meat-type chickens and turkeys. One cause of such poultry leg problems is traced to a defect arising in the growing end of leg bones called tibia, which partially fail to become bone, making the ends prone to breakage and infection. This review summarizes the possible causes of the origin of this defect, and measures that have been used to prevent this problem.
Technical Abstract: Leg problems are major production related health and welfare problems in young poultry. A variety of skeletal, muscular, and neuropathic factors can contribute to 'leg weakness' in chickens and turkeys, with skeletal problems being the most identified cause of lameness. Over the years, selective breeding, better management, and nutritional practices have controlled different leg problems; however, some problems such as tibial dyschondroplasia (TD) still occur frequently. Since TD is responsible for a number of 'leg problems' including pain, fracture, and bone weakness, this review will be limited to tibial dyschondroplasia. Up to 30 % of chickens and 90% of turkeys have been reported to be affected with tibial dyschondroplasia. TD is considered to be a metabolic cartilage disease in poultry in which parts of growth plate cartilage fail to form bone leading to the retention of a thickened plug of dead cartilage in the proximal end of the tibial and tibio-tarsal bones. Consequently, the growth plate becomes prone to fracture, infection, and deformed bone development. Birds with TD show frequent unwillingness to walk. Thus TD is a leading cause of lameness, mortality, and carcass condemnations. Although thought, to be related to fast growth the exact cause of TD is not known. There is no evidence of TD having an infectious etiology. This review deals with the physiopathological aspects of TD and some of the intervention measures that have been used to circumvent this problem.